PAPERS

by International Journal of Drug Policy – Volume 139, May 2025 – Brandon del Pozo et al.

Highlights
  • Studies show an association between police opioid seizures and fatal overdose.
  • This model presents physical and behavioral causes of this positive relationship.
  • Reducing the disruptive outcomes of police opioid seizures can reduce overdose.
  • Police opioid seizures can worsen the problem of overdose they intend to address.

Abstract

Context

Police seizures of illicit opioids remain a dominant strategy for addressing problematic substance use and overdose in the United States and throughout the world, yet qualitative accounts and quantitative analyses exhibit positive associations between police opioid seizures and ensuing risk of fatal overdose at the local level of individual incidents. Since these associations run counter to the commonly held belief that removing potent illicit substances from the community is protective of overdose, a causal model is needed to demonstrate this association and convey the overdose risks that follow from police opioid seizures.

Methods

Leveraging well-established biological and psychological outcomes of opioid use disorder and opioid supply interruption, our analysis presents the Police Opioid Seizure Temporal Risk (POSTeR) Model, an individual-level casual model that begins at the point of opioid dependence, introduces an interruption to an individual’s supply of opioids as the result of a police drug seizure, and presents the physical and behavioral outcomes that increase the ensuing temporal risk of fatal overdose.

Results

The aftermath of a police opioid seizure can increase a person’s risk of fatal overdose. The urgent need to prevent or reduce acute opioid withdrawal symptoms leads people to seek a replacement supply, while reduced opioid tolerance resulting from post-seizure involuntary abstinence combines with the uncertain potency of a replacement supply of illicit opioids to significantly increase the difficulty of administering a safe but effective dose. In the face of these hazards, people in withdrawal often have a reduced aversion to risk, prompting them to consume this uncertain dose in a manner that increases their exposure to overdose.

Conclusions

Strategies that emphasize police opioid seizures as an acceptable way to reduce the prevalence of illicit drugs in a community without accounting for the elevated risk of fatal overdose that results can worsen one of the most significant problems they are meant to address.

Introduction

A growing body of evidence shows that when a person is dependent on opioids, temporarily interrupting their supply of the drug exposes them to an increased risk of overdose (Hochstatter et al., 2023Mark & Parish, 2019Williams et al., 2020). The first studies about interruptions originating from police drug seizures explored this assertion qualitatively, finding that people problematically dependent on opioids reported this increased risk when asked about their personal experiences (Carroll et al., 2020Rhodes et al., 2019Victor et al., 2020). Conversely, these and other studies found people who use drugs (PWUD) with steady access to a supplier they could trust, who provided a basically consistent supply, could warn of inconsistencies, and who might supply naloxone, was protective of overdose (Carroll et al., 2020Hedden-Clayton et al., 2024). More recently, quantitative analyses have found a statistically significant spatiotemporal association between police opioid seizures and overdose during a multiyear periods in Indianapolis, Indiana (Ray et al., 2023), and San Francisco, California (Kral, et al., 2025). In accordance with studies that show ecological associations at the state and county levels (Cano et al., 2024), the analysis found that fatal overdoses doubled within three weeks of the police seizure, in a radius of up to 500 m from the seizure’s site, and this association held when considering all quantities of opioids seized, regardless of whether they were taken from a dealer or an individual who uses drugs (Ray et al., 2023).
Many people find the conclusion that police drug seizures increase overdose risk strongly counterintuitive, considering that governments act to interrupt the supply of illicit drugs to ostensibly reduce risk and save lives. To that end, the presumption is that reducing the quantity of illicit drugs in circulation and interrupting their consumption by people dependent on opioids is believed to reduce risk. But at least in the proximate sense, the evidence does not bear this presumption out. To address this gap between emerging research findings and many people’s intuitions, and to promote the rigorous interrogation of this proposition, this paper presents the discrete causal model by which increased exposure to overdose arises from the aftermath of a police drug seizure, a phenomenon that has critical implications for our present public health and drug enforcement policies. In doing so, it intends to bolster our understanding of the health outcomes of police drug enforcement and suggest ways to interrupt the causal chain to reduce overdose mortality. Barring such a model, the evidence we produce to explore this relationship will continue to face its inherent limitations. Qualitative research conveys the lived experience of increased exposure to overdose in the aftermath of police drug seizures with nuance, but the method inherently precludes broad generalizability. In contrast, quantitative analyses of administrative data can demonstrate statistically significant associations, but do not readily illuminate the causal pathways that suggest where to effectively intervene. Both veins of research would benefit from the development of a model that conveys how personal experience and quantitative correlation can be understood as causation. By presenting such a model here, this paper provides guidance about where future research on this topic should go, and what intervention designs might look like.
The model we present takes policing as its primary focus. It concerns the events that we commonly understand to be police drug seizures: the arrest of people for drug possession, the seizure of contraband drugs that people preemptively discard to avoid arrest by police, and the arrest of distributors and suppliers accompanied by the seizure of their drugs as evidence. It does not distinguish between the volume or target of the seizure; it could consist of the arrest of an individual person and the seizure of their own supply, or the seizure of a dealer one or more steps up the supply chain. The inclusion criteria for the model are only that opioids are seized by police, and in a manner that ultimately interrupts supply at an individual level. The model therefore operates at these lower geographic resolutions, during the relatively short time frames considered in Ray et al. (2023) and Kral et al. (2025), and does not intend to offer explanatory power across larger ecologies such as cities, counties, or states, or over longer periods of time.
The model here takes up overdose as the exclusive outcome of interest, although there is evidence that police drug seizures can increase the risk of other harms as well. In the aftermath of police contact, people may change the way they consume drugs, for example, speeding the act of injection or sharing syringes (Cooper et al., 2005Werb et al., 2008), thereby increasing the risk of abscess and infectious disease (Baker et al., 2020). To keep our causal model as direct and compelling as possible, these other outcomes will not be its focus. In the same vein, while the model here pertains to policing, and is not intended for general application across the criminal justice system. Release from a period of incarceration is a prime example of another event that substantially increases risk of overdose (Binswanger et al., 20112007), and researchers have presented the corresponding conceptual framework (Joudrey et al., 2019), while emphasizing the particular role of fentanyl in generating these overdoses (Brinkley-Rubinstein et al., 2018). We intend to complement this research with a pragmatic realist account (Cherryholmes, 1992) of overdose risks that occur upstream, at the point of police encounters, prior to a period of imprisonment. In its realist approach, our account asserts that prevalent scientific and behavioral theories accurately describe the aspects of the world they were created to explain (Leplin, 1984Psillos, 2005). We further assert that their individual explanatory mechanisms can combine to produce an accurate, predictive understanding of an overall phenomenon (Leplin, 1984), in this case, increased overdose risk after a police drug seizure. In this way, our approach is in the tradition of scientific realist evaluation (Pawson & Tilley, 1997), where outcomes arise from interactions between mechanisms and their social contexts, and causal mechanisms can be reliably identified through reductionist theorizing (Jagosh, 2020). The model’s pragmatism lies in providing insights and recommendations that acknowledge the current political and social contexts of substance use and policing.
The paper will proceed as follows: it will present widely accepted principles of pharmacology, accounts of how opioid dependency biologically influences the behavior of PWUD, and research about how both the mechanics and social dynamics of policing and substance use further affect these behaviors. Taken in sum, we will argue they combine to elevate overdose risk, and we will present these relationships in a graphical model, i.e., a causal diagram (Greenland & Brumback, 2002) entitled the Police Opioid Seizure Temporal Risk (POSTeR) Model. We close by discussing several policy responses to the risks the model presents, stressing that there are potential ways to mitigate overdose risks that result from seizures, although they vary in feasibility and acceptability given individual contexts and political climates. We then discuss POSTeR Model’s limitations and suggest avenues for further research.

Principles underlying overdose as a result of drug seizures

There are five factors that drive our model, each one an evidence-based premise that combines to increase fatal overdose risk when a personal drug supply is interrupted by a police drug seizure. They may present as contributory causes that are insufficient to decisively increase fatal overdose on their own, but that synthesize to do so. In that sense, they build on each other to produce increased risk. The principles are as follows:

  • 1)
    Supply interruption sends people who are physically dependent on opioids into withdrawal, and the most common outcome is that they will avoid or reduce the condition with a replacement supply of opioids (Frank et al., 2023Hall et al., 2024). Opioid dependence is defined by the physical experience of opioid withdrawal, its psychological toll, and the ways in which they guide and modify behavior (Pergolizzi Jr et al., 2020). The most common responses to the onset of opioid withdrawal are to avoid it, reduce it, or reverse it (Bardwell et al., 2021Frank et al., 2023Mateu-Gelabert et al., 2010), which sets the stage for the challenges presented by the other principles below. For many people, relief requires gaining access to a replacement supply of opioids (which could include treatment medications) or being forced to endure a period of detoxification that is, by all accounts, extremely painful and difficult to bear (Dunn et al., 2023Shah & Huecker, 2018). Its symptoms can last weeks (Ware & Dunn, 2023), and are potentially life-threatening (El-Sabawi, 2024), and therefore motivate strong survival behaviors. The idea that a person with problematic opioid dependence can detoxify by enduring a few days of discomfort reflects a deep misunderstanding of the physiological processes and changes to the body and brain that have occurred when a person is heavily dependent on opioids (Monroe & Radke, 2023). In response, some may attempt to manage the symptomatic presentations of their withdrawal by means such as benzodiazepines, sedatives, cannabis, or other substances, which may provide some relief to individual symptoms without alleviating withdrawal themselves, and which may present the additional risks discussed in Principle 5 below.
  • 2)
    Supply interruption reduces a person’s tolerance of opioids to a degree they cannot measure with precision, making dosing more hazardous. Withdrawal, in and of itself, is insufficient to elevate a person’s overdose risk. If a person were to know the dose necessary to alleviate it, and had reliable access to that dose, the resulting risk would be reduced. An initial challenge, therefore, is establishing a safe dose, since even short interruptions in the supply of opioids affect a person’s tolerance of the substance. As prolonged use generally increases tolerance, such that greater quantities are necessary to avoid withdrawal, produce a euphoric effect, or simply maintain bodily homeostasis (Dumas & Pollack, 2008Freye & Latasch, 2003), interruptions have the opposite effect (Kesten et al., 2022), which is why physicians may alter the dose of patients who use prescribed opioids if there is cause to believe they have diminished tolerance (Gökçınar et al., 2022Jeffery et al., 2020).
    It is critical to note, however, that several factors affect the actual loss of tolerance, from genetic predispositions to body composition (Byanyima et al., 2023Lötsch et al., 2004Na et al., 2024Wilder-Smith, 2005), preventing the precise measurement of this reduction. While these variables and a lack of research prevent accurate predictions about the tolerance lost by a particular person after a given period of time, the warnings provided to patients about resuming opioid use after discharge from inpatient detoxification advise that a potentially fatal loss of tolerance can occur within a few days (META PHI, 2024). In sum, when a person resumes consumption, it will be with a tolerance for opioids that is reduced by an uncertain amount, making dosing much more a matter of estimation than it would otherwise be.
  • 3)
    The replacement supply of illicitly produced opioids sought in the aftermath of a seizure event is likely to be of a different, uncertain potency than the interrupted one, further compounding the hazards of dosing. While an indeterminate reduction in tolerance prevents a person from gauging the dose necessary to safely and effectively address withdrawal symptoms, the replacement opioids procured in an illicit market compound this risk by being of an unknown potency regardless (Rosenblum et al., 2020). In saying this, it is critical to note that we do not mean the new supply is likely to be more potent. In presenting our model to nonspecialist audiences at practitioner-oriented conferences as an accompaniment to quantitative findings about the relationship between police opioid seizures and overdose, one misconception that frequently arose was that initial heroin supplies were replaced with a resupply of fentanyl. Our model does not depend on pharmaceutically produced opioids or heroin being replaced by fentanyl. Instead, it presumes that fentanyl has saturated the nation’s illicit opioid markets (Zoorob, 2019Zoorob et al., 2024), is what people who use illicit opioids are likely to consume, and what replacement supplies most likely consist of. The variability in potency that powers the model here arises from the heterogeneity in which illicit opioids are cut for distribution to the end user (Ivsins et al., 2020Larnder et al., 2022Tobias et al., 2021), and the unsuspected presence of fentanyl in counterfeit analgesic pills (Friedman & Ciccarone, 2025O’Donnell et al., 2023). Since illicit manufacturing and packaging processes are not carried out to any standard, or with reliable precision, barring the illicit consumption of pharmaceutically produced opioid analgesics, there will most likely be variance between the potency of an initial supply of illicit opioids and its replacement.
  • 4)
    People experiencing opioid withdrawal have a reduced aversion to risk, causing them to discount these hazards. Finally, while PWUD who use drugs often understand the preceding problems, the risks they pose are often insufficient to deter them from consuming replacement opioids, or doing so in a safer, more cautious manner (Hall et al., 2024). It is well-documented that the symptoms of opioid withdrawal range from extreme discomfort to acute pain and trauma (Bluthenthal et al., 2020). The motivation to reduce these symptoms is compelling, and can lead people to take risks solely for the need to escape the sensation of withdrawal (Frank et al., 2023). Such risks are wide-ranging, and while many do not apply to this model, they illustrate the powerful forces at work. For example, people may engage in criminal activity to obtain funds for drugs, patronize unfamiliar drug dealers with uncertain reputations, use replacement substances of unknown quality (perhaps using them by a new and unfamiliar route of administration), and engage in unprotected, risky sex work. In our model, however, we posit that one of the risks a person will be significantly less averse to is consuming a replacement opioid supply of an uncertain potency, and doing so in a more risky manner than if they were not experiencing withdrawal (Mateu-Gelabert et al., 2010), such as by rushing consumption, neglecting to test the dose for potency, or to ensure other people are present in the event of an emergency, preferably with naloxone on hand. In other words, not only is a person in these circumstances likely to encounter an uncertain replacement supply that will have an unknown interaction with their newly-reduced tolerance, but they will be less averse to consuming it regardless, and to doing so with few or reduced protective measures, even if they are aware of the attendant risks.
  • 5)
    Efforts at self-medication after a police opioid seizure can also increase risk of overdose. If a person loses their supply of opioids and begins to experience withdrawal, other factors may contribute to their overall overdose risk in addition to ones directly tied to a sequence of withdrawal, loss of tolerance, replacement supplies of uncertain potency, and reduced aversion to risk. For example, people may seek sedatives or other substances to alleviate symptoms until they can resume opioid use or fully detoxify, such as by taking prescribed or illicit benzodiazepines or kratom (Boyer et al., 2008Preiss et al., 2022). This alternative poses its own set of risks. Benzodiazepines compound the respiratory depression of opioids, and can cause overdose if they are consumed together or in close succession (Sun et al., 2017). Moreover, the illicit market for sedatives has been heavily compromised by counterfeit pills (Friedman & Ciccarone, 2025), introducing the dangers of uncertain dosing discussed above (O’Donnell et al., 2023).
There is also an ancillary factor that plays a role in the model: the margin of error for correctly dosing fentanyl and other powerful synthetic opioids is very small. The challenge of safely dosing illicitly-supplied fentanyl is driving the present wave of the nation’s overdose epidemic (Zoorob, 2019Zoorob et al., 2024), since a comparatively small difference in the volume of this powerful synthetic in a given dose, or its presence in other substances, can spell the difference between safe use and overdose for many consumers. Not only does dosing vary by supply source, merchant, and batch (given the ad-hoc means of preparing and packaging drugs for smuggling and consumption), but for any unit of difference in the amount of opioid in a supply, the dose is going to be much more potent if it is a unit of fentanyl than some type of less potent alternative. We consider this an ancillary factor because the model suggests people whose supply of illicit opioids are interrupted by a police seizure will suffer an increased risk of fatal overdose regardless of the type of opioid involved. Rather, highly potent synthetic opioids such as fentanyl greatly increase the magnitude of this risk because any given unit of inconsistency represents a much greater variance in potency than the variance per unit found in heroin or pharmaceutically produced analgesic pills.

The causal model

The POSTeR Model proceeds through the eleven parts presented in Fig. 1 as follows. The figure’s solid arrows represent causal relationships with no alternatives in the model, and the dotted arrows represent possible branches. Green arrows signal ways to lower risk, and red signals a pathway to elevated risk. The underlying principles presented above appear in the figure both when they first manifest, and then when they combine to ultimately produce elevated overdose risk.

Fig. 1. The Police Opioid Seizure Temporal Risk (POSTeR) Model of increased exposure to fatal overdose.

Parts 1 through 4 present the basic stasis of consistent supply for people who have transitioned from opioid use to a state of dependence. A person with opioid dependence (1) exhibits increasing physical and psychological dependence on opioids (2), as well as an increasing pharmacological tolerance for the effects of the drug (2). As their tolerance increases, the general consistency of their supply (3) allows them to adjust their dose accordingly. There is still risk to this behavior, including instances of polydrug use that can introduce unpredictable variables (Peppin et al., 2020) and the inherent instability of an illicit drug supply (Holland et al., 2024), but this general consistency in comparison to a seizure event means that the person’s opioid supply is not exceedingly difficult to dose as needed, thereby reducing overdose risk (Carroll et al., 2020). Overdose may still occur, but these protective factors make it less likely to be fatal (4), or imprecise dosing may not be sufficient to alleviate withdrawal and lead to the risks that arise from repeat dosing (4). The result is the continued cycle of opioid dependence as described above, which can last for years or decades. People may exit this cycle over time, in which case they would leave the model by completing the withdrawal period and not re-initiating use, or by entering treatment (5). It is worth noting most people who are dependent on opioids do not fatally overdose (Degenhardt et al., 2011), can age out of problematic use (Jones et al., 2020Kelly et al., 2017), may contend with intermittent cycles of substance use and recovery over the course of years or decades (Hser et al., 20012015), and may enter remission of their own accord (Mocenni et al., 2019).
For the person actively dependent on opioids, the path toward an elevated exposure to fatal overdose begins with the type of supply interruption that results from a police opioid seizure (6). The interruption could be the result of an arrest of the person, or their supplier; either event deprives the person of the opioids necessary to maintain their cycle of use and suffices to bring about the physical effects of involuntary abstinence: withdrawal and decreased tolerance (7). These effects produce efforts to avoid withdrawal with a new opioid supply or self-manage it using sedatives or cannabis combined with reduced aversion to the risks associated with consuming these substances (8). The result is seeking a replacement substance of uncertain potency, especially if it is from a new dealer, although this variance is ultimately dependent on the structure and sources of the community’s drug supply network (9). Consuming the replacement supply constitutes an elevated hazard because it occurs at the nexus of two risk factors and a catalyst: a reduced but indeterminate tolerance to opioids, an uncertain potency that precludes accurate dosing (compounded by not knowing what that dose should be in light of lowered tolerance), and the reduced aversion to risk that comes with avoiding or escaping opioid withdrawal (10). This reduced aversion means that even if a person apprehends the pending hazards, they will disregard them, and/or engage in the additional risk behaviors described in the next section. This results in a significantly increased exposure to the risk of fatal overdose (11).
At any point in the model, a person can attempt to enter treatment, and if it was effective, they would leave this causal pathway. A return to use, however, will place them back in the pathway at (9), facing overdose risk. While many factors motivate a person’s return to use, from social pressures to trauma, pain, stress, and deeply-ingrained triggers (Childress et al., 1988Dennis, 2016Massaly et al., 2016), the decision necessarily indicates they have become less averse to the risks of opioid misuse. Since their new drug supply will be of an unknown potency, and their tolerance will be significantly reduced by some indeterminate amount, it may affect them in unknown ways. This accords with research that a return to use after a period of abstinence poses an elevated risk of overdose compared to the risks a person faced if they were consistently supplied when they were dependent on opioids (Hser et al., 2015Kumar 2016). The model as related here is therefore neither directed, nor acyclic. People can remain in a basic stasis given a consistent supply of opioids, although escalating frequency and volume of use as dependence and tolerance increase, and treatment can either remove them from the cycle entirely, or, with a nonfatal relapse, can return them to the provisional stasis expressed by steps (1) through (4) of the model.

Other behavioral responses to police drug seizures

Our model is principally driven by physiological factors. For example, reduced aversion to risk arises from the need to limit acute physical withdrawal symptoms. There are other behavioral factors, however, that emerge from a risk calculus that is not driven by biological and pharmacological concerns but instead result from decisions meant to reduce the probability of additional supply interruptions by police, or tactics to quickly reduce or reverse withdrawal that constitute riskier behaviors. We describe five of them here and note in step (10) that they fit our model as additional causes of risk at the point of consumption that compound those arising from the causal process described above.

  • Use in private places. In order to avoid the attention of police, especially when a prior seizure was the result consuming drugs in public, people who use drugs may shift to doing in more secluded or private places, such as indoors, in tents, or in vehicles. Using in private spaces decreases the likelihood that someone who is overdosing will be discovered and revived in time to avert death or irreversible injury.
  • Using alone. Regardless of whether the person is using in public or not, solitary use increases the risk of fatal overdose. Many people consume drugs alone to protect themselves from exposure to police or to limit their visibility to other people, who may call police or otherwise express the stigma associated with drug use (Hanoa et al., 2024). When someone is in withdrawal, using alone rather than seeking out trusted people who can observe the results may be a response to the need for rapid abatement of physical symptoms, which can increase such risk-taking behavior (Rosen et al., 2023).
  • Electing not to keep naloxone on hand. PWUD and their associates may believe carrying naloxone elevates the suspicion of police and may increase the risk of a seizure (Bennett et al., 2020Smyth, 2017). If that is the case, PWUD may elect not to have it on hand in the hopes of averting seizures, creating the risk that it will not be available to avert a fatal overdose.
  • Rushed consumption. If a person believes they have no option but to consume drugs in public, but a prior seizure leads them to fear police intervention, they may rush the process of consumption (Suen et al., 2022Ti et al., 2015), which runs counter to the harm reduction adage of “start low, go slow” (Aleixo et al., 2024Collins et al., 2024). When consuming a new supply of drugs, a user can test a small quantity of the substance and then adjust the dose as its potency becomes clear, but rushed consumption increases risk as people use a larger amount sooner, either to avoid arrest or to abate withdrawal.
  • Hesitance to seek help for an overdose. People present at the scene of an overdose may be hesitant to seek help if it ultimately means calling 9–1–1, for fear that police will respond and make arrests (Weisenthal et al., 2022). People in recent contact with police that resulted in a drug seizure may likewise hesitate to seek help when they witness an overdose or call 9–1–1 if they witness one, out of the fear of arrest and another drug seizure (Byles et al., 2024van der Meulen et al., 2021). This may lead them to hope the overdose passes without turning fatal rather than try to reverse it. When they do call, people may downplay or obscure the fact that an overdose emergency is occurring (Atkins et al., 2024). Although this may result in medical personnel being dispatched without police, it may also delay the administration of naloxone of police officers who were poised to arrive first (Pourtaher et al., 2022White et al., 2022), elevating the risk of death or serious morbidities.

Implications for policy and practice

The POSTeR Model allows us to examine the points at which overdose risk can be averted or reduced. We present them along a general arc from the interventions that are likely to be the most feasible and acceptable given the present policy environment to the ones that would require more significant shifts in norms, laws, and culture, with the interventions requiring the most significant shifts likely to be the ones that offer the greatest potential to reduce the overdose risks described by this model. In sum, these interventions work by either preventing the move from risky use (10) to fatal overdose (11) by shunting people back toward a comparatively safer stasis or better equipping them with safer supplies (1–4) by referring them to medications to treat opioid dependence (5), or moving further upstream and preventing disruptive supply interruptions (6) in the first place, promoting the ability of people with opioid dependence to consume drugs with a greater level of consistency prior to entering treatment (5), which is in and of itself a possible intervention. Another possibility, as discussed above, is that a person may eventually desist from substance use over time (Jones et al., 2020Kelly et al., 2017), an outcome common to many problematic social behaviors (Sampson & Laub, 1993), since most people with opioid dependence do not fatally overdose (Degenhardt et al., 2019). Given this approach, the following are possible changes to policy and practice that would prevent, interrupt, or reduce overdose risk related to opioid seizures.

Cautionary publicity about police drug seizures, especially notable incidents

Official acknowledgement that police drug seizures can increase risk of overdose would alert people dependent on opioids to the impending hazards and empower them to better manage the risks. Such an acknowledgment could also pave the way for warnings about particularly notable seizure incidents. For example, public officials in Manchester, New Hampshire issued a warning to the community that police had made a significant high-level drug seizure, and deployed overdose response teams to the area concerned as a protective measure, emphasizing both harm reduction measures and linkages to MOUD (Barndollar, 2023McFadden, 2023). In doing so, they explicitly cited the Ray et al. (2023) study that associated police drug enforcement with increased overdose. Such public measures remain rare, however, since they hinge on the still counterintuitive recognition that police drug seizures, despite the goal of reducing harm, can have the proximate effect of increasing them.

Linkage to MOUD

Linking people with opioid dependence to the medications that can effectively treat it interrupts the pathway to overdose by removing the risks associated with consuming illicit opioids of any potency (National Academies of Sciences Engineering & Medicine, 2019). In our model, it forecloses overdose risk by statically positioning the person at step (5). It does not, however, address the risks faced by people who are pre-contemplative about treatment and seek a replacement supply as withdrawal sets in, which will be most of the population of concern at any given time. Moreover, as our model reflects, relapse from treatment back to substance use places a person at elevated risk by moving them through the model to (10), as a person will resume substance use with a supply of unknown potency and a diminished but unknown tolerance as discussed above. Linkage to MOUD also requires that there be sufficient and immediate access to medications in the aftermath of a seizure.
Despite these limitations, linkage to MOUD in the aftermath of a police drug seizure will remain an appealing policy option because it is the least contested and controversial response: it signals a person’s efforts to make a decisive change in their own exposure to overdose risk that is less susceptible to the stigma and biases that typically accompany harm reduction efforts and legal reforms. Despite this appeal, as a response that intends to prevent overdose and save lives, linkage to MOUD will not offer protection to most people whose drug supply is interrupted by a police opioid seizure. Even the most robust, low-barrier linkages to MOUD will only impact people who actively seek out the medication or choose to engage with the treatment that is offered to them. This is a small minority of the at-risk population of PWUD at any time, most of whom are not contemplating treatment and would not accept MOUD if it were offered to them.
Because successful engagement with MOUD requires a change in behaviors entrenched by habits and biological dependence, assessing where an intervention offers its protections among the Stages of Change (Norcross et al., 2011Prochaska & Norcross, 2001) can clarify the subpopulation of PWUD it is most likely to reach, and help assess the collective reach of an array of measures. By such an analysis, MOUD does not reach people in a state of precontemplation, i.e., the majority of PWUD at a given time (Mann, 2023Patton & Best, 2024). As illustrated in Fig. 2, the interventions below are more likely to fill the resulting gap by offering protection from overdose prior to a decision to change drug consumption habits or enter recovery. It suggests the most effective lifesaving response is a comprehensive one.

Fig. 2. Interventions to prevent overdose in the aftermath of a police drug seizure mapped onto the Stages of Change.

Community naloxone distribution

While the distribution of naloxone to lay persons in the community for the purposes of overdose reversal has gained increasing political and cultural acceptance, its success depends on saturating at risk communities with a quantity of naloxone substantial enough to be used in a meaningful number of overdose events. Success in this regard would require a large, sustained investment in naloxone programs targeted to PWUD and the people who are present with them when they consume drugs (Doe-Simkins & Wheeler, 2025). At the individual level, community naloxone distribution would interrupt the model when two conditions are satisfied: a person uses drugs in the presence of someone who abstains from risky drug use or coordinates their own use to prevent simultaneous overdose, and that person has access to, or can feasibly summon a bystander with naloxone. Meeting these two conditions, moves people from instances of dangerous use (10) back toward stasis (1–4). Given Ray et al. (2023)’s findings that overdoses increase withing 500 m of a seizure event over the following weeks, the targeted distribution of community naloxone in the aftermath of a seizure could be particularly effective.

Access to harm reduction services and education

Harm reduction interventions would directly supply people dependent on opioids with naloxone and the knowledge necessary for its effective administration, in doing so reducing risk among people well prior to the point of substantial change in their drug use behavior (see Fig. 2). As people in drug-using communities facing greatly elevated overdose risks, this manner of naloxone distribution has the potential to be more effective than widespread distribution or distribution to first responders (Townsend et al., 2020) by making the medication more likely to be present at the times and places where overdose occur, especially if PWUD are more likely to consume drugs together, rather than in the presence of non-using community members. Harm reduction services can also offer education and training about the importance of “going slow” (i.e., not rushing consumption), and not consuming drugs alone, while innovative measures include prescribing medications such as single-dose buprenorphine (Ahmadi et al., 20182020) or using cannabis or sedatives as a temporary form of withdrawal support (Meacham et al., 2022Wiese & Wilson-Poe, 2018), thereby reducing the risks that come with withdrawal-motivated behaviors. Together, these interventions can reduce the probability that a person proceeds from step (10) of the model to fatal overdose (11) by shunting them back toward comparative stasis (1–4), and decreasing the incidence of other risky behaviors that can occur after a seizure discussed above. Harm reduction services can also provide people dependent on opioids with linkage to treatment (5).

Drug checking services

Analyses of the composition of drugs performed by community drug checking programs can likewise reduce overdose risk by providing reliable information about what a replacement substance may contain Green et al. (2022).They may be especially useful if a person resorts to a replacement substance such as opioid pills, or non-opioids such as benzodiazepines for the purposes of managing withdrawal symptoms before resupply, both of which are likely to be counterfeit and contain unpredictable amounts of fentanyl. As with other harm reduction services, the knowledge gained from drug checking could be leveraged to promote safer use behaviors, which can move people from steps (10) to steps (1–4) rather than (11), providing protection not only in cases if uncertain potency, but when PWUD utilize other substances to try to mitigate the effects of withdrawal.

Overdose prevention centers

Places where people consume drugs under supervision and are revived if they overdose, offer the potential to eliminate the risk of fatal overdose after a person with a reduced, uncertain tolerance uses drugs of uncertain potency. As with other harm reduction services, the user is fully exposed to the risks of supply interruption as a result of seizure (10) but mitigates them by preventing what would otherwise be a fatal overdose (11) either through an effective reversal, or preventive measures, moving the person to point (4) in the model. Similar efforts may also reduce risk through remote observation, such as via phone, app, biometric sensors, or motion detectors (Lombardi et al., 2023).

Decriminalization of drug possession

Attempted in Oregon 2021 and subsequently reversed in 2024, decriminalization could partially mitigate the hazards of a supply interruption (6) for people dependent on opioids. It would do so by preventing or limiting the duration of the supply interruptions that occur when PWUD are arrested for possession and detained or possibly incarcerated, which are associated with increased risk of overdose (Victor et al., 2022Zhang et al., 2022). It would not, however, prevent the interruptions that come from the apprehension of drug sellers and the seizure of their inventory, since the law did not decriminalize the distribution of drugs. In this way, successful decriminalization programs that still enforce laws against drug dealing like the one implemented in Portugal would not eliminate the risks of our model. Rather, they would lessen incidence of personal drug seizures, and the duration of supply interruptions from incarceration, thereby lessening symptoms of withdrawal and reductions in tolerance (7). The Portuguese system of decriminalization also offers immediate, no-cost linkage to medications that treat opioid dependence (5), lowering the risks of a supply interruption through that pathway as well (Laqueur, 2015Rego et al., 2021). The very low rate of overdose in Portugal, where heroin rather than fentanyl remains the principal source of illicit opioids, may support the hypothesis that the severity of the overdose risk described by our model is greatly increased by fentanyl’s potency, and small margin of error in dosing.

Safer supply

The consistent and uninterrupted provision of opioids of known potency to people with opioid dependence, such as analgesics or pharmaceutically manufactured heroin Ivsins et al. (2020), could limit overdose by keeping people in comparative stasis (1–4) rather than subjecting them to supply interruptions (6). While some Canadian jurisdictions have embarked on such an initiative (Young et al., 2022), the programs have high barriers for enrollment, serve small numbers of clients, and have faced implementation hurdles (Karamouzian et al., 2023), limiting their ability to reduce the overdose risk resulting from drug seizures in the larger population. The rationale for safer supply also suggests that our model may see fewer overdoses if the illicit opioids were the pharmaceutically produced analgesics that were the origin of the present opioid epidemic, although erratically dosed counterfeit pills, which have proliferated throughout the illicit opioid market (Friedman & Ciccarone, 2025Green et al., 2022), would likely confound such a reduction.

Legalization and regulation

As with safer supply, legalization and regulation would bring the manufacture of recreationally used opioids under a regime that would closely monitor their consistency and potency and provide a means for commercial distribution that would preclude dealer-related supply interruptions. This would do two things: prevent the supply interruptions arising from police drug seizures in the first place (6) and ensure that the drugs consumed by people were regulated to the extent that their potency was consistent and well-known, regardless of whether a user experiences some type of interrupted supply or not (3 or 9).
Legalization, especially when accompanied by safer supply practices, would also likely lessen the circumstances in which people experienced withdrawal and reductions in tolerance due to extended supply interruptions (7), providing several means to escape the causal pathway from a supply interruption to fatal overdose (Emerson & Haden, 2021). It would also likely decrease the frequency of several other behaviors that contribute to overdose risk, such as rushed use, clandestine use, and variance across suppliers and between batches. Regardless of the theoretical effectiveness of this measure, it is critical to note that all of this is said without regard to the political reality that legalization is currently the least likely of the drug policy interventions discussed here to be implemented, due to a pronounced lack of political and cultural acceptance of the idea.

Discussion

The extent to which police drug seizures impact the broader community in terms of the availability and consistency of the drug supply is ultimately unknown, likely to be highly dependent on local contexts, and deserves further study. We do know, however, that police opioid seizures certainly affect the person the drugs are taken from, and their direct connections, and our model explains the elevated overdose risk that results. The strength of the POSTeR Model lies in its reliance on well-known features of opioid dependence and withdrawal, and a well-established understanding of certain basic mechanics of the illicit drug market. That people who consistently consume opioids will experience increasingly acute dependence and greater tolerance is not open to debate, and neither is the intense desire—or physiological need—for people dependent on opioids to avoid or mitigate withdrawal, which is a known motivator of risky behavior (Frank et al., 2023). The same can be said of the decreased opioid tolerance that comes from abstinence, whether voluntary or involuntary. The inconsistency in the potency and contents of the illicit drug supply in the case of heroin and fentanyl are also well-established, which underlies the main argument for safer supply initiatives (Ivsins et al., 2020).
In showing how these factors come together, the model moves from anecdotal accounts and quantitative research to a logic model that illustrates the causal chain between a drug seizure, the ensuing supply interruption, and increased exposure to overdose, underwriting our prior spatiotemporal analysis of the association between the two. If the four premises presented at the outset of this paper are correct, then they are sufficient to establish the validity of the model. It is important to recall that this validity does not depend on an actual increase in fatal overdose, but an increase in its risk, which can then be reduced by taking the appropriate precautions. We posit that many fatal overdoses occur because the desire to avoid withdrawal in the aftermath of a supply interruption is very strong, and often the reason people do not take the recommended precautions. The behavioral factors presented after the formal model further exacerbate this risk, but it does not depend on them for its validity.
Despite such strengths, our model has limitations that call for both caution and further research. Although it is an ancillary aspect of or model, we do not know how much of an elevated overdose risk can be attributed a general variance in the composition of the opioid supply, versus a variance in the composition of the fentanyl supply in particular, where small changes can yield comparably large increases in potency. The makeshift production processes employed by the illicit market, which can take place in private residences and other crude, repurposed spaces, is far removed from a proper pharmaceutical manufacturing operation, resulting in variance in the volume of the active opioid per dose. We hypothesize that compared to pharmaceutically produced and heroin-based opioids, powerful illicitly packaged synthetics such as fentanyl are inherently more difficult to safely dose, since even the smallest variations in the volume of the active opioid could yield great differences in potency.
It is also worth noting that the POSTeR Model only considers the near-term spatiotemporal effects of police drug seizures. The research findings that motivated this model considered overdose up to three weeks after a police drug seizure (Ray et al., 2023), and POSTeR Model is meant to provide a causal explanation for events on this time horizon. It does not examine the long-term effects of drug seizures on a community, especially large ones that might have a more significant impact on the drug market. So, while we are unaware of any police drug seizure that was significant enough to have a durable effect on the price and/or availability of illicit drugs in the US, our model is not meant to describe mid- to long-term effects. It therefore cannot rule out the possibility that drug seizures of a size and type sufficient to cause a sustained supply shortage may foreclose the induction of new drug users, or promote treatment seeking among existing users, therefore lowering the community’s overall rate of opioid dependence, or the extent to which this may offset the negative effects we describe here at the population level. Given the constant occurrence of police drug seizures across the nation, and the persistence and worsening of the overdose crisis, we would hypothesize this population level effect is minimal in comparison to the elevated risk of overdose.
Relatedly, as a model that draws on data from urban centers, it is unclear how the overdose risks it produces could be exacerbated or reduced by seizures in rural areas which may pose unique concerns (Dunn et al., 2016). The considerably greater distances and smaller populations involved in rural illicit drug distribution may matter (Fadanelli et al., 2020), as may economic precarity, which can limit options for replacement supplies (Pear et al., 2019). They could relate to longer timeframes for resupply that increase withdrawal symptoms with reduced access to harm reduction resources, or it may increase the likelihood that a replacement substance comes from a different supply chain with an inherently different or more volatile potency. Conversely, the tight-knit nature of small rural populations may yield more transparency and trust across dealer networks. More research is necessary to understand how geography affects the model.
Another limitation to the POSTeR Model is that it describes the effects of a supply interruption at the individual level, which can be caused by either a direct encounter with a police officer that results in an arrest of the PWUD, or the police takedown of a distributor who supplies a significant number of people in the community. In either case, the logic of the model is identical, and indicates an increase in overdose risk, but it does not distinguish between the intensity, duration, and breadth of the risk in different cases. It also does not distinguish how the risk is experienced by individuals in different ways, such as sex workers, unhoused people, or those with the financial resources or networks of trusted dealers that may better insulate them from supply interruptions. While these differences should be researched to further refine the model, one of its strengths may be its versatility across cases and populations. That said, the POSTeR Model does not account for the complexities of polysubstance use, i.e., the co-use of depressants and stimulants, or of different drug types within each class. Polysubstance use, which is increasingly common among people who use opioids (Cicero et al., 2020Lim et al., 2021), can exacerbate overdose risks (Pergolizzi Jr et al., 2021), and our model does not account for these interaction effects.
Critically, this analysis does not adjudicate the competing priorities that drive narcotics enforcement and police drug seizures in many communities. There may be reasons for enforcement and the accompanying seizures that communities and their elected officials find compelling despite their iatrogenic effects. For example, police seizures might provide a way to reduce serious violence among drug suppliers, or a drug selling operation may have a significant negative impact on the public order of a neighborhood, and there is a strong desire among community members for the police to reduce or eliminate it. The role of policies and laws in addressing these issues—or failing to do so—is complex and far beyond the scope of this paper. What our model does do, however, is suggest that there may be serious negative health outcomes associated with law enforcement to address these concerns, even though the approach may have community support, and be culturally ingrained in our approach to problematic substance use. If that is the case, it is incumbent upon communities to account for these outcomes. It is counter-intuitive that drug seizures can increase overdose risk, making the public’s recalcitrance is understandable, so the causal model discussed here may offer a critical means to foster a public understanding that could shape future support for evidence-based drug policy proposals.
The fact that policing routinely creates conditions sufficient for fatal overdose, and that they occur with considerable frequency, suggests the proposed model is a critical component of understanding how policing exacerbates the health risks faced by people with opioid dependence. In doing so, it demonstrates a significant tension between the police role of protection and rescue, in which they are expected to prioritize the sanctity of human life in a manner broadly consistent with public health (del Pozo, 2022Goulka et al., 2021), and the potentially fatal risks generated by their principal strategy for addressing problematic substance use.

Conclusion

The POSTeR Model contributes to the body of knowledge about how criminal justice interventions intended to address the effects of addiction and overdose can have iatrogenic consequences that worsen health outcomes of people dependent on opioids. It is a problem that manifests across the criminal justice system. In the case of imprisonment, for example, the moral consequences of punishment are meant to be complemented by a period of detoxification and abstinence intended to promote recovery. Despite the underleveraged potential for evidence-based treatment to lessen these risks (Berk et al., 2022), this type of forced abstinence is neither effective nor safe for the people it is imposed on: release from jail or prison is believed to be one of the highest periods of overdose risk for people dependent on opioids (Binswanger et al., 20132007). By the account here, the drug seizures by police that precede incarceration, whether they are from an individual who possesses drugs for personal use or someone with large quantities intended for distribution, comprise another mechanism that can increase fatal overdose despite being intended to reduce it. It is critical that future research continues to explore this outcome, assesses its prevalence across settings, estimates the magnitude of the effect, discerns which variables are protect against risk, and brings greater clarity to the risks imposed at the individual and community levels. While it is possible that police view the reduction in supply that results from drug seizures as prima facie evidence of a successful outcome, this model and the accompanying research suggest this is not the case if a reduced supply is meant to deliver the proximate public health goal of mortality reduction.
If research continues to exhibit a positive relationship between seizures and overdose, legalization and regulation of opioids would broadly incentivize the drug market to reduce or eliminate products of uncertain potency, decisively lowering the overdose risks resulting from uncertain dosing, as well as moderate the risky behaviors that result from the fear of drug seizures. Legalization, however, has yet to be even a remotely feasible political possibility in the United States, as nascent efforts at more modest forms of decriminalization were met with resistance, implemented poorly, and eventually repealed (del Pozo, 2024Kim, 2024Smiley-McDonald et al., 2023). It is likely that police drug seizures will remain a core feature of our response to illicit substances, and that such enforcement efforts will intensify, as the criminal enforcement of drug possession holds perpetual appeal in communities that hope it will reduce risk. To safeguard health, it is critical that we understand the full range of consequences for these and other policies based on police drug seizures.

Declaration of competing interest

The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:
Brandon del Pozo reports financial support was provided by National Institute on Drug Abuse. Traci Green reports financial support was provided by NIH National Institute of General Medical Sciences. Bradley Ray reports was provided by Centers for Disease Control and Prevention. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Source: https://www.sciencedirect.com/science/article/pii/S095539592500088X
by DFAF – Save Our Society From Drugs <clincoln-dfaf.org@shared1.ccsend.com> 10 April 2025

 

Rather than investing in prevention strategies and expanding access to treatment and recovery services, British Columbia, Canada, chose to enact radical harm reduction policies—policies that are now being linked to a significant worsening of the opioid crisis.

In March 2020, British Columbia launched its safer opioid supply policy, allowing physicians and nurse practitioners to prescribe pharmaceutical-grade opioids to individuals at risk of overdose. Then, in January 2023, the province implemented a decriminalization policy, removing criminal penalties for possession of small quantities (up to 2.5g) of drugs including opioids, cocaine, methamphetamine, and MDMA.

The result? A public health disaster.

Hospitalizations due to opioid poisoning increased by 33% (93 additional hospitalizations) following the rollout of the safer supply program. After decriminalization was added, these hospitalizations rose another 58% (164 more hospitalizations), relative to the pre-policy period.

The safer opioid supply guidelines allowed prescribers to offer powerful opioids such as up to 14 hydromorphone tablets per day and two oral morphine (80 to 240 mg) capsules per day, with the option of supervised ingestion at the prescriber’s discretion. While advocates argue that these policies shield people from contaminated street drugs, a critical question remains: Who is tracking where these powerful drugs end up—and what’s being done to move people into treatment and recovery?

The evidence is troubling. Diversion is happening. Only about 3% of opioid users have accessed these so-called safer opioids. This means the vast majority of high-dose prescriptions may be going unused by intended recipients—fueling black market activity and increasing the risk of exposure for opioid-naïve individuals, especially youth. Rather than reduce harm, these diverted drugs may be driving overdose and addiction deeper into communities.

Decriminalization only exacerbates the issue by removing legal consequences, making it harder for law enforcement to respond and opening the door for increased public use, street-level trafficking, and easier circulation of diverted substances.

As for opioid-related deaths, there were increases during the safer supply period, although these findings lost statistical significance after deeper analysis. Nonetheless, the trend raises serious concerns, especially given the surge in hospitalizations.

The authors also noted rising reports of public drug use, which contributed to the government’s decision to recriminalize drug use in public spaces—a walk-back of the initial policy.

These policies may have been introduced with good intentions, but the outcomes are clear: they are not working. By prioritizing access to drugs over prevention, treatment, and accountability, British Columbia has intensified the crisis it sought to solve.

If other jurisdictions consider similar approaches, British Columbia’s experience should serve as a warning—not a model.

 

Source:  https://doi.org/10.1001/jamahealthforum.2025.0101

 

Comment by NDPA: The health-promoting benefit of prevention before treatment is well-founded. The latin root of the word ‘prevention’ is ‘praevenire’ which means ‘to come before’ – not ‘during’ or ‘after’ – reactive policies which have their place, but are at best ‘repair jobs’. The PreVenture program is to be welcomed in this context, and we wish it every success. Peter Stoker, Director, National Drug Prevention Alliance (UK).

PreVenture program has reduced odds by focusing on risky personality traits: study

A drug prevention program that began in Montreal has been found to reduce the risk of substance use disorders in teens by offering them tools and strategies to cope with personality traits like impulsivity and anxiety.

“If a young person is reporting very high levels of these traits, they’re more likely to use substances as a way to manage those traits,” said Patricia Conrod, founder of the PreVenture program, who is also a psychiatry professor at the Université de Montréal and a scientist at Sainte-Justine hospital in Montreal.

A recent study in the American Journal of Psychiatry looked at the impact of PreVenture in 31 Montreal-area high schools over a five-year period.

The study found the program helped reduce the growth in the odds of substance use disorder by 35 per cent year over year, compared with a control group.

Conrod told CBC News that the odds of developing a substance use disorder increase as students get older.

The program focuses on such traits as impulsivity, sensation seeking, anxiety sensitivity and hopelessness — all of which may lead teens to turn to substance use to cope. During two 90-minute workshops given in Grade 7, students gain insight into their own personalities and tools to manage them.

The program uses cognitive behavioural therapy, interactive exercises and group discussions to find personality-specific coping strategies.

‘I can deal with them, so I feel better’

Fara Thifault, 13, a Grade 7 student at Collège de Montréal, participated in a workshop last fall.

“I didn’t realize I had negative thoughts, and when I did that [workshop], I realized, ‘Yeah I get them a lot and this is how I can deal with them, so I feel better,'” she said.

Grade 10 student Romane Roussel, 16, said the workshops helped her, too.

“I’m less impulsive now because I use some techniques, I take a breather,” she said.

Conrod said while a growing body of evidence supports the PreVenture program and others like it, schools across the country need sustained funding, including from federal and provincial governments, to deliver them more widely.

“Some substance use disorders are preventable, and we should be making sure that young people have access to the programs and the resources they need,” she said.

The program is currently available in schools in five Canadian provinces, including Quebec, Ontario and British Colombia, as well as in several U.S. states.

“It’s a little bit harder for policy-makers to put the money towards prevention knowing they may not see the benefits — and there will be benefits in many of these cases, but they’re not going to see them for several years,” she said in an interview.

Schwartz was part of a team that examined school-based prevention programs around the world, including PreVenture.

“There’s been a long history of using programs that haven’t necessarily been effective,” she said. “What’s happening now is that policy-makers are increasingly turning to the research evidence.”

What’s missing, Schwartz said, is funding to maintain programs and put them in place more widely.

Prevention before treatment

Justin Phillips’s son Aaron died of a heroin overdose in 2013, when he was 20, in Indianapolis. She described him as an “impulsive, sensation-seeking kid.”

He once skateboarded off the roof of her house, Phillips recalled, but said he was also very sensitive and sometimes anxious.

These are all traits, she said, that young people and their families don’t always have the tools to recognize and manage.

“Had we had these tools, I absolutely believe things would have been different,” she said in an interview.

The year after her son’s death, Phillips founded an organization called Overdose Lifeline to support other families dealing with addiction and to promote prevention. She is also involved with PreVenture, training people to deliver the workshops and working to bring the program to more communities in the United States.

Source: https://www.cbc.ca/news/health/teens-drug-use-prevention-study-1.7470849

Dangerous but common misconceptions can prevent crucial early addiction treatment.

Key points:

  • Misconceptions and the ignoring of research-based evidence prevent crucial early treatment of addiction.
  • Drugs of abuse cause health, life, and relationship problems with many long-lasting effects.
  • Teen and young adult drug prevention is necessary and needs funding.

Research published in high-quality peer-reviewed journals reveals key information on the realities of addiction, exposing pervasive myths and misconceptions, as in these examples.

False Belief 1: Drug experimentation is normal for teens and shouldn’t alarm parents.

Drug use and experimentation among teens often is ignored by many—even parents, who then may be unaware that any use places adolescent brains in jeopardy. For today’s teens, life often feels overwhelming, but avoiding alcohol, tobacco, marijuana, and other drugs is their one best choice to promote continued healthy physical and mental development. Preventing or delaying all teenage substance use not only reduces their current risks for depression, psychosis, and school/learning problems, but it also significantly decreases their probability of addiction as adults.

Harvard’s Sharon Levy, MD, MPH, and founding National Institute of Drug Abuse Director Robert DuPont, MD, strongly advocate a zero-tolerance approach to youth substance use. They emphasize that no amount of drug use is safe for young people. They promote the One Choice initiative encouraging adolescents to avoid substance use: alcohol, tobacco, marijuana, and other drugs.

It’s now known that THC in marijuana interferes with the developing brain circuits responsible for regulating behavior, leading to increased risk-taking and poor decision-making. Even infrequent teen use can impede judgment, increasing the probability of risky behaviors and accidents. Adolescents also are more likely than adults to develop cannabis use disorder (CUD) due to their heightened neuroplasticity during this developmental stage. The resulting impairment may lead to academic underperformance and problematic interpersonal relationships.

False Belief 2: Addiction is a personal weakness.

Addiction is not about people being weak-minded. It’s far more complicated. Becoming addicted depends on the drug used, dose, route, frequency, and risk factors like ages of users. Also, the same drug at the same dose affects people differently because of personal differences, as well as the presence/absence of traumatic past life experiences.

Yale’s Joel Gelernter identified genetic variants associated with vulnerability to addictions. However, genetic characteristics themselves interact with environmental factors in developing substance use disorders (SUDs). As Nora Volkow, director of NIDA, has said, “Addiction is a complex disease of a complex brain; ignoring this fact will only hamper our efforts to find effective solutions …”

False Belief 3: People must hit “rock bottom” to recover from addiction.

No, no, and no! Roadside alcohol testing has prevented thousands of deaths and helped many people with alcohol use disorders (AUD) obtain help, sometimes by coercion of courts. About 50 percent of those arrested for DUI have an AUD. Users often deny they have a problem with drugs or alcohol and believe they are truthful. But they are lying to themselves.

Addiction is a chronic, relapsing condition driven by changes in brain circuitry, particularly in areas controlling reward, stress, and decision-making. While some people seek help after suffering dire consequences, others are compelled into treatment by the courts, based on a past offense. Waiting to hit “rock bottom” increases major risks of harming the person’s relationships, job, and health—and strengthens the hold of the drug over the person.

False Belief 4: Addiction treatment never works.

Researchers from the University of British Columbia and Harvard Medical School recently analyzed survey data from nearly 57,000 participants in 21 countries over 19 years, providing clear data. They discovered that the number-one barrier to treatment was addicted people themselves: Most were in denial and did not recognize they needed treatment.

Alcoholics Anonymous is often successful, non-judgmentally providing new members a roadmap, role models, hope, and social connections. Successful people actively involved in AA complain that their friends kept asking them why they “weren’t cured yet” since they went to so many meetings. But going to meetings is what works.

Even among experts, there’s no consensus on what constitutes successful treatment. To some, success is that the person is still alive and hasn’t been rushed to the emergency room because of an overdose in the past 6 months or year. To others, it is taking treatment medications. And to still others, only abstinence and a full resumption of all family and work obligations counted as success.

Another issue is that most people with SUDs have multiple addictions. Even when they overdosed, most took multiple drugs. It’s also true that many people come to treatment also needing treatment for other medical, addiction, and psychiatric problems. Yet only rarely are patients evaluated and treated for all issues.

False Belief 5: Overdoses of drugs don’t cause brain damage.

Drugs of abuse can harm the brain. Overdose survivors may suffer from undetected brain damage and hypoxic brain injury caused by opioid-induced respiratory depression. As a society, we better understand hypoxia as associated with drowning or choking than its much more common occurrence in drug overdoses with loss of consciousness.

Recent studies estimate that at least half of people using opioids have illicitly experienced a non-fatal overdose or witnessed an overdose. People who regularly use drugs are at elevated risk of brain injury due to accidents, fights, and overdoses. A single fentanyl overdose could cause hypoxia, brain injury, and memory and concentration problems.

Overdoses with counterfeit pills, cocaine, methamphetamine, xylazine, or heroin usually also include fentanyl, making neurologically compromising overdoses more common.

Summary

Myths and misconceptions increase stigma and decrease the likelihood that someone with an addictive illness will receive prompt, effective treatment. We need early intervention and treatment during the preaddiction phase. Bottom line: Preventing teen and young adult use is crucial.

Mark Gold M.D.

Mark S. Gold, M.D., is a pioneering researcher, professor, and chairman of psychiatry at Yale, the University of Florida, and Washington University in St Louis. His theories have changed the field, stimulated additional research, and led to new understanding and treatments for opioid use disorders, cocaine use disorders, overeating, smoking, and depression.

Source: https://www.psychologytoday.com/intl/blog/addiction-outlook/202502/5-common-false-beliefs-about-drug-use-users-and-addiction

OPENING STATEMENT BY AUTHOR: Dec 31, 2024

Drug Free Australia has launched a new Substack where we start out with the foundational failure of Australia’s 1985 Harm Minimisation experiment which has literally seen thousands of families (5,400 between 2000 and 2007 alone) needlessly grieving for a lost loved one – all directly as a result of our adoption of Harm Reduction measures.  If you think this is fanciful, you need to look at the cold, hard evidence.

If you live in another country, this is precisely a drug policy approach you need to fight to avoid and you may need to use this data to do it.

Gary Christian, President, Drug Free Australia. Phone: 0422 163 141

In 2022 the White House Office of National Drug Control Strategy (ONDCP) published its first National Drug Control Strategy, which outlined seven goals to be achieved by 2025. On December 30, 2024, the ONDCP released the National Drug Control Strategy Performance Review System (PRS) Report—essentially a progress update on the Biden administration response to the overdose crisis between 2020 and 2022.

Though the ONDCP published an updated Strategy in May 2024, the new PRS report is intended to span data through 2022, corresponding to the original version. It has a tendency to veer into data from more recent years, however, which reflect a turnaround in overdose rates and as such look a lot better than the years the report is meant to cover.

The seven goals outlined in the original Strategy contain 25 objectives, most of which are assessed as on track. Five are already completed; five are behind schedule.

Viewed in the context of the recent drop in overdose mortality, the PRS updates would suggest that reducing drug-related deaths doesn’t actually require reducing access to drugs, but that’s probably beyond the scope of the ONDCP’s analysis.

 

Goal 1: Less drug use

The first objective for this goal was to reduce overdose deaths by 13 percent by 2025. The most recent Centers for Disease Control and Prevention data show a decrease of 16.9 percent, which according to the report is “[t]hanks in significant part to actions by the Administration.”

The second objective was to reduce prevalence of substance use disorders (SUD) specific to opioids, methamphetamine and cocaine by 25 percent.

The ONDCP attributed cocaine use disorder to 0.5 percent of the population in 2021, based on responses to the 2021 National Drug Use Survey. Which evolved between 2020 and 2021, and identifies different SUD by somewhat convoluted means, but the ONDCP doesn’t acknowledge non-problematic use of those substances and so approached use and SUD as the same thing. It attributed methamphetamine use disorder to 0.6 percent of the population, and opioid use disorder to 2 percent.

Per 2022 data, there’s been no change in baseline use of cocaine and meth. Opioid use increased to 2.2 percent, meaning “accelerated action” would be needed to finish on time.

 

Goal 2: More prevention

While the previous goal applied to ages 12 and up, this goal of ensuring that “Prevention efforts are increased in the the United States,” refers to youth drinking and vaping.

The first objective was to get youth alcohol consumption, measured by past 30-day use, under 6.5 percent by 2025. Data show that between 2021 and 2022 the rate decreased from 7.2 percent to 6.8 percent, which put it on track.

The second objective was to reduce youth use of nicotine vapes by 15 percent by 2025. Data show that in 2021, around 7.6 percent of middle- and high-school students reported having vaped within the past month. In 2022 this rose to 9.4, but the target for 2025 was anything under 11.1, so ONDCP considers this objective already met and the 2022 increase doesn’t change that.

 

Goal 3: More harm reduction

The first objective here was an 85-percent increase in the number of counties disproportionately affected by overdose that had at least one syringe service program (SSP). Data show that in 2020, 130 counties with high overdose death rates had at least one SSP; by 2022 this had increased to 180 counties, which was on track for the ONDCP goal of 241 counties by 2025.

The second objective was a 25-percent increase in SSP offering “some type of drug safety checking support service.” The 2025 target of 21.3 percent had already been met by 2021, but over the next year the number of SSP offering drug-checking services nearly doubled—2022 data show 46.7 percent of SSP met that criteria.

However, “some type” of drug-checking refers largely to fentanyl test strips, which are most useful to people who do not regularly use opioids. The more useful drug-checking service for people who do regularly use opioids—the population that SSP primarily serve—is on-site forensic analysis. This requires more expensive equipment, to which only a handful of SSP have access.

 

Goal 4: More treatment

The first objective was a 100-percent increase in admissions to treatment facilities among people considered at high risk for overdose involving opioids, methamphetamine or cocaine. This doesn’t include methadone maintenance or outpatient buprenorphine prescriptions. In 2021, treatment facilities reported 637,589 admissions among people using primarily opioids, methamphetamine, cocaine or other “synthetics,” which was already about one-third short of the target for that year. In 2022 admissions dropped to 604,096.

The second objective was to ease the shortage of behavioral health providers by 70 percent. The PRS report finds that this been pretty steadily on track and is projected to stay that way.

 

Goal 5: More recovery initiatives

The first objective here is to have at least 14 states operating a “recovery-ready workplace initiative” by 2025. The term refers to a Biden administration push for more equitable employment policies for workers with substance use disorder, which led to the creation of a national Recovery-Friendly Workplace Initiative in 2023. Data show this goal was met in 2022 with 16 states reporting a qualifying initiative, up from 13 in 2021.

The second objective was to increase the number peer-led recovery organizations to at least 194. This has been completed, as there were 232 as of 2022.

The third objective was to increase the number of recovery high schools to at least 47, which was on track with 45 operational as of 2022.

The fourth objective was to increase the number of collegiate recovery programs to at least 165, which was similarly on track with 149 as of 2022.

The fifth and final objective was to have at least 8,600 residential recovery programs operational by 2025. This too was on track as of 2022, with 7,957 programs.

 

Goal 6: “Criminal justice reform efforts include drug policy matters”

Despite the extremely broad title, this goal had pretty narrow objectives. The first was to have 80 percent of drug courts complete equity and inclusion trainings by 2025. As of 2022 we were at 19 percent, considerably behind schedule. The PRS report attributes this to a combination of COVID-19 pandemic restrictions and bureaucratic restrictions, which it expects to resolve.

The second objective was a 100-percent increase in access to medications for opioid use disorder (MOUD) in federal Bureau of Prisons facilities, and a 50-percent increase for in state prisons and local jails.

The PRS report does not differentiate between access to methadone and buprenorphine, which have been shown to decrease overdose risk, and naltrexone—which has been shown to increase overdose risk, and of the three Food and Drug Administration-approved MOUD is by far the favorite among corrections departments. With that in mind, the ONDCP goal is on track for federal and state prisons.

“Currently, there is no single data source that can be used to track progress in increasing the percent of local jails offering MOUD,” the report states. “For illustrative purposes, [the figure below] shows the estimated percent of local jails offering MOUD in the United States from 2019 to 2022.”

 

 

Goal 7: Less drugs

The first objective for this goal was a 365-percent increase in the “number of targets identified in counternarcotics Executive Orders and related asset freezes and seizures made by law enforcement.” This refers to people and entities associated with transnational drug-trafficking organizations. Per the report, 46 had been identified by 2022, and the administration was on track to identify 96 by 2025.

The second objective was a 14-percent increase in the number of people convicted of felonies as a result of Drug Enforcement Administration investigations using data from the Financial Crimes Enforcement Network (FinCEN). Per the DEA, as of 2022 it had used FinCEN data in investigations that led to the convictions of 6,529 people. This surpassed the goal of 5,775 people convicted by 2025.

The third objective was to have at least 70 percent of the DEA’s active priority investigations “linked to the Sinaloa or Jalisco New Generation cartels, or their enablers.” This was also on track, at 62 percent in 2022.

The fourth objective was to decrease “potential production” of cocaine by 10 percent, and that of heroin by 30 percent.

“The United States Government is internally realigning responsibility for conducting illicit crop estimates. As a result of the change in responsibility, there will be a temporary gap in data for 2022 and 2023,” the report states in reference to both cocaine and heroin. “This gap in data does not reflect a change in priorities.”

Potential cocaine production was decreased only slightly between 2020 and 2021, but was projected to be on track as of 2021.

“[I]t is important to note that provisional estimates of drug overdose deaths involving cocaine for the 12-month period ending in July 2024 were 14.1 percent lower compared to a year prior,” the ONDCP added. “The Administration will continue its efforts to reduce the supply of cocaine.”

Heroin interdiction was not on track, but the ONDCP made the same statement verbatim for heroin-involved deaths.

The fifth objective was to have a total of at least 14 incident reports—like seizures or stopped shipments—involving fentanyl precursors from China or India. From 2021 to 2022 the number dropped from 11 to two, but the ONDCP notes that this data is voluntarily reported by other entities and as such is unreliable. And also that preliminary estimates for 2023 look a lot higher.

Source: https://filtermag.org/ondcp-national-drug-control-strategy/

Tulsa World
Aug 25, 2024

The Cherokee Nation’s approach to substance abuse recovery is harm reduction, which has drawn criticism from some who work in addiction recovery.

“Harm reduction is a pretty controversial topic. A lot of people feel it can be enabling drug users. It can feel counterproductive and counter intuitive,” said Jennifer Steward, director of the University of Tulsa’s Behavioral Health Clinic.

In a Tulsa World interview, Steward said the controversial aspect comes from the fact that harm reduction does not encourage abstinence from drug use, which makes it different from traditional substance abuse rehabilitation programs. Harm reduction instead focuses on keeping active drug users alive, with considerations for their health and safety.

The Cherokee Nation harm reduction program utilizes a mobile unit that brings supplies to drug-users on the streets: clean needles, cotton swabs and Narcan, which can reduce cravings and combat a potentially fatal overdose.

Steward said many harm reduction programs also provide a safe, clean environment to partake in drug use, free of disease such as HIV or hepatitis C, with staff ready to assist in case of overdose.

Cherokee Nation prevention specialist Coleman Cox said that his tribe recognized the potential for addiction among the Cherokee people after being exposed to the opioid epidemic is “far reaching and the latest in a long line of injustices brought upon indigenous peoples.”

According to the Centers for Disease Control, in 2021 the highest rate of drug overdose deaths was in American Indian and Alaskan Native individuals. Data from the Substance Abuse and Mental Health Services Administration indicates 5.1% of Natives have misused opioids, which can include prescribed pain-relief medications, hydrocodone, oxycodone, fentanyl and heroin.

“We bent the opioid industry to a settlement for the harm it inflicted, and we are making the opioid industry help pay for every single penny of this facility,” said Cherokee Nation Chief Chuck Hoskin Jr. in reference to their treatment facility they broke ground for Thursday morning.

The Cherokee Nation received a Substance Abuse and Mental Health Services Administration grant last year for harm-reduction services. They now operate a storefront at 214 N. Bliss Ave. in Tahlequah. It is open not only to tribal members but also to the public, and all participants can remain anonymous.

The new facility that the tribe broke ground on this week is a $25 million dollar addiction treatment center just outside of Tahlequah.

The Cherokee Nation’s Public Health and Wellness Fund Act of 2021 dedicated $100 million in settlement funds from opioid and e-cigarette lawsuits for a variety of public health programs.

Cox said harm reduction meets people where they are at in their addiction. This means that if the user does not want to seek rehabilitative services, they do not have to. Rehabilitation services may be recommended, but they are not a requirement.

“Harm reduction is more than Narcan and clean needles. It’s treating others how they want to be treated — with dignity, respect and value, without conditions,” said Cox.

Evan White, a member of the Absentee Shawnee tribe, is the director of Native American research at Laureate Institute for Brain Research in Tulsa. He has worked with various tribal behavioral health programs through his research.

“Harm reduction is a model that has a strong evidence base for good outcomes,” he said, “especially in substance use disorders.”

White believes harm reduction could be attractive to Native communities as it values a person’s autonomy.

“I see a consistent value of a person as an individual within Native communities. Healing is an important part of the process in these cultural spaces, even though there is a lot of stigma around substance abuse in our broader society,” he said.

For Native individuals with substance abuse issues, White said participating in cultural activities may enhance self-control and mindfulness.

The Cherokee Nation’s program provides opportunities for Native people in recovery to partake in cultural activities.

“We planted a Three Sisters Garden: corn, beans and gourds,” said Cox. “Corn provides the bean a pathway for growth. Beans give back by imparting nitrogen to the soil. Gourd provides protection and covers the ground. Three different things working in harmony. Body, mind and spirit.”

Members of the program get to adopt a plant, name it and tend to it. Cox said the vegetables are not for eating, however.

“They are meant to harvest seeds for the future bounty, beyond what we can see now. Just like when our members come to us for whatever kind of help, we plant a seed that one day they will harvest a healthier life,” he said.

Cox said the harm reduction staff launched a new chapter of “wellbriety movement” that they call “recovery rez.” It’s a cultural approach to the traditional 12-step recovery plan.

“At Recovery Rez they begin with prayer and fellowship meal, then smudge and hold a talking circle guided by the passing of an eagle feather from speaker to speaker. They close out the evening with a drum circle and singing. All are welcome, and citizens don’t need to be in recovery to benefit from the cultural protective factors,” said Cox.

Steward said it can be difficult to view harm reduction as a substance abuse program because harm reduction focuses on the long-term.

“The goal is to help someone be ready to engage in rehabilitation later on, but in order to do that, they have to be alive,” she said.

According to Cherokee Nation spokeswoman Julie Hubbard, the tribe’s harm reduction program has had 3,099 encounters for service, and it has 1,049 members currently. The number of people who still inject drugs within the program is 743. The amount of lives saved at the program from Narcan distribution is 44.

August 4, 2024

Lifestyle changes—including eating fruits, vegetables, and whole grains—can help patients, especially those with diabetes or hypertension, improve outcomes.

Robert Ostfeld, MD, ScM, director of preventive cardiology at Montefiore Health System and professor of medicine at Albert Einstein College of Medicine in New York sat down with Drug Topics ahead of the American Society for Preventive Cardiology Congress on CVD Prevention to discuss the role that dietary patterns and nutrition decisions play in living a healthful lifestyle.

Drug Topics: What specific nutrients or dietary patterns have been shown to benefit patients with hypertension and diabetes, and how can this information be incorporated into patient counseling?

Robert Ostfeld, MD, ScM: That’s a very important question. A healthful diet, of course, can very positively impact cardiometabolic health—including blood pressure, diabetes, [and] lipids—and cardiovascular health and overall health in general.

Reassuringly, there is broad [alignment] in terms of what defines a healthful dietary pattern. For example, multiple medical societies—like the American Heart Association, the American College of Cardiology, the American Society for Preventive Cardiology, the Canadian Cardiovascular Society, the European Society of Cardiology—are all broadly aligned; consuming more plant-based nutrition, less ultra-processed foods, less red and processed meats, is helpful both cardiometabolically and [for] cardiovascular health overall.

Unfortunately, that recommendation hasn’t necessarily percolated down well, at least into the US. There was an interesting recent analysis where from the NHANES database—the National Health and Nutrition Examination Survey database—published in 2021, where they looked at a little over 11,000 people…where they used 5 elements to define diet. One element was consuming at least 4 and a half servings of fruits and vegetables a day, at least 3 servings of whole grains each day, low sugar or sweetened beverage consumption, low salt consumption, and 2 servings of fatty fish each week. If you had 0 or 1 of those, then they felt you had a poor diet; 2 or 3 an intermediate [diet], and 4 or 5, an ideal dietary pattern. About 75% of the US has a poor, 0 to 1 of those [elements] dietary pattern; 25% [have] intermediate, and 0.7% of the US has an ideal dietary pattern.

READ MORE: Food Is Medicine: Pharmacists Can Advance Policies for Healthier Communities

There’s a huge gap between where we are and where we could. You could ask, “Does it even really matter?” Of course it does. In this study, they modeled if everyone adopted an ideal dietary pattern—so 4 or 5 of those 5 elements—for 1 year, what would happen? Well, it was estimated that cardiovascular event rates would fall by about 42%. The gap matters. There’s randomized prospective cohort data that eating a healthful dietary pattern, more plant based [and] aligned with American College of Cardiology and American Heart Association recommendations, can also be helpful for high blood pressure, particularly the DASH [Dietary Approaches to Stop Hypertension] dietary pattern for high cholesterol, the dietary portfolio pattern, which is a high fiber plant based diet, and also, similar recommendations broadly for diabetes.

What I should reinforce is, it’s not really that there’s 1 diet for high blood pressure, high cholesterol, and diabetes. They’re really broadly aligned that consuming more healthful, plant-based foods—fruits, vegetables, whole grains, beans, lentils—less ultra-processed foods and less red and processed meats, is helpful for all of the above: cardiovascular health and cardiometabolic health.

Drug Topics: How can patients be supported in overcoming common barriers to healthy eating, such as budget constraints and limited access to nutritious foods, in the management of hypertension and diabetes?

Ostfeld: Helping the individual patient in the office embrace a more healthful diet can be a challenge. Society does not make…it easy for the healthy choice to be the easy choice. And behavior change, getting someone to change how they eat, how they live, can be very, very difficult. These are big hurdles that we face.

As an individual practitioner, it can be overwhelming to overcome some of these things; at least we can try and start. As an individual [health care provider], you’ll have your team around you who can support you and reinforce your message. Nurses, support staff, and registered dietitians can be incredibly helpful to reinforce and educate about this topic.

In the clinic specifically, I will try to find a specific reason that the patient may be interested in living more healthfully. Maybe they want to lose weight or improve their skin complexion, maybe they want to lower their blood pressure, lower their cholesterol, come off a medication… Whatever the case may be, I try to highlight how consistently eating more healthfully can address that particular issue. I will give them some very specific steps—some simple specific steps, because everyone’s busy and there’s so much information to take in—that they can hopefully do when they get home to live more healthily. I have a handout that I give them that I try to keep very simple.

Sometimes in clinic, because we’re all so busy, I’ll just say, “Let’s just start with 222.” [That’s] 2 servings of green leafy vegetables a day, 2 servings of fruit each day, 2 servings of other vegetables each day: 222. I’ll do that a little bit weirdly, deliberately, so they’ll remember it. Then when they go home, depending on where they live, there may be more or [fewer] access or cost issues. [I’ll explain that] for ease, [they] could cook in bulk; we certainly don’t have to buy, you know, organic green juices. You can get frozen vegetables, frozen fruits, big sacks of potatoes, oatmeal, and beans, and those things can be much less expensive and more doable.

Another way to help patients adopt a more healthful lifestyle is—there may be the hurdle of costs here—but there are services that can deliver meals, healthful meals, to patients; they may be able to access registered dieticians, and of course there are multiple online resources that are free for patients. The Physicians Committee for Responsible Medicine has a 21-day kickstart for more plant-based nutrition should, the [health care provider] feel that that’s appropriate for the patient. There are a variety of resources that people can have access to; some may cost a little bit more, but some are also free. The American College of Lifestyle Medicine also has multiple online resources.

Source: https://www.drugtopics.com/view/q-a-examining-the-key-drivers-of-a-healthful-lifestyle

Teams from Boyle Street Community Services had been assigned to walk around the Stanley Milner Library, downtown malls and pedways and the LRT system. Their duties focused on responding to drug poisonings but they also helped educate business owners, pick up needles and refer people to services.

The city funded the first phase of the pilot, which began in the spring of 2022, then extended its funding in December 2023, but Jen Flaman, deputy city manager of community services, told city council in a May 27 memo that there were no administrative funds available to extend it further.

The memo said the city submitted a funding request to the provincial government but was unsuccessful and has applied to a Health Canada program but has not heard back.

The pilot cost $3.3 million, and included funding for a data analyst at Boyle Street.

Marliss Taylor, who is Boyle Street’s director of Streetworks and health services and oversaw the pilot, said it was a success.

She said the teams responded to more than 440 drug poisonings, distributed more than 20,000 naloxone kits, disposed of more than 7,000 sharp objects, and referred 2,500 people to detox or supervised consumption services.

“We absolutely were able to save some lives and I think that’s critically important,” Taylor said.

‘It never gets easier,’ says overdose prevention nurse, Tabatha Plesuk, a nurse based at the Stanley Milner Library in Edmonton. She said the teams also helped security guards and demonstrated friendly, respectful ways of interacting with vulnerable people in public places.

EMS responses to opioid-related events surged in Edmonton in recent years and a record 1,867 people died in Alberta because of opioid poisoning last year.

Though the rate of drug poisoning deaths in the province has slowed since 2023, Taylor said the number of overdoses in Edmonton is still high. According to the province’s substance use surveillance data, there were 148 drug poisoning deaths in the city between January and March of this year.

Taylor said she is worried about what could happen if the overdose prevention teams stop running.

“What we don’t want is for people to be injured or die of an unintentional drug overdose in spaces where people are not sure how to react,” she said.

In an emailed statement, Michelle Steele, a city spokesperson, said the teams were funded as a response to the worsening drug poisoning crisis in 2022 “with the recognition that the funding was not permanent.”

The city memo said funding ended on June 30 and the team’s services would be closing, but Taylor said the teams are still working for now.

She said Boyle Street is seeking other funding sources, with help from nearby businesses and organizations.

Madeleine Cummings

Madeleine Cummings is a reporter with CBC Edmonton. She covers local news for CBC Edmonton’s web, radio and TV platforms. You can reach her at madeleine.cummings@cbc.ca.

Source: https://www.cbc.ca/news/canada/edmonton/edmonton-stops-funding-drug-overdose-prevention-pilot-1.7254667

“We know that the ‘Just Say No’ campaign doesn’t work. It’s based in pure risks, and that doesn’t resonate with teens,” said developmental psychologist Bonnie Halpern-Felsher, PhD, a professor of pediatrics and founder and executive director of several substance use prevention and intervention curriculums at Stanford University. “There are real and perceived benefits to using drugs, as well as risks, such as coping with stress or liking the ‘high.’ If we only talk about the negatives, we lose our credibility.”

Partially because of the lessons learned from D.A.R.E., many communities are taking a different approach to addressing youth substance use. They’re also responding to very real changes in the drug landscape. Aside from vaping, adolescent use of illicit substances has dropped substantially over the past few decades, but more teens are overdosing than ever—largely because of contamination of the drug supply with fentanyl, as well as the availability of stronger substances (Most reported substance use among adolescents held steady in 2022, National Institute on Drug Abuse).

“The goal is to impress upon youth that far and away the healthiest choice is not to put these substances in your body, while at the same time acknowledging that some kids are still going to try them,” said Aaron Weiner, PhD, ABPP, a licensed clinical psychologist based in Lake Forest, Illinois, and immediate past-president of APA’s Division 50 (Society of Addiction Psychology). “If that’s the case, we want to help them avoid the worst consequences.”

While that approach, which incorporates principles of harm reduction, is not universally accepted, evidence is growing for its ability to protect youth from accidental overdoses and other consequences of substance use, including addiction, justice involvement, and problems at school. Psychologists have been a key part of the effort to create, test, and administer developmentally appropriate, evidence-based programs that approach prevention in a holistic, nonstigmatizing way.

“Drugs cannot be this taboo thing that young people can’t ask about anymore,” said Nina Christie, PhD, a postdoctoral research fellow in the Center on Alcohol, Substance Use, and Addictions at the University of New Mexico. “That’s just a recipe for young people dying, and we can’t continue to allow that.”

Changes in drug use

In 2022, about 1 in 3 high school seniors, 1 in 5 sophomores, and 1 in 10 eighth graders reported using an illicit substance in the past year, according to the National Institute on Drug Abuse’s (NIDA) annual survey (Monitoring the Future: National Survey Results on Drug Use, 1975–2022: Secondary School Students, NIDA, 2023 [PDF, 7.78MB]). Those numbers were down significantly from prepandemic levels and essentially at their lowest point in decades.

Substance use during adolescence is particularly dangerous because psychoactive substances, including nicotine, cannabis, and alcohol, can interfere with healthy brain development (Winters, K. C., & Arria, A., Prevention Research, Vol. 18, No. 2, 2011). Young people who use substances early and frequently also face a higher risk of developing a substance use disorder in adulthood (McCabe, S. E., et al., JAMA Network Open, Vol. 5, No. 4, 2022). Kids who avoid regular substance use are more likely to succeed in school and to avoid problems with the juvenile justice system (Public policy statement on prevention, American Society of Addiction Medicine, 2023).

“The longer we can get kids to go without using substances regularly, the better their chances of having an optimal life trajectory,” Weiner said.

The drugs young people are using—and the way they’re using them—have also changed, and psychologists say this needs to inform educational efforts around substance use. Alcohol and cocaine are less popular than they were in the 1990s; use of cannabis and hallucinogens, which are now more salient and easier to obtain, were higher than ever among young adults in 2021 (Marijuana and hallucinogen use among young adults reached all-time high in 2021, NIDA).

“Gen Z is drinking less alcohol than previous generations, but they seem to be increasingly interested in psychedelics and cannabis,” Christie said. “Those substances have kind of replaced alcohol as the cool thing to be doing.”

Young people are also seeing and sharing content about substance use on social media, with a rise in posts and influencers promoting vaping on TikTok and other platforms (Vassey, J., et al., Nicotine & Tobacco Research, 2023). Research suggests that adolescents and young adults who see tobacco or nicotine content on social media are more likely to later start using it (Donaldson, S. I., et al., JAMA Pediatrics, Vol. 176, No. 9, 2022).

A more holistic view

Concern for youth well-being is what drove the well-intentioned, but ultimately ineffective, “mad rush for abstinence,” as Robert Schwebel, PhD, calls it. Though that approach has been unsuccessful in many settings, a large number of communities still employ it, said Schwebel, a clinical psychologist who created the Seven Challenges Program for treating substance use in youth.

But increasingly, those working to prevent and treat youth substance use are taking a different approach—one that aligns with principles Schwebel helped popularize through Seven Challenges.

A key tenet of modern prevention and treatment programs is empowering youth to make their own decisions around substance use in a developmentally appropriate way. Adolescents are exploring their identities (including how they personally relate to drugs), learning how to weigh the consequences of their actions, and preparing for adulthood, which involves making choices about their future. The Seven Challenges Program, for example, uses supportive journaling exercises, combined with counseling, to help young people practice informed decision-making around substance use with those processes in mind.

“You can insist until you’re blue in the face, but that’s not going to make people abstinent. They ultimately have to make their own decisions,” Schwebel said.

Today’s prevention efforts also tend to be more holistic than their predecessors, accounting for the ways drug use relates to other addictive behaviors, such as gaming and gambling, or risky choices, such as fighting, drag racing, and having unprotected sex. Risk factors for substance use—which include trauma, adverse childhood experiences, parental history of substance misuse, and personality factors such as impulsivity and sensation seeking—overlap with many of those behaviors, so it often makes sense to address them collectively.

[Related: Psychologists are innovating to tackle substance use]

“We’ve become more sophisticated in understanding the biopsychosocial determinants of alcohol and drug use and moving beyond this idea that it’s a disease and the only solution is medication,” said James Murphy, PhD, a professor of psychology at the University of Memphis who studies addictive behaviors and how to intervene.

Modern prevention programs also acknowledge that young people use substances to serve a purpose—typically either social or emotional in nature—and if adults expect them not to use, they should help teens learn to fulfill those needs in a different way, Weiner said.

“Youth are generally using substances to gain friends, avoid losing them, or to cope with emotional problems that they’re having,” he said. “Effective prevention efforts need to offer healthy alternatives for achieving those goals.”

Just say “know”

At times, the tenets of harm reduction and substance use prevention seem inherently misaligned. Harm reduction, born out of a response to the AIDS crisis, prioritizes bodily autonomy and meeting people where they are without judgment. For some harm reductionists, actively encouraging teens against using drugs could violate the principle of respecting autonomy, Weiner said.

On the other hand, traditional prevention advocates may feel that teaching adolescents how to use fentanyl test strips or encouraging them not to use drugs alone undermines the idea that they can choose not to use substances. But Weiner says both approaches can be part of the solution.

“It doesn’t have to be either prevention or harm reduction, and we lose really important tools when we say it has to be one or the other,” he said.

In adults, harm reduction approaches save lives, prevent disease transmission, and help people connect with substance use treatment (Harm Reduction, NIDA, 2022). Early evidence shows similar interventions can help adolescents improve their knowledge and decision-making around drug use (Fischer, N. R., Substance Abuse Treatment, Prevention, and Policy, Vol. 17, 2022). Teens are enthusiastic about these programs, which experts often call “Just Say Know” to contrast them with the traditional “Just Say No” approach. In one pilot study, 94% of students said a “Just Say Know” program provided helpful information and 92% said it might influence their approach to substance use (Meredith, L. R., et al., The American Journal of Drug and Alcohol Abuse, Vol. 47, No. 1, 2021).

“Obviously, it’s the healthiest thing if we remove substance use from kids’ lives while their brains are developing. At the same time, my preference is that we do something that will have a positive impact on these kids’ health and behaviors,” said Nora Charles, PhD, an associate professor and head of the Youth Substance Use and Risky Behavior Lab at the University of Southern Mississippi. “If the way to do that is to encourage more sensible and careful engagement with illicit substances, that is still better than not addressing the problem.”

One thing not to do is to overly normalize drug use or to imply that it is widespread, Weiner said. Data show that it’s not accurate to say that most teens have used drugs in the past year or that drugs are “just a part of high school life.” In fact, students tend to overestimate how many of their peers use substances (Dumas, T. M., et al., Addictive Behaviors, Vol. 90, 2019Helms, S. W., et al., Developmental Psychology, Vol. 50, No. 12, 2014).

A way to incorporate both harm reduction and traditional prevention is to customize solutions to the needs of various communities. For example, in 2022, five Alabama high school students overdosed on a substance laced with fentanyl, suggesting that harm reduction strategies could save lives in that community. Other schools with less reported substance use might benefit more from a primary prevention-style program.

At Stanford, Halpern-Felsher’s Research and Education to Empower Adolescents and Young Adults to Choose Health (REACH) Lab has developed a series of free, evidence-based programs through community-based participatory research that can help populations with different needs. The REACH Lab offers activity-based prevention, intervention, and cessation programs for elementary, middle, and high school students, including curricula on alcohol, vaping, cannabis, fentanyl, and other drugs (Current Problems in Pediatric and Adolescent Health Care, Vol. 52, No. 6, 2022). They’re also working on custom curricula for high-risk groups, including sexual and gender minorities.

The REACH Lab programs, including the comprehensive Safety First curriculum, incorporate honest discussion about the risks and benefits of using substances. For example: Drugs are one way to cope with stress, but exercise, sleep, and eating well can also help. Because many young people care about the environment, one lesson explores how cannabis and tobacco production causes environmental harm.

The programs also dispel myths about how many adolescents are using substances and help them practice skills, such as how to decline an offer to use drugs in a way that resonates with them. They learn about the developing brain in a positive way—whereas teens were long told they can’t make good decisions, Safety First empowers them to choose to protect their brains and bodies by making healthy choices across the board.

“Teens can make good decisions,” Halpern-Felsher said. “The equation is just different because they care more about certain things—peers, relationships—compared to adults.”

Motivating young people

Because substance use and mental health are so intertwined, some programs can do prevention successfully with very little drug-focused content. In one of the PreVenture Program’s workshops for teens, only half a page in a 35-page workbook explicitly mentions substances.

“That’s what’s fascinating about the evidence base for PreVenture,” said clinical psychologist Patricia Conrod, PhD, a professor of psychiatry at the University of Montreal who developed the program. “You can have quite a dramatic effect on young people’s substance use without even talking about it.”

PreVenture offers a series of 90-minute workshops that apply cognitive behavioral insights upstream (addressing the root causes of a potential issue rather than waiting for symptoms to emerge) to help young people explore their personality traits and develop healthy coping strategies to achieve their long-term goals.

Adolescents high in impulsivity, hopelessness, thrill-seeking, or anxiety sensitivity face higher risks of mental health difficulties and substance use, so the personalized material helps them practice healthy coping based on their personality type. For example, the PreVenture workshop that targets anxiety sensitivity helps young people learn to challenge cognitive distortions that can cause stress, then ties that skill back to their own goals.

The intervention can be customized to the needs of a given community (in one trial, drag racing outstripped substance use as the most problematic thrill-seeking behavior). In several randomized controlled trials of PreVenture, adolescents who completed the program started using substances later than peers who did not receive the intervention and faced fewer alcohol-related harms (Newton, N. C., et al., JAMA Network Open, Vol. 5, No. 11, 2022). The program has also been shown to reduce the likelihood that adolescents will experiment with illicit substances, which relates to the current overdose crisis in North America, Conrod said (Archives of General Psychiatry, Vol. 67, No. 1, 2010).

“People shouldn’t shy away from a targeted approach like this,” Conrod said. “Young people report that having the words and skills to manage their traits is actually helpful, and the research shows that at behavioral level, it really does protect them.”

As young people leave secondary school and enter college or adult life, about 30% will binge drink, 8% will engage in heavy alcohol use, and 20% will use illicit drugs (Alcohol and Young Adults Ages 18 to 24, National Institute on Alcohol Abuse and Alcoholism, 2023SAMHSA announces national survey on drug use and health (NSDUH) results detailing mental illness and substance use levels in 2021). But young people are very unlikely to seek help, even if those activities cause them distress, Murphy said. For that reason, brief interventions that leverage motivational interviewing and can be delivered in a school, work, or medical setting can make a big difference.

In an intervention Murphy and his colleagues are testing, young adults complete a questionnaire about how often they drink or use drugs, how much money they spend on substances, and negative things that have happened as a result of those choices (getting into an argument or having a hangover, for example).

In an hour-long counseling session, they then have a nonjudgmental conversation about their substance use, where the counselor gently amplifies any statements the young person makes about negative outcomes or a desire to change their behavior. Participants also see charts that quantify how much money and time they spend on substances, including recovering from being intoxicated, and how that stacks up against other things they value, such as exercise, family time, and hobbies.

“For many young people, when they look at what they allocate to drinking and drug use, relative to these other things that they view as much more important, it’s often very motivating,” Murphy said.

A meta-analysis of brief alcohol interventions shows that they can reduce the average amount participants drink for at least 6 months (Mun, E.Y., et al., Prevention Science, Vol. 24, No. 8, 2023). Even a small reduction in alcohol use can be life-altering, Murphy said. The fourth or fifth drink on a night out, for example, could be the one that leads to negative consequences—so reducing intake to just three drinks may make a big difference for young people.

Conrod and her colleagues have also adapted the PreVenture Program for university students; they are currently testing its efficacy in a randomized trial across multiple institutions.

Christie is also focused on the young adult population. As a policy intern with Students for Sensible Drug Policy, she created a handbook of evidence-based policies that college campuses can use to reduce harm among students but still remain compliant with federal law. For example, the Drug Free Schools and Communities Act mandates that higher education institutions formally state that illegal drug use is not allowed on campus but does not bar universities from taking an educational or harm reduction-based approach if students violate that policy.

“One low-hanging fruit is for universities to implement a Good Samaritan policy, where students can call for help during a medical emergency and won’t get in trouble, even if illegal substance use is underway,” she said.

Ultimately, taking a step back to keep the larger goals in focus—as well as staying dedicated to prevention and intervention approaches backed by science—is what will help keep young people healthy and safe, Weiner said.

“What everyone can agree on is that we want kids to have the best life they can,” he said. “If we can start there, what tools do we have available to help?”

 

The use of psychoactive substances among children and young people is one of today’s challenges. In order to solve this problem by acting in a coordinated manner, this academic year Vilnius city municipality, in cooperation with the Ministry of the Interior of the Republic of Lithuania, implemented a pilot model for the prevention of drug use and distribution by minors in schools. The project was implemented in three schools of the capital – Antakalnis, Vasilijaus Kačialovos and Vilnius Jesuit high schools.

“Initiating this project, we aimed to increase the safety of students in educational institutions and their entrances, to include in the project all persons participating in the student’s life and, most importantly, to respond to the needs of minors. The problem of psychoactive substance use among young people is not only in Vilnius, so we paid a lot of attention to the sharing of good practices between municipalities,” said Agneta Ladek, Deputy Minister of the Ministry of the Interior of the Republic of Lithuania.

In implementing the project, the Vilnius City Municipality relied on the international primary prevention model Planet Youth, based on scientific and practical evidence, which was implemented in the capital in 2020. One of the key aspects of the model is a community-based approach that fosters positive relationships between children and their families, peers, educators and other adults.

“Building a strong community—of children, parents, or teachers—is the healthiest and wisest way to promote children’s well-being and help them grow into mature individuals who make healthy choices.” It has been scientifically proven that children and teenagers who are surrounded by a positive environment, who have good relations with teachers and parents, use or consider using legal and illegal psychoactive substances much less often,” said Simona Bieliūnė, the vice-mayor of the city of Vilnius.

It is planned that the activities tested during the project will continue to be implemented in other schools of the capital. This will contribute to the consistent implementation of prevention of the use and distribution of psychoactive substances and will help to form healthy lifestyle habits.

Implementation of projects to strengthen school communities

The pilot model project was implemented in three schools of the capital – Antakalnis, Vasilijaus Kačialovos and Vilnius Jesuit high schools. Realizing the extent of the problem of the use and distribution of psychoactive substances among schoolchildren, the heads of educational institutions do not shy away from talking about it publicly and looking for solutions.

“Every year, students from about 30 different educational institutions come to the first classes of the high school, so it is natural that attitudes and attitudes differ. With the start of the new academic year, we face great challenges in order to familiarize students and their parents with the rules in force at our school, and their observance,” said Anželika Keršinskienė, director of Vilnius Antakalnis Gymnasium.

When planning the preventive measures for the implementation of the project, we were guided by the data of each school’s “Planet Youth” study on the extent of psychoactive substance use, children’s psychological resilience, trends in relations with parents, peers, teachers and other factors related to the use of psychoactive substances – common goals are achieved by adapting to unique school situations. After the initiation of the project, data-based individual prevention plans were created and the conditions for their implementation were created, as well as preventive activity planning, financing and implementation practices suitable for the entire municipality were tested.

All the schools that participated in the project note that the project allowed the school communities – administration, teachers, students and their parents – to focus, helped to become more active and strengthen mutual relations.

“During the project, the funds allocated by the municipality allowed our school to expand and renovate the student’s leisure spaces, install smoke detectors, partially covered the costs of fencing the school’s territory. We are happy that the students willingly got involved in the activities, initiated and created social advertisements themselves, but our most important achievement is that our school community started to speak “one language”, said Roza Dimentova, director of Vilnius V. Kačialovos Gymnasium.

“As part of the project, we established 6 student clubs according to their interests on the initiative of the students. Parents and teachers were involved in the activities. Such clubs, such as astronomy, politics or games, bring all participants together and encourage increased student engagement in extracurricular activities. We plan to continue these activities and expand them next year as well,” said Vilnius Jesuit High School director S. Edita Šicaite.

In the pilot model discussion – insights from the professionals

During the implementation of the pilot model for the prevention of underage drug use and distribution in schools, the Vilnius Public Health Office, police representatives, as well as experts from the Icelandic “Planet Youth” model joined the project activities together with the Vilnius City Municipality.

In the discussion of the pilot model, representatives of the municipality for the first time presented footage of the network of free services for the use of psychoactive substances in the city of Vilnius, which will be distributed to doctors and teachers. An informational publication has been created so far, which can be accessed at the address paslaugosjaunimui.lt.

The coordinator of the Vilnius Public Health Office presented the project activities implemented in pilot schools and the importance of student research results in planning targeted prevention measures at different levels of the community.

In the discussion of the pilot model, a tool for assessing the security of school infrastructure was also presented, as well as additional measures for the prevention of the use and distribution of psychoactive substances.

Source: https://madeinvilnius.lt/en/news/city/pilot-model-of-prevention-of-drug-use-and-distribution-by-minors-in-schools-was-implemented-in-Vilnius

The following Complaint was sent to BBC by David Raynes of the NDPA – the response is shown underneath the Complaint summary herein.

David judges the BBC response to be “very defensive, but a partial win” for NDPA.

************

BBC Radio programme – ‘PM’, Radio 4, 27 October 2022

Complaint

This edition of PM included a sequence prompted by Germany’s plan to legalise
recreational cannabis. A listener complained about the absence of an alternative view and a
lack of impartiality on the part of the presenter . The ECU considered whether the
programme met BBC standards for due impartiality.

Outcome

The presenter, Evan Davis, explained that other countries (including Canada) had already
taken this step, as well as many states in the USA. He introduced a report from New York
by a correspondent describing “how life has changed there” and then interviewed Professor
Akwasi Owusu-Bempah of Toronto University, described as an expert in drugs policy. In his
final question Mr Davis asked him “in three words” whether other countries should follow
Canada’s example: “Are you basically thinking it’s worked?”. Professor Owusu-Bempah
replied “Do it now, those are my three words” prompting laughter from Mr Davis.
In the ECU’s view the decriminalisation and/or legalisation of cannabis possession is a
controversial subject in the UK, even if the controversy is not “active” in the sense of there
being legislation before Parliament or immediate prospect of it. However, the question of
the social effects of legislation is not, on its own terms, a matter of controversy, and is open
to empirical exploration. It was therefore legitimate for the programme to question an
expert on those aspects, and there was no need for an alternative viewpoint in that
connection.
Taken as a whole the sequence highlighted negative as well as positive social consequences
of changing the law. The presenter’s laughter should be seen in the context of the succinct
nature of the response rather than any expression of a personal view. But in posing his final
question, he invited an opinion on a matter of controversy. Professor Owusu-Bempah
having expressed unqualified support for immediate legalisation, in the ECU’s view there
was a need to remind listeners of the existence of opposing opinions

BBC conclusion: 
Part Upheld

*******

British Broadcasting Corporation British Broadcasting Corporation BBC Wogan House, Level 1, 99 Great Portland
Street, London W1A 1AA
Telephone: 020 8743 8000 Email: ecu@bbc.co.uk

BBC

Executive Complaints Unit
David Raynes
pheon@cix.co.uk

Ref: CAS-7325932
2 March 2023

Dear Mr Raynes
PM, Radio 4, 27 October 2022
Thank you for your email to the Executive Complaints Unit about an item in this
edition of PM on a plan to legalise recreational cannabis use in Germany. The
presenter, Evan Davis, explained that other countries (including Canada) had already
taken this step, as well as many states in the USA. He introduced a report from New
York by a correspondent describing “how life has changed there”. She detailed the
proliferation of cannabis sellers in the city and the greater evidence of its use. He then
interviewed Professor Akwasi Owusu-Bempah of Toronto University, described as an
expert in drugs policy. He was asked how the law applied in Canada, the effect on
consumption, the relationship between the illegal trade and overall crime, and the
relation between the police and “certain groups” in the light of a “huge” drop in arrests
and convictions for the possession of cannabis. The professor observed that, in line
with the aims of the legislators, legal sales in cannabis had overtaken illegal sales. Mr
Davis then asked him “in three words” whether other countries should follow Canada’s
example: “Are you basically thinking it’s worked?”. Professor Owusu-Bempah replied
“Do it now, those are my three words”, prompting laughter from Mr Davis.
You complained about the absence of an alternative view in the item, drew attention
to reported ill effects on mental health from cannabis consumption and pointed to the
possible risks to younger listeners who might have heard the question of legalisation
discussed in these terms. You also objected to Mr Davis’ laughter.
The BBC’s Editorial Guidelines on impartiality say:
When dealing with ‘controversial subjects’, we must ensure a wide range of
significant views and perspectives are given due weight and prominence,
particularly when the controversy is active.
I would regard the decriminalisation and/or legalisation of cannabis possession as
being a controversial subject in this country, even if the controversy is not “active” in
the sense of there being legislation before Parliament or any immediate prospect of it.

However, the question of the social effects of legislation is not, on its own terms, a
matter of controversy, and is open to empirical exploration. I think it was therefore
legitimate for Mr Davis to question Professor Owusu-Bempah on those aspects, and
that there was no need for an alternative viewpoint in that connection. Taken as a
whole the piece highlighted negative as well as positive social consequences of
changing the law and seen through that prism was therefore more nuanced than you
suggest. But by posing his final question, as to whether other countries, including the
UK, should follow Canada’s example, Mr Davis invited an opinion on a matter of
controversy. Professor Owusu-Bempah having expressed unqualified support for
immediate legalisation, I think there was a need at least to remind listeners of the
existence of opposing opinions, preferably with some reference to the arguments here
in this country. In the absence of that or the inclusion of an alternative view elsewhere
in the item, I agree there was a breach of the BBC’s standards of impartiality and I am
upholding this element of your complaint.
On your point about the possible risk to children, the PM programme is aimed at an
adult audience – its average age is 60 – and accordingly I do not believe its output
should be judged on the basis of its potential effect on children. As for Mr Davis’
laughter at the end of the interview, I can see how it might have struck you as “humour
from a top and admired presenter about the concept of harmful cannabis legalisation in
the UK”. To my ear, though, it sounded like amused surprise at the fact that Professor
Owusu-Bempah, having been told “we’re entirely out of time”, had so precisely met his
request to state his opinion “in three words”. I am therefore not upholding these
aspects of your complaint.
Thank you for bringing this to the attention of the ECU. Please accept my apology for
this breach of standards. I attach a summary of the finding intended for publication on
the complaints pages of bbc.co.uk, at https://www.bbc.co.uk/contact/recent-ecu. It
will appear there later today. Meanwhile, as this letter represents the BBC’s final view
on your complaint, it is now open to you to take it to the broadcasting regulator,
Ofcom, if you are dissatisfied. You can find details of how to contact Ofcom and the
procedures it will apply at https://www.ofcom.org.uk/tv-radio-and-on-demand/howto-report-a-complaint. Alternatively, you can write to Ofcom, Riverside House, 2a
Southwark Bridge Road, London SE1 9HA, or telephone either 0300 123 3333 or 020
7981 3040. Ofcom acknowledges all complaints received.
Yours sincerely
Fraser Steel
Head of the Executive Complaints Unit

Source: David Raynes, NDPA.

In its 2023 Annual Report, the International Narcotics Control Board:

– finds that online drug trafficking has increased the availability of drugs on the illicit market;

– warns that patient safety is at risk from illicit Internet pharmacies selling drugs without a prescription directly to the consumer;

– highlights the daunting task facing law enforcement authorities to monitor and prosecute online drug activities;

– sees opportunities to use the Internet and social media for drug use prevention campaigns and to improve access to drug treatment services;

– encourages governments to use the full range of INCB tools and programmes to assist in their efforts to counter exploitation of the Internet for drug trafficking; and

– voices concern about the persistent regional disparities in availability and consumption of licit drugs for the treatment of pain.

VIENNA, 5 March (UN Information Service) – The evolving landscape of online drug trafficking is presenting new challenges to drug control, says the International Narcotics Control Board (INCB) in its Annual Report. There are also opportunities to use the Internet for drug use prevention and treatment to safeguard people’s health and welfare, the Board says.

The increased availability of illicit drugs on the Internet, the exploitation by criminal groups of online platforms including social media, and the increased risk of overdose deaths due to the online presence of fentanyl and other synthetic opioids are some of the key challenges for drug control in the Internet era.

“We can see that drug trafficking is not just carried out on the dark web. Legitimate e-commerce platforms are being exploited by criminals too. We encourage governments to work with the private sector and INCB projects to prevent and detect trafficking of drugs and other dangerous substances online,” said Jallal Toufiq, the President of INCB.

Using social media and other online platforms means drug traffickers can advertise their products to large global audiences. Various conventional social media platforms are being used as local marketplaces and inappropriate content is widely accessible to children and adolescents.

Encryption methods, anonymous browsing on the darknet and cryptocurrencies are commonly used to avoid detection, posing difficulties for prosecuting online trafficking offences. Offenders can move their activities to territories with less intensive law enforcement action or lighter sanctions or base themselves in countries where they can evade extradition. The sheer scale of online activity is an added complication. In one case in France, law enforcement authorities collected more than 120 million text messages from 60,000 mobile phones.

Patient safety is at risk from illicit Internet pharmacies which sell drugs without a prescription directly to consumers. It is impossible for consumers to know whether the drugs are counterfeit, unapproved or even illegal. The global trade in illicit pharmaceuticals is estimated to be worth 4.4 billion USD.

Opportunities for drug treatment and prevention

The Board sees opportunities to use online platforms to prevent non-medical use of drugs, raise awareness about the harms of drug use and support public health campaigns. Governments can use social media platforms to conduct drug use prevention campaigns to prevent substance misuse among young people in particular.

“There are opportunities to use social media and the Internet to prevent drug use, raise awareness of its harms and improve access to drug treatment services,” said INCB President Toufiq, “At the same time we are concerned about the increasing use of social media to market drugs including to children and the ways that criminals are exploiting online platforms for illicit activities.”

Telemedicine and Internet pharmacies could improve access to healthcare and help reach patients with drug use disorders and deliver drug treatment services to more people. Online platforms could also be used for sharing information about adverse consequences of drug use and communicating warnings of adulterated drugs which could save lives.

International cooperation essential to tackle this growing trend

The global nature of online platforms makes collaborative efforts vitally important for identifying new threats and developing effective responses.

INCB is encouraging voluntary cooperation between governments and online industries to tackle the misuse of legitimate e-commerce platforms for drug trafficking. Its initiatives such as the GRIDS programme have led to drug seizures and arrests as well as criminal networks being dismantled.

The manufacturing, marketing, movement and monetization industries are particularly vulnerable to being exploited by those trafficking in dangerous substances. The Board says that increased cooperation is needed between governments, international organizations, regulatory authorities and the private sector to meet these evolving challenges.

Persistent disparities in access to medicines for the treatment of pain

In many parts of the world there is not enough affordable morphine available to meet medical needs. These persistent regional disparities in opioid analgesics used for pain treatment are not due to a shortage of opiate raw materials but rather in part due to inaccurate estimates of the actual medical needs of their populations. Levels of consumption of pain relief medicine remain highest in Europe and North America.

There was an acute need for medicines containing internationally controlled substances in 2023 for people caught up in natural disasters and emergencies related to climate change and conflict. INCB urges governments to use simplified control procedures in such situations to ensure unimpeded availability of these medicines.

Notable developments in illicit drug supply

In Afghanistan, illicit opium poppy cultivation and heroin production declined dramatically. INCB says that alternative livelihoods need to be offered to affected farmers who may not have other sources of income.

The opioid crisis continues to have serious consequences in North America with the number of deaths that involved synthetic opioids other than methadone continuing to increase, reaching more than 70,000 in 2021.

Drug trafficking organizations continue to expand their operations in the Amazon Basin into illegal mining, illegal logging and wildlife trafficking.

Record levels of illicit coca bush cultivation were recorded in Colombia and Peru, rising by 13 percent and 18 per cent respectively. Seizures of cocaine reached a record level in 2021 in West and Central Africa, a significant transit region for cocaine.

Several European countries have continued to establish regulated markets for cannabis for non-medical purposes. These programmes do not appear to be consistent with the drug control conventions.

South Asia appears to be increasingly being targeted for the trafficking of methamphetamine illicitly manufactured in Afghanistan to Europe and Oceania.

Pacific island States have transformed from solely transit sites along drug trafficking routes to destination markets for synthetic drugs. This is posing significant challenges to communities and their public health systems.

Precursors report

As part of international efforts to prevent illicit drug manufacturers from replacing certain controlled chemicals with closely related substitutes, the Board is recommending that a total of 16 amphetamine-type stimulant precursors (two series of closely related chemicals) are put under international control.

Two fentanyl precursors have also been assessed and recommended for international control by INCB, following a request made by the United States. The Precursors report also shows a surge in non-controlled fentanyl precursors in North America in 2023.

The Commission on Narcotic Drugs will vote at its session in March on placing all 18 substances under international control, through placement in Table I of the 1988 Convention.

INCB is concerned about the lack of audits and inspections in certain free trade zones which are susceptible to misuse for illicit activities. The Board calls on governments to ensure proper oversight over these zones to prevent them being exploited for precursor trafficking.

***

INCB is the independent, quasi-judicial body charged with promoting and monitoring Government compliance with the three international drug control conventions: the 1961 Single Convention on Narcotic Drugs, the 1971 Convention on Psychotropic Substances, and the 1988 Convention against Illicit Traffic in Narcotic Drugs and Psychotropic Substances. Established by the Single Convention on Narcotic Drugs of 1961, the thirteen members of the Board are elected in a personal capacity by the Economic and Social Council for terms of five years. 

 

Source: https://unis.unvienna.org/unis/en/pressrels/2024/unisnar1481.html

ABSTRACT

Parental cannabis use has been associated with adverse neurodevelopmental outcomes in offspring, but how such phenotypes are transmitted is largely unknown. Using reduced representation bisulphite sequencing (RRBS), we recently demonstrated that cannabis use is associated with widespread DNA methylation changes in human and rat sperm. Discs-Large Associated Protein 2 (DLGAP2), involved in synapse organization, neuronal signaling, and strongly implicated in autism, exhibited significant hypomethylation (p < 0.05) at 17 CpG sites in human sperm. We successfully validated the differential methylation present in DLGAP2 for nine CpG sites located in intron seven (p < 0.05) using quantitative bisulphite pyrosequencing. Intron 7 DNA methylation and DLGAP2 expression in human conceptal brain tissue were inversely correlated (p < 0.01). Adult male rats exposed to delta-9-tetrahydrocannabinol (THC) showed differential DNA methylation at Dlgap2 in sperm (p < 0.03), as did the nucleus accumbens of rats whose fathers were exposed to THC prior to conception (p < 0.05). Altogether, these results warrant further investigation into the effects of preconception cannabis use in males and the potential effects on subsequent generations.

KEYWORDS: Cannabis, sperm, DNA methylation, autism, heritability

Introduction

Cannabis sativa is the most commonly used illicit psychoactive drug in the United States (U.S.) and Europe [1]. In the U.S., 11 states and Washington D.C. have legalized the recreational use of cannabis and 33 states have legalized the use of medicinal cannabis [2,3]. Since 1995, cannabis potency (defined as the concentration of the psychoactive cannabis component delta-9-tetrahydrocannabinol, or THC, in the sample [4]) has consistently risen from ~4% to as high as 32% in some states [2,5,6]. Changes in cannabis potency have been accompanied by changes in attitudes about cannabis and patterns of cannabis use. Between 2002 and 2014, the percentage of adults in the U.S. who perceived cannabis use as risky declined from 50% to 33% [6]. During this same period, the percentage of U.S. adults who believed cannabis to have no risk rose from 6% to 15% [6]. According to a 2015 Survey on Drug Use and Health, 52.5% of men in the U.S. of reproductive age (≥18) have reported cannabis use at some point in their lives, making cannabis exposure especially relevant for potential future fathers [711].

Given the increased prevalence of cannabis use in the U.S., studies are beginning to focus on the effects of use on the health and development of offspring. Prenatal cannabis exposure via maternal use during pregnancy is associated with decreased infant birth weight, an increased likelihood to require the neonatal intensive care unit, and the potential for an impaired fetal immune system compared to those infants who are not exposed during gestation [1,12]. In rodent studies, rat pups born to parents who were both exposed to THC during adolescence had increased heroin-seeking behaviour later in life, a phenotype that was accompanied by epigenetic changes in the nucleus accumbens [1315]. These studies and others have begun to highlight the potential for intergenerational consequences of cannabis exposure [16]. Identifying the mechanism that underlies these changes is critical as cannabis use continues to increase across the U.S.

The environment impacts the integrity and maintenance of the epigenome such that it is now viewed as a molecular archive of past exposures [17]. While the majority of environmental epigenetic studies are focused on the impact of the inutero environment on the epigenome and health of the child, it has become apparent that the exposure history of the father must also be considered – specifically the impact of his exposures on the sperm epigenome. Studies have shown that exposure to phthalates, pesticides, nutritional deficiencies, and obesity can all induce potentially heritable changes in the sperm epigenome [1824]. It is likely that other common and emerging exposures, including cannabis, may also contribute to disruption of sperm DNA methylation in a similar fashion, and that such changes could be transmitted to the subsequent generation.

Using reduced representation bisulphite sequencing (RRBS) our group recently demonstrated that cannabis use in humans, and THC exposure in rats, is associated with decreased sperm concentrations and widespread changes in sperm DNA methylation [25]. Of the regions identified in humans, Discs-Large Associated Protein 2 (DLGAP2) exhibited significant hypomethylation in the sperm of cannabis-exposed men compared to controls (p < 0.05). DLGAP2, a membrane-associated protein located in the post-synaptic density of neurons, plays a key role in synapse organization and neuronal signaling [26]. Dysregulation of DLGAP2 is associated with various neurological and psychiatric disorders, such as autism spectrum disorder (ASD) and schizophrenia [2629]. In our prior screen, we identified 17 differentially methylated CpG sites within DLGAP2 in the sperm of cannabis-exposed men compared to controls. DLGAP2 was just one of 46 genes with greater than 10 CpG sites showing significantly altered DNA methylation in the sperm of cannabis users compared to controls, out of the 2,077 genes we identified as having altered DNA methylation. The first objective of this study was to validate our preliminary RRBS findings for DLGAP2 using quantitative bisulphite pyrosequencing. Our second objective was to determine the functional association between DNA methylation and gene expression of DLGAP2 to better understand how cannabis use might affect this relationship. To determine the possible intergenerational effects of paternal cannabis use, our third objective was to determine if Dlgap2 was differentially methylated in the sperm of rats exposed to THC versus controls, and if so, whether or not these changes were intergenerationally heritable.

Results

DLGAP2 is hypomethylated in sperm from cannabis users versus controls by Reduced Representation Bisulphite Sequencing (RRBS)

Our prior study [25] revealed 17 differentially methylated sites by RRBS in the sperm of cannabis users compared to controls for the DLGAP2 gene. Table S1 lists all 17 of these sites and their genomic coordinates. Figure 1a graphically demonstrates the significant hypomethylation of nine of these sites that are clustered together in the seventh intron of this gene. DLGAP2 is schematically shown in Figure 1b, including the exon-intron structure, position of CpG islands, transcription start site and the region of interest in intron 7 within the context of the gene body, with an inset showing the nucleotide sequence analysed in this study.

Validation of DLGAP2 RRBS methylation data

To confirm the methylation differences that were initially detected using RRBS, we designed a bisulphite pyrosequencing assay for the DLGAP2 intron 7 region (see Figure 1b) which captures 10 CpG sites, nine of which were identified as significantly differentially methylated using RRBS. We first validated pyrosequencing assay performance using defined mixtures of fully methylated and unmethylated human genomic DNAs. The measured levels of methylation by pyrosequencing showed good agreement between the amount of input methylation levels and the amount of methylation detected (r2 = 0.99 and p = 0.0003) (Figure 1c). These results confirmed the linearity of the assay in the ability to detect increasing amounts of DNA methylation at this region across the full range of possible methylation values, and indicate that the assay is suitable for use with biological specimens.

The DLGAP2 intron 7 region is not an imprinting control region (ICR)

DLGAP2 is paternally expressed in the testis, biallelically expressed in the brain, and has low expression elsewhere in the body [30]. Since DLGAP2 is known to be genomically imprinted in testis [30], and since the imprint control region for this gene has not yet been defined, we sought to determine if the region of interest in intron 7 is part of the DLGAP2 imprint control region (ICR). The methylation at ICRs is established during epigenome reprogramming in the primordial germ cells in embryonic development. Male and female gametes exhibit divergent methylation at ICRs, and this methylation profile is maintained through subsequent post-fertilization epigenetic reprogramming and in somatic cells throughout the life course. Therefore, we expected that if the DLGAP2 intron 7 region is an ICR, the diploid testis tissues from human conceptuses would exhibit approximately 50% methylation due to the complete methylation of one allele at this region and the complete lack of methylation at the other allele. Human conceptal testes tissues (n = 3) showed an average of 72.5% methylation at the DLGAP2 intron 7 region (Figure 1d). This finding, of higher than anticipated and variable levels of methylation, is inconsistent with ICR status.

Bisulphite pyrosequencing validates the RRBS methylation data in human sperm

We next performed quantitative bisulphite pyrosequencing on the same sperm DNA samples from cannabis users and controls as those used to generate the RRBS data to confirm the loss of methylation present at the intron 7 region of DLGAP2. All nine CpG sites that were hypomethylated in the cannabis users by RRBS were also found to be hypomethylated by bisulphite pyrosequencing, as well as an additional CpG site that was captured in the assay design (p < 0.05 for all 10 sites) (Figure 2). Following Bonferroni correction of the p value to adjust for multiple comparisons (p < 0.005), CpG sites 1,2,3,5,7,8,9, and 10 remained significant. From this pyrosequencing assay we observed methylation differences of 7–15% between the sperm of the cannabis users (n = 8) compared to controls (n = 7). Correlation of the RRBS and pyrosequencing data for each individual CpG site showed significant agreement at all sites analysed (p < 0.02 for all sites; Figure S1). All CpG sites showed a significant loss of methylation in accordance with the direction of change observed by RRBS for these same CpG sites.

Methylation of DLGAP2 intron 7 is inversely correlated with DLGAP2 expression

Given that we observed significant loss of intron 7 DLGAP2 DNA methylation in sperm of cannabis users relative to non-users, we next examined the relationship between DNA methylation and gene expression in the brain, where this gene’s function is critical. We used 28 conceptal brain tissues to examine the relationship between DNA methylation and mRNA expression. Expression levels were normalized to the lowest expressing sample, and the relationship between DNA methylation and mRNA expression was calculated with a Pearson correlation. We found that as methylation increased in this region, mRNA expression decreased significantly (p < 0.05) (Figure 3a). Knowing that there are sex differences in autism spectrum disorder (ASD), and that dysregulation of DLGAP2 is associated with ASD [26], we sought to determine if there were any sex differences in the methylation-expression relationship in these tissues. To investigate this, we ran the correlation for males (n = 15) and females (n = 13) independently. The inverse relationship between methylation and expression was evident for both males and females, but this relationship was significant only in females (p = 0.006) (Figure 3b, c).

Intergenerational inheritance of altered Dlgap2 DNA methylation

We next sought to investigate Dlgap2 using data obtained from our prior study [25] to determine if there was any differential methylation of Dlgap2 in THC versus control rats that was not initially identified using the imposed thresholds of that study. We were particularly interested in the potential for intergenerational transmission and to determine if route of THC exposure affected DNA methylation at this gene. The pilot study rats [25] were given THC via oral gavage (to mimic oral ingestion of drug) while subsequent studies dosed rats via intraperitoneal injection (to mimic inhalation of drug). From the rats administered THC via oral gavage versus controls, we identified a region of Dlgap2 that showed differential methylation by the RRBS analysis that contains eight CpG sites. This region is in the first intron of Dlgap2, in a CpG island that spans the first exon of this gene as well (schematic of the gene structure and sequence of this region shown in Figure 4a). We validated the rat Dlgap2 pyrosequencing assay using commercially available rat DNA of defined methylation status. The results showed good agreement between the input methylation and the amount of methylation detected by pyrosequencing (r2 = 0.92, p = 0.01) (Figure 4b).

We were able to demonstrate intergenerational inheritance of an altered DNA methylation pattern in Dlgap2. Comparing the average methylation for exposed and unexposed sperm for each CpG site revealed that sites 2,3,4 and 6 of the eight CpG sites analysed were significantly hypomethylated in the sperm of rats exposed via injection to 4mg/kg THC compared to controls (p = 0.03 to p = 0.005) (Figure 4c). CpG site 6 remained significant after Bonferroni correction (p < 0.006). The same region of Dlgap2 was then analysed in the hippocampus and nucleus accumbens of rats whose fathers were exposed to control or 4mg/kg THC. While CpG site 7 was significantly hypomethylated (p < 0.05) in the hippocampus of the offspring (Figure 5a), this site was not identified as differentially methylated in the sperm of THC exposed rats, and therefore we could not conclude that this change was transmitted as the result of changes present in the exposed sperm. In the nucleus accumbens, however, significant hypomethylation (p = 0.02) at CpG site 2 was detected in the offspring (Figure 5b), one of the same sites identified in the sperm of THC exposed rats. We also found that there was an inverse relationship between DNA methylation and expression of Dlgap2 in the nucleus accumbens, though not statistically significant likely due to the small sample size available in this study (n = 6 exposed, n = 8 unexposed; Figure S2).

Discussion

In this study, we examined the effects of regular male cannabis use on human sperm DNA methylation, at DLGAP2. Our RRBS study initially identified 17 CpG sites in DLGAP2 that were differentially methylated in the sperm of cannabis users compared to controls. Of the sites that were initially identified, nine of them all reside together in the seventh intron of this gene, though not in a defined CpG island. To first confirm the RRBS data, we performed quantitative bisulphite pyrosequencing for the nine clustered CpG sites. We were able to capture an additional CpG site with careful assay design for a total of ten CpG sites analysed via bisulphite pyrosequencing. We successfully validated the RRBS findings, confirming that there was significant hypomethylation among these ten sites with cannabis use. We confirmed a significant inverse correlation between methylation and expression at this region in human conceptal brain tissues.

To begin to determine whether or not the effects of cannabis on sperm are heritable, we analysed sperm from THC exposed and control male rats, as well as the hippocampus and nucleus accumbens from offspring of THC exposed and control males for changes in DNA methylation at Dlgap2. Rats exposed to THC were given a dose (4mg/kg THC for 28 days) that is pharmacodynamically equivalent to daily cannabis use to resemble frequent use in humans. We identified significant hypomethylation at Dlgap2 in the sperm of exposed rats as compared to controls. This hypomethylated state was also detected in the nucleus accumbens of rats born to THC exposed fathers compared to controls, supporting the potential for intergenerational inheritance of an altered sperm DNA methylation pattern. While the changes in the degree of methylation are small in the rats (0.5–0.7%), we previously reported that fractional changes in methylation can significantly influence the degree to which the gene’s expression is altered [31].

DLGAP2 is a member of the DLGAP family of scaffolding proteins located in the post-synaptic density (PSD) of neurons. The PSD is a protein-dense web that lies under the postsynaptic membrane of neurons and facilitates excitatory glutamatergic signaling in the central nervous system [26,32]. DLGAP2 functions to transmit neuronal signals across synaptic junctions and helps control downstream signaling events [26,32]. Due to its important role in PSD signaling, even small changes in the expression of DLGAP2 can have severe consequences [26,32]. Of particular relevance, DLGAP2 has been linked to schizophrenia and importantly, has been identified as an autism candidate gene [27,28,33,34]. Differential methylation of DLGAP2 is reported in the brain of individuals with autism, and has been linked to post-traumatic stress disorder in rats [27,35]. Knockout of Dlgap2 in mice results in abnormal social behaviour, increased aggressive behaviour, and learning deficits [36].

Studies are increasingly showing associations between cannabis use and various neuropsychiatric and behavioural disorders including anxiety, depression, cognitive deficits, autism, psychosis, and addiction [2,6,7,9,14,3739]. Research looking into the effects of THC exposure found that rat pups born to parents who were exposed to THC during adolescence showed increased effort to self-administer heroin compared to those born to unexposed parents [13]. This increase in addictive behaviour was driven by THC-induced changes in DNA methylation, occurring in the striatum, including the nucleus accumbens [14,15]. One of the genes whose methylation was altered by parental THC exposure was Dlgap2 [15]. Recently, a group from Australia analysed datasets from two independent cohorts to examine the relationship between cannabis legalization in the U.S. and ASD incidence. They determined there was a strikingly significant positive association between cannabis legalization and increased ASD incidence. Further, the study authors predicted that there will be a 60% increase in excess ASD cases in states with legal cannabis by 2030, and deemed ASD the most common form of cannabis-associated clinical teratology [40].

It is estimated that the ratio of boys with ASD to girls with ASD is 4:1 which led us to stratify our analysis looking at the relationship between DNA methylation and gene expression by sex [41,42]. The results of our methylation-expression analyses demonstrated a significant association in females but not males. While we don’t know the ASD status of these samples, there are several reasons why this may be the case. First, there are certain genes that confer a stronger ASD phenotype in girls compared to boys [41,42]. Thus, while we see the trend in both sexes, it is possible that dysregulation of this gene may manifest phenotypically more in girls. Alternatively, it may be that the regulatory relationship between methylation and expression is retained in females while altered methylation further exacerbates an already fragile relationship in males. Overall, this data confirms that the region of DNA methylation within DLGAP2 that was differentially methylated in the sperm of cannabis users compared to controls is functionally important in the brain.

DLGAP2 is an imprinted gene that exhibits paternal expression in the testis, biallelic expression in the brain, and low expression elsewhere in the body [30]. Because the methylation established at imprinted genes resists post-fertilization epigenetic reprogramming [4345], this supports the possibility that changes in methylation at DLGAP2 in sperm could be transmitted to the next generation. However, given that the region in intron 7 is not an ICR, it is unlikely that this would be a potential mechanism for intergenerational inheritance of an altered methylation pattern at this region. However, it has recently been discovered that a subset of genes termed ‘escapees’ are able to escape primordial germ cell (PGC) and post-fertilization reprogramming events [46,47], providing a mechanism for epigenetic changes incurred by sperm to be passed on to the subsequent generation.

Processes in the PSD are sensitive to endocannabinoids [26,4851], which suggests that these processes are potentially sensitive to exogenous cannabinoids, such as THC and cannabis. This is especially important as cannabis legalization and use are increasing dramatically across the U.S. It is estimated that 22% of American adults currently use cannabis, of which 63% are regular users (≥1–2 times per month) [710]. Among regular users 55% are males and over half of all men over 18 have reported cannabis use in their lifetime [710]. Importantly, this age range includes individuals of reproductive age. Since almost half of all pregnancies in the U.S. are unplanned, there is concern that many pregnancies may occur during a time when one, or both, parents are using or are exposed to cannabis [52].

Our results provide novel findings about the effects of paternal cannabis use on the methylation status of an ASD candidate gene, a disorder whose rates continue to climb, but whose precise aetiologies remain unknown. Studies are beginning to show that there is a potential for paternal intergenerational inheritance. In particular, epigenetic changes in umbilical cord blood of babies born to obese fathers were also found in the sperm of obese men. This study is the first to demonstrate that there are changes present in the sperm epigenome of cannabis users at a gene involved in ASD.

The results of this study have several limitations. The sample size was small, which might limit generalization of the study findings. However, even though our sample size was small, we were able to identify common pathways that were differentially methylated in both human and rat sperm, highlighting the potential specificity of these effects [25]. We did not account for a wide variety of potential confounders such as various lifestyle habits, sleep, diet/nutrition, exercise, etc, given that their influence on the sperm DNA methylome is largely unknown. Larger studies are required to confirm these findings. In the conceptal tissues we were only able to analyse whole brain, rather than the areas where DLGAP2 is most highly expressed such as the hippocampus and the striatum, which could have diluted the strength of the results.

Strengths of the study included that we used a highly quantitative method to confirm the methylation status that was measured by RRBS. This study was the first demonstration of the association between cannabis use and substantial hypomethylation of DLGAP2 in human sperm. Additionally, we are able to confirm a functional relationship between methylation and expression in a relevant target tissue, and have shown that the relationship between methylation and expression is weakened in males, which could bear relevance to the sexual dimorphism in the prevalence of autism. This is the first demonstration of potential heritability of altered methylation resulting from preconceptional paternal THC exposure. Given the increasing legalization and use of cannabis in the U.S., our results underscore a need for larger studies to determine the potential for heritability of DLGAP2 methylation changes in the human F1 generation and beyond. It will also be important to examine how cannabis-associated methylation changes relate to neurobehavioral phenotypes

Source:   Epigenetics. 2020; 15(1-2): 161–173.

Published online 2019 Aug 26. doi: 10.1080/15592294.2019.1656158

(-)-Trans-Δ9-tetrahydrocannabinol (Δ9-THC) is the main compound responsible for the intoxicant activity of Cannabis sativa L. The length of the side alkyl chain influences the biological activity of this cannabinoid. In particular, synthetic analogues of Δ9-THC with a longer side chain have shown cannabimimetic properties far higher than Δ9-THC itself. In the attempt to define the phytocannabinoids profile that characterizes a medicinal cannabis variety, a new phytocannabinoid with the same structure of Δ9-THC but with a seven-term alkyl side chain was identified.

The natural compound was isolated and fully characterized and its stereochemical configuration was assigned by match with the same compound obtained by a stereoselective synthesis. This new phytocannabinoid has been called (-)-trans-Δ9-tetrahydrocannabiphorol (Δ9-THCP). Along with Δ9-THCP, the corresponding cannabidiol (CBD) homolog with seven-term side alkyl chain (CBDP) was also isolated and unambiguously identified by match with its synthetic counterpart. The binding activity of Δ9-THCP against human CB1 receptor in vitro (Ki=1.2nM) resulted similar to that of CP55940 (Ki=0.9nM), a potent full CB1 agonist. In the cannabinoid tetrad pharmacological test, Δ9-THCP induced hypomotility, analgesia, catalepsy and decreased rectal temperature indicating a THC-like cannabimimetic activity.
The presence of this new phytocannabinoid could account for the pharmacological properties of some cannabis varieties difficult to explain by the presence of the sole Δ9-THC.

Cannabis sativa has always been a controversial plant as it can be considered as a lifesaver for several pathologies including glaucoma and epilepsy, an invaluable source of nutrients, an environmentally friendly raw material for manufacturing and textiles, but it is also the most widely spread illicit drug in the world, especially among young adults
.
Its peculiarity is its ability to produce a class of organic molecules called phytocannabinoids, which derive from an enzymatic reaction between a resorcinol and an isoprenoid group. The modularity of these two parts is the key for the extreme variability of the resulting product that has led to almost 150 different known phytocannabinoids. The precursors for the most commonly naturally occurring phytocannabinoids are olivetolic acid and geranyl pyrophosphate, which take part to a condensation reaction leading to the formation of cannabigerolic acid (CBGA). CBGA can be then converted into either tetrahydrocannabinolic acid (THCA) or cannabidiolic acid (CBDA) or cannabichromenic acid (CBCA) by the action of a specific cyclase enzyme. All phytocannabinoids are biosynthesized in the carboxylated form, which can be converted into the corresponding decarboxylated (or neutral) form by heat.

The best known neutral cannabinoids are undoubtedly Δ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD), the former being responsible for the intoxicant properties of the cannabis plant, and the latter being active as antioxidant, anti-inflammatory, anti-convulsant, but also as antagonist of THC negative effects.
All these cannabinoids are characterized by the presence of an alkyl side chain on the resorcinol moiety made of five carbon atoms. However, other phytocannabinoids with a different number of carbon atoms on the side chain are known and they have been called varinoids (with three carbon atoms), such as cannabidivarin (CBDV) and Δ9-tetrahydrocannabivarin (Δ9 -THCV), and orcinoids (with one carbon atom), such as cannabidiorcol (CBD-C1) and tetrahydrocannabiorcol (THC-C1)7. Both series are biosynthesized in the plant as the specific ketide synthases have been identified.
Our research group has recently reported the presence of a butyl phytocannabinoid series with a four-term alkyl chain, in particular cannabidibutol (CBDB) and Δ9-tetrahydrocannabutol (Δ9-THCB), in CBD samples derived from hemp and in a medicinal cannabis variety. Since no evidence has been provided for the presence of plant enzymes responsible for the biosynthesis of these butyl phytocannabinoids, it has been suggested that they might derive from microbial ω-oxidation and decarboxylation of their corresponding five-term homolog.
The length of the alkyl side chain has indeed proved to be the key parameter, the pharmacophore, for the biological activity exerted by Δ9-THC on the human cannabinoid receptor CB1 as evidenced by structure-activity relationship (SAR) studies collected by Bow and Rimondi. In particular, a minimum of three carbons is necessary to bind the receptor, then the highest activity has been registered with an eight-carbon side chain to finally decrease with a higher number of carbon atoms. Δ8-THC homologs with more than five carbon atoms on the side chain have been synthetically produced and tested in order to have molecules several times more potent than Δ9-THC.
To the best of our knowledge, a phytocannabinoid with a linear alkyl side chain containing more than five carbon atoms has never been reported as naturally occurring. However, our research group disclosed for the first time the presence of seven-term homologs of CBD and Δ9-THC in a medicinal cannabis variety, the Italian FM2, provided by the Military Chemical Pharmaceutical Institute in Florence.

The two new phytocannabinoids were isolated and fully characterized and their absolute configuration was confirmed by a stereoselective synthesis. According to the International Non-proprietary Name (INN), we suggested for these CBD and THC analogues the name “cannabidiphorol” (CBDP) and “tetrahydrocannabiphorol” (THCP), respectively. The suffix “-phorol” comes from “sphaerophorol”, common name for 5-heptyl-benzen-1,3-diol, which constitutes the resorcinol moiety of these two new phytocannabinoids.
A number of clinical trials and a growing body of literature provide real evidence of the pharmacological potential of cannabis and cannabinoids on a wide range of disorders from sleep to anxiety, multiple sclerosis, autism and neuropathic pain20–23. In particular, being the most potent psychotropic cannabinoid, Δ9-THC is the main focus of such studies.

In light of the above and of the results of the SAR studies, we expected that THCP is endowed of an even higher binding affinity for CB1 receptor and a greater cannabimimetic activity than THC itself. In order to investigate these pharmacological aspects of THCP, its binding affinity for CB1 receptor was tested by a radioligand in vitro assay and its cannabimimetic activity was assessed by the tetrad behavioral tests
in mice.
Results
Identifcation of cannabidiphorol (CBDP) and Δ9-tetrahydrocannabiphorol (Δ9-THCP) by liquid chromatography coupled to high-resolution mass spectrometry (LC-HRMS).

The FM2 ethanolic extract was analyzed by an analytical method recently developed for the cannabinoid profiling of this medicinal cannabis variety. As the native extract contains mainly the carboxylated forms of phytocannabinoids as a consequence of a cold extraction25, part of the plant material was heated to achieve decarboxylation where the predominant forms are neutral phytocannabinoids.

The advanced analytical platform of ultra-high performance liquid chromatography coupled to high resolution Orbitrap mass spectrometry was employed to analyze the FM2 extracts and study the fragmentation spectra of the analytes under investigation. The precursor ions of the neutral derivatives cannabidiphorol (CBDP) and Δ9-tetrahydrocannabiphorol (Δ9-THCP), 341.2486 for the [M-H]− and 343.2632 for the [M+H]+, showed an elution time of 19.4 min for CBDP and 21.3 min for Δ9-THCP (Fig. 1a).
Their identification was confirmed by the injection of a mixture (5 ng/mL) of the two chemically synthesized CBDP and Δ9-THCP (Fig. 1b) as it will be described later. As for their carboxylated counterpart, the precursor ions of the neutral forms CBDP and Δ9-THCP break in the same way in ESI+mode, but they show a different fragmentation pattern in ESI− mode. Whilst Δ9-THCP shows only the precursor ion [M-H]− (Fig. 1d), CBDP molecule generates the fragments at m/z 273.1858 corresponding to a retro Diels-Alder reaction, and 207.1381
corresponding to the resorcinol moiety after the break of the bond with the terpenoid group (Fig. 1c). It is noteworthy that for both molecules, CBDP and Δ9-THCP, each fragment in both ionization modes differ exactly by an ethylene unit (CH2)2 from the corresponding five-termed homologs CBD and THC.

Moreover, the longer elution time corroborates the hypothesis of the seven-termed phytocannabinoids considering the higher lipophilicity of the latter.

Source: https://www.nature.com/articles/s41598-019-56785-1 December 2019

Nearly 10% of cannabis users in the United States report using it for medicinal purposes.
As of August 2019, 33 states and the District of Columbia have initiated policies allowing the use of cannabis or cannabinoids for the management of specific medical conditions.
Yet, the federal government still classifies cannabis as illegal, complicating its medical use and research into its effectiveness as a treatment for the various conditions purported to benefit from cannabis pharmacotherapy. Because of this conflict and restrictions on cannabis research, evidence of the efficacy of cannabis to manage various diseases is often lacking.

This article updates a review published in the June 23, 2015, issue of JAMA2 and describes newer evidence regarding what is known and not known about the efficacy of cannabis and cannabinoids for managing various conditions.

Indications for Therapeutic Use Approved by the US Food and Drug Administration
Cannabis has numerous cannabinoids, the most notable being tetrahydrocannabinol, which accounts for its psychoactive effects. Individual cannabinoids have unique pharmacologic profiles enabling drug development to manage various conditions without having the cognitive effects typically associated with cannabis.

Only a few cannabinoids have high-quality evidence to support their use and are approved for medicinal use by the US Food and Drug Administration (FDA). The cannabinoids dronabinol and nabilone were approved by the FDA for chemotherapy-induced nausea and vomiting in 1985, with dronabinol gaining an additional indication for appetite stimulation in conditions that cause weight loss, such as AIDS, in 1992. Recently, a third cannabinoid, cannabidiol (CBD), was approved by the FDA for the management of 2 forms of pediatric epilepsy, Dravet syndrome and Lennox-Gastaut syndrome, based on the strength of positive randomized clinical trials (RCTs).

Other Medical Indications
Cannabinoids are often cited as being effective for managing chronic pain. The National Academies of Science, Engineering, and Medicine examined this issue and found that there was conclusive or substantial evidence that cannabis or cannabinoids effectively managed chronic pain, based on their expert committee’s assessment that the literature on this topic had many supportive findings from good-quality studies with no credible opposing findings.

The panel relied on a single meta-analysis of 28 studies, few of which were from the United States, that assessed a variety of diseases and compounds. Although they concluded that cannabinoids effectively managed pain, the CIs associated with these findings were large, suggesting unreliability in the meta-analysis results.
A more recent meta-analysis of 91 publications found cannabinoids to reduce pain 30% more than placebo (odds ratio, 1.46 [95% CI, 1.16 1.84]), but had a number needed to treat for chronic pain of 24 (95% CI, 15-61) and a number needed to harm of 6 (95% CI, 5-8).While a moderate level of evidence supports these recommendations, most studies of the efficacy of cannabinoids on pain are for neuropathic pain, with relatively few high-quality studies examining other types of pain. Taken together, at best, there is only inconclusive evidence that cannabinoids effectively manage chronic pain, and large numbers of patients must receive treatment with cannabinoids for a few to benefit, while not many need to receive treatment to result in harm.
There is strong evidence to support relief of symptoms of muscle spasticity resulting from multiple sclerosis from cannabinoids as reported by patients, but the association is much weaker when outcomes are measured by physicians. There is insufficient evidence to support or refute claims that cannabinoids provide relief for spinal cord injury–related muscle spasms.

Recent Clinical Trials
Two multicenter, international trials with substantial numbers of patients (n = 120 and n = 171) demonstrated the efficacy of CBD as an add-on drug to manage some seizure disorders. Over 14 weeks, 20mg/kg of CBD significantly reduced the median frequency of convulsive seizures in children and young adults with Dravet syndrome as well as the estimated median difference in monthly drop seizures between CBD and placebo in patients with Lennox-Gastaut syndrome. Although promising, these results were found in relatively uncommon disorders and the studies were limited by the use of subjective end points and incomplete blinding that is typical of cannabinoid studies because these drugs have readily identifiable side effects.
Numerous other medical conditions, including Parkinson disease, posttraumatic stress disorder, and Tourette syndrome, have a hypothetical rationale for the use of cannabis or cannabinoids as pharmacotherapy based on cannabinoid effects on spasticity, anxiety, and density of cannabinoid receptors in areas implicated in development of tics, such as the basal ganglia and cerebellum. The strength of the evidence supporting the use of cannabinoids for these diseases is weak because most studies of patients with these diseases have been small, often uncontrolled, or crossover studies.

Few pharmaceutical companies are conducting cannabinoid trials. Thus, it is not likely that additional cannabinoids will be approved by the FDA in the near future. Public interest in cannabis and cannabinoids as pharmacotherapy continues to increase, as does the number of medical conditions for which patients are utilizing cannabis and CBD, despite insufficient evidence to support this trend.

Neurologic Adverse Effects Are Better Defined Than Physical Adverse Effects
Acute cannabis use is associated with impaired learning, memory, attention, and motor coordination, areas that can affect important activities of daily living, such as driving. Acute cannabis use can also affect judgment, potentially resulting in users making risky decisions that they would not otherwise make. While there is consensus that acute cannabis use results in cognitive deficits, residual cognitive effects persisting after acute intoxication are still debated, especially for individuals who used cannabis regularly as adolescents.

Chronic cannabis use is associated with an increased risk of psychiatric illness and addiction. There is a significant association— possibly a causal relationship—between cannabis use and the development of psychotic disorders, such as schizophrenia, particularly among heavy users. Chronic cannabis use can lead to cannabis use disorder (CUD) and contributes to impairment in work, school, and relationships in up to 31% of adult users.  Regular cannabis use at levels associated with CUD (near-daily use of more than one eighth ounce of cannabis per week) is associated with worsening functional status, including lower income, greater need for socio-economic assistance, criminal behavior, unemployment, and decreased life satisfaction.

Cannabis use is associated with adverse perinatal outcomes as well; a 2019 study showed the crude rate of preterm birth was 12.0% among cannabis users and 6.1% among nonusers (risk difference, 5.88% [95% CI, 5.22%-6.54%]).

Inadequate Evidence Supporting the Use of Cannabinoids for Many Medical Conditions
The quality of the evidence supporting the use of cannabinoids is suboptimal. First, studies assessing pain and spasticity are difficult to conduct, in part because of heterogeneity of the outcome measures used in these studies. Second, most RCTs that have evaluated cannabinoid clinical outcomes were small, with fewer than 100 participants in each, and small trials may overestimate treatment effects. Third, the timeframe for most studies is too short to assess the long-term effects of these medications. Fourth, tolerance, withdrawal, and potential for drug-drug interactions may affect the usefulness of cannabis, and these phenomena are not well understood for cannabinoids.

The lack of high-quality evidence results in outsized claims of the efficacy of cannabinoids for numerous medical conditions. There is a need for well-designed, large, multisite RCTs of cannabis or cannabinoids to resolve claims of efficacy for conditions for which there are claims of efficacy not supported by high quality evidence, such as pain and spasticity.

Conclusions
Insufficient evidence exists for the use of medical cannabis for most conditions for which its use is advocated. Despite the lack of evidence, various US state governments have recommended cannabis for the management of more than 50 medical conditions. Physicians may be appropriately reticent to recommend medical cannabis for their patients because of the limited scientific evidence supporting its use or because cannabis remains illegal in federal law. Cannabis is useful for some conditions, but patients who might benefit may not get appropriate treatment because of insufficient awareness regarding the evidence supporting its use or confusion from federal law deeming cannabis illegal.

Source: Medical Use of Cannabis in 2019 | Clinical Pharmacy and Pharmacology | JAMA | JAMA Network August 2019

Abstract

The molecular composition of the cannabinoid type 1 (CB1) receptor complex beyond the classical G-protein signaling components is not known. Using proteomics on mouse cortex in vivo, we pulled down proteins interacting with CB1 in neurons and show that the CB1 receptor assembles with multiple members of the WAVE1 complex and the RhoGTPase Rac1 and modulates their activity. Activation levels of CB1 receptor directly impacted on actin polymerization and stability via WAVE1 in growth cones of developing neurons, leading to their collapse, as well as in synaptic spines of mature neurons, leading to their retraction. In adult mice, CB1 receptor agonists attenuated activity-dependent remodeling of dendritic spines in spinal cord neurons in vivo and suppressed inflammatory pain by regulating the WAVE1 complex. This study reports novel signaling mechanisms for cannabinoidergic modulation of the nervous system and demonstrates a previously unreported role for the WAVE1 complex in therapeutic applications of cannabinoids.

Abstract

Background

Whilst cannabis commercialization is occurring rapidly guided by highly individualistic public narratives, evidence that all congenital anomalies (CA) increase alongside cannabis use in Canada, a link with 21 CA’s in Hawaii, and rising CA’s in Colorado indicate that transgenerational effects can be significant and impact public health. It was therefore important to study Northern New South Wales (NNSW) where cannabis use is high.

Methods

Design: Cohort. 2008–2015. Setting: NNSW and Queensland (QLD), Australia. Participants. Whole populations. Exposures. Tobacco, alcohol, cannabis. Source: National Drug Strategy Household Surveys 2010, 2013. Main Outcomes. CA Rates. NNSW-QLD comparisons. Geospatial and causal regression.

Results

Cardiovascular, respiratory and gastrointestinal anomalies rose with falling tobacco and alcohol but rising cannabis use rates across Queensland. Maternal age NNSW-QLD was not different (2008–2015: 4265/22084 v. 96,473/490514 > 35 years/total, Chi.Sq. = 1.687, P = 0.194). A higher rate of NNSW cannabis-related than cannabis-unrelated defects occurred (prevalence ratio (PR) = 2.13, 95%C.I. 1.80–2.52, P = 3.24 × 10− 19). CA’s rose more potently with rising cannabis than with rising tobacco or alcohol use. Exomphalos and gastroschisis had the highest NNSW:QLD PR (6.29(2.94–13.48) and 5.85(3.54–9.67)) and attributable fraction in the exposed (84.11%(65.95–92.58%) and 82.91%(71.75–89.66%), P = 2.83 × 10− 8 and P = 5.62 × 10− 15). In multivariable geospatial models cannabis was significantly linked with cardiovascular (atrial septal defect, ventricular septal defect, tetralogy of Fallot, patent ductus arteriosus), genetic (chromosomal defects, Downs syndrome), gastrointestinal (small intestinal atresia), body wall (gastroschisis, diaphragmatic hernia) and other (hypospadias) (AVTPCDSGDH) CA’s. In linear modelling cannabis use was significantly linked with anal stenosis, congenital hydrocephalus and Turner syndrome (ACT) and was significantly linked in borderline significant models (model P < 0.1) with microtia, microphthalmia, and transposition of the great vessels. At robust and mixed effects inverse probability weighted multivariable regression cannabis was related to 18 defects. 16/17 E-Values in spatial models were > 1.25 ranging up to 5.2 × 1013 making uncontrolled confounding unlikely.

Conclusions

These results suggest that population level CA’s react more strongly to small rises in cannabis use than tobacco or alcohol; cardiovascular, chromosomal, body wall and gastrointestinal CA’s rise significantly with small increases in cannabis use; that cannabis is a bivariate correlate of AVTPCDSGDH and ACT anomalies, is robust to adjustment for other substances; and is causal.

Source: Broad Spectrum Epidemiological Contribution of Cannabis, Tobacco and Alcohol to the Teratological Profile of Northern New South Wales: Geospatial and Causal Inference Analysis | Research Square November 2020

Sometimes when your son or daughter is struggling with substance use, it feels like you’ve tried absolutely everything to help. What if you’ve nearly given up hope?

In this short video, Master Addictions Counselor Mary Ann Badenoch, LPC, offers some new ways to think about opportunities for change. For example, instead of focusing on the end goal, be sure to notice the small victories along the way. This can lead to larger positive change and help you remain hopeful.

Cancer is a word that conjures up many images. It is a varied disease that affects many people and can leave families distraught. There are fortunately treatments for a large number of these cancers, which work by restricting tumour growth and inducing cell death. However, there are cancers which pose more of a challenge, and so finding new drugs that can fight these ones becomes even more important.

The methods for discovering and developing new drugs, or chemotherapies, simply fall into two camps. The more recent approach has been the design of drugs with a particular molecular target in mind. This is arguably best exemplified by the drug imatinib, notably used to eat leukaemia. After scientists understood that the BCR-ABL hybrid gene was the cause of a certain type of leukaemia it allowed them to develop pharmacological ways to specifically counteract it – by inhibiting the signals inside the cancer cell used to grow and divide. The drug that was born to much fanfare and arguably revolutionised drug development.

Continued improvements in the understanding of the mechanisms inside cells that are hijacked by cancer have helped to improve the way that compounds are designed and then tested clinically. Those that are able to restore the normal function of the signalling pathways disrupted by cancer are an attractive target for drug development.

At least three major pharmaceutical players are in a fight to negate the cancer-supporting action of AKT, for example. This protein kinase – a key regulator of cell function – is a central player in determining cell proliferation and growth, and is intimately linked with a number of other cell communications systems that all work in unison to support a cancer developing. Its level is over-expressed in a number of cancers, and is linked to a poorer prognosis. Consequently, therapeutic interventions to counteract its effects are particularly attractive and potentially lucrative.

Isolating the compound

It was however, never like this. Before the mystery of cancer was opened up, drug discovery was empirical in nature. Through antiquity, a range of flora were said to cure ailments and, using these anecdotes as guides, active ingredients have been extracted, purified and improved. This has been successful, and a number of drugs now form normal members of the pharmacopeia, including aspirin, which was isolated from the white willow, and less familiar anti-cancer drugs such as etoposide, irinotecan and taxol, which were derived from mayapples, camptotheca trees and Pacific yews. There is no doubt of their value in treatment and they’ve been used successfully for over 40 years.

Then there is the cannabis plant. The putative medicinal property of cannabis has been known for some time; indeed, history records show they were used to ease symptoms of gout, malaria and even childbirth. However, the fundamental issue with using cannabis in its whole form as a medicine is its psychoactive properties, so it would make sense to identify the important anti-cancer parts and remove the psychoactive components. Cannabinoids are these. They number around 80, with cannabidiol (CBD) and tetrahydrocannabinol (THC) the two lead medicinal candidates. However, unlike the mayapple and Pacific yew, their development has been seriously curtailed.

Cannabis. M a n u e l, CC BY

It’s likely that the widespread use of cannabis as a recreational drug has affected research into the potential in cannabis – and the result was death by association. I wonder how the early development of CBD and THC would have progressed if it was known by any other name.

Chequered pasts

Drugs with chequered pasts have found redemption; take the thalidomide story. This drug was infamously linked to babies born with deformations; however, serendipitous observations of improvements in leprosy in a patient taking thalidomide in 1965 led to the discovery that it also had important effects on the immune system. Refinements to the chemistry of the drug were made and the result was a new family of drugs that are valuable tools in anti-cancer research and treatment.

The story emphasises the point that medicinal potential of drugs should be seen objectively and guided scientifically. Cannabinoids and cannabis are not the same thing – it’s just that cannabinoids are derived from cannabis. Cannabinoids possess anti-cancer properties, which they achieve through their fundamental interactions with proteins embedded in the signalling pathways in cells that are now seen as particularly interesting for research.

In addition to this direct anti-cancer action, cannabinoids also have the capacity to disrupt the ability of cancer to feed itself by a process called angiogenesis as well as being able to modulate the immune system to make it more hostile towards cancer. Furthermore, CBD and THC appear to support the activity and efficacy of other chemotherapy drugs. Indeed, we recently showed that the cancer-killing property of radiotherapy was dramatically enhanced when cannabinoids were used in combination with this treatment – certain forms of brain cancer were reduced to sizes that were difficult to detect. Taken together, all of these features show a profile with great anti-cancer potential.

However slow things have been, a sea-change has been occurring; there is a palpable sense that legislators are becoming open to the scientific evidence that suggests cannabinoids may possess medicinal quality. Clinical trials using various forms of cannabinoids are now taking place in a number of countries, and we all await the results of these studies.

I hope to be able to change the answer that I give to patients who contact me to ask: “do you think I should be using cannabinoids for my cancer?” from the negative to the affirmative. My frustrating answer has always been it is too early to say, as promising laboratory data has not yet been confirmed by objective clinical studies. This is not a criticism of the drug development system, as convincing clinical trials are needed to ensure patients are given drugs that have been thoroughly tested to ensure the best chance of them fighting their disease.

The flip side of those who passionately shout for the “legalisation of cannabis” is that their call may inadvertently hamper the medical development of cannabinoids, which is a shame. My aim is to deliver a drug that can be used in patients with cancer. And for a headache, no one would suggest you chew on a white willow plant, especially when you could be taking an aspirin. The same is true of cannabis and cannabinoids.

Source:    https://theconversation.com/profiles/wai-liu-144882 

Recent data from the Kollins lab (‘Cannabinoid exposure and altered DNA methylation in rat and human sperm’ Epigenetics 2018; 13: 1208–1221) indicated epigenetic effects of cannabis use on sperm in man parallel those in rats and showed substantial shifts in both hypo- and hyper-DNA methylation with the latter predominating. This provides one likely mechanism for the transgenerational transmission of epigenomic instability with sperm as the vector. It therefore contributes important pathophysiological insights into the probable mechanisms underlying the epidemiology of prenatal cannabis exposure potentially explaining diverse features of cannabis-related teratology including effects on the neuraxis, cardiovasculature, immune stimulation, secondary genomic instability and carcinogenesis related to both adult and pediatric cancers.

The potentially inheritable and therefore multigenerational nature of these defects needs to be carefully considered in the light of recent teratological and neurobehavioural trends in diverse jurisdictions such as the USA nationally, Hawaii, Colorado, Canada, France and Australia, particularly relating to mental retardation, age-related morbidity and oncogenesis including inheritable cancerogenesis. Increasing demonstrations that the epigenome can respond directly and in real time and retain memories of environmental exposures of many kinds implies that the genome-epigenome is much more sensitive to environmental toxicants than has been generally realized. Issues of long-term multigenerational inheritance amplify these concerns. Further research particularly on the epigenomic toxicology of many cannabinoids is also required.

Introduction

Physiology and pathobiology of the epigenome and its complex interactions with the genome, metabolome and immunometabolome, and cannabinoid physiopharmacology represents some of the most exciting areas of modern biological research. Type 1 and 2 cannabinoid receptors (CB1R and CB2R) are involved in a host of endogenous processes with potential therapeutic applications in numerous fields as diverse as pain, nausea, temperature regulation and weight control amongst others. Several recent detailed structural descriptions of the CB1R and CB2R complexed with high affinity agonists and antagonists, and pathways for the bulk biological synthesis of cannabinoids open the way to the rational design of high affinity molecules to differentially modulate these key receptors which are involved in a host of endogenous processes with diverse potential therapeutic applications. The use of exogenous cannabinoid compounds that bind to CB1R and CB2R may however also produce unwanted side effects including through modulation of DNA methylation states.

Within each nucleated cell, 2 m of DNA is normally stored coiled around four histones known as a nucleosome. A total of 147 bases of DNA are wrapped twice around two sets of H2A, H2B, H3 and H4 which together form the histone octamer. The bases of DNA itself may have a methyl group (CH3-) attached to them, usually to cytosine-phosphate-guanine (CpG), which when it occurs in the region of the gene promoter, blocks the transcription machinery and prevents the gene from becoming activated. The tails of the four histone proteins protrude from the central globular core and normally bind by electrostatic forces to the coiled DNA. Addition of an acetyl group to these histone tails, particularly on H3 and H4, disrupts the salt bridges opening up the DNA code for active transcription. Histone tails can also be methylated or indeed be modified by many groups (mono-, di- and trimethyl, acetyl, phosphoryl, crotonyl, citrulline, ubiquitin and ADP-ribosyl, etc.) which control gene transcription . DNA is transcribed into RNA some of which is made into the many proteins from which our bodies are made. However, much of the RNA also has purely informatic roles, and short and long non-coding RNA’s (ncRNA) controls DNA availability and transcription, RNA processing and splicing and can form a scaffold upon which layers of DNA regulation can be built. These various mechanisms, DNA methylation, post-translational modification of histone tails, nucleosome positioning, histone replacement, nuclear positioning and ncRNA’s form the basis of epigenetic regulation and appear to undergo an ‘epigenetic conversation’ amongst these different layers.

Chromatin loops are extruded through cohesin rings giving rise to transcription factories (topologically active domains) where different regions of the DNA including proximal promoters and distal enhancers are brought into close proximity to control transcription either on the same chromosome (in cis) or sometimes on nearby chromosomes (in trans). Super-enhancers, enhancer cross-talk, and extensive 3D remodelling of euchromatin looping during development are also described.

Moreover, a variety of studies in animals and several epidemiological studies in humans show that the epigenetic code can form a mechanism for inheritable changes across generations from both father and mother to subsequent generations which do not involve changes in the genetic code itself. Such epigenetic inheritance has been shown clinically for starvation, obesity, bariatric surgery and for tobacco and alcohol consumption. It has also been demonstrated in rodents for alcohol, cocaine and opioids, and in rodents’ immune system, nucleus accumbens and sperm following cannabinoid exposure in the parents.

If DNA is thought of as the cells’ bioinformatic ‘hardware’ then the epigenome can be considered its programming ‘software’. The epigenome controls gene expression and is key to cell differentiation into different tissue fates, different states of cellular differentiation, to cellular reprogramming into induced pluripotential stem cell states, cancer, numerous neuropsychiatric diseases including addiction, immune, metabolic and brain memory, aging, and the response of the cell to changes in its environment by way of gene-environment interactions including the development of so-called ‘epigenetic scars’.

This powerful informatic system has recently been shown to have a host of unforeseen capabilities. It has been shown that histone tails sense oxygen tension rapidly within 1 h with resulting modification of gene expression cassettes. Lysine (K) demethylase 5A (KDM5A) is a Jumanji-C domain containing molecular dioxygenase which is inactivated by hypoxia in a hypoxia-inducible factor-independent manner, controls H3K4me3 and H3K36me3 histone trimethylations and governs the transcriptome expression several hours after brief hypoxia. Similarly, KDM6A is also an oxygen sensitive dioxygenase and histone demethylase which controls H3K27me3. Its blockade by hypoxia interferes with cell differentiation and maintains cells in an undifferentiated state. Since the ten eleven translocase enzymes and are key demethylators of DNA and are dioxygenases also sensitive to profound hypoxia, and since hypoxia exists in most stem cell niches and at the centre of many tumours, such histone- and DNA-centred mechanisms are likely to be important in stem cell, aging, cellular differentiation and cancer biology.

Epigenomic regulation of tumour immunometabolome

Similarly, one of the great paradoxes of cancer biology is the presence within tumours of numerous effector T-cells which are able to expand and eradicate large metastatic tumours effectively, but do not do so within clinical cancers. It was recently shown that this effect is due to the very elevated nucleocytosolic potassium level within tumour lymphocytes which stalls metabolism and runs down acetyl-coenzyme A levels, the main acetyl donor for histone acetylation and induces a form of calorie restriction (like starvation) including autophagy and mitophagy and impairs the normal mTOR (mammalian target of rapamycin)-dependent T-cell receptor-mediated activation response. This program was mediated by reduced levels of H3K9 and H3K27 acetylation. Hence, tumour lymphocyte anergy and stemness were both mediated epigenetically and were shown to be reversible when the immunometabolic defect was corrected either genetically or by substrate supplementation. This work elegantly demonstrates the close relationship between the metabolic state of cells, cell differentiation state and starvation response, the control of cell fate by the epigenetic landscape and disease outcome.

Metabolomic supply of epigenetic substrate

Several studies similarly link the supply of metabolic intermediates required as inputs by the epigenetic machinery to epigenetic state and downstream gene control. Indeed, the well-known supplementation of staple foods by folic acid is believed to act because of the central role played by this vitamin in the methyl cycle and the supply of single carbon units to the methylation machinery for DNA and histones. A moments reflection shows that expression of the DNA of the mitochondria and the DNA of the nucleus need to be tightly coordinated to supply the correct number of subunits for the complex machineries of the mitochondrion including electron transport. This mitonuclear balance acts at several levels including RNA transfer, metabolic substrate (acetyl-coenzyme A, nicotinamide mononucleotide) transfer and the control of the epigenetic regulators PARP (polyadenosineribosyl polymerase) and Sirt1 (a major histone deacetylase).

Cannabinoid signalling impacts mitochondria

As noted above the identification of CB1R and CB2R on the plasma membrane has been a major milestone in cellular cannabinoid physiology. It is less well known that CB1R’s also exist on the mitochondrial outer membrane, and that the inner and outer leaflet of the mitochondria, together with the intermembrane space host the same cannabinoid transduction machinery as the plasmalemma. Neuronal mitochondrial CB1R’s have been implicated in memory and several critical neural processes. Hence, the well-substantiated findings that diverse cannabinoids generally suppress mitochondrial activity (in neurons, lung, liver and sperm), lower the mitochondrial transmembrane potential and interfere with oxidative phosphorylation carry major epigenetic implications not only for mitonuclear balance and trafficking including the mitochondrial stress response, but also for the supply of the requisite metabolic intermediates in terms of acetyl-coenzyme A which is an absolute requirement for histone acetylation and normal gene activation.

Histone serotonylation and dopaminylation

Serotonin, which has long been implicated in mood dysregulation and drug addiction was recently shown to act as a novel post-translational modification of the tail of H3 at lysine 4 via serotonylation where it increases the binding of the transcription machinery and allows correct cell differentiation. It is likely that dopamine will soon be similarly implicated.

Almost accompanying the modern bioinformatic explosion of knowledge related to the sequencing of the human genome has been a parallel increase in knowledge of the complexities and intricacies of epigenomic regulation. Nowhere is this more evident than in cancer. Indeed, it has become apparent that there are numerous forms of cross-talk, interaction and cross-regulation between the genome and the epigenome and the two are in fact highly inter-related. This is of particular relevance to chromosomal integrity and cancerogenic mechanisms. Several mechanisms have been described for such interactions including alterations of DNA methylation, altered cytosine hydroxymethylation, alteration of TERT function which is a key catalytic component of the telomerase enzyme which protects chromosome ends and altered architecture of enhancers and their looping interactions with promoters which control gene expression. Indeed, pharmacological modulation of the bromodomain ‘readers’ of epigenomic information has become a very exciting area within modern cancer therapeutic research , and forms an area into which large pharmaceutical companies are presently investing several billion dollars.

Gamete cannabinoid epigenomics – Murphy et. al

In this powerful context, the masterful epigenetic work from the Kollins laboratory of Murphy and colleagues was situated. These workers studied 12 control men who self-reported no psychoactive drug use in the last 6 months, and 12 subjects who reported more than weekly use of cannabis only, with all results confirmed by urine toxicology and ultra performance liquid chromatography/tandem mass spectrometry and enzyme immunoassay. In parallel two groups of 9-week-old male rats were administered solvent or 2 mg/kg THC by gastric lavage for 12 days prior to sacrifice and the epididymis was harvested. Sperm were assayed by the ‘swim out’ method where sperm swam out into normal saline bath solution. Cannabis exposed men had lower sperm counts, and it was found that there was differential sperm DNA methylation at 6,640 CpG sites including at 3,979 CpG islands in gene promoters where methylation was changed by more than 10% (which is alot). Significant changes were in both the hypomethylation and hypermethylation direction were noted with the changes in the hypomethylation group being more marked across the genome and at gene promoters. Pathways in cancer (including the BRAF, PRCACA, APC2 PIK3R2, LAMA1, LAMB1, AKT1 and FGF genes), hippo pathways (which are also important in cancer and in embryonic body pattern formation), the MAP kinase pathway (also involved in growth and cancer), AMPA, NMDA and kainate glutamate receptor subunits, and the Wnt genes 3A, 5A, 9A, 10A (involved in cancer and in body patterning and morphogensis) were found to be particularly affected. A dose–response effect was demonstrated at 183 CpG sites on 177 genes including the PTG1R gene which encodes the prostacyclin (a powerful vasodilator and antithrombotic agent) receptor which was down-regulated.

Twenty-three genes involved in platelet activation and 21 genes involved in glutamate metabolism were also modulated. LAMB1, whose gene product laminin B has been implicated in progeria and is increasingly implicated in genetic ageing pathways through its role in nuclear positioning of chromatin and the maintenance of heterochromatin (including female X-chromosome inactivation) in an inactive state inside the nuclear membrane, and its role in establishing integrity of the nuclear envelope, was also identified.

Results in the rats closely paralleled those found in humans. Fifty-five genes were found to overlap between altered sperm methylation patterns and a previous study of brain Nuclear Accumbens DNA methylation in prenatally cannaboid exposed rats which showing increased heroin self-administration, a highly statistically significant result. These results support the hypothesis that the transgenerational transmission of defects following pre-conceptual exposure to cannabis found in the immune system and limbic system of the brain including increased tendency for drug use in later life in rodents may be transmitted through alterations in the DNA methylation of the male germ line. More work is clearly needed in this area with exhaustive epigenetic, transcriptomic and genomic characterization of these results with larger sample sizes and in other species.

Cannabis – cancer links

Mechanistically these results have very far-reaching implications indeed and appear to account for much of the epidemiologically documented associations of cannabis use. Cannabis has been associated with cancer of the mouth and throat, lung, bladder, leukaemia, larynx, prostate and cervix and in four out of four studies with testicular teratomas with a relative risk of three in meta-analysis. Cannabis has also been implicated with increased rates of the childhood cancers acute lymphocytic leukaemia, acute myeloid leukaemia, acute myelomonocytic leukaemia, neuroblastoma and rhabdomyosarcoma.

These are believed to be due to inheritable genetic or epigenetic problems from the parents, albeit the mechanism of such transmission was not understood in the pre-epigenomic era. Results of Murphy and colleagues may potentially explain mechanistically much of the epidemiologically documented morbidity that has in the past been associated with cannabis use. As noted, cannabis contains the same tars as tobacco and also several known genotoxic compounds, and is also immunoactive. Such actions imply several mechanisms by which cannabis may be implicated in carcinogenic mechanisms.

That cannabis is associated with heritable paediatric cancers where the parents themselves do not harbour such tumours is suggestive evidence that non-genetic and likely epigenetic mechanisms are involved in the childhood cancers which are observed. Detailed delineation of such putative pathways will require further research.

Cannabis has also been shown to be associated with increased rates of gastroschisis in seven of seven studies to examine this association. This pathology, where the bowels of the neonate protrude through the abdominal wall usually to the right of the umbilicus, is believed to be due to a disruption of blood flow to the forming abdominal wall. If cannabinoid exposure powerfully activates platelets through multiple mechanisms and disrupts major vasodilator systems such as the prostacyclin receptor then such a pathway could well damage the tiny blood vessels of the developing foetus and account for the development of gastroschisis. Cannabis use in adults has been linked with both myocardial infarction and stroke possibly by similar mechanisms. It has been shown elsewhere that cannabis use can also stimulate inflammation and be proinflammatory.

Epigenomics of foetal alcohol syndrome

Indeed, foetal alcohol syndrome disorder (FASD) is said to be mediated in part by the CB1R , to be epigenetically mediated, and to comprise amongst other features small heads, microcephaly, impaired visuospatial coordination and to be commonly associated with ventricular septal defect and atrial septal defect all of which have been described in association with prenatal cannabis exposure. However, the facial features of FASD are not described in the congenital cannabis literature.

Cannabis and congenital anomalies

Indeed, one Hawaiian statewide epidemiological report found elevated rates of 21 congenital defects in prenatally cannabis exposed infants. Whilst this paper is unique in the literature it helps explain much about the presently reported patterns of congenital anomalies across USA in relation to atrial septal defect, Downs’ syndrome, Trisomy 18, ventricular septal defect, limb reduction defects, anotia, gastroschisis and autism, all of which crude rates are more common in states with liberal cannabis policies. Similar morbidity patterns were observed in Canada with crude rates of all congenital defects, gastroschisis, total cardiovascular defects and orofacial clefts more common in areas with higher cannabis use. The Colorado birth defects registry has also reported a three-fold increase in the crude (unadjusted) rate of atrial septal defects 2000–2014 spanning the period of cannabis legalization together with increases of 30% or more over the same period in crude rates of total cardiovascular defects, ventricular septal defects, Down’s syndrome and anencephaly. This is highly significant as atrial septal defect has only been found to be linked with cannabis in the Hawaiian study, suggesting that our list of cannabis-related defects is as yet incomplete. As mentioned above the putative link between atrial septal defect and cannabis use has also been found in the generality of states across the USA. It should also be noted that according to a major nationally representative recurrent survey the use of all other drugs in Colorado fell during this period, making cannabis the most likely pharmacological suspect for the surge in congenital anomalies.

These findings are also consistent with data arising from France, wherein three separate regions which have permitted cannabis to be used as feed for the dairy industry calves are born without legs, and an increase in the rate of phocomelia (no arms) in human infants has similarly been observed. In the French northeast region of Ain which is adjacent to Switzerland, the crude rate of phocomelia is said to be elevated 58 times above background, whilst in nearby Switzerland which has not permitted cannabis to be used as a feed crop no such anomalies are observed.

Neuroteratogenesis and beyond

The above comments in relation to epigenetic modulation of the glutamate system have been shown in recent studies to be related to many neuropsychiatric disorders. However, the recent demonstration at least in insects that glutamate could also act as a key morphogen in body patterning processes and major organ formation may have much wider implications well beyond the neuraxis Cannabis and epigenetic ageing.

The finding of overall DNA hypomethylation by Murphy’s group carries particular significance especially in the context of disordered lamin B metabolism. Chronic inflammation is known to be a major risk factor for carcinogenesis in humans in many organs including the skin, oropharynx, bronchi, lungs, oesophagus, stomach, pancreas, liver, biliary tree, colon, bladder and prostate. Inflammatory conditions are invariably strongly pro-oxidative and damage to DNA is not unusual. Because CpGs in gene promoters are more often largely unmethylated and therefore exposed the guanine in these positions is a common target for oxidative damage. Oxo-guanine is strongly mutagenic. This form of DNA damage recruits the maintenance DNA methyltransferase DNMT1 from the gene body to the gene promoter. There DNMT1 recruits Sirt1, a histone deacetylase which tends to epigenetically silence gene expression, and also EZH2 part of the polycomb repressive complexes 2 and 4 which epigenetically silences gene expression and tends to spread the silencing of chromatin. Hence, one of the end results of this form of oxidative DNA damage is to move the DNA methylation from the gene bodies to the gene promoters, thereby hypermethylating the promoters, the CpG Island Methylator Phenotype (CIMP) and hypomethylating the gene bodies and intergenic regions. By this epigenetic means chronic inflammation and tobacco smoke have been shown to induce widespread epigenomic field change right across tissues such as colon, bronchi or bone marrow. Furthermore, this mechanism moves gene expression from the control of histone modification to DNA methylation which tends to be more fixed and less plastic than histone alterations. Such findings are consistent with a previous demonstration of accelerated ageing in cannabis exposed clinical populations.

Epigenomic control of mobile transposable genetic elements

Reducing the global level of DNA methylation also has the effect of reducing the control of mobile transposable repeat elements in the genome. Forty-two per cent of the human genome has been shown to be comprised of these mobile elements of various varieties. Long Interspersed Repeat Elements (LINE-1) are believed to be retroviral repeat elements which long ago became incorporated in the genome and are able when expressed to induce their own reverse transcription back into the genome via endogenous reverse transcriptases. For this reason, they are also called ‘jumping genes.’ Because they become randomly incorporated into the genome after reverse transcription their activity is very damaging to genetic integrity. Whilst retrotransposon mobility is normally controlled by three mechanisms these defences can be overcome in advanced cellular senescence. The presence of double-stranded DNA (dsDNA) in the cytoplasm is strongly stimulating for the immune system and stimulates a type-1 interferon proinflammatory response, which further exacerbates the cycle and directly drives the Senescence Associated Secretory Phenotype (SASP) of advanced senescence and the ‘inflamm-aging’ which is well described in advanced age. Accelerated ageing in patients exposed clinically to cannabis has previously been described using a well validated metric of arterial stiffness. Whilst neither Murphy nor Watson found evidence following cannabinoid exposure for altered methylation of repeat elements the presence of chronic inflammation in the context of widespread preneoplastic change and documented neoplasia suggest that this newly described ageing mechanism might well merit further investigation.

These changes are likely exacerbated by several classical descriptions that cannabinoids reduce the overall level of histone protein synthesis. Since the overall length of DNA does not change this is likely to further open up the genome to dysregulated transcription. Severe morphological abnormalities of human and rodent sperm have been reported.

Similarly classical descriptions exist of grossly disrupted mitoses, particularly in oocytes, which are said to be seriously deficient in DNA repair machinery. Morishima reported as long ago as 1984, evidence of nuclear blebs and bridges due to deranged meiotic divisions in cannabinoid-exposed rodent oocytes . Similar blebs and bridges have been reported by others. It has since been shown that these nuclear blebs represent areas of weakness of the nuclear membrane which are often disrupted spilling their contents into the cytoplasm. They are also a sign of nuclear ageing.

Cannabinoids and micronuclei

Cannabis has long been known to test positive in the micronuclear assay due to interference with the function of the mitotic spindle. This is a major cause of chromosomal disruption and downstream severe genetic damage in surviving cells, has previously been linked with teratogenesis and carcinogenesis, and which is also potently proinflammatory by releasing dsDNA into the cytoplasm and stimulating cGAS-STING (Cyclic GMP-AMP synthase – STimulator of INterferon Gamma) signalling and downstream innate immune pathways.

Cytoplasmic dsDNA has also been shown to be an important factor driving the lethal process of cancer metastasis.

Cannabis and wnt signalling

The findings of Murphy in relation to Wnt signalling are also of great interest. It has been found by several investigators that prenatal cannabis exposure is related to encephalocoele or anencephaly defects. Non-canonical Wnt signalling has been shown to control the closure of the anterior neuropore providing a mechanistic underpinning for this fascinating finding. Wnt signalling has also been implicated in cancer development in numerous studies and in controlling limb development which have been previously linked with cannabis exposure (as noted above).

Cannabis and autism

It was recently demonstrated that the rising use of cannabis parallels the rising incidence of autism in 50 of 51 US states and territories including Washington D.C., and that cannabis legalization was associated with increased rates of autism in legal states. Several cannabinoids in addition to Δ9-tetrahydrocannabinol (THC) were implicated in such actions including cannabidiol, cannabinol, cannabichromene, cannabigerol and tetrahydrocannabivarin. A rich literature demonstrates the impacts of epigenomics on brain development and its involvement in autistic spectrum disorders. Whether cannabis is acting by epigenetic or other routes including those outlined above remains to be demonstrated. Further research is indicated.

Cannabidiol and other cannabinoids

These findings raise the larger issue of the extent to which the described changes reflect the involvement of THC as compared to other cannabinoids in the more general genotoxicity and epigenotoxicity of both oral (edible) and inhaled (smoked) cannabis. THC, cannabidiol, cannabidivarin, and cannabinol have previously been shown to be genotoxic to chromosomes and associated with micronucleus development. American cannabis has been selectively bred for its THC content and the ratio of THC to cannabidiol (CBD) was noted to have increased from 14:1 to 80:1 1998–2018. However in more recent times, cannabidiol is being widely used across the USA for numerous (nonmedical) recommendations.

Cannabidiol is known to inhibit mitochondrial oxidative phosphorylation including calcium metabolism which is known to have a negative effect on genome maintenance and is believed to secondarily restrict the supply of acetyl and other groups for epigenetic modifications. Cannabidiol is known to act via CB1R’s particularly at higher doses. Cannabidiol acts via PPARγ (Peroxisome Proliferator Activator Receptor) which is a nuclear receptor which is implicated in various physiological and pathological states including adipogenesis, obesity, diabetes, atherogenesis, neurodegenerative disease, fertility and cancer. In a human skin cell culture experiment, cannabidiol was shown to act via CB1R’s as a transcriptional repressor by increasing the level of global DNA methylation by enhancing the expression of the maintenance DNA methylase DNMT1 which in turn suppressed the expression of skin differentiation genes and returned the cells to a less differentiated state. One notes, importantly, that this DNA hypermethylation paralleled exactly the changes reported by Murphy for THC hypermethylation. The de-differentiation reported or implied in both studies is clearly a more proliferative and proto-oncogenic state. Hence, while more research is clearly required to carefully delineate the epigenetic actions of cannabidiol, its activity at CB1R’s, its mitochondrial inhibitory action, its implication of PPARγ and particularly its THC-like induction of epigenetic and cellular de-differentiation, together with its implication in chromosomal fragmentation and micronucleus induction would suggest that caution is prudent whilst the results of further research are awaited.

Other cannabinoid receptors and notch signalling

The above discussion is intended to be indicative and suggestive rather than exhaustive as the cannabinoids’ pharmacological effects are very pleiotropic, partly because CB1R’s, CB2R’s – and six other cannabinoid sensing receptors are widely distributed across most tissues. One notes that the mechanisms described above do not obviously account for very important finding that in both Colorado and Canada increasing rates of cannabis use were associated with higher rates of total congenital cardiovascular disease. One observes that in both cases the cited rise in rates refers to an elevation of crude rates unadjusted for other covariates. This finding is important for several reasons not the least of which is that cardiovascular disease is the commonest class of congenital disorders. It may be that this action is related to the effects of cannabinoids binding high-density endovascular CB1R’s from early in foetal life and interacting with the notch signalling system. Notch is a key morphogen involved in the patterning particularly of the brain, heart, vasculature and haemopoietic systems and also in many cancers. Notch signalling both acts upon the epigenome and is acted upon by the epigenome both in benign (atherosclerotic and haemopoietic) and cancerous (ovarian, biliary, colonic, leukaemic) diseases. Clearly in view of their salience, the interactions between cannabinoids and both notch and Wnt signalling pathways constitute fertile areas for ongoing research.

Conclusion

In short the timely paper by Murphy and colleagues nicely fills the gap between extant studies documenting that pre-conception exposure to cannabis is related to widespread changes in epigenetic regulation of the immune and central nervous systems and confirms that male germ cells are a key vector of this inheritance and has given new gravity to epidemiological data on the downstream teratological manifestations of prenatal cannabinoid exposure. The reasonably close parallels in findings between rats and man confirm the usefulness of this experimental model. Since guinea pigs and white rabbits are known to form the most predictive preclinical models for human teratogenicity studies it would be prudent to investigate how epigenomic results in these species compared to those identified in man and rodents. Finally the considerable and significant clinical teratogenicity of cannabis, including its very substantial neurobehavioural teratogenicity imply that such studies need to be prioritized by the research community and the research resourcing community alike, particularly if the alarming findings of recent European experience in terms of cannabinoids allowed in the food chain is not to be repeated elsewhere. Indeed, the recent passage of the nearly $USD1trillion USA Farm Act which encourages hemp to be widely grown for general use together with the advent in some US cafés of ‘hempburgers’ and ‘cannabis cookies’ would appear to have ushered in just such an era. Hemp oil has recently been marketed in Australian supermarkets completely unsupervised. Meanwhile, the rapidly accumulating and stellar discoveries relating to the pathobiology of the epigenome and its remarkable bioinformatical secrets continue to be of general medical and community importance. In some areas, particularly relating to the epigenotoxicology of the non-THC cannabinoids, further research is clearly indicated, especially in view of the widespread use and relatively innocuous reputation of cannabis derivates including particularly cannabidiol.

Such issues suggest that in the pharmacologically exciting era of the development of novel intelligently designed cannabinoids intended for human therapeutics, considerations of genomic and epigenomic toxicity including mutagenicity, teratogenicity, carcinogenicity, pro-ageing and heritable multigenerational effects warrant special caution and attention prior to the widespread exposure of whole populations either to phytocannabinoids or to their synthetic derivatives. Equally, the possibility of locus-specific epigenetic medication development as modifiers of the epigenetic reading, writing and erasing machinery suggests that very exciting developments are also beginning in this area.

Author Note

While this paper was in review our paper examining the epidemiological pattern and trends of Colorado birth defects of 2000-2014 and entitled “Cannabis Teratology Explains Current Patterns of Coloradan Congenital Defects: The Contribution of Increased Cannabinoid Exposure to Rising Teratological Trends” was accepted by the journal Clinical Pediatrics. It provides further details and confirmation on some of the issues discussed in the present paper. It also contains a detailed ecological investigation of the role of cannabidiol at the epidemiological level which confirms and extends the mechanistic observations and the quantitative remarks relating to the epidemiology of birth defects in Colorado made in the present manuscript. The interested reader may also wish to consult this resource.

Source: https://www.tandfonline.com/doi/full/10.1080/15592294.2019.1633868 July 2019

January 2019 • Volume 48, Number 1 • Alex Berenson
Alex Berenson Author, Tell Your Children: The Truth About Marijuana, Mental Illness, and Violence

The following is adapted from a speech delivered on January 15, 2019, at Hillsdale College’s Allan P. Kirby, Jr. Center for Constitutional Studies and Citizenship in Washington, D.C.

Seventy miles northwest of New York City is a hospital that looks like a prison, its drab brick buildings wrapped in layers of fencing and barbed wire. This grim facility is called the Mid-Hudson Forensic Psychiatric Institute. It’s one of three places the state of New York sends the criminally mentally ill—defendants judged not guilty by reason of insanity.
Until recently, my wife Jackie—Dr. Jacqueline Berenson—was a senior psychiatrist there. Many of Mid-Hudson’s 300 patients are killers and arsonists. At least one is a cannibal. Most have been diagnosed with psychotic disorders like schizophrenia that provoked them to violence against family members or strangers.
A couple of years ago, Jackie was telling me about a patient. In passing, she said something like, Of course he’d been smoking pot his whole life.
Of course? I said.
Yes, they all smoke.

So marijuana causes schizophrenia?
I was surprised, to say the least. I tended to be a libertarian on drugs. Years before, I’d covered the pharmaceutical industry for The New York Times. I was aware of the claims about marijuana as medicine, and I’d watched the slow spread of legalized cannabis without much interest.
Jackie would have been within her rights to say, I know what I’m talking about, unlike you. Instead she offered something neutral like, I think that’s what the big studies say. You should read them.
So I did. The big studies, the little ones, and all the rest. I read everything I could find. I talked to every psychiatrist and brain scientist who would talk to me. And I soon realized that in all my years as a journalist I had never seen a story where the gap between insider and outsider knowledge was so great, or the stakes so high.

I began to wonder why—with the stocks of cannabis companies soaring and politicians promoting legalization as a low-risk way to raise tax revenue and reduce crime—I had never heard the truth about marijuana, mental illness, and violence.
***
Over the last 30 years, psychiatrists and epidemiologists have turned speculation about marijuana’s dangers into science. Yet over the same period, a shrewd and expensive lobbying campaign has pushed public attitudes about marijuana the other way. And the effects are now becoming apparent.
Almost everything you think you know about the health effects of cannabis, almost everything advocates and the media have told you for a generation, is wrong.
They’ve told you marijuana has many different medical uses. In reality marijuana and THC, its active ingredient, have been shown to work only in a few narrow conditions. They are most commonly prescribed for pain relief. But they are rarely tested against other pain relief drugs like ibuprofen—and in July, a large four-year study of patients with chronic pain in Australia showed cannabis use was associated with greater pain over time.
They’ve told you cannabis can stem opioid use—“Two new studies show how marijuana can help fight the opioid epidemic,” according to Wonkblog, a Washington Post website, in April 2018— and that marijuana’s effects as a painkiller make it a potential substitute for opiates. In reality, like alcohol, marijuana is too weak as a painkiller to work for most people who truly need opiates, such as terminal cancer patients. Even cannabis advocates, like Rob Kampia, the co-founder of the Marijuana Policy Project, acknowledge that they have always viewed medical marijuana laws primarily as a way to protect recreational users.

As for the marijuana-reduces-opiate-use theory, it is based largely on a single paper comparing overdose deaths by state before 2010 to the spread of medical marijuana laws— and the paper’s finding is probably a result of simple geographic coincidence. The opiate epidemic began in Appalachia, while the first states to legalize medical marijuana were in the West. Since 2010, as both the epidemic and medical marijuana laws have spread nationally, the finding has vanished. And the United States, the Western country with the most cannabis use, also has by far the worst problem with opioids.
Research on individual users—a better way to trace cause and effect than looking at aggregate state-level data—consistently shows that marijuana use leads to other drug use. For example, a January 2018 paper in the American Journal of Psychiatry showed that people who used cannabis in 2001 were almost three times as likely to use opiates three years later, even after adjusting for other potential risks.
Most of all, advocates have told you that marijuana is not just safe for people with psychiatric problems like depression, but that it is a potential treatment for those patients. On its website, the cannabis delivery service Eaze offers the “Best Marijuana Strains and Products for Treating Anxiety.” “How Does Cannabis Help Depression?” is the topic of an article on Leafly, the largest cannabis website. But a mountain of peer-reviewed research in top medical journals shows that marijuana can cause or worsen severe mental illness, especially psychosis, the medical term for a break from reality. Teenagers who smoke marijuana regularly are about three times as likely to develop schizophrenia, the most devastating psychotic disorder.

After an exhaustive review, the National Academy of Medicine found in 2017 that “cannabis use is likely to increase the risk of developing schizophrenia and other psychoses; the higher the use, the greater the risk.” Also that “regular cannabis use is likely to increase the risk for developing social anxiety disorder.”
***
Over the past decade, as legalization has spread, patterns of marijuana use—and the drug itself—have changed in dangerous ways.
Legalization has not led to a huge increase in people using the drug casually. About 15 percent of Americans used cannabis at least once in 2017, up from ten percent in 2006, according to a large federal study called the National Survey on Drug Use and Health. (By contrast, about 65 percent of Americans had a drink in the last year.) But the number of Americans who use cannabis heavily is soaring. In 2006, about three million Americans reported using cannabis at least 300 times a year, the standard for daily use. By 2017, that number had nearly tripled, to eight million, approaching the twelve million Americans who drank alcohol every day. Put another way, one in 15 drinkers consumed alcohol daily; about one in five marijuana users used cannabis that often.
Cannabis users today are also consuming a drug that is far more potent than ever before, as measured by the amount of THC—delta-9-tetrahydrocannabinol, the chemical in cannabis responsible for its psychoactive effects—it contains. In the 1970s, the last time this many Americans used cannabis, most marijuana contained less than two percent THC. Today, marijuana routinely contains 20 to 25 percent THC, thanks to sophisticated farming and cloning techniques—as well as to a demand by users for cannabis that produces a stronger high more quickly. In states where cannabis is legal, many users prefer extracts that are nearly pure THC. Think of the difference between near-beer and a martini, or even grain alcohol, to understand the difference.

These new patterns of use have caused problems with the drug to soar. In 2014, people who had diagnosable cannabis use disorder, the medical term for marijuana abuse or addiction, made up about 1.5 percent of Americans. But they accounted for eleven percent of all the psychosis cases in emergency rooms—90,000 cases, 250 a day, triple the number in 2006. In states like Colorado, emergency room physicians have become experts on dealing with cannabis-induced psychosis.
Cannabis advocates often argue that the drug can’t be as neurotoxic as studies suggest, because otherwise Western countries would have seen population-wide increases in psychosis alongside rising use. In reality, accurately tracking psychosis cases is impossible in the United States. The government carefully tracks diseases like cancer with central registries, but no such registry exists for schizophrenia or other severe mental illnesses.

On the other hand, research from Finland and Denmark, two countries that track mental illness more comprehensively, shows a significant increase in psychosis since 2000, following an increase in cannabis use. And in September of last year, a large federal survey found a rise in serious mental illness in the United States as well, especially among young adults, the heaviest users of cannabis.
According to this latter study, 7.5 percent of adults age 18-25 met the criteria for serious mental illness in 2017, double the rate in 2008. What’s especially striking is that adolescents age 12-17 don’t show these increases in cannabis use and severe mental illness.

A caveat: this federal survey doesn’t count individual cases, and it lumps psychosis with other severe mental illness. So it isn’t as accurate as the Finnish or Danish studies. Nor do any of these studies prove that rising cannabis use has caused population-wide increases in psychosis or other mental illness. The most that can be said is that they offer intriguing evidence of a link.
Advocates for people with mental illness do not like discussing the link between schizophrenia and crime. They fear it will stigmatize people with the disease. “Most people with mental illness are not violent,” the National Alliance on Mental Illness (NAMI) explains on its website. But wishing away the link can’t make it disappear. In truth, psychosis is a shockingly high risk factor for violence. The best analysis came in a 2009 paper in PLOS Medicine by Dr.Seena Fazel, an Oxford University psychiatrist and epidemiologist. Drawing on earlier studies, the paper found that people with schizophrenia are five times as likely to commit violent crimes as healthy people, and almost 20 times as likely to commit homicide.

NAMI’s statement that most people with mental illness are not violent is of course accurate, given that “most” simply means “more than half”; but it is deeply misleading. Schizophrenia is rare. But people with the disorder commit an appreciable fraction of all murders, in the range of six to nine percent.
“The best way to deal with the stigma is to reduce the violence,” says Dr. Sheilagh Hodgins, a professor at the University of Montreal who has studied mental illness and violence for more than 30 years.

The marijuana-psychosis-violence connection is even stronger than those figures suggest. People with schizophrenia are only moderately more likely to become violent than healthy people when they are taking antipsychotic medicine and avoiding recreational drugs. But when they use drugs, their risk of violence skyrockets. “You don’t just have an increased risk of one thing—these things occur in clusters,” Dr. Fazel told me.

Along with alcohol, the drug that psychotic patients use more than any other is cannabis: a 2010 review of earlier studies in Schizophrenia Bulletin found that 27 percent of people with schizophrenia had been diagnosed with cannabis use disorder in their lives. And unfortunately—despite its reputation for making users relaxed and calm—cannabis appears to provoke many of them to violence.
A Swiss study of 265 psychotic patients published in Frontiers of Forensic Psychiatry last June found that over a three-year period, young men with psychosis who used cannabis had a 50 percent chance of becoming violent. That risk was four times higher than for those with psychosis who didn’t use, even after adjusting for factors such as alcohol use. Other researchers have produced similar findings. A 2013 paper in an Italian psychiatric journal examined almost 1,600 psychiatric patients in southern Italy and found that cannabis use was associated with a ten-fold increase in violence.

The most obvious way that cannabis fuels violence in psychotic people is through its tendency to cause paranoia—something even cannabis advocates acknowledge the drug can cause. The risk is so obvious that users joke about it and dispensaries advertise certain strains as less likely to induce paranoia. And for people with psychotic disorders, paranoia can fuel extreme violence. A 2007 paper in the Medical Journal of Australia on 88 defendants who had committed homicide during psychotic episodes found that most believed they were in danger from the victim, and almost two-thirds reported misusing cannabis—more than alcohol and amphetamines combined.

Yet the link between marijuana and violence doesn’t appear limited to people with pre-existing psychosis. Researchers have studied alcohol and violence for generations, proving that alcohol is a risk factor for domestic abuse, assault, and even murder. Far less work has been done on marijuana, in part because advocates have stigmatized anyone who raises the issue. But studies showing that marijuana use is a significant risk factor for violence have quietly piled up. Many of them weren’t even designed to catch the link, but they did. Dozens of such studies exist, covering everything from bullying by high school students to fighting among vacationers in Spain.

In most cases, studies find that the risk is at least as significant as with alcohol. A 2012 paper in the Journal of Interpersonal Violence examined a federal survey of more than 9,000 adolescents and found that marijuana use was associated with a doubling of domestic violence; a 2017 paper in Social Psychiatry and Psychiatric Epidemiology examined drivers of violence among 6,000 British and Chinese men and found that drug use—the drug nearly always being cannabis—translated into a five-fold increase in violence.

Today that risk is translating into real-world impacts. Before states legalized recreational cannabis, advocates said that legalization would let police focus on hardened criminals rather than marijuana smokers and thus reduce violent crime. Some advocates go so far as to claim that legalization has reduced violent crime. In a 2017 speech calling for federal legalization, U.S. Senator Cory Booker said that “states [that have legalized marijuana] are seeing decreases in violent crime.” He was wrong.

The first four states to legalize marijuana for recreational use were Colorado and Washington in 2014 and Alaska and Oregon in 2015. Combined, those four states had about 450 murders and 30,300 aggravated assaults in 2013. Last year, they had almost 620 murders and 38,000 aggravated assaults—an increase of 37 percent for murders and 25 percent for aggravated assaults, far greater than the national increase, even after accounting for differences in population growth.

Knowing exactly how much of the increase is related to cannabis is impossible without researching every crime. But police reports, news stories, and arrest warrants suggest a close link in many cases. For example, last September, police in Longmont, Colorado, arrested Daniel Lopez for stabbing his brother Thomas to death as a neighbour watched. Daniel Lopez had been diagnosed with schizophrenia and was “self-medicating” with marijuana, according to an arrest affidavit.

In every state, not just those where marijuana is legal, cases like Lopez’s are far more common than either cannabis or mental illness advocates acknowledge. Cannabis is also associated with a disturbing number of child deaths from abuse and neglect—many more than alcohol, and more than cocaine, methamphetamines, and opioids combined—according to reports from Texas, one of the few states to provide detailed information on drug use by perpetrators.

These crimes rarely receive more than local attention. Psychosis-induced violence takes particularly ugly forms and is frequently directed at helpless family members. The elite national media prefers to ignore the crimes as tabloid fodder. Even police departments, which see this violence up close, have been slow to recognize the trend, in part because the epidemic of opioid overdose deaths has overwhelmed them.
So the black tide of psychosis and the red tide of violence are rising steadily, almost unnoticed, on a slow green wave.
***
For centuries, people worldwide have understood that cannabis causes mental illness and violence—just as they’ve known that opiates cause addiction and overdose. Hard data on the relationship between marijuana and madness dates back 150 years, to British asylum registers in India. Yet 20 years ago, the United States moved to encourage wider use of cannabis and opiates.
In both cases, we decided we could outsmart these drugs—that we could have their benefits without their costs. And in both cases we were wrong. Opiates are riskier, and the overdose deaths they cause a more imminent crisis, so we have focused on those. But soon enough the mental illness and violence that follow cannabis use will also be too widespread to ignore.

Whether to use cannabis, or any drug, is a personal decision. Whether cannabis should be legal is a political issue. But its precise legal status is far less important than making sure that anyone who uses it is aware of its risks. Most cigarette smokers don’t die of lung cancer. But we have made it widely known that cigarettes cause cancer, full stop. Most people who drink and drive don’t have fatal accidents. But we have highlighted the cases of those who do.
We need equally unambiguous and well-funded advertising campaigns on the risks of cannabis. Instead, we are now in the worst of all worlds. Marijuana is legal in some states, illegal in others, dangerously potent, and sold without warnings everywhere.

But before we can do anything, we—especially cannabis advocates and those in the elite media who have for too long credulously accepted their claims—need to come to terms with the truth about the science on marijuana. That adjustment may be painful. But the alternative is far worse, as the patients at Mid-Hudson Forensic Psychiatric Institute—and their victims—know.

Source: Imprimis January 2019 • Volume 48, Number 1

You’re aware America is under siege, fighting an opioid crisis that has exploded into a public-health emergency. You’ve heard of OxyContin, the pain medication to which countless patients have become addicted. But do you know that the company that makes Oxy and reaps the billions of dollars in profits it generates is owned by one family?

The newly installed Sackler Courtyard at London’s Victoria and Albert Museum is one of the most glittering places in the developed world. Eleven thousand white porcelain tiles, inlaid like a shattered backgammon board, cover a surface the size of six tennis courts. According to the V&A;’s director, the regal setting is intended to serve as a “living room for London,” by which he presumably means a living room for Kensington, the museum’s neighborhood, which is among the world’s wealthiest. In late June, Kate Middleton, the Duchess of Cambridge, was summoned to consecrate the courtyard, said to be the earth’s first outdoor space made of porcelain; stepping onto the ceramic expanse, she silently mouthed, “Wow.”

The Sackler Courtyard is the latest addition to an impressive portfolio. There’s the Sackler Wing at New York’s Metropolitan Museum of Art, which houses the majestic Temple of Dendur, a sandstone shrine from ancient Egypt; additional Sackler wings at the Louvre and the Royal Academy; stand-alone Sackler museums at Harvard and Peking Universities; and named Sackler galleries at the Smithsonian, the Serpentine, and Oxford’s Ashmolean. The Guggenheim in New York has a Sackler Center, and the American Museum of Natural History has a Sackler Educational Lab. Members of the family, legendary in museum circles for their pursuit of naming rights, have also underwritten projects of a more modest caliber—a Sackler Staircase at Berlin’s Jewish Museum; a Sackler Escalator at the Tate Modern; a Sackler Crossing in Kew Gardens. A popular species of pink rose is named after a Sackler. So is an asteroid.

The Sackler name is no less prominent among the emerald quads of higher education, where it’s possible to receive degrees from Sackler schools, participate in Sackler colloquiums, take courses from professors with endowed Sackler chairs, and attend annual Sackler lectures on topics such as theoretical astrophysics and human rights. The Sackler Institute for Nutrition Science supports research on obesity and micronutrient deficiencies. Meanwhile, the Sackler institutes at Cornell, Columbia, McGill, Edinburgh, Glasgow, Sussex, and King’s College London tackle psychobiology, with an emphasis on early childhood development.

The Sacklers’ philanthropy differs from that of civic populists like Andrew Carnegie, who built hundreds of libraries in small towns, and Bill Gates, whose foundation ministers to global masses. Instead, the family has donated its fortune to blue-chip brands, braiding the family name into the patronage network of the world’s most prestigious, well-endowed institutions. The Sackler name is everywhere, evoking automatic reverence; the Sacklers themselves, however, are rarely seen.

The descendants of Mortimer and Raymond Sackler, a pair of psychiatrist brothers from Brooklyn, are members of a billionaire clan with homes scattered across Connecticut, London, Utah, Gstaad, the Hamptons, and, especially, New York City. It was not until 2015 that they were noticed by Forbes, which added them to the list of America’s richest families. The magazine pegged their wealth, shared among twenty heirs, at a conservative $14 billion. (Descendants of Arthur Sackler, Mortimer and Raymond’s older brother, split off decades ago and are mere multi-millionaires.) To a remarkable degree, those who share in the billions appear to have abided by an oath of omertà: Never comment publicly on the source of the family’s wealth.

That may be because the greatest part of that $14 billion fortune tallied by Forbes came from OxyContin, the narcotic painkiller regarded by many public-health experts as among the most dangerous products ever sold on a mass scale. Since 1996, when the drug was brought to market by Purdue Pharma, the American branch of the Sacklers’ pharmaceutical empire, more than two hundred thousand people in the United States have died from overdoses of OxyContin and other prescription painkillers. Thousands more have died after starting on a prescription opioid and then switching to a drug with a cheaper street price, such as heroin. Not all of these deaths are related to OxyContin—dozens of other painkillers, including generics, have flooded the market in the past thirty years. Nevertheless, Purdue Pharma was the first to achieve a dominant share of the market for long-acting opioids, accounting for more than half of prescriptions by 2001.

According to the Centers for Disease Control, fifty-three thousand Americans died from opioid overdoses in 2016, more than the thirty-six thousand who died in car crashes in 2015 or the thirty-five thousand who died from gun violence that year. This past July, Donald Trump’s Commission on Combating Drug Addiction and the Opioid Crisis, led by New Jersey governor Chris Christie, declared that opioids were killing roughly 142 Americans each day, a tally vividly described as “September 11th every three weeks.” The epidemic has also exacted a crushing financial toll: According to a study published by the American Public Health Association, using data from 2013—before the epidemic entered its current, more virulent phase—the total economic burden from opioid use stood at about $80 billion, adding together health costs, criminal-justice costs, and GDP loss from drug-dependent Americans leaving the workforce. Tobacco remains, by a significant multiple, the country’s most lethal product, responsible for some 480,000 deaths per year. But although billions have been made from tobacco, cars, and firearms, it’s not clear that any of those enterprises has generated a family fortune from a single product that approaches the Sacklers’ haul from OxyContin.

Even so, hardly anyone associates the Sackler name with their company’s lone blockbuster drug. “The Fords, Hewletts, Packards, Johnsons—all those families put their name on their product because they were proud,” said Keith Humphreys, a professor of psychiatry at Stanford University School of Medicine who has written extensively about the opioid crisis. “The Sacklers have hidden their connection to their product. They don’t call it ‘Sackler Pharma.’ They don’t call their pills ‘Sackler pills.’ And when they’re questioned, they say, ‘Well, it’s a privately held firm, we’re a family, we like to keep our privacy, you understand.’ ”

The family’s leaders have pulled off three of the great marketing triumphs of the modern era: The first is selling OxyContin; the second is promoting the Sackler name; and the third is ensuring that, as far as the public is aware, the first and the second have nothing to do with one another.

To the extent that the Sacklers have cultivated a reputation, it’s for being earnest healers, judicious stewards of scientific progress, and connoisseurs of old and beautiful things. Few are aware that during the crucial period of OxyContin’s development and promotion, Sackler family members actively led Purdue’s day-to-day affairs, filling the majority of its board slots and supplying top executives. By any assessment, the family’s leaders have pulled off three of the great marketing triumphs of the modern era: The first is selling OxyContin; the second is promoting the Sackler name; and the third is ensuring that, as far as the public is aware, the first and the second have nothing to do with one another.


If you head north on I-95 through Stamford, Connecticut, you will spot, on the left, a giant misshapen glass cube. Along the building’s top edge, white lettering spells out ONE STAMFORD FORUM. No markings visible from the highway indicate the presence of the building’s owner and chief occupant, Purdue Pharma.

Originally known as Purdue Frederick, the first iteration of the company was founded in 1892 on New York’s Lower East Side as a peddler of patent medicines. For decades, it sustained itself with sales of Gray’s Glycerine Tonic, a sherry-based liquid of “broad application” marketed as a remedy for everything from anemia to tuberculosis. The company was purchased in 1952 by Arthur Sackler, thirty-nine, and was run by his brothers, Mortimer, thirty- six, and Raymond, thirty-two. The Sackler brothers came from a family of Jewish immigrants in Flatbush, Brooklyn. Arthur was a headstrong and ambitious provider, setting the tone—and often choosing the path—for his younger brothers. After attending medical school on Arthur’s dime, Mortimer and Raymond followed him to jobs at the Creedmoor psychiatric hospital in Queens. There, they coauthored more than one hundred studies on the biochemical roots of mental illness. The brothers’ research was promising—they were among the first to identify a link between psychosis and the hormone cortisone—but their findings were mostly ignored by their professional peers, who, in keeping with the era, favored a Freudian model of mental illness.

Concurrent with his psychiatric work, Arthur Sackler made his name in pharmaceutical advertising, which at the time consisted almost exclusively of pitches from so-called “detail men” who sold drugs to doctors door-to-door. Arthur intuited that print ads in medical journals could have a revolutionary effect on pharmaceutical sales, especially given the excitement surrounding the “miracle drugs” of the 1950s—steroids, antibiotics, antihistamines, and psychotropics. In 1952, the same year that he and his brothers acquired Purdue, Arthur became the first adman to convince The Journal of the American Medical Association, one of the profession’s most august publications, to include a color advertorial brochure.

In the 1960s, Arthur was contracted by Roche to develop an advertising strategy for a new antianxiety medication called Valium. This posed a challenge, because the effects of the medication were nearly indistinguishable from those of Librium, another Roche tranquilizer that was already on the market. Arthur differentiated Valium by audaciously inflating its range of indications. Whereas Librium was sold as a treatment for garden- variety anxiety, Valium was positioned as an elixir for a problem Arthur christened “psychic tension.” According to his ads, psychic tension, the forebear of today’s “stress,” was the secret culprit behind a host of somatic conditions, including heartburn, gastrointestinal issues, insomnia, and restless-leg syndrome. The campaign was such a success that for a time Valium became America’s most widely prescribed medication—the first to reach more than $100 million in sales. Arthur, whose compensation depended on the volume of pills sold, was richly rewarded, and he later became one of the first inductees into the Medical Advertising Hall of Fame.

As Arthur’s fortune grew, he turned his acquisitive instincts to the art market, quickly amassing the world’s largest private collection of ancient Chinese artifacts. According to a memoir by Marietta Lutze, his second wife, collecting, exhibiting, owning, and donating art fed Arthur’s “driving necessity for prestige and recognition.” Rewarding at first, collecting soon became a mania that took over his life. “Boxes of artifacts of tremendous value piled up in numerous storage locations,” she wrote, “there was too much to open, too much to appreciate; some objects known only by a packing list.” Under an avalanche of “ritual bronzes and weapons, mirrors and ceramics, inscribed bones and archaic jades,” their lives were “often in chaos.” “Addiction is a curse,” Lutze noted, “be it drugs, women, or collecting.”

When Arthur donated his art and money to museums, he often imposed onerous terms. According to a memoir written by Thomas Hoving, the Met director from 1967 to 1977, when Arthur established the Sackler Gallery at the Metropolitan Museum of Art to house Chinese antiquities, in 1963, he required the museum to collaborate on a byzantine tax-avoidance maneuver. In accordance with the scheme, the museum first soldArthur a large quantity of ancient artifacts at the deflated 1920s prices for which they had originally been acquired. Arthur then donated back the artifacts at 1960s prices, in the process taking a tax deduction so hefty that it likely exceeded the value of his initial donation. Three years later, in connection with another donation, Arthur negotiated an even more unusual arrangement. This time, the Met opened a secret chamber above the museum’s auditorium to provide Arthur with free storage for some five thousand objects from his private collection, relieving him of the substantial burden of fire protection and other insurance costs. (In an email exchange, Jillian Sackler, Arthur’s third wife, called Hoving’s tax-deduction story “fake news.” She also noted that New York’s attorney general conducted an investigation into Arthur’s dealings with the Met and cleared him of wrongdoing.)

In 1974, when Arthur and his brothers made a large gift to the Met—$3.5 million, to erect the Temple of Dendur—they stipulated that all museum signage, catalog entries, and bulletins referring to objects in the newly opened Sackler Wing had to include the names of all three brothers, each followed by “M.D.” (One museum official quipped, “All that was missing was a note of their office hours.”)

Hoving said that the Met hoped that Arthur would eventually donate his collection to the museum, but over time Arthur grew disgruntled over a series of rankling slights. For one, the Temple of Dendur was being rented out for parties, including a dinner for the designer Valentino, which Arthur called “disgusting.” According to Met chronicler Michael Gross, he was also denied that coveted ticket of arrival, a board seat. (Jillian Sackler said it was Arthur who rejected the board seat, after repeated offers by the museum.) In 1982, in a bad breakup with the Met, Arthur donated the best parts of his collection, plus $4 million, to the Smithsonian in Washington, D. C.


Arthur’s younger brothers, Mortimer and Raymond, looked so much alike that when they worked together at Creedmoor, they fooled the staff by pretending to be one another. Their physical similarities did not extend to their personalities, however. Tage Honore, Purdue’s vice-president of discovery of research from 2000 to 2005, described them as “like day and night.” Mortimer, said Honore, was “extroverted—a ‘world man,’ I would call it.” He acquired a reputation as a big-spending, transatlantic playboy, living most of the year in opulent homes in England, Switzerland, and France. (In 1974, he renounced his U. S. citizenship to become a citizen of Austria, which infuriated his patriotic older brother.) Like Arthur, Mortimer became a major museum donor and married three wives over the course of his life.

Mortimer had his own feuds with the Met. On his seventieth birthday, in 1986, the museum agreed to make the Temple of Dendur available to him for a party but refused to allow him to redecorate the ancient shrine: Together with other improvements, Mortimer and his interior designer, flown in from Europe, had hoped to spiff up the temple by adding extra pillars. Also galling to Mortimer was the sale of naming rights for one of the Sackler Wing’s balconies to a donor from Japan. “They sold it twice,” Mortimer fumed to a reporter from New York magazine. Raymond, the youngest brother, cut a different figure—“a family man,” said Honore. Kind and mild-mannered, he stayed with the same woman his entire life. Lutze concluded that Raymond owed his comparatively serene nature to having missed the worst years of the Depression. “He had summer vacations in camp, which Arthur never had,” she wrote. “The feeling of the two older brothers about the youngest was, ‘Let the kid enjoy himself.’ ”

Raymond led Purdue Frederick as its top executive for several decades, while Mortimer led Napp Pharmaceuticals, the family’s drug company in the UK. (In practice, a family spokesperson said, “the brothers worked closely together leading both companies.”) Arthur, the adman, had no official role in the family’s pharmaceutical operations. According to Barry Meier’s Pain Killer, a prescient account of the rise of OxyContin published in 2003, Raymond and Mortimer bought Arthur’s share in Purdue from his estate for $22.4 million after he died in 1987. In an email exchange, Arthur’s daughter Elizabeth Sackler, a historian of feminist art who sits on the board of the Brooklyn Museum and supports a variety of progressive causes, emphatically distanced her branch of the family from her cousins’ businesses. “Neither I, nor my siblings, nor my children have ever had ownership in or any benefit whatsoever from Purdue Pharma or OxyContin,” she wrote, while also praising “the breadth of my father’s brilliance and important works.” Jillian, Arthur’s widow, said her husband had died too soon: “His enemies have gotten the last word.”


The Sacklers have been millionaires for decades, but their real money—the painkiller money—is of comparatively recent vintage. The vehicle of that fortune was OxyContin, but its engine, the driving power that made them so many billions, was not so much the drug itself as it was Arthur’s original marketing insight, rehabbed for the era of chronic-pain management. That simple but profitable idea was to take a substance with addictive properties—in Arthur’s case, a benzo; in Raymond and Mortimer’s case, an opioid—and market it as a salve for a vast range of indications.

In the years before it swooped into the pain-management business, Purdue had been a small industry player, specializing in over-the-counter remedies like ear-wax remover and laxatives. Its most successful product, acquired in 1966, was Betadine, a powerful antiseptic purchased in industrial quantities by the U. S. government to prevent infection among wounded soldiers in Vietnam. The turning point, according to company lore, came in 1972, when a London doctor working for Cicely Saunders, the Florence Nightingale of the modern hospice movement, approached Napp with the idea of creating a timed-release morphine pill. A long-acting morphine pill, the doctor reasoned, would allow dying cancer patients to sleep through the night without an IV. At the time, treatment with opioids was stigmatized in the United States, owing in part to a heroin epidemic fueled by returning Vietnam veterans. “Opiophobia,” as it came to be called, prevented skittish doctors from treating most patients, including nearly all infants, with strong pain medication of any kind. In hospice care, though, addiction was not a concern: It didn’t matter whether terminal patients became hooked in their final days. Over the course of the seventies, building on a slow-release technology the company had already developed for an asthma medication, Napp created what came to be known as the “Contin” system. In 1981, Napp introduced a timed-release morphine pill in the UK; six years later, Purdue brought the same drug to market in the U. S. as MS Contin.

“The Sacklers have hidden their connection to their product,” said Keith Humphreys, a professor of psychiatry at Stanford University School of Medicine. “They don’t call it ‘Sackler Pharma.’ They don’t call their pills ‘Sackler pills.’”

MS Contin quickly became the gold standard for pain relief in cancer care. At the same time, a number of clinicians associated with the burgeoning chronic-pain movement started advocating the use of powerful opioids for noncancer conditions like back pain and neuropathic pain, afflictions that at their worst could be debilitating. In 1986, two doctors from Memorial Sloan Kettering hospital in New York published a fateful article in a medical journal that purported to show, based on a study of thirty-eight patients, that long-term opioid treatment was safe and effective so long as patients had no history of drug abuse. Soon enough, opioid advocates dredged up a letter to the editor published in The New England Journal of Medicine in 1980 that suggested, based on a highly unrepresentative cohort, that the risk of addiction from long-term opioid use was less than 1 percent. Though ultimately disavowed by its author, the letter ended up getting cited in medical journals more than six hundred times.

As the country was reexamining pain, Raymond’s eldest son, Richard Sackler, was searching for new applications for Purdue’s timed-release Contin system. “At all the meetings, that was a constant source of discussion—‘What else can we use the Contin system for?’ ” said Peter Lacouture, a senior director of clinical research at Purdue from 1991 to 2001. “And that’s where Richard would fire some ideas—maybe antibiotics, maybe chemotherapy—he was always out there digging.” Richard’s spitballing wasn’t idle blather. A trained physician, he treasured his role as a research scientist and appeared as an inventor on dozens of the company’s patents (though not on the patents for OxyContin). In the tradition of his uncle Arthur, Richard was also fascinated by sales messaging. “He was very interested in the commercial side and also very interested in marketing approaches,” said Sally Allen Riddle, Purdue’s former executive director for product management. “He didn’t always wait for the research results.” (A Purdue spokesperson said that Richard “always considered relevant scientific information when making decisions.”)

Perhaps the most private member of a generally secretive family, Richard appears nowhere on Purdue’s website. From public records and conversations with former employees, though, a rough portrait emerges of a testy eccentric with ardent, relentless ambitions. Born in 1945, he holds degrees from Columbia University and NYU Medical School. According to a bio on the website of the Koch Institute for Integrative Cancer Research at MIT, where Richard serves on the advisory board, he started working at Purdue as his father’s assistant at age twenty-six before eventually leading the firm’s R&D; division and, separately, its sales and marketing division. In 1999, while Mortimer and Raymond remained Purdue’s co-CEOs, Richard joined them at the top of the company as president, a position he relinquished in 2003 to become cochairman of the board. The few publicly available pictures of him are generic and sphinxlike—a white guy with a receding hairline. He is one of the few Sacklers to consistently smile for the camera. In a photo on what appears to be his Facebook profile, Richard is wearing a tan suit and a pink tie, his right hand casually scrunched into his pocket, projecting a jaunty charm. Divorced in 2013, he lists his relationship status on the profile as “It’s complicated.”

When Purdue eventually pleaded guilty to felony charges in 2007 for criminally “misbranding” OxyContin, it acknowledged exploiting doctors’ misconceptions about oxycodone’s strength.

Richard’s political contributions have gone mostly to Republicans—including Strom Thurmond and Herman Cain—though at times he has also given to Democrats. (His ex-wife, Beth Sackler, has given almost exclusively to Democrats.) In 2008, he wrote a letter to the editor of The Wall Street Journaldenouncing Muslim support for suicide bombing, a concern that seems to persist: Since 2014, his charitable organization, the Richard and Beth Sackler Foundation, has donated to several anti-Muslim groups, including three organizations classified as hate groups by the Southern Poverty Law Center. (The family spokesperson said, “It was never Richard Sackler’s intention to donate to an anti-Muslim or hate group.”) The foundation has also donated to True the Vote, the “voter-fraud watchdog” that was the original source for Donald Trump’s inaccurate claim that three million illegal immigrants voted in the 2016 election.

Former employees describe Richard as a man with an unnerving intelligence, alternately detached and pouncing. In meetings, his face was often glued to his laptop. “This was pre-smartphone days,” said Riddle. “He’d be typing away and you would think he wasn’t even listening, and then all of the sudden his head would pop up and he’d be asking a very pointed question.” He was notorious for peppering subordinates with unexpected, rapid-fire queries, sometimes in the middle of the night. “Richard had the mind of someone who’s going two hundred miles an hour,” said Lacouture. “He could be a little bit disconnected in the way he would communicate. Whether it was on the weekend or a holiday or a Christmas party, you could always expect the unexpected.”

Richard also had an appetite for micromanagement. “I remember one time he mailed out a rambling sales bulletin,” said Shelby Sherman, a Purdue sales rep from 1974 to 1998. “And right in the middle, he put in, ‘If you’re reading this, then you must call my secretary at this number and give her this secret password.’ He wanted to check and see if the reps were reading this shit. We called it ‘Playin’ Passwords.’ ” According to Sherman, Richard started taking a more prominent role in the company during the early 1980s. “The shift was abrupt,” he said. “Raymond was just so nice and down-to-earth and calm and gentle.” When Richard came, “things got a lot harder. Richard really wanted Purdue to be big—I mean really big.”

To effectively capitalize on the chronic-pain movement, Purdue knew it needed to move beyond MS Contin. “Morphine had a stigma,” said Riddle. “People hear the word and say, ‘Wait a minute, I’m not dying or anything.’ ” Aside from its terminal aura, MS Contin had a further handicap: Its patent was set to expire in the late nineties. In a 1990 memo addressed to Richard and other executives, Purdue’s VP of clinical research, Robert Kaiko, suggested that the company work on a pill containing oxycodone, a chemical similar to morphine that was also derived from the opium poppy. When it came to branding, oxycodone had a key advantage: Although it was 50 percent stronger than morphine, many doctors believed—wrongly—that it was substantially less powerful. They were deceived about its potency in part because oxycodone was widely known as one of the active ingredients in Percocet, a relatively weak opioid- acetaminophen combination that doctors often prescribed for painful injuries. “It really didn’t have the same connotation that morphine did in people’s minds,” said Riddle.

A common malapropism led to further advantage for Purdue. “Some people would call it oxy-codeine” instead of oxycodone, recalled Lacouture. “Codeine is very weak.” When Purdue eventually pleaded guilty to felony charges in 2007 for criminally “misbranding” OxyContin, it acknowledged exploiting doctors’ misconceptions about oxycodone’s strength. In court documents, the company said it was “well aware of the incorrect view held by many physicians that oxycodone was weaker than morphine” and “did not want to do anything ‘to make physicians think that oxycodone was stronger or equal to morphine’ or to ‘take any steps . . . that would affect the unique position that OxyContin’ ” held among physicians.

Purdue did not merely neglect to clear up confusion about the strength of OxyContin. As the company later admitted, it misleadingly promoted OxyContin as less addictive than older opioids on the market. In this deception, Purdue had a big assist from the FDA, which allowed the company to include an astonishing labeling claim in OxyContin’s package insert: “Delayed absorption, as provided by OxyContin tablets, is believed to reduce the abuse liability of a drug.”

The theory was that addicts would shy away from timed-released drugs, preferring an immediate rush. In practice, OxyContin, which crammed a huge amount of pure narcotic into a single pill, became a lusted-after target for addicts, who quickly discovered that the timed-release mechanism in OxyContin was easy to circumvent—you could simply crush a pill and snort it to get most of the narcotic payload in a single inhalation. This wasn’t exactly news to the manufacturer: OxyContin’s own packaging warned that consuming broken pills would thwart the timed-release system and subject patients to a potentially fatal overdose. MS Contin had contended with similar vulnerabilities, and as a result commanded a hefty premium on the street. But the “reduced abuse liability” claim that added wings to the sales of OxyContin had not been approved for MS Contin. It was removed from OxyContin in 2001 and would never be approved again for any other opioid.

The year after OxyContin’s release, Curtis Wright, the FDA examiner who approved the pharmaceutical’s original application, quit. After a stint at another pharmaceutical company, he began working for Purdue. In an interview with Esquire, Wright defended his work at the FDA and at Purdue. “At the time, it was believed that extended-release formulations were intrinsically less abusable,” he insisted. “It came as a rather big shock to everybody—the government and Purdue—that people found ways to grind up, chew up, snort, dissolve, and inject the pills.” Preventing abuse, he said, had to be balanced against providing relief to chronic-pain sufferers. “In the mid-nineties,” he recalled, “the very best pain specialists told the medical community they were not prescribing opioids enough. That was not something generated by Purdue—that was not a secret plan, that was not a plot, that was not a clever marketing ploy. Chronic pain is horrible. In the right circumstances, opioid therapy is nothing short of miraculous; you give people their lives back.” In Wright’s account, the Sacklers were not just great employers, they were great people. “No company in the history of pharmaceuticals,” he said, “has worked harder to try to prevent abuse of their product than Purdue.”


Purdue did not invent the chronic-pain movement, but it used that movement to engineer a crucial shift. Wright is correct that in the nineties patients suffering from chronic pain often received inadequate treatment. But the call for clinical reforms also became a flexible alibi for overly aggressive prescribing practices. By the end of the decade, clinical proponents of opioid treatment, supported by millions in funding from Purdue and other pharmaceutical companies, had organized themselves into advocacy groups with names like the American Pain Society and the American Academy of Pain Medicine. (Purdue also launched its own group, called Partners Against Pain.) As the decade wore on, these organizations, which critics have characterized as front groups for the pharmaceutical industry, began pressuring health regulators to make pain “the fifth vital sign”—a number, measured on a subjective ten-point scale, to be asked and recorded at every doctor’s visit. As an internal strategy document put it, Purdue’s ambition was to “attach an emotional aspect to noncancer pain” so that doctors would feel pressure to “treat it more seriously and aggressively.” The company rebranded pain relief as a sacred right: a universal narcotic entitlement available not only to the terminally ill but to every American.

The company rebranded pain relief as a sacred right: a universal narcotic entitlement available not only to the terminally ill but to every American. By 2001, annual OxyContin sales had surged past $1 billion.

OxyContin’s sales started out small in 1996, in part because Purdue first focused on the cancer market to gain formulary acceptance from HMOs and state Medicaid programs. Over the next several years, though, the company doubled its sales force to six hundred—equal to the total number of DEA diversion agents employed to combat the sale of prescription drugs on the black market—and began targeting general practitioners, dentists, OB/GYNs, physician assistants, nurses, and residents. By 2001, annual OxyContin sales had surged past $1 billion. Sales reps were encouraged to downplay addiction risks. “It was sell, sell, sell,” recalled Sherman. “We were directed to lie. Why mince words about it? Greed took hold and overruled everything. They saw that potential for billions of dollars and just went after it.” Flush with cash, Purdue pioneered a high-cost promotion strategy, effectively providing kickbacks—which were legal under American law—to each part of the distribution chain. Wholesalers got rebates in exchange for keeping OxyContin off prior authorization lists. Pharmacists got refunds on their initial orders. Patients got coupons for thirty- day starter supplies. Academics got grants. Medical journals got millions in advertising. Senators and members of Congress on key committees got donations from Purdue and from members of the Sackler family.

It was doctors, though, who received the most attention. “We used to fly doctors to these ‘seminars,’ ” said Sherman, which were, in practice, “just golf trips to Pebble Beach. It was graft.” Though offering perks and freebies to doctors was hardly uncommon in the industry, it was unprecedented in the marketing of a Schedule II narcotic. For some physicians, the junkets to sunny locales weren’t enough to persuade them to prescribe. To entice the holdouts—a group the company referred to internally as “problem doctors”—the reps would dangle the lure of Purdue’s lucrative speakers’ bureau. “Everybody was automatically approved,” said Sherman. “We would set up these little dinners, and they’d make their little fifteen-minute talk, and they’d get $500.”

Between 1996 and 2001, the number of OxyContin prescriptions in the United States surged from about three hundred thousand to nearly six million, and reports of abuse started to bubble up in places like West Virginia, Florida, and Maine. (Research would later show a direct correlation between prescription volume in an area and rates of abuse and overdose.) Hundreds of doctors were eventually arrested for running pill mills. According to an investigation in the Los Angeles Times, even though Purdue kept an internal list of doctors it suspected of criminal diversion, it didn’t volunteer this information to law enforcement until years later.

As criticism of OxyContin mounted through the aughts, Purdue responded with symbolic concessions while retaining its volume-driven business model. To prevent addicts from forging prescriptions, the company gave doctors tamper-resistant prescription pads; to mollify pharmacists worried about robberies, Purdue offered to replace, free of charge, any stolen drugs; to gather data on drug abuse and diversion, the company launched a national monitoring program called RADARS.

Critics were not impressed. In a letter to Richard Sackler in July 2001, Richard Blumenthal, then Connecticut’s attorney general and now a U. S. senator, called the company’s efforts “cosmetic.” As Blumenthal had deduced, the root problem of the prescription-opioid epidemic was the high volume of prescriptions written for powerful opioids. “It is time for Purdue Pharma to change its practices,” Blumenthal warned Richard, “not just its public-relations strategy.”

It wasn’t just that doctors were writing huge numbers of prescriptions; it was also that the prescriptions were often for extraordinarily high doses. A single dose of Percocet contains between 2.5 and 10mg of oxycodone. OxyContin came in 10-, 20-, 30-, 40-, and 80mg formulations and, for a time, even 160mg. Purdue’s greatest competitive advantage in dominating the pain market, it had determined early on, was that OxyContin lasted twelve hours, enough to sleep through the night. But for many patients, the drug lasted only six or eight hours, creating a cycle of crash and euphoria that one academic called “a perfect recipe for addiction.” When confronted with complaints about “breakthrough pain”—meaning that the pills weren’t working as long as advertised—Purdue’s sales reps were given strict instructions to tell doctors to strengthen the dose rather than increase dosing frequency.

Sales reps were encouraged to downplay addiction risks. “It was sell, sell, sell,” recalled Sherman. “We were directed to lie. Why mince words about it?”

Over the next several years, dozens of class-action lawsuits were brought against Purdue. Many were dismissed, but in some cases Purdue wrote big checks to avoid going to trial. Several plaintiffs’ lawyers found that the company was willing to go to great lengths to prevent Richard Sackler from having to testify under oath. “They didn’t want him deposed, I can tell you that much,” recalled Marvin Masters, a lawyer who brought a class-action suit against Purdue in the early 2000s in West Virginia. “They were willing to sit down and settle the case to keep from doing that.” Purdue tried to get Richard removed from the suit, but when that didn’t work, the company settled with the plaintiffs for more than $20 million. Paul Hanly, a New York class-action lawyer who won a large settlement from Purdue in 2007, had a similar recollection. “We were attempting to take Richard Sackler’s deposition,” he said, “around the time that they agreed to a settlement.” (A spokesperson for the company said, “Purdue did not settle any cases to avoid the deposition of Dr. Richard Sackler, or any other individual.”)

When the federal government finally stepped in, in 2007, it extracted historic terms of surrender from the company. Purdue pleaded guilty to felony charges, admitting that it had lied to doctors about OxyContin’s abuse potential. (The technical charge was “misbranding a drug with intent to defraud or mislead.”) Under the agreement, the company paid $600 million in fines and its three top executives at the time—its medical director, general counsel, and Richard’s successor as president—pleaded guilty to misdemeanor charges. The executives paid $34.5 million out of their own pockets and performed four hundred hours of community service. It was one of the harshest penalties ever imposed on a pharmaceutical company. (In a statement to Esquire, Purdue said that it “abides by the highest ethical standards and legal requirements.” The statement went on: “We want physicians to use their professional judgment, and we were not trying to pressure them.”)

Fifty-three thousand Americans died from opioid overdoses in 2016, more than the thirty-six thousand who died in car crashes in 2015 or the thirty-five thousand who died from gun violence that year.

No Sacklers were named in the 2007 suit. Indeed, the Sackler name appeared nowhere in the plea agreement, even though Richard had been one of the company’s top executives during most of the period covered by the settlement. He did eventually have to give a deposition in 2015, in a case brought by Kentucky’s attorney general. Richard’s testimony—the only known record of a Sackler speaking about the crisis the family’s company helped create—was promptly sealed. (In 2016, STAT, an online magazine owned by Boston Globe Media that covers health and medicine, asked a court in Kentucky to unseal the deposition, which is said to have lasted several hours. STAT won a lower-court ruling in May 2016. As of press time, the matter was before an appeals court.)

In 2010, Purdue executed a breathtaking pivot: Embracing the arguments critics had been making for years about OxyContin’s susceptibility to abuse, the company released a new formulation of the medication that was harder to snort or inject. Purdue seized the occasion to rebrand itself as an industry leader in abuse-deterrent technology. The change of heart coincided with two developments: First, an increasing number of addicts, unable to afford OxyContin’s high street price, were turning to cheaper alternatives like heroin; second, OxyContin was nearing the end of its patents. Purdue suddenly argued that the drug it had been selling for nearly fifteen years was so prone to abuse that generic manufacturers should not be allowed to copy it.

On April 16, 2013, the day some of the key patents for OxyContin were scheduled to expire, the FDA followed Purdue’s lead, declaring that no generic versions of the original OxyContin formulation could be sold. The company had effectively won several additional years of patent protection for its golden goose.


Opioid withdrawal, which causes aches, vomiting, and restless anxiety, is a gruesome process to experience as an adult. It’s considerably worse for the twenty thousand or so American babies who emerge each year from opioid-soaked wombs. These infants, suddenly cut off from their supply, cry uncontrollably. Their skin is mottled. They cannot fall asleep. Their bodies are shaken by tremors and, in the worst cases, seizures. Bottles of milk leave them distraught, because they cannot maneuver their lips with enough precision to create suction. Treatment comes in the form of drops of morphine pushed from a syringe into the babies’ mouths. Weaning sometimes takes a week but can last as long as twelve. It’s a heartrending, expensive process, typically carried out in the neonatal ICU, where newborns have limited access to their mothers.

But the children of OxyContin, its heirs and legatees, are many and various. The second- and third-generation descendants of Raymond and Mortimer Sackler spend their money in the ways we have come to expect from the not-so-idle rich. Notably, several have made children a focus of their business and philanthropic endeavors. One Sackler heir helped start an iPhone app called RedRover, which generates ideas for child-friendly activities for urban parents; another runs a child- development center near Central Park; another is a donor to charter-school causes, as well as an investor in an education start-up called AltSchool. Yet another is the founder of Beespace, an “incubator for emerging nonprofits,” which provides resources and mentoring for initiatives like the Malala Fund, which invests in education programs for women in the developing world, and Yoga Foster, whose objective is to bring “accessible, sustainable yoga programs into schools across the country.” Other Sackler heirs get to do the fun stuff: One helps finance small, interesting films like The Witch; a second married a famous cricket player; a third is a sound artist; a fourth started a production company with Boyd Holbrook, star of the Netflix series Narcos; a fifth founded a small chain of gastropubs in New York called the Smith.

Holding fast to family tradition, Raymond’s and Mortimer’s heirs declined to be interviewed for this article. Instead, through a spokesperson, they put forward two decorated academics who have been on the receiving end of the family’s largesse: Phillip Sharp, the Nobel-prize-winning MIT geneticist, and Herbert Pardes, formerly the dean of faculty at Columbia University’s medical school and CEO of New York-Presbyterian Hospital. Both men effusively praised the Sacklers’ donations to the arts and sciences, marveling at their loyalty to academic excellence. “Once you were on that exalted list of philanthropic projects,” Pardes told Esquire, “you were there and you were in a position to secure additional philanthropy. It was like a family acquisition.” Pardes called the Sacklers “the nicest, most gentle people you could imagine.” As for the family’s connection to OxyContin, he said that it had never come up as an issue in the faculty lounge or the hospital break room. “I have never heard one inch about that,” he said.

Pardes’s ostrichlike avoidance is not unusual. In 2008, Raymond and his wife donated an undisclosed amount to Yale to start the Raymond and Beverly Sackler Institute for Biological, Physical and Engineering Sciences. Lynne Regan, its current director, told me that neither students nor faculty have ever brought up the OxyContin connection. “Most people don’t know about that,” she said. “I think people are mainly oblivious.” A spokesperson for the university added, “Yale does not vet donors for controversies that may or may not arise.”

In May, a dozen lawmakers in Congress sent a bipartisan letter to the World Health Organization warning that Sackler-owned companies were preparing to flood foreign countries with legal narcotics.

The controversy surrounding OxyContin shows little sign of receding. In 2016, the CDC issued a startling warning: There was no good evidence that opioids were an effective treatment for chronic pain beyond six weeks. There was, on the other hand, an abundance of evidence that long-term treatment with opioids had harmful effects. (A recent paper by Princeton economist Alan Krueger suggests that chronic opioid use may account for more than 20 percent of the decline in American labor-force participation from 1999 to 2015.) Millions of opioid prescriptions for chronic pain had been written in the preceding two decades, and the CDC was calling into question whether many of them should have been written at all. At least twenty-five government entities, ranging from states to small cities, have recently filed lawsuits against Purdue to recover damages associated with the opioid epidemic.

The Sacklers, though, will likely emerge untouched: Because of a sweeping non-prosecution agreement negotiated during the 2007 settlement, most new criminal litigation against Purdue can only address activity that occurred after that date. Neither Richard nor any other family members have occupied an executive position at the company since 2003.

The American market for OxyContin is dwindling. According to Purdue, prescriptions fell 33 percent between 2012 and 2016. But while the company’s primary product may be in eclipse in the United States, international markets for pain medications are expanding. According to an investigation last year in the Los Angeles Times, Mundipharma, the Sackler-owned company charged with developing new markets, is employing a suite of familiar tactics in countries like Mexico, Brazil, and China to stoke concern for as-yet-unheralded “silent epidemics” of untreated pain. In Colombia, according to the L.A. Times, the company went so far as to circulate a press release suggesting that 47 percent of the population suffered from chronic pain.

Napp is the family’s drug company in the UK. Mundipharma is their company charged with developing new markets.

In May, a dozen lawmakers in Congress, inspired by the L.A. Timesinvestigation, sent a bipartisan letter to the World Health Organization warning that Sackler-owned companies were preparing to flood foreign countries with legal narcotics. “Purdue began the opioid crisis that has devastated American communities,” the letter reads. “Today, Mundipharma is using many of the same deceptive and reckless practices to sell OxyContin abroad.” Significantly, the letter calls out the Sackler family by name, leaving no room for the public to wonder about the identities of the people who stood behind Mundipharma.

The final assessment of the Sacklers’ global impact will take years to work out. In some places, though, they have already left their mark. In July, Raymond, the last remaining of the original Sackler brothers, died at ninety-seven. Over the years, he had won a British knighthood, been made an Officer of France’s Légion d’Honneur, and received one of the highest possible honors from the royal house of the Netherlands. One of his final accolades came in June 2013, when Anthony Monaco, the president of Tufts University, traveled to Purdue Pharma’s headquarters in Stamford to bestow an honorary doctorate. The Sacklers had made a number of transformational donations to the university over the years—endowing, among other things, the Sackler School of Graduate Biomedical Sciences. At Tufts, as at most schools, honorary degrees are traditionally awarded on campus during commencement, but in consideration of Raymond’s advanced age, Monaco trekked to Purdue for a special ceremony. The audience that day was limited to family members, select university officials, and a scrum of employees. Addressing the crowd of intimates, Monaco praised his benefactor. “It would be impossible to calculate how many lives you have saved, how many scientific fields you have redefined, and how many new physicians, scientists, mathematicians, and engineers are doing important work as a result of your entrepreneurial spirit.” He concluded, “You are a world changer.”

Source: https://www.esquire.com/news-politics/a12775932/sackler-family-oxycontin/ October 2017

For those who are still concerned about ‘evidence based science’ and ‘best medical and pharmaceutical practice’…the following ‘open letter’ with attachments was sent to all Federal Senators, NSW and Victorian Premiers last week. 

Dear Senator,
 
In the coming weeks/months, you will no doubt be presented with a Bill to consider changing both law and process to permit a new version of ‘medical marijuana’. On behalf of our Institute and a concerned public I would like you to carefully consider the following.

Firstly I write with some concerns about the consultation conducted on behalf of Victorian State government by the VLRC in Melbourne on May 6th this year and the now subsequent recommendations that have emerged from this very small Melbourne meeting (Less than 60 people in attendance! – This issue was directly raised with Victorian Health Minister earlier this year).

Whilst we gleaned from radio interviews with VLRC representatives prior to the consultation that the public discussions on the potential introduction of a new form ‘medical marijuana’ (different to existing medicinal forms of cannabis derived pharmaceuticals already in the Australian market) were not for changing laws to suit a particular agenda. It was instead implied that the purpose was to look at potential redundancies that might hinder best practice.  It was to be, for all intents and purposes an unbiased mechanism to: glean evidence, perspectives, opinions and ideas from the general public for consideration in the higher and more important discussion of wise, evidence based, best healthcare practice before making any move on the release of another version of therapeutic cannabis.

Conversely, our affiliate/colleagues experience of the very small Melbourne consultation did not reflect any of the above expectation. Rather those of our affiliates who attended observed the following:

  1. A seemingly deliberately emotively charged atmosphere, in favour of getting cannabis legalised for medical purposes. The tone seemed to be set to that end from the outset.
  2. The meeting was facilitated by representatives of the VLRC who appeared to have a bias toward the legalisation of ‘medical marijuana’ in manner that suited the self-medicating option, regardless of evidence based science.
  3. When attempts were made to present evidence contrary to the seemingly predetermined agenda of these facilitators, they were either quickly shut down (if they dared to speak in the first place) or continually ignored; apparently, dissenting opinions were not welcome. Whilst at the same time, proponents for ‘self-medication’ use of cannabis were given complete and unfettered access to the floor, producing statements such as:“Many, many people have been cured – from just about anything and everything.”
    “What would you rather have – infertility or 35 seizures a day?”
    “Random workplace drug testing is wrong.”Not only are these statements (now on record) outrageous, they are also utterly unsubstantiated by any legitimate clinical trial. This very small contingent of pro-cannabis lobbyists were permitted to simply spruik anecdotes with no evidence based presentation yet also had their evidenced-deprived opinions affirmed and validated by the facilitators.
  4. The facilitators appeared to infer that the Government (of Victoria, at least) already has legislation in place with this current ‘consultation’ process simply in play to validate those changes and therefore it is in essence a forgone conclusion. There was also a strong indication that either the A.M.A. or T.G.A. recommendations or processes would be ignored and negated wherever possible by simple legal changes.

Senator, it is a concern that if this particular experience of ours was repeated in other consultations with the same consensus manufacturing agenda, then this consultative process is a travesty.

If a government negates not only good evidence based science, but also established protective, best practice medical processes to enable a legal rite of passage for self-medication, it is placing itself at an extremely high risk of litigation. Future law-suits are likely, from the ‘victims’ of self-medicating regimes who will cite the changes in law that were NOT based on proper clinical trial or TGA and AMA recommendations and protocols.  When emotionally charged vitriol combines with vote chasing and misguided sympathies, it is the recipients of these untested substances that will be the final casualties – especially children! Compassion and wisdom dictate that all fair and democratic processes be engaged to maximise help and minimise harm, especially to children who will be the ones at greatest risk of an ill-advised self-medicating regime.

Senator, for purposes of clarification about the possible national legalisation of ‘another’ route/process/protocol for medicines are you able to confirm or deny that:

  1. The representations by the facilitators at the Melbourne consultation are in fact reflective of the pre-ordained intent of the public consultation documented above in not only Victoria, but other States and Territories?
  2. If not, will a review of the practice/method/behaviours be made into this particular process and subsequently the clearly questionable recommendations that have emerged from such narrow, non-evidence based and seemingly biased processes?
  3. A fair and proper representation of all views on this matter be gleaned from these meetings/consultations and interpreted and represented fairly without prejudice?
  4. A.M.A. and T.G.A. processes and protocols for best practice on medicines will be upheld and engaged, or simply ignored and by-passed?

Finally Senator, it is of grave concern that a pattern seems to be emerging from this ‘populist’ process, that best practice, evidence based protocols may simply be ignored and by passed.  If this is indeed the plan and the use of VLRC type agencies is the vehicle to do so, then the following must be raised.

The Dalgarno Institute ask:

  • Do you want your government and your ministerial role to be linked with a poorly considered and non-evidenced based process that enables a self-medicating policy – particularly for the ones the State has greatest responsibility to protect – the children?
  • Will your government and ministerial role be the ones who in so ignoring proper clinical processes facilitate a quasi-health regime that will precipitate immediate and long term unwanted side effects that can then be later subject to litigation and class-actions?
  • If an unqualified and unproven self-medicating mechanism is sanctioned and approved by government, and the inevitable damage (particularly to children) emerges, will the taxpayers of Australia have to fund the damages of an ill-conceived and non-TGA/AMA approved medical practice? Or will there be iron-clad caveats in place that ensure those who chose to use their own version of ‘medicine’ be the only ones liable for the outcomes of it, and not place further healthcare and monetary burden on the vast majority of tax-payers who have sought to follow best evidence-based and prescriptive practices?
  • If proper clinical trials and T.G.A and A.M.A. processes and protocols are negated or circumvented and a ‘new’ or ‘alternative’ process for registering, manufacturing, prescribing and dispensing marijuana as medicine be put in place, then how will you/your government  address the following important questions.
    • Who will be ‘growing’ and preparing this ‘medicine’?
    • Who will monitor content and quality of ‘medicine’?
    • Who will determine dosage rates and quantities?
    • What mechanisms will be in place to ensure quality control is followed?
    • What mechanisms will be in place to ensure, movement, dispensing and use of this ‘medicine’ is done without risk to non-patients?
    • Who will be able to prescribe this ‘medicine’ – Doctors, pharmacists, naturopaths, nurses, and counsellors? Who will monitor this process and ensure total safety?
    • What community safe-guards will be in place to ensure this new ‘medicine’ will not be misused?
    • Will the ‘medicine’ come in edible or smoked form and what safeguards will be in play around such a ‘medicine delivery’ system?
    • Will there be advertising and public promotion of this new form of ‘medicine’? Will that be strictly monitored to ensure no misinformation will mislead the public?
    • Which government department will oversee this process and how many more new protocols, processes, staff and finance will be required to set up this new vehicle for ‘medicine’ identification and management?
    • Who will be paying for this new and added cost?

We at Dalgarno Institute and its growing coalition remain very concerned for the overwhelming majority of Australians who are being kept in the dark about this new and illegitimate push to change evidence based processes and the laws that ensure those processes are protected. We are looking to you, in your role, to ensure that there is a genuine and robust pursuit of best medical and health practice outcomes for all Australians, particularly the most vulnerable – the young, very sick and disadvantaged – and that any mechanism that seeks to undermine that platform not be permitted to emerge under any circumstance.  Science and best health practice, NOT lawyers should determine pharmaceutical best practice.

I have also attached just a very small sample of the volumes of evidence-based data currently in the scientific space that raise clear warnings about a ‘new’ and untested version of cannabis as medicine. Please avail yourself of them and consult the people who do know better, compassion and good government demands it.
We look forward to receiving your response.

Sincerely Yours, 

Shane Varcoe
Executive Director
Dalgarno Institute

You can read our compassionate policy stance on M.M titled ‘CANNABIS AS MEDICINE? CAUTION NEEDED’!

https://dalgarnoinstitute.org.au/index.php/advocacy/dalgarno-aod-policy/86-open-letter-to-all-australian-politicians-regarding-new-version-of-medicinal-cannabis

Source: Email from Dalgarno Institute

September 2017

Thomas M. Nappe, DO* and Christopher O. Hoyte, MD

Abstract

Since marijuana legalization, pediatric exposures to cannabis have increased. To date, pediatric deaths from cannabis exposure have not been reported. The authors report an 11-month-old male who, following cannabis exposure, presented with central nervous system depression after seizure, and progressed to cardiac arrest and died. Myocarditis was diagnosed post-mortem and cannabis exposure was confirmed.

Given the temporal relationship of these two rare occurrences – cannabis exposure and sudden death secondary to myocarditis in an 11-month-old – as well as histological consistency with drug-induced myocarditis without confirmed alternate causes, and prior reported cases of cannabis-associated myocarditis, a possible relationship exists between cannabis exposure in this child and myocarditis leading to death. In areas where marijuana is commercially available or decriminalized, the authors urge clinicians to preventively counsel parents and to include cannabis exposure in the differential diagnosis of patients presenting with myocarditis.

INTRODUCTION

Since marijuana legalization, pediatric exposures to cannabis have increased, resulting in increased pediatric emergency department (ED) visits. Neurologic toxicity is most common after pediatric exposure; however, gastrointestinal and cardiopulmonary toxicity are reported. According to a retrospective review of 986 pediatric cannabis ingestions from 2005 to 2011, pediatric exposure has been specifically linked to a multitude of symptoms including, but not limited to, drowsiness, lethargy, irritability, seizures, nausea and vomiting, respiratory depression, bradycardia and hypotension.Prognosis is often reassuring. 

Specific myocardial complications related to cannabis toxicity that are well documented in adolescence through older adulthood include acute coronary syndrome, cardiomyopathy, myocarditis, pericarditis, dysrhythmias and cardiac arrest. To date, there are no reported pediatric deaths from myocarditis after confirmed, recent cannabis exposure. The authors report an 11-month-old male who, following cannabis exposure, presented in cardiac arrest after seizure and died. Myocarditis was diagnosed post-mortem and cannabis exposure was confirmed. Analyses of serum cannabis metabolites, post-mortem infectious testing, cardiac histopathology, as well as clinical course, support a potential link between the cannabis exposure and myocarditis that would justify preventive parental counseling and consideration of urine drug screening in this reported setting.

CASE REPORT

An 11-month-old male with no known past medical history presented to the ED with central nervous system (CNS) depression and then went into cardiac arrest. The patient was lethargic for two hours after awakening that morning and then had a seizure. During the prior 24–48 hours, he was irritable with decreased activity and was later retching. He was noted to be healthy before developing these symptoms. Upon arrival in the ED, he was unresponsive with no gag reflex. Vital signs were temperature 36.1° Celsius, heart rate 156 beats per minute, respiratory rate 8 breaths per minute, oxygen saturation 80% on room air.

Physical exam revealed a well-nourished, 20.5 lb., 11-month-old male, with normal development, no trauma, normal oropharynx, normal tympanic membranes, no lymphadenopathy, tachycardia, clear lungs, normal abdomen and Glasgow Coma Scale rating of 4. He was intubated for significant CNS depression and required no medications for induction or paralysis. Post-intubation chest radiograph is shown in Image 2. He subsequently became bradycardic with a heart rate in the 40s with a wide complex rhythm. Initial electrocardiogram (ECG) was performed and is shown in Image 1.

He then became pulseless, and cardiopulmonary resuscitation was initiated. Laboratory analysis revealed sodium 136 mmol/L, potassium 7.7 mmol/L, chloride 115 mmol/L, bicarbonate 8.0 mmol/L, blood urea nitrogen 24 mg/dL, creatinine 0.9 mg/dL, and glucose 175 mg/dL Venous blood gas pH was 6.77. An ECG was repeated (Image 3). He received intravenous fluid resuscitation, sodium bicarbonate infusion, calcium chloride, insulin, glucose, ceftriaxone and four doses of epinephrine. Resuscitation continued for approximately one hour but the patient ultimately died.

Initial electrocardiogram demonstrating wide-complex tachycardia.

Post-intubation chest radiograph. Measurement indicates distance of endotracheal tube tip above carina.

Repeat electrocardiogram showing disorganized rhythm, peri-arrest.

Further laboratory findings in the ED included a complete blood count (CBC) with differential, liver function tests (LFTs), one blood culture and toxicology screen. CBC demonstrated white blood cell count 13.8 K/mcL with absolute neutrophil count of 2.5 K/mcL and absolute lymphocyte count of 10.7 K/mcL, hemoglobin 10.0 gm/dL, hematocrit 34.7%, and platelet count 321 K/mcL. LFTs showed total bilirubin 0.6 mg/dL, aspartate aminotransferase 77 IU/L, and alanine transferase 97 IU/U. A single blood culture from the right external jugular vein revealed aerobic gram-positive rods that were reported two days later as Bacillus species (not Bacillus anthracis). Toxicology screening revealed urine enzyme-linked immunosorbent assay positive for tetrahydrocannabinol-carboxylic acid (THC-COOH) and undetectable serum acetaminophen and salicylate concentrations. Route and timing of exposure to cannabis were unknown.

Autopsy revealed a non-dilated heart with normal coronary arteries. Microscopic examination showed a severe, diffuse, primarily lymphocytic myocarditis, with a mixed cellular infiltrate in some areas consisting of histiocytes, plasma cells, and eosinophils. Myocyte necrosis was also observed. There was no evidence of concomitant bacterial or viral infection based on post-mortem cultures obtained from cardiac and peripheral blood, lung pleura, nasopharynx and cerebrospinal fluid. Post-mortem cardiac blood analysis confirmed the presence of Δ-9-carboxy-tetrahydrocannabinol (Δ-9-carboxy-THC) at a concentration of 7.8 ng/mL. Additional history disclosed an unstable motel-living situation and parental admission of drug possession, including cannabis.

DISCUSSION

As of this writing, this is the first reported pediatric death associated with cannabis exposure. Given the existing relationship between cannabis and cardiovascular (CV) toxicity, as well as the temporal progression of events, post-mortem analysis, and previously reported cases of cannabis-induced myocarditis, the authors propose a relationship between cannabis exposure in this patient and myocarditis, leading to cardiac arrest and ultimately death. This occurrence should justify consideration of urine drug screening for cannabis in pediatric patients presenting with myocarditis of unknown etiology in areas where cannabis is widely used. In addition, parents should be counseled regarding measures to prevent such exposures.

The progressive clinical presentation of this patient during the prior 24–48 hours, including symptoms of somnolence, lethargy, irritability, nausea, seizure and respiratory depression are consistent with previously documented, known complications of recent cannabis exposure in the pediatric population. It is well known that common CV effects of cannabis exposure include tachycardia and decreased vascular resistance with acute use and bradycardia in more chronic use. These effects are believed to be multifactorial, and evidence suggests that cannabinoid effect on the autonomic nervous system, peripheral vasculature, cardiac microvasculature, and myocardial tissue and Purkinje fibers are all likely contributory. The pathogenesis of myocarditis is not fully understood. In general, myocarditis results from direct damage to myocytes from an offending agent such as a virus, or in this case, potentially a toxin. The resulting cellular injury leads to a local inflammatory response. Destruction of cardiac tissue may result in myocyte necrosis and arrhythmogenic activity, or cellular remodeling in chronic myocarditis.

Autopsy findings in this patient were consistent with noninfectious myocarditis as a cause of death. The histological findings of myocyte necrosis with mature lymphocytic mixed cellular infiltrate are consistent with drug-induced, toxic myocarditis.The presence of THC metabolites in the patient’s urine and serum, most likely secondary to ingestion, is the only uncovered risk factor in the etiology for his myocarditis. This is highly unlikely attributable to passive exposure.

It is difficult to extrapolate a specific time of cannabis ingestion given the unknown dose of THC, the individual variability of metabolism and excretion, as well as the lack of data on this topic in the pediatric population and post-mortem redistribution (PMR) kinetics. However, the THC metabolite detected in the patient’s blood, Δ-9-carboxy-THC, is known to peak in less than six hours and be detectable for at least a day, while the parent compound, tetrahydrocannabinol (THC), is expected to rapidly metabolize and distribute much more quickly, being potentially undetectable six hours after exposure in an infrequent user. 

The parent compound was below threshold for detection in this patient’s blood. In addition, if cannabis ingestion occurred the day of presentation, it would have been more likely that THC would have been detected with its metabolite after PMR. Given this information, the authors deduce that cannabis consumption occurred within the recent two to six days, assuming this was a single, acute high-potency ingestion. This time frame would overlap with the patient’s symptomatology and allow time for the development of myocarditis, thus supporting cannabis as the etiology.

The link between cannabis use and myocarditis has been documented in multiple teenagers and young adults. In 2008 Leontiadis reported a 16-year-old with severe heart failure requiring a left ventricular assist device, associated with biopsy-diagnosed myocarditis.The authors attributed the heart failure to cannabis use of unknown chronicity. In 2014 Rodríguez-Castro reported a 29-year-old male who had two episodes of myopericarditis several months apart.Each episode occurred within two days of smoking cannabis.In 2016, Tournebize reported a 15-year-old male diagnosed with myocarditis, clinically and by cardiac magnetic resonance imaging, after initiating regular cannabis use eight months earlier. There were no other causes for myocarditis, including infectious, uncovered by these authors, and no adulterants were identified in these patients’ consumed marijuana.Unlike our patient, all three of these previously reported patients recovered.

In the age of legalized marijuana, children are at increased risk of exposure, mainly through ingestion of food products, or “edibles.”These products are attractive in appearance and have very high concentrations of THC, which can make small exposures exceptionally more toxic in small children.

Limitations in this report include the case study design, the limitations on interpreting an exact time, dose and route of cannabis exposure, the specificity of histopathology being used to classify etiology of myocarditis, and inconsistent blood culture results. The inconsistency in blood culture results also raises concern of a contributing bacterial etiology in the development of myocarditis, lending to the possibility that cannabis may have potentially induced the fatal symptomatology in an already-developing silent myocarditis. However, due to high contaminant rates associated with bacillus species and negative subsequent blood cultures, the authors believe this was more likely a contaminant. In addition, the patient had no source of infection on exam or recent history and was afebrile without leukocytosis. All of his subsequent cultures from multiple sites were negative.

CONCLUSION

Of all the previously reported cases of cannabis-induced myocarditis, patients were previously healthy and no evidence was found for other etiologies. All of the prior reported cases were associated with full recovery. In this reported case, however, the patient died after myocarditis-associated cardiac arrest. Given two rare occurrences with a clear temporal relationship – the recent exposure to cannabis and the myocarditis-associated cardiac arrest – we believe there exists a plausible relationship that justifies further research into cannabis-associated cardiotoxicity and related practice adjustments. In states where cannabis is legalized, it is important that physicians not only counsel parents on preventing exposure to cannabis, but to also consider cannabis toxicity in unexplained pediatric myocarditis and cardiac deaths as a basis for urine drug screening in this setting.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5965161/ March 2017

The medical marijuana market is in a downward spiral as businesses, lured by big money, shift to recreational

At the height of the medical marijuana industry there were 420 dispensaries in Oregon. Now there are only eight.

In 2015, Erich Berkovitz opened his medical marijuana processing company, PharmEx, with the intention of getting sick people their medicine. His passion stemmed from his own illness. Berkovitz has Tourette syndrome, which triggers ticks in his shoulder that causes chronic pain. Cannabis takes that away.

Yet in the rapidly changing marijuana landscape, PharmEx is now one of three medical-only processors left in the entire state of Oregon.

On the retail end, it’s also grim. At the height of the medical marijuana industry in 2016, there were 420 dispensaries in Oregon available to medical cardholders. Today, only eight are left standing and only one of these medical dispensaries carries Berkovitz’s products.

Ironically, Oregon’s medical marijuana market has been on a downward spiral since the state legalized cannabis for recreational use in 2014. The option of making big money inspired many medical businesses to go recreational, dramatically shifting the focus away from patients to consumers. In 2015, the Oregon Liquor Control Commission (OLCC) took over the recreational industry. Between 2016 and 2018, nine bills were passed that expanded consumer access to marijuana while changing regulatory procedures on growing, processing and packaging.

In the shuffle, recreational marijuana turned into a million-dollar industry in Oregon, while the personalized patient-grower network of the medical program quietly dried up.

Now, sick people are suffering.

“For those patients that would need their medicine in an area that’s opted out of recreational sales, and they don’t have a grower or they’re not growing on their own, it does present a real access issue for those individuals,” said André Ourso, an administrator for the Center for Health Protection at the Oregon Health Authority. The woes of the Oregon Medical Marijuana Program (OMMP) were outlined in a recently published report by the Oregon Health Authority. The analysis found the program suffers from “insufficient and inaccurate reporting and tracking,” “inspections that did not keep pace with applications”, and “insufficient funding and staffing”.

Operating outside of Salem, Oregon, PharmEx primarily makes extracts – a solid or liquid form of concentrated cannabinoids. Through his OMMP-licensed supply chain, he gets his high dose medicine to people who suffer from cancer, Crohn’s, HIV and other autoimmune diseases. Many are end-of-life patients.

These days, most recreational dispensaries sell both consumer and medical products, which are tax-free for cardholders. The problem for Berkovitz is that he’s only medically licensed. This means recreational dispensaries can’t carry his exacts. Legally, they can

only sell products from companies with an OLCC license. Since issuing almost 1,900 licenses, the OLCC has paused on accepting new applications until further notice.

Limits on THC – a powerful active ingredient in cannabis products – are also an issue, according to Berkovitz. With the dawn of recreational dispensaries, the Oregon Health Authority began regulating THC content. A medical edible, typically in the form of a sweet treat, is now capped at 100mg THC, which Berkovitz says is not enough for a really sick person.

“If you need two 3000mg a day orally and you’re capped at a 100mg candy bar, that means you need 20 candy bars, which cost $20 a pop,” he said. “So you’re spending $400 a day to eat 20 candy bars.”

“The dispensaries never worked for high dose patients, even in the medical program,” continued Berkovitz. “What worked was people who grew their own and were able to legally process it themselves, or go to a processor who did it at a reasonable rate.”

But with increased processing and testing costs, and a decrease on the number of plants a medical grower can produce, patients are likely to seek cannabis products in a more shadowy place – the black market.

“All the people that we made these laws for – the ones who are desperately ill – are being screwed right now and are directed to the black market,” said Karla Kay, the chief of operations at PharmEx.

Kay, who also holds a medical marijuana card for her kidney disease, said some patients she knows have resorted to buying high dose medical marijuana products illegally from local farmers markets – in a state that was one of the first to legally establish a medical cannabis industry back in 1998.

Moreover, the networks between medical patients, growers and processors have diminished.

The OMMP maintains a record of processors and the few remaining dispensaries, but no published list of patients or grow sites – a privacy right protected under Oregon law, much to the chagrin of law enforcement.

According to the Oregon Health Authority’s report, just 58 of more than 20,000 medical growers were inspected last year.

In eastern Oregon’s Deschutes county, the sheriff’s office and the district attorney have repeatedly requested the location of each medical marijuana grower in their county. They’ve been consistently denied by the Oregon Health Authority.

Recently, the sheriff has gone as far as hiring a detective to focus solely on enforcing marijuana operations.

“There is an overproduction of marijuana in Oregon and the state doesn’t have adequate resources to enforce the laws when it comes to recreational marijuana, medical marijuana, as well as ensuring the growth of hemp is within the THC guidelines,” said the Deschutes sheriff, Shane Nelson. As of last February, the state database logged 1.1m pounds of cannabis flower, as reported by the Willamette Week in April. That’s three times what residents buy in a year, which means the excess is slipping out of the regulated market. To help curb the trend, senate bill 1544 was passed this year to funnel part of the state’s marijuana tax revenues into the Criminal Justice Commission and provide the funding needed to go after the black market, especially when it comes to illicit Oregon weed being smuggled to other states. The program’s priority is “placed on rural areas with lots of production and diversion, and little law enforcement”, said Rob Bovett, the legal counsel with the Association of Oregon Counties, who crafted the bill.

In a May 2018 memo on his marijuana enforcement priorities, Billy J Williams, a US attorney for the district of Oregon, noted that “since broader legalization took effect in 2015, large quantities of marijuana from Oregon have been seized in 30 states, most of which continue to prohibit marijuana.”

As of 1 July, however, all medical growers that produce plants for three or more patients – about 2,000 growers in Oregon – must track their marijuana from seed-to-sale using the OLCC’s Cannabis Tracking System.

Berkovitz, however, is looking to cut out the middle man (namely dispensaries) to keep PharmEx afloat. “The only way the patients are going to have large, high doses of medicine is if we revive the patient-grower networks. They need to communicate with each other. No one’s going to get rich, but everybody involved will get clean medicine from the people they trust at a more affordable rate.”

Source: https://www.theguardian.com/society/2018/jul/31/oregon-cannabis-medical-marijuana-problems-sick-people

There are several principal pathways to inheritable genotoxicity, mutagenicity and teratogenes is induced by cannabis which are known and well established at this time including the following.
These three papers discuss different aspects of these effects.

1) Stops Brain Waves and Thinking The brain has both stimulatory and inhibitory pathways.  GABA is the main brain inhibitory pathway. Brain centres talk to each other on gamma (about 40 cycles/sec) and theta frequencies (about 5 cycles/sec), where the theta waves are  used as the carrier waves for the gamma wave which then interacts like harmonics in music.
The degree to which the waves are in and out of phase carries information which can be monitored externally. GABA (γ-aminobutyric acid) inhibition is key to the generation of the synchronized firing which underpins these various brain oscillations. These GABA transmissions are controlled presynaptically by type 1 cannabinoid receptors (CB1R’s) and CB1R stimulation shuts them down. This is why cannabis users forget and fall asleep.

2) Blocks GABA Pathway and Brain Formation GABA is also a key neurotransmitter in  brain formation in that it guides and direct neural stem cell formation and transmission and development and growth of the cerebral cortex and other major brain areas. Gamma and theta  brain waves also direct neural stem cell formation, sculpting and connectivity.

Derangements then of GABA physiology imply that the brain will not form properly. Thin frontal cortical  plate measurements have been shown in humans prenatally exposed to cannabis by fMRI.
This implies that their brains can never be structurally normal which then explains the long lasting and persistent defects identified into adulthood.

3) Epigenetic Damage DNA not only carries the genetic hardware of our genetic code but it also carries the software of the code which works like traffic lights along the sequence of DNA bases to direct when to switch the genes on and off. This is known as the “epigenetic code”.

Fetal alcohol syndrome is believed to be due to damage to the software epigenetic code. The long lasting intellectual, mood regulation, attention and concentration defects which have been described after in utero cannabis exposure in the primary, middle and high schools and as college age young adults are likely due to these defects. Epigenetics “sets in stone” the errors of brain structure made in (2) above.

4) Arterial Damage. Cannabis has a well described effect to damage arteries through (CB1R’s) (American Heart Association 2007) which they carry in high concentration (Nature Reviews Cardiology 2018). In adults this causes heart attack (500% elevation in the first hour after smoking), stroke, severe cardiac arrhythmias including sudden cardiac death; but in developing babies CB1R’s acting on the developing heart tissues can lead to at least six major cardiac defects (Atrial- ventricular- and mixed atrio-ventricular and septal defects, Tetralogy of Fallot, Epstein’s deformity amongst others), whilst constriction of various babies’ arteries can lead to serious side effects such as gastroschisis (bowels hanging out) and possibly absent limbs (in at least one series).

5) Disruption of Mitotic Spindle. When cells divide the separating chromosomes actually slide along “train tracks” which are long chains made of tubulin. The tubulin chains are called “microtubules” and the whole football-shaped structure is called a “mitotic spindle”. Cannabis inhibits tubulin formation, disrupting microtubules and the mitotic spindle causing the separating chromosomes to become cut off in tiny micronuclei, where they eventually become smashed up and pulverized into “genetic junk”, which leads to foetal malformations, cancer and cell death. High rates of Down’s syndrome, chromosomal anomalies and cancers in cannabis exposed babies provide clinical evidence of this.

6) Defective Energy Generation & Downstream DNA Damage DNA is the crown jewel of the cell and its most complex molecule. Maintaining it in good repair is a very energy intensive process. Without energy DNA cannot be properly maintained. Cannabis has been known to reduce cellular energy production by the cell’s power plants, mitochondria, for many decades now. This has now been firmly linked with increased DNA damage, cancer formation and aging of the cells and indeed the whole organism. As it is known to occur in eggs and sperm, this will also damage the quality of the germ cells which go into forming the baby and lead directly to damaged babies and babies lost and wasted through spontaneous miscarriage and therapeutic termination for severe deformities.

7) Cancer induction Cannabis causes 12 cancers and has been identified as a carcinogen by the California Environmental Protection agency (2009). This makes it also a mutagen. 4 of these cancers are inheritable to children; i.e. inheritable carcinogenicity and mutagenicity. All four studies in testicular cancer are strongly positive (elevation by three fold). Carcinogen = mutagen = teratogen.

8) Colorado’s Teratology Profile. From the above described teratological profile we would expect exactly the profile of congenital defects which have been identified in Colorado (higher total defects and heart defects, and chromosomal defects) and Ottawa in Canada (long lasting and persistent brain damage seen on both functional testing and fMRI brain scans in children exposed in utero) where cannabis use has become common.

Gastroschisis was shown to be higher in all seven studies looking at this; and including in Canada, carefully controlled studies. Moreover in Australia, Canada, North Carolina, Colorado, Mexico and New Zealand, gastroschisis and sometimes other major congenital defects cluster where cannabis use is highest. Colorado 2000-2013 has experienced an extra 20,152 severely abnormal births above the rates prior to cannabis liberalization which if applied to the whole USA would equate to more than 83,000 abnormal babies live born annually (and probably about that number again therapeutically aborted); actually much more since both the number of users and concentration of cannabis have risen sharply since 2013, and cannabis has been well proven to be much more severely genotoxic at higher doses.

9) Cannabidiol is also Genotoxic and tests positive in many genotoxicity assays, just as tetrahydrocannabinol does.

10) Births defects registry data needs to be open and transparent and public. At present it is not. This looks too much like a cover up.

Source: Email from Dr Stuart Reece to Drug Watch International members May 2018

Eleonora Patsenker, Ph.D. and Felix Stickel, M.D., Ph.D.

Mounting evidence indicates that the endocannabinoid (EC) system (ECS) plays an important role in various liver diseases including viral hepatitis, nonalcoholic fatty liver disease (NAFLD), alcoholic liver disease, hepatic encephalopathy, and autoimmune hepatitis. The ECS also impacts on involved processes such as hepatic hemodynamics, nutrient intake and turnover, and ischemia/reperfusion (I/R) after liver transplantation. Although this involvement is undisputed, therapeutic implications regarding the ECS are just beginning to emerge; so far, no approved drug
acting specifically on the ECS is available.

Source: https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/cld.527 2016

 

 

Source:

http://www.pnas.org/content/109/40/E2657

July 2012

By William Ross Perlman, Ph.D., CMPP, NIDA Notes Contributing Writer

This research:

  • Identified a gene variant that promotes impulsive behavior and enhanced responses to heroin in rats.
  • Linked the corresponding human gene variant to increased risk for impulsivity and drug use.

People who are highly impulsive and those diagnosed with ADHD are at increased risk for substance use disorders (SUD). Recent research implicates a variant of the gene for a protein called cAMP-response element modulator (CREM) in these associations. Drs. Michael L. Miller and Yasmin L. Hurd from the Icahn School of Medicine at Mount Sinai in New York, with colleagues from several other institutions, showed that the gene variant promotes impulsive and hyperactive behavior in both animals and humans, and can contribute to a person’s risk for developing SUD.

Of Rats…

The Icahn researchers began their investigations with a strain of rats that exhibit impulsive behaviors resembling human attention-deficit/hyperactivity disorder (ADHD). Initial experiments confirmed that, compared with a strain (Western Kyoto) of rats that are not known for impulsivity, these “spontaneously hypertensive” (SH) rats:

  • Were more impatient to receive rewards, fidgeted more while waiting to receive rewards, ran around more, and were more attracted to novel experiences.
  • Self-administered more heroin and, when it was made unavailable, gave up seeking it less readily.  
  • Had enhanced elevation of dopamine levels in response to heroin.

The researchers screened the rats’ DNA for genetic differences that might contribute to these behavioral differences. The results revealed that the two strains carried different variants of the gene for CREM. As a result, the SH rats had lower concentrations of CREM in the core of the nucleus accumbens—a key brain region governing reward and movement.

…And People

 

Figure 1. A CREM Gene Variant Increases HyperactivityHyperactivity scores were higher in ADHD subjects than in control subjects. In addition, ADHD subjects who carried at least one copy of the less highly expressed A variant (i.e., with the G/A or A/A CREM genotype) reported significantly higher hyperactivity than did those carrying only the more highly expressed G variant (i.e., with the G/G genotype). Genotype had no effect on hyperactivity in non-ADHD control subjects

The researchers used genetic and behavioral evidence from previous studies conducted by other researchers to demonstrate that the corresponding variant in the human CREM gene similarly predisposes people to impulsivity. This variant occupies approximately the same position on the human gene that the rodent variant occupies on the rodent gene. At this site, known as rs12765063, the CREM gene exists in two versions—called A and G—and the A variant dials down CREM production. In one study, preschool children with the A variant were found to be more distractible and to engage in more dangerous activities than peers with only the G variant (Figure 1). In another, among adolescents with ADHD, those who carried the A variant reported more symptomatic hyperactivity than those who did not.

The researchers further found that by promoting impulsivity, the variant raises the risk of drug use. Thus, in two studies of adolescents, neither the A variant alone nor ADHD alone increased the risk for drug use, but the two together did. The first analysis looked at adolescents with ADHD, and found higher rates of drug use among those with the A variant than among those with only the G variant. The second analysis looked at adolescents who had the A variant of rs12765063 and histories of childhood ADHD. It found that those whose childhood ADHD still persisted reported more use of alcohol, tobacco, marijuana, and prescription stimulants than those who had outgrown their ADHD (Figure 2). Moreover, those who no longer had ADHD reported no more drug use than a comparison group who did not carry the A variant.

 

Figure 2. The A Variant of the CREM Gene Is Associated With Increased Drug Use in People With Persistent ADHD Among a cohort whose childhood ADHD persisted through adolescence, those with the CREM A variant reported more drug use than those with only the G variant. Genotype was not linked to risk for drug use in people without ADHD (i.e., those who never had ADHD or those with remitted ADHD).

A Key to Prevention and Treatment?

Dr. Hurd suggests that CREM may be a key link between impulsivity and vulnerability to addiction. Understanding these relationships may help identify new ways of treating or preventing SUD. The protein is known to regulate multiple gene networks and their biological functions, and to influence the growth of structures that neurons use to communicate with each other.

Dr. Hurd says, “These results highlight that CREM is a mediating factor between impulsivity and substance abuse vulnerability. It brings attention to CREM in the nucleus accumbens as a regulator of impulsive action and structural plasticity.”

The study was supported by NIH grants DA015446, DA030359, DA006470, DA038954, DA031559, and DA007135.

Source: https://www.drugabuse.gov/news-events/nida-notes/2018/06/gene-links-impulsivity-drug-use-vulnerability June 2018

Introduction by Theodore M. Pinkert, M.D., J.D.

The study of the consequences of maternal drug abuse represents one of the most compelling areas of research in the drug abuse field. The potential victims of this problem have no say in the maternal behaviors, which may place them at risk. Therefore, it is incumbent upon the research community to attempt to delineate the potential hazards to the fetus, the newborn, the infant, and the child, so that deficits may be identified in sufficient time to compensate, where possible, with specific treatment interventions.

The purpose of this volume is to focus attention on recent studies of the effects of maternal substance abuse on offspring. The material presented includes reviews of animal data, as well as the results of large interdisciplinary clinical studies, which were originally presented on September 24th and 25th, 1984, at a National Institute on Drug Abuse Technical Review sponsored by the Divisions of Preclinical and Clinical Research. (The papers presented in the preclinical portion of this meeting will be published in a separate volume, entitled Prenatal Drug Exposure: Kinetics and Dynamics.)

     In the opening chapter of this monograph, Dr. Donald Hutchings defines the field of study known as behavioral teratology and provides a conceptual and historical framework that facilitates an understanding of what inferences may reasonably be drawn from both the animal and clinical literature. His studies in behavioral teratology integrate developmental toxicology and teratology with developmental psychology and focus on a variety of neurobehavioral changes that are crucial to the development and maturation of the individual.

The next chapter, by Dr. Ernest Abel, elaborates on the difficulties inherent in attempting to understand the interactive nature of the maternal and fetoplacental units. Through a careful review of his own work, and that of others, he provides important insights into the limitations and strengths of both epidemiological and clinical studies. He also points out the value of animal studies in providing the methodological rigor necessary (in combination with the human studies) to establish the most convincing demonstration of causality when adverse pregnancy outcomes are suspected from one or more chemical agents. Then he reviews the effects of marijuana (A5—THC) on pregnant animals and their offspring and discusses both the results and the methodological pitfalls to be avoided in these studies.

     In the following chapter, Dr. Nancy Day and her colleagues analyze the problems faced by clinical researchers in obtaining reliable and valid results using the instruments and techniques currently employed in prenatal research. The two major challenges identified are: (1) When questionnaire formats are used, do subjects understand the questions and report accurately? and (2) How does one obtain accurate measures of complex and changing events (substance abuse patterns) for specific time periods which coincide with different stages of fetal vulnerability, so that the prediction of biological effects can be made with a high degree of probability?

In the same chapter, the authors suggest techniques for eliciting accurate patterns of maternal drug intake and describe how these techniques are implemented in their current research on the effects of maternal marijuana and alcohol use during pregnancy. The value of the assessment instruments they have developed is that they measure both the quantity and frequency of drug intake in a manner that more closely resembles the way subjects naturally organize their own memory of substance use——in terms of both language and sequence. The authors also elaborate other techniques which are designed to overcome accuracy problems created either by the patient’s deliberate misrepresentation of past drug intake or by their flawed recall of remote events. These techniques include the bogus pipeline, which attempts to overcome misrepresentation of drug use, and the breakdown of prepregnancy and first trimester events into specific time intervals to aid in more accurate recall of the quantity and frequency of drug use.

     The next chapter, by Katherine Tennes and colleagues, describes the results of a large clinical study on the effects of prenatal marijuana exposure. Participating women responded to structured questionnaires about themselves, their habits (substance abuse, nutritional, etc.), and the habits of the father, if known. After delivery, infants were examined for birth measurements, physical anomalies, and muscle tone, and the Brazelton Neonatal Behavioral Assessment Scale was administered. At 1 year of age, the infant’s physical parameters were reexamined and they were evaluated on the Bayley Infant Scale of Mental and Motor Development and Behavior Checklist. One finding of this study is that maternal marijuana use decreased from previous levels of consumption as the pregnancy advanced. At delivery, no significant differences in 12 indices of obstetrical complications were detected that could not be attributed to parity, or to the amount of pain—relieving medication administered (although users of marijuana required more pain—relieving medication than nonusers). Heavy marijuana use was found to be associated with an increase in male over female offspring, but with a decrease in infant length at birth. No increase in teratogenicity, or decrease in APGAR or Brazelton scores, was associated with prenatal marijuana use. No significant differences were detected in physical measurements or Bayley scores at 1 year. The authors point out that some of their outcome data are in disagreement with previous clinical studies, and they explore possible reasons for the difference in results. In addition, the authors caution that studies examining the effects of maternal marijuana use on more complex cognitive functioning in offspring have yet to be performed.

     In the next chapter, Dr. Peter Fried reports on another major clinical study of maternal marijuana use, but in a population with significantly different demographics than the previous study. Among his findings were that gestation was shortened by maternal marijuana use and that there were neurobehavioral effects, as measured by altered visual responses and changes in state regulation (heightened tremors and startles), in the newborn. Although not yet completed, studies employing neuro- opthalmological and electrophysiological testing suggested that prenatal exposure to marijuana might delay maturation of the visual system. In agreement with the Tennes study, there were no differences in rates of miscarriage, obstetrical complications. APGAR scores, or teratological effects between the marijuana—using population and the comparison group. (Studies of both animal and human populations which suggest different results are presented and discussed.)

In addition, data collected from developmental tests administered to the infants at 6—month intervals after birth failed to discriminate infants of marijuana—using mothers from either matched controls or the general population. Dr. Fried cautions that it is not at all clear whether neurological findings present at birth are transient, or compensated for by maturation. He suggests the possibility that the tests currently used to measure developmental neurological disturbances in the newborn and neonate may not have
sufficient discriminatory sensitivity to detect subtle differences that may remain in the older, marijuana—exposed infant or child.

     In the next chapter, Drs. Rosen and Johnson review their findings on the prenatal effects and postnatal consequences to the offspring of methadone—maintained mothers. Their results include analyses of methadone’s effects upon the neonatal and infant periods of development, and they present recent data from their oldest cohorts of children, who are now in the 4— to 7—year—old age range. Among the effects on offspring of methadone—maintained mothers was a higher incidence of small—for—gestational—age infants, and infants below the third percentile in head circumference.

In addition, the maternal methadone dose and the length of time on methadone had a positive correlation with a higher incidence of obstetrical complications, decreased birth weight, and decreased infant performance on certain Brazelton measures. Neurological and developmental testing continued to reveal significant differences between methadone—exposed children and a comparison group through the 36—month evaluations. These differences included an increased incidence of abnormal reflexes, nystagmus, infections, abnormal muscle tone, and delayed developmental milestones among the methadone—exposed infants. As the children reached school age, those who did poorly neuro— developmentally at earlier evaluations continued to do poorly. A trend toward lower scores in receptive language evaluations was evident among the methadone—exposed children.

Their neurological evaluations demonstrated a higher prevalence of abnormalities of fine and gross motor coordination, poor balance, decreased attention span, hyperactivity, and speech and language delays. There was also a higher incidence of referrals for behavioral and academic problems. However, as the comparison group of children (a population selected from women in a low socioeconomic status similar to that of the methadone—maintained mothers) approached school age, they too began to show poor performance in testing. This raises important questions about the interaction between prenatal environments and the socioeconomic status of the child in the postnatal environment.

     In the following chapter, Dr. Ira Chasnoff compares the effects on offspring of the maternal use of narcotic versus nonnarcotic substances. Unique in this group of reports, his study is an attempt to distinguish the in utero effects of narcotic use (methadone and pentazocine/tripelennamine groups), from non— narcotic drug use (including a small group of women whose primary drug of abuse was phencyclidine EPCPJ, and another group with mixed sedative/hypnotic exposure, including marijuana). Although the number of subjects in each group was small, infants exposed in utero to narcotic substances showed fairly consistent decreases in birth weight, length, and head circumference from both the sedative/hypnotic group and the comparison group.

The methadone—exposed group of neonates also demonstrated deficits in auditory orientation and motor maturity. Infants exposed to both narcotic and nonnarcotic drugs showed decrements in state regulation, and infants exposed to PCP showed increased state liability and poor consolability when compared to all other drug—exposed groups. As was manifested in the preceding Rosen and Johnson material, the scores of the comparison group of infants began to fall away from the normal range toward that of the drug—exposed infants by 24 months of age.

     In the last chapter, Dr. Barry Zuckerman reviews the developmental consequences of maternal drug use. He describes the features compatible with the fetal alcohol syndrome and discusses research which suggests that these features may reflect a final common pathway of numerous agents (Including drugs of abuse), rather than a specific teratogenic effect of alcohol.

In addition, the author stresses the importance to developmental outcome studies of repeated assessments over time, and he suggests the application of newer physiologic techniques such as evoked responses, Brain Electrical Activity Mapping (BEAM),
Positron Emission Tomography (PET Scan), and Nuclear Magnetic Resonance (NMR), to enhance our understanding of the effects of prenatal drug exposure.

     In summary, much remains to be learned about the specific developmental effects of a variety of commonly used and abused drugs. The research community has not yet exhausted the potential for the development and application of new testing techniques and Instruments that will help us to identify the scope of subtle cognitive and motor effects caused by prenatal drug exposure.

Beyond these refinements lies the possibility of understanding the particular mechanisms through which these drugs exert their effects. It is the hope of those who participated in the conference that what lies herein will stimulate research into the many unanswered questions In this area.

Source and link to full articles:

https://archives.drugabuse.gov/sites/default/files/monograph59_0.pdf

Introduction by Cora Lee Wetherington, Vincent L. Smeriglio, and Loretta P. Finnegan

For several years the use of drugs during pregnancy, particularly cocaine, has been a major public health issue because of the concern about possible adverse behavioral effects on the neonate and the developing child. While many popular press publications have warned of the severe adverse effects of prenatal drug exposure, the scientific literature has been less clear on this issue, in part because of complex methodological issues that confront research in this field.
    On July 12 and 13, 1993, the National Institute on Drug Abuse conducted a technical review at which researchers reviewed the state of the art regarding behavioral assessments of offspring prenatally exposed to abused drugs. Presenters identified and addressed the complex methodological issues that abound in both human and animal studies designed to assess behavioral effects of prenatal drug exposure, and they stressed the caveats involved in drawing causal conclusions from associations between maternal drug abuse and adverse behavioral outcomes in the offspring. This research monograph is based upon revisions of presentations made at that technical review. The fundamental aim of this research monograph is to clarify the methodological issues for future research in this field, to provide caution in the interpretation of research findings, and to suggest future research directions.

Link to source and full articles:

https://archives.drugabuse.gov/sites/default/files/monograph164_0.pdf  1996

PHE publications gateway number: 2016490 December 2016

Executive summary

Alcohol is a prominent commodity in the UK marketplace. It is widely used in numerous social situations. For many, alcohol is associated with positive aspects of life; however, there are currently over 10 million people drinking at levels which increase their risk of health harm. Among those aged 15 to 49 in England, alcohol is now the leading risk factor for ill-health, early mortality and disability and the fifth leading risk factor for ill health across all age groups. Since 1980, sales of alcohol in England and Wales have increased by 42%, from roughly 400 million litres in the early 1980s, with a peak at 567 million litres in 2008, and a subsequent decline.

This growth has been driven by increased consumption among women, a shift to higher strength products, and increasing affordability of alcohol, particularly through the 1980s and 1990s. Over this period, the way in which alcohol is sold and consumed also changed. In 2016 there were 210,000 license premises in England and Wales, a 4% increase on 2010. There has been a shift in drinking location such that most alcohol is now bought from shops and drunk at home.

Although consumption has declined in recent years, levels of abstinence have also increased. Consequently, it is unclear how much of the decline is actually related to drinkers consuming less alcohol and how much to an increasing proportion of the population not drinking at all. In recent years, many indicators of alcohol-related harm have increased.

There are now over 1 million hospital admissions relating to alcohol each year, half of which occur in the lowest three socioeconomic deciles. Alcohol-related mortality has also increased, particularly for liver disease which has seen a 400% increase since 1970, and this trend is in stark contrast to much of Western Europe. In England, the average age at death of those dying from an alcohol-specific cause is 54.3 years. The average age of death from all causes is 77.6 years.

More working years of life are lost in England as a result of alcohol-related deaths than from cancer of the lung, bronchus, trachea, colon, rectum, brain, pancreas, skin, ovary, kidney, stomach, bladder and prostate, combined.

Despite this burden of harm, some positive trends have emerged over this period, particularly indicators which relate to alcohol consumption among those aged less than 18 years, and there have been steady reductions in alcohol-related road traffic crashes. The public health burden of alcohol is wide ranging, relating to health, social or economic harms. These can be tangible, direct costs (including costs to the health, criminal justice and welfare systems), or indirect costs (including the costs of lost productivity due to absenteeism, unemployment, decreased output or lost working years due to premature pension or death).

Harms can also be intangible, and difficult to cost, including those assigned to pain and suffering, poor quality of life or the emotional The Public Health Burden of Alcohol and the Effectiveness and Cost-Effectiveness of Alcohol Control Policies: An evidence review 7 distress caused by living with a heavy drinker. The spectrum of harm ranges from those that are relatively mild, such as drinkers loitering near residential streets, through to those that are severe, including death or lifelong disability. Many of these harms

impact upon other people, including relationship partners, children, relatives, friends, co-workers and strangers. In sum, the economic burden of alcohol is substantial, with estimates placing the annual cost to be between 1.3% and 2.7% of annual GDP.

Few studies report costs on the magnitude of harm to people other than the drinker, so the economic burden of alcohol consumption is generally underestimated. Crucially, the financial burden which alcohol-related harm places on society is not reflected in its market price, with taxpayers picking up a larger amount of the overall cost compared to the individual drinkers. This should provide impetus for governments to implement effective policies to reduce the public health impact of alcohol, not only because it is an intrinsically desirable societal goal, but because it is an important aspect of economic growth and competitiveness. Reflecting three key influencers of alcohol consumption – price (affordability), ease of purchase (availability) and the social norms around its consumption (acceptability) – an extensive array of policies have been developed with the primary aim of reducing the public health burden of alcohol. The present review evaluates the effectiveness and cost-effectiveness of each of these policy approaches.

Source: https://assets.publishing.service.gov.uk/government/uploads 2016

Sydney Parliament House, 09.07.2018

Cannabis has been greatly oversold by a left leaning press controlled by globalist and centralist forces while its real and known dangers have not been given appropriate weight in the popular press. In particular its genotoxic and teratogenic potential on an unborn generation for the next hundred years has not been aired or properly weighed in popular forums.

These weighty considerations clearly take cannabis out of the realm of personal choice or individual freedoms and place it squarely in the realm of the public good and a matter with which the whole community is rightly concerned and properly involved.

Cannabinoids are a group of 400 substances which occur only in the leaves of the Cannabis sativa plant where they are used by the plants as toxins and poisons in natural defence against other plants and against herbivores.

Major leading world experts such as Dr Nora Volkow, Director of the National Institute of Drug Abuse at NIH 1, Professor Wayne Hall, Previous Director of the Sydney Based National Drug and Alcohol Research Centre at UNSW 2, and Health Canada 3 – amongst many others – are agreed that cannabis is linked with the following impressive lists of toxicities:

1) Cannabis is addictive, particularly when used by teenagers

2) Cannabis affects brain development

3) Cannabis is a gateway to other harder drug use

4) Cannabis is linked with many mental health disorders including anxiety, depression,

psychosis, schizophrenia and bipolar disorder

5) Cannabis alters and greatly impairs the normal developmental trajectory – getting a

job, finishing a course and forming a long term stable relationship 4-11

6) Cannabis impairs driving ability 12

7) Cannabis damages the lungs

8) Cannabis is immunosuppressive

9) Cannabis is linked with heart attack, stroke and cardiovascular disease

10) Cannabis is commonly more potent in recent years, with forms up to 30% being widely available in many parts of USA, and oils up to 100% THC also widely available.

Serious questions have also been raised about its involvement in 12 different cancers, increased Emergency Room presentations and exposures of developing babies during pregnancy. It is with this latter group that the present address is mainly concerned.

Basic Physiology and Embryology Cells make energy in dedicated organelles called mitochondria. Mitochondrial energy, in the form of ATP, is known to be involved in both DNA protection and control of the immune system. This means that when the cell’s ATP is high DNA maintenance is good and the genome is intact. When cellular ATP drops DNA maintenance is impaired, DNA breaks remain unsealed, and cancers can form. Also immunity is triggered by low ATP.

As organisms age ATP falls by half each 20 years after the age of 20. Mitochondria signal and shuttle to the cell nucleus via several pathways. Not only do cells carry cannabinoid receptors on their surface, but they also exist, along with their signalling machinery, at high density on mitochondria themselves 13-19. Cannabis, and indeed all addictive drugs, are known to impair this cellular energy generation and thus promote the biochemical aging process 14-16,19,20. Most addictions are associated with increased cancers, increased infections and increased clinical signs of ageing 21-34.

The foetal heart forms very early inside the mother with a heartbeat present from day 21 of human gestation. The heart forms by complicated pathways, and arises from more than six groups of cells inside the embryo 35,36. First two arteries come together, they fold, then flex and twist to give the final shape of the adult heart. Structures in the centre of the heart mass called endocardial cushions grow out to form the heart valves between the atria and ventricles and parts of the septum which grows between the two atria and ventricles. These cardiac cushions, and their associated conoventricular ridges which grow into and divide the cardiac outflow tract into left and right halves, all carry high density cannabinoid type 1 receptors (CB1R’s) and cannabis is known to be able to interfere with their growth and development.CB1R’s appear on foetal arteries from week nine of human gestation 37.

The developing brain grows out in a complex way in the head section 35,36. Newborn brain cells are born centrally in the area adjacent to the central ventricles of the brain and then migrate along pathways into the remainder of the brain, and grow to populate the cortex, parietal lobes, olfactory lobes, limbic system, hypothalamus and hippocampus which is an important area deep in the centre of the temporal lobes where memories first form.

Developing bipolar neuroblasts migrate along pathways and then climb out along 200 million guide cells, called radial glia cells, to the cortex of the brain where they sprout dendrites and a major central axon which are then wired in to the electrical network in a “use it or lose it”, “cells that fire together wire together” manner.

The brain continues to grow and mature into the 20’s as new neurons are born and surplus dendrites are pruned by the immune system. Cannabinoids interfere with cellular migration, cellular division, the generation of newborn neurons and all the classes of glia, axonal pathfinding, dendrite sprouting, myelin formation around axons and axon tracts and the firing of both inhibitory and stimulatory synapses 14-16,19,20,38-40. Cannabinoids interfere with gene expression directly, via numerous epigenetic means, and via immune perturbation.

Cannabinoids also disrupt the mechanics of cell division by disrupting the mitotic spindle on which chromosomal separation occurs, causing severe genetic damage and frank chromosomal mis-segregation, disruption, rupture and pulverization 41-43.

Cannabis was found to be a human carcinogen by the California Environmental Protection agency in 2009 44. This makes it a likely human teratogen (deforms babies). Importantly, while discussion continues over some cancers, it bears repeating that a positive association between cannabis and testicular cancer was found in all four studies which investigated this question 45-49.

Cannabis Teratogenesis

The best animal models for human malformations are hamsters and rabbits. In rabbits cannabis exhibits a severe spectrum of foetal abnormalities when applied at high dose including shortened limbs, bowels hanging out, spina bifida and exencephaly (brain hanging out). There is also impaired foetal growth and increased foetal loss and resorption 50,51.

Many of these features have been noted in human studies 52. In 2014 Centres for Disease Control Atlanta Georgia reported increased rates of anencephaly (no brain, usually rapid death) gastroschisis (bowels hanging out), diaphragmatic hernia, and oesophageal narrowing 53,54. The American Heart Association and the American Academy of Pediatrics reported in 2007 an increased rate of ventricular septal defect and an abnormality of the tricuspid valve (Ebstein’s anomaly) 55. Strikingly, a number of studies have shown that cannabis exposure of the father is worse than that of the mother 56. In Colorado atrial septal defect is noted to have risen by over 260% from 2000-2013 (see Figure 1; note close correlation (correlation coefficient R = 0.95, P value = 0.000066) between teenage cannabis use and rising rate of major congenital anomalies in Colorado to 12.7%, or 1 in 8 live births, a rate four times higher than the USA national average !) 57.

And three longitudinal studies following children exposed to cannabis in utero have consistently noted abnormalities of brain growth with smaller brains and heads – persisting into adult life – and deficits of cortical and executive functioning persistent throughout primary, middle and high schools and into young adult life in the early 20’s 58-63. An Australian MRI neuroimaging study noted 88% disconnection of cortical wiring from the splenium to precuneus which are key integrating and computing centres in the cerebral cortex 38,39,64. Chromosomal defects were also found to be elevated in Colorado (rose 30%) 57, in Hawaii 52 in our recent analysis of cannabis use and congenital anomalies across USA, and in infants presenting from Northern New South Wales to Queensland hospitals 65. And gastroschisis shows a uniform pattern of elevation in all recent studies which have examined it (our univariate meta-analysis) 52,54,66-71.

Interestingly the gastroschisis rate doubled in North Carolina in just three years 1997-2001 72, but rose 24 times in Mexico 73 which for a long time formed a principal supply source for Southern USA 74. Within North Carolina gastroschisis and congenital heart defects closely followed cannabis distribution routes 74-76. In Canada a remarkable geographical analysis by the Canadian Government has shown repeatedly that the highest incidence of all anomalies – including chromosomal anomalies – occurs in those northern parts where most cannabis is smoked 77,78.

Congenital anomalies forms the largest cause of death of babies in the first year of life. The biggest group of them is cardiovascular defects. Since cannabis affects several major classes
of congenital defects it is obviously a major human teratogen. Its heavy epigenetic footprint,
by which it controls gene expression by controlling DNA methylation and histone modifications 79-81, imply that its effects will be felt for the next three to four generations – that is the next 100 years 82,83. Equally obviously it is presently being marketed globally as a major commodity apparently for commercial – or ideological – reasons. Since cannabis is clearly contraindicated in several groups of people including:

1) Babies

2) Children

3) Adolescents

4) Car drivers

5) Commercial Drivers – Taxis, Buses, Trains,

6) Pilots of Aeroplanes

7) Workers – Manual Tools, Construction, Concentration Jobs

8) Children

9) Adolescents

10) Males of Reproductive age

11) Females of Reproductive age

12) Pregnancy

13) Lactation

14) Workers

15) Older People – Mental Illness

16) Immunosuppressed

17) Asthmatics – 80% Population after severe chest infection

18) People with Personal History of Cancer

19) People with Family History of Cancer

20) People with Personal History of Mental Illness

21) People with Family History of Mental Illness

22) Anyone or any population concerned about ageing effects 34

… cannabis legalization is not likely to be in the best interests of public health.

Concluding Remarks

In 1854 Dr John Snow achieved lasting public health fame by taking the handle off the Broad Street pump and saving east London from its cholera epidemic, based upon the maps he drew of where the cholera cases were occurring – in the local vicinity of the Broad Street pump.

Looking across the broad spectrum of the above evidence one notices a trulyremarkable concordance of the evidence between:

1) Preclinical studies in

i) Rabbits and

ii) Hamsters

2) Cellular and biological mechanisms, particularly relating to:

i) Brain development

ii) Heart development

iii) Blood vessel development

iv) Genetic development

v) Abnormalities of chromosomal segregation

i. Downs syndrome

ii. Turners syndrome

iii. Trisomy 18

iv. Trisomy 13

vi) Cell division / mitotic poison / micronucleus formation

vii) Epigenetic change

viii) Growth inhibition

3) 84Cross-sectional Epidemiological studies, especially from:

i) Canada 77,85

ii) USA 86,87

iii) Northern New South Wales 65,88 4) Longitudinal studies from 58:

i) Ottawa 59-63

ii) Pittsburgh

iii) Netherlands

Our studies of congenital defects in USA have also shown a close concordance of congenital anomaly rates for 23 defects with the cannabis use rate indexed for the rising cannabis concentration in USA, and mostly in the three major classes of brain defects, cardiovascular defects and chromosomal defects, just as found by previous investigators in Hawaii 52.

Of no other toxin to our knowledge can it be said that it interferes with brain growth and development to the point where the brain is permanently shrunken in size or does not form at all. The demonstration by CDC twice that the incidence of anencephaly (no brain) is doubled by cannabis 53,54 implies that anencephaly is the most severe end of the neurobehavioural teratogenicity of cannabis and forms one end of a continuum with all the other impairments which are implied by the above commentary.

(Actually when blighted ova, foetal resorptions and spontaneous abortion are included in the teratological profile anencephaly is not the most severe end of the teratological spectrum – that is foetal death). It is our view that with the recent advent of high dose potent forms of cannabis reaching the foetus through both maternal and paternal lines major and clinically significant neurobehavioural teratological presentations will become commonplace, and might well become all but universal in infants experiencing significant gestational exposure.

One can only wonder if the community has been prepared for such a holocaust and tsunami amongst its children?

It is the view of myself and my collaborators that these matters are significant and salient and should be achieving greater airplay in the public discussion proceeding around the world at this time on this subject.

Whilst cannabis legalization may line the pockets of the few it will clearly not be in the public interest in any sense; and indeed the public will be picking up the bill for this unpremeditated move for generations to come. Oddly – financial gain seems to be one of the primary drivers of the present transnational push. When the above described public health message gets out amongst ambitious legal fraternities, financial gain and the threat of major medico-legal settlements for congenital defects – will quickly become be the worst reason for cannabis legalization.

Indeed it can be argued that the legalization lobby is well aware of all of the above concerns – and their controlled media pretend debate does not allow such issues to air in the public forum. The awareness of these concerns is then the likely direct reason that cannabis requires its own legislation. As noted in the patient information leaflet for the recently approved Epidiolex (cannabidiol oil for paediatric fits) the US Food and Drug Administration (FDA) is well aware of the genotoxicity of cannabinoids.

The only possible conclusion therefore is that the public is deliberately being duped. To which our only defence will be to publicize the truth.

Source: Summary of Address to Sydney Parliament House, 09.07.2018 by Professor Dr. Stuart Reece, Clinical Associate Professor, UWA Medical School. University of Western Australia

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Authors: Mücke M, Weier M, Carter C, Copeland J, Degenhardt L, Cuhls H, Radbruch L, Häuser W, Conrad R.

Abstract

We provide a systematic review and meta-analysis on the efficacy, tolerability, and safety of cannabinoids in palliative medicine. The Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, PsycINFO, PubMed, Scopus, and http://clinicaltrials.gov, and a selection of cancer journals were searched up until 15th of March 2017.

     Of the 108 screened studies, nine studies with a total of 1561 participants were included. Overall, the nine studies were at moderate risk of bias. The quality of evidence comparing cannabinoids with placebo was rated according to Grading of Recommendations Assessment, Development, and Evaluation as low or very low because of indirectness, imprecision, and potential reporting bias.

     In cancer patients, there were no significant differences between cannabinoids and placebo for improving caloric intake (standardized mean differences [SMD]:

0.2 95% confidence interval [CI]: [-0.66, 1.06] P = 0.65),

appetite (SMD: 0.81 95% CI: [-1.14, 2.75]; P = 0.42),

nausea/vomiting (SMD: 0.21 [-0.10, 0.52] P = 0.19),

>30% decrease in pain (risk differences [RD]: 0.07 95% CI: [-0.01, 0.16]; P = 0.07),

or sleep problems (SMD: -0.09 95% CI: [-0.62, 0.43] P = 0.72).

     In human immunodeficiency virus (HIV) patients, cannabinoids were superior to placebo for weight gain (SMD: 0.57 [0.22; 0.92]; P = 0.001) and appetite (SMD: 0.57 [0.11; 1.03]; P = 0.02) but not for nausea/vomiting (SMD: 0.20 [-0.15, 0.54]; P = 0.26).

     Regarding side effects in cancer patients, there were no differences between cannabinoids and placebo in symptoms of dizziness (RD: 0.03 [-0.02; 0.08]; P = 0.23) or poor mental health (RD: -0.01 [-0.04; 0.03]; P = 0.69), whereas in HIV patients, there was a significant increase in mental health symptoms (RD: 0.05 [0.00; 0.11]; P = 0.05).

     Tolerability (measured by the number of withdrawals because of adverse events) did not differ significantly in cancer (RD: 1.15 [0.80; 1.66]; P = 0.46) and HIV patients (RD: 1.87 [0.60; 5.84]; P = 0.28). Safety did not differ in cancer (RD: 1.12 [0.86; 1.46]; P = 0.39) or HIV patients (4.51 [0.54; 37.45]; P = 0.32) although there was large uncertainty about the latter reflected in the width of the CI. In one moderate quality study of 469 cancer patients with cancer-associated anorexia, megestrol was superior to cannabinoids in improving appetite, producing >10% weight gain and tolerability.

     In another study comparing megestrol to dronabinol in HIV patients, megestrol treatment led to higher weight gain without any differences in tolerability and safety. We found no convincing, unbiased, high quality evidence suggesting that cannabinoids are of value for anorexia or cachexia in cancer or HIV patients.

Source: https://www.ncbi.nlm.nih.gov/pubmed/29400010  February 2018

Cannabis’ effects on diabetes unclear – by Dr. Elizabeth Ko & Dr. Eve Glazier – Ask the Doctors  column, August 4, 2018 –  Ask the Doctors, c/0 Media Relations, UCLA Health, 924 Westwood Blvd. Suite 350, Los Angeles, CA  90095

Question:  I have Type 1 diabetes and have used marijuana for years to control my blood sugar.  I’ve seen my blood sugar drop 100 points in five minutes with marijuana, faster than my Humalog insulin can manage.  Why is that?  Will medical marijuana ever go mainstream?

Answer:  Marijuana, or cannabis, contains more than 100 active chemical compounds.  Known as cannabinoids, each behaves differently in the body.  As the number of states that allow the use of cannabis for medical purposes continues to grow, so does the body of evidence that many of the compounds found within the plant have therapeutic potential.

     The challenge to investigate medical claims regarding cannabis is that it remains illegal at the federal level.  Research is subject to numerous restrictions.  Even so, various studies and clinical trials are moving forward.

     We found that you’re not alone in noticing its effect on blood sugar.  However, much of what we found is anecdotal evidence, which lacks scientific rigor.  The study of cannabis and its potential effects on diabetes is in the early stages, which much of the work done in mice and on donated tissue samples.

     Until researchers are able to work extensively with human populations, the how and why of the effects of cannabis on the complex physiologic processes encompassed by diabetes will remain educated guesses.

     Preliminary research suggests that certain cannabinoids may help with glucose control.  Some studies have found that cannabis can have a positive effect on insulin resistance.  A study published in 2016 in a journal of the American Diabetes Association found that THCV, one of the cannabinoids that are not psychoactive, improved glycemic control in some individuals with Type 2 diabetes.  Another study that same year drew a link between cannabidiol, a compound in cannabis, and a decrease in inflammation of the pancreas.  In an observational study using data from the federal Centers for Disease Control and Prevention, researchers found the incidence of diabetes among regular cannabis users to be measurably lower than that of the population at large.

     The results of several other recent studies contradict a number of these pro-cannabis findings.  So, basically, the jury is still out.

     Although cannabis shows promise in the area of diabetes, science has yet to catch up with the claims being made.  In the research that has been done, the reason for the effects of cannabis is not yet fully understood.  Interest in the subject is strong, though, and continues to grow.

From “Ask the Doctors” – typed-copied from printed Erie Times-News (Erie, Pa.), August 4, 2018 (www.GoErie.com

Response by Prof. Stuart Reece to FDA

Link to FDA

https://www.federalregister.gov/documents/2018/04/09/2018-07225/international-drug-scheduling-convention-on-psychotropic-substances-single-convention-on-narcotic

Source: Dr Stuart Reece’s original response letter to the FDA:

03 FDA Federal Register Submission for WHO Review and Consideration – Genotoxicity Teratogenicity Concise 2  April 2018

The proliferation of retail boutiques in California did not really bother him, Evan told me, but the billboards did. Advertisements for delivery, advertisements promoting the substance for relaxation, for fun, for health. “Shop. It’s legal.” “Hello marijuana, goodbye hangover.” “It’s not a trigger,” he told me. “But it is in your face.”

When we spoke, he had been sober for a hard-fought seven weeks: seven weeks of sleepless nights, intermittent nausea, irritability, trouble focusing, and psychological turmoil. There were upsides, he said, in terms of reduced mental fog, a fatter wallet, and a growing sense of confidence that he could quit. “I don’t think it’s a ‘can’ as much as a ‘must,'” he said.

Evan, who asked that his full name not be used for fear of the professional repercussions, has a self-described cannabis-use disorder. If not necessarily because of legalization, but alongside legalization, such problems are becoming more common: The share of adults with one has doubled since the early aughts, as the share of cannabis users who consume it daily or near-daily has jumped nearly 50 percent-all “in the context of increasingly permissive cannabis legislation, attitudes, and lower risk perception,” as the National Institutes of Health put it.

Public-health experts worry about the increasingly potent options available, and the striking number of constant users. “Cannabis is potentially a real public-health problem,” said Mark A. R. Kleiman, a professor of public policy at New York University. “It wasn’t obvious to me 25 years ago, when 9 percent of self-reported cannabis users over the last month reported daily or near-daily use. I always was prepared to say, ‘No, it’s not a very abusable drug. Nine percent of anybody will do something stupid.’ But that number is now [something like] 40 percent.” They argue that state and local governments are setting up legal regimes without sufficient public-health protection, with some even warning that the country is replacing one form of reefer madness with another, careening from treating cannabis as if it were as dangerous as heroin to treating it as if it were as benign as kombucha.

But cannabis is not benign, even if it is relatively benign, compared with alcohol, opiates, and cigarettes, among other substances. Thousands of Americans are finding their own use problematic-in a climate where pot products are getting more potent, more socially acceptable to use, and yet easier to come by, not that it was particularly hard before.

For Keith Humphreys, a professor of psychiatry and behavioral sciences at Stanford University, the most compelling evidence of the deleterious effects comes from users themselves. “In large national surveys, about one in 10 people who smoke it say they have a lot of problems. They say things like, ‘I have trouble quitting. I think a lot about quitting and I can’t do it. I smoked more than I intended to. I neglect responsibilities.’ There are plenty of people who have problems with it, in terms of things like concentration, short-term memory, and motivation,” he said. “People will say, ‘Oh, that’s just you fuddy-duddy doctors.’ Actually, no. It’s millions of people who use the drug who say that it causes problems.”

Users or former users I spoke with described lost jobs, lost marriages, lost houses, lost money, lost time. Foreclosures and divorces. Weight gain and mental-health problems. And one other thing: the problem of convincing other people that what they were experiencing was real. A few mentioned jokes about Doritos, and comments implying that the real issue was that they were lazy stoners. Others mentioned the common belief that you can be “psychologically” addicted to pot, but not “physically” or “really” addicted. The condition remains misunderstood, discounted, and strangely invisible, even as legalization and white-marketization pitches ahead.

The country is in the midst of a volte-face on marijuana. The federal government still classifies cannabis as Schedule I drug, with no accepted medical use. (Meth and PCP, among other drugs, are Schedule II.) Politicians still argue it is a gateway to the use of things like heroin and cocaine. The country still spends billions of dollars fighting it in a bloody and futile drug war, and still arrests more people for offenses related to cannabis than it does for all violent crimes combined.

Yet dozens of states have pushed ahead with legalization for medical or recreational purposes, given that for decades physicians have argued that marijuana’s health risks have been overstated and its medical uses overlooked; activists have stressed prohibition’s tremendous fiscal cost and far worse human cost; and researchers have convincingly argued that cannabis is far less dangerous than alcohol. A solid majority of Americans support legalization nowadays.

Academics and public-health officials, though, have raised the concern that cannabis’s real risks have been overlooked or underplayed-perhaps as part of a counter-reaction to federal prohibition, and perhaps because millions and millions cannabis users have no problems controlling their use. “Part of how legalization was sold was with this assumption that there was no harm, in reaction to the message that everyone has smoked marijuana was going to ruin their whole life,” Humphreys told me. It was a point Kleiman agreed with. “I do think that not legalization, but the legalization movement, does have a lot on its conscience now,” he said. “The mantra about how this is a harmless, natural, and non-addictive substance-it’s now known by everybody. And it’s a lie.”

Thousands of businesses, as well as local governments earning tax money off of sales, are now literally invested in that lie. “The liquor companies are salivating,” Matt Karnes of GreenWave Advisors told me. “They can’t wait to come in full force.” He added that Big Pharma was targeting the medical market, with Wall Street, Silicon Valley, food businesses, and tobacco companies aiming at the recreational market.

Sellers are targeting broad swaths of the consumer market-soccer moms, recent retirees, folks looking to replace their nightly glass of chardonnay with a precisely dosed, low-calorie, and hangover-free mint. Many have consciously played up cannabis as a lifestyle product, a gift to give yourself, like a nice crystal or an antioxidant face cream. “This is not about marijuana,” one executive at the California retailer MedMen recently argued. “This is about the people who use cannabis for all the reasons people have used cannabis for hundreds of years. Yes for recreation, just like alcohol, but also for wellness.”

Evan started off smoking with his friends when they were playing sports or video games, lighting up to chill out after his nine-to-five as a paralegal at a law office. But that soon became couch-lock, and he lost interest in working out, going out, doing anything with his roommates. Then came a lack of motivation and the slow erosion of ambition, and law school moving further out of reach. He started smoking before work and after work. Eventually, he realized it was impossible to get through the day without it. “I was smoking anytime I had to do anything boring, and it took a long time before I realized that I wasn’t doing anything without getting stoned,” he said.

His first attempts to reduce his use went miserably, as the consequences on his health and his life piled up. He gained nearly 40 pounds, he said, when he stopped working out and cooking his own food at home. He recognized that he was just barely getting by at work, and was continually worried about getting fired. Worse, his friends were unsympathetic to the idea that he was struggling and needed help. “[You have to] try to convince someone that something that is hurting you is hurting you,” he said.

Other people who found their use problematic or had managed to quit, none of whom wanted to use their names, described similar struggles and consequences. “I was running two companies at the time, and fitting smoking in between running those companies. Then, we sold those companies and I had a whole lot of time on my hands,” one other former cannabis user told me. “I just started sitting around smoking all the time. And things just came to a halt. I was in terrible shape. I was depressed.”

Lax regulatory standards and aggressive commercialization in some states have compounded some existing public-health risks, raised new ones, and failed to tamp down on others, experts argue. In terms of compounding risks, many cite the availability of hyper-potent marijuana products. “We’re seeing these increases in the strength of cannabis, as we are also seeing an emergence of new types of products,” such as edibles, tinctures, vape pens, sublingual sprays, and concentrates, Ziva Cooper, an associate professor of clinical neurobiology in the Department of Psychiatry at Columbia University Medical Center, told me. “A lot of these concentrates can have up to 90 percent THC,” she said, whereas the kind of flower you could get 30 years ago was far, far weaker. Scientists are not sure how such high-octane products affect people’s bodies, she said, but worry that they might have more potential for raising tolerance, introducing brain damage, and inculcating dependence.

As for new risks: In many stores, budtenders are providing medical advice with no licensing or training whatsoever. “I’m most scared of the advice to smoke marijuana during pregnancy for cramps,” said Humphreys, arguing that sellers were providing recommendations with no scientific backing, good or bad, at all.

In terms of long-standing risks, the lack of federal involvement in legalization has meant that marijuana products are not being safety-tested like pharmaceuticals; measured and dosed like food products; subjected to agricultural-safety and pesticide standards like crops; and held to labelling standards like alcohol. (Different states have different rules and testing regimes, complicating things further.)

Health experts also cited an uncomfortable truth about allowing a vice product to be widely available, loosely regulated, and fully commercialized: Heavy users will make up a huge share of sales, with businesses wanting them to buy more and spend more and use more, despite any health consequences.

“The reckless way that we are legalizing marijuana so far is mind-boggling from a public-health perspective,” Kevin Sabet, an Obama administration official and a founder of the non-profit Smart Approaches to Marijuana, told me. “The issue now is that we have lobbyists, special interests, and people whose motivation is to make money that are writing all of these laws and taking control of the conversation.”

This is not to say that prohibition is a more attractive policy, or that legalization has proven a public-health disaster. “The big-picture view is that the vast majority of people who use cannabis are not going to be problematic users,” said Jolene Forman, an attorney at the Drug Policy Alliance. “They’re not going to have a cannabis-use disorder. They’re going to have a healthy relationship with it. And criminalization actually increases the harms related to cannabis, and so having like a strictly regulated market where there can be limits on advertising, where only adults can purchase cannabis, and where you’re going to get a wide variety of products makes sense.”

Still, strictly regulated might mean more strictly regulated than today, at least in some places, drug-policy experts argue. “Here, what we’ve done is we’ve copied the alcohol industry fully formed, and then on steroids with very minimal regulation,” Humphreys said. “The oversight boards of a number of states are the industry themselves. We’ve learned enough about capitalism to know that’s very dangerous.”

A number of policy reforms might tamp down on problem use and protect consumers, without quashing the legal market or pivoting back to prohibition and all its harms. One extreme option would be to require markets to be non-commercial: The District of Columbia, for instance, does not allow recreational sales, but does allow home cultivation and the gifting of marijuana products among adults. “If I got to pick a policy, that would probably be it,” Kleiman told me. “That would be a fine place to be if we were starting from prohibition, but we are starting from patchwork legalization. As the Vermont farmer says, I don’t think you can get there from here. I fear its time has passed. It’s generally true that the drug warriors have never missed an opportunity to miss an opportunity.”

There’s no shortage of other reasonable proposals, many already in place or under consideration in some states. The government could run marijuana stores, as in Canada. States could require budtenders to have some training or to refrain from making medical claims. They could ask users to set a monthly THC purchase cap and remain under it. They could cap the amount of THC in products, and bar producers from making edibles that are attractive to kids, like candies. A ban or limits on marijuana advertising are also options, as is requiring cannabis dispensaries to post public-health information.

Then, there are THC taxes, designed to hit heavy users the hardest. Some drug-policy experts argue that such levies would just push people from marijuana to alcohol, with dangerous health consequences. “It would be like saying, ‘Let’s let the beef and pork industries market and do whatever they wish, but let’s have much tougher restrictions on tofu and seitan,'” said Mason Tvert of the Marijuana Policy Project. “In light of the current system, where alcohol is so prevalent and is a more harmful substance, it is bad policy to steer people toward that.” Yet reducing the commercial appeal of all vice products-cigarettes, alcohol, marijuana-is an option, if not necessarily a popular one.

Perhaps most important might be reintroducing some reasonable skepticism about cannabis, especially until scientists have a better sense of the health effects of high-potency products, used frequently. Until then, listening to and believing the hundreds of thousands of users who argue marijuana is not always benign might be a good start.

Source: info@learnaboutsam.org   20th August 2018

www.learnaboutsam.org

In 2016, Gov. Greg Abbott announced a $9.75 million grant to McKesson Corporation. Now, Texas is among the states investigating the giant drug distributor’s role in a growing opioid crisis

In the early months of 2016, as U.S. overdose deaths were on track to break records and the number of Texas infants born addicted to opioid painkillers climbed steadily higher, Gov. Greg Abbott was courting a massive pharmaceutical company, McKesson, with a multimillion-dollar offer.

At the time, the two stories — Texas public health officials grappling with an overdose epidemic while the governor’s office worked on economic development — seemed unrelated. When Abbott announced he would give McKesson a $9.75 million grant from the state’s Enterprise Fund to woo the pharmaceutical distributor into expanding its operations in North Texas, he mostly received favorable news coverage for promising nearly 1,000 jobs to the local Irving economy.

But as the state and nation’s focus on the opioid crisis has sharpened in recent months, McKesson and other drug companies have come under legal scrutiny and the deal has put Abbott in an uncomfortable position.

Texas has since joined a multistate investigation into pharmaceutical companies, including McKesson, over whether they are responsible for feeding the nation’s opioid crisis and whether they broke any laws in the process. Several Texas counties have moved to sue McKesson and other companies for economic damages, alleging that manufacturers downplayed addiction risks and their distributors failed to track suspicious orders that flooded communities with pills.

The state grant to McKesson, worth about $10,000 for each job it brought to North Texas, is the largest Abbott has doled out from the Enterprise Fund, the controversial deal-closing incentives program created in 2004 under former Gov. Rick Perry. No U.S. state or local government has publicly given McKesson a more generous grant since 2000, according to data compiled by Good Jobs First, a Washington D.C.-based group that tracks government subsidies and other economic incentives.

In statements at the time, Abbott said the company’s expansion would “serve as an invaluable contribution to the Texas economy.”

But if Texas decides to sue McKesson, as several of its counties have, lawyers for the state will likely argue the opposite has happened — at least in the context of the company’s distribution of opioids. Across the country, local and state governments have begun to argue they are bearing the financial burden associated with opioid addiction.

One state lawmaker suggested Abbott’s office should have more closely scrutinized McKesson’s record before issuing the grant — even though the grant happened more than a year before Attorney General Ken Paxton announced Texas was joining the multistate investigation.

“There needs to be better oversight here,” said state Rep. Joe Moody, an El Paso Democrat and member of the new House panel examining the opioid crisis. “You’re in the middle of the opioid crisis, and we’re issuing an enormous grant that comprises a significant amount of grants this company is getting across the country.” 

Abbott’s office did not respond to repeated requests for comment.

Faced with the lawsuits and investigations, McKesson — headquartered in San Francisco but with a sizable Texas footprint — has denied any wrongdoing and insisted it is trying to work toward halting the opioid crisis, not fuel it.

“Our partnership with the state remains strong,” said Kristin Chasen, a company spokeswoman. “We certainly agree that the opioid epidemic is a national public health crisis, and we’re cooperatively having lots of conversations with AG Paxton and the others involved in the multistate investigation.”

A nationwide emergency

Opioids are a family of drugs that include prescription painkillers like hydrocodone as well as illicit drugs like heroin. Last Thursday, President Donald Trump declared a nationwide emergency to address the surging human and financial toll of opioid addiction.

U.S. drug overdose deaths in 2015 far outnumbered deaths from auto accidents or guns, and opioids account for more than 60 percent of overdose deaths — nearly 100 each day, according to the U.S. Centers for Disease Control. That death toll has quadrupled over the past two decades. 

“Beyond the shocking death toll, the terrible measure of the opioid crisis includes the families ripped apart and, for many communities, a generation of lost potential and opportunity,” Trump said Thursday

In Texas, opioids have claimed proportionately fewer lives than in other states, and the growth of opioid-related deaths has been slower, according to U.S. mortality data. Still, the casualties in Texas — 1,107 accidental opioid poisoning deaths in 2016 — have seized the attention of state policymakers.

Last week, Texas House Speaker Joe Straus ordered lawmakers to form a select committee on opioids and substance abuse to examine an issue that he said has had a “devastating impact on many lives.” The announcement came after Paxton joined a 41-state investigation into whether a slew of drug manufacturers and distributors broke any laws in allegedly fueling the crisis.

“This is a public safety and public health issue. Opioid painkiller abuse and related overdoses are devastating families here in Texas and throughout the country,” Paxton said when he announced the probe in June.

Some Texas counties have already taken the drug companies to court.

In late September, Upshur County, population about 40,000, sued a slew of painkiller manufacturers and distributors — including McKesson. Seeking to recoup an unspecified amount in financial damages, the East Texas county argues the drug companies broadly “ignored science and consumer health for profits,” meaning the county “continues to spend large sums combatting the public health crisis created by [a] negligent and fraudulent marketing campaign.”

More specifically, the suit argues McKesson and other distributors “did nothing” to address the “alarming and suspicious” overprescription of drugs.

Bowie County, a rural slice of East Texas nudging Arkansas, has since joined the lawsuit, with other East Texas counties expected to follow. El Paso County isalso mulling legal action, and Bexar County, home to San Antonio, has announced plans to sue.

In an interview last week, Bexar County Judge Nelson Wolff said he couldn’t immediately offer a complete list of companies his county would target, but “I’m sure McKesson is one of them.”

Wolff chuckled when asked about the company’s grant from the state. “That’d give us $10 million more that we could get out of their hides in our lawsuit, if you look at it that way.”

In teaming up to probe drug companies, some experts suggest governments are following a playbook similar to one used during the 1990s to sue tobacco companies for their role in fueling a costly health crisis — an effort that resulted in a settlement yielding more than $15 billion for Texas alone.

“It’s like a polluter externalizing all his risk,” said Mike Papantonio, a Florida-based lawyer with experience in tobacco litigation. 

“He makes a lot of money because he pours the poison right into the river,” said Papantonio, who now organizes a legal conference for groups interested in suing pharmaceutical companies. “The shareholders love it, but then the taxpayers have to come back and fix it.”

“McKesson is a great company”

At the April grand opening of the new McKesson campus in Las Colinas, near Irving, local leaders gathered alongside Abbott and company executives for a ribbon-cutting at the $157 million, 525,000-square foot campus.

“McKesson is a great company,” Abbott said on the stage of a large meeting room at the newly renovated headquarters. 

“I am proud of the work McKesson is doing,” he went on, “and make a commitment of my own to continue to ensure Texas attracts further business and expanding enterprise.”

Beth Van Duyne, then the mayor of Irving, now a U.S. Housing and Urban Development administrator under Trump, defended the city’s decision to give the pharmaceutical company a more than $2 million incentives package on top of the state’s Enterprise Fund gift.

“Having to offer incentives is always a difficult decision to make, but as long as the return on that investment is strong, we can support it,” Van Duyne said in a video recorded from the grand opening.

Even though the promise of taxpayer funds came before Paxton launched his investigation, Moody, the Democratic lawmaker, said Abbott’s office should more carefully vet companies before granting them taxpayer money, and in McKesson’s case, it should have considered the drug company’s alleged role in the opioid crisis.

“We know there’s a problem with drug distribution. These drugs being taken out of the regular route, finding their way into other people’s hands — leading to deaths, leading to overdoses,” he said, later adding, “I don’t think it’s unrealistic to ask that to be part of the evaluation at all. Part of the conversation of growing the economy is what types of companies, businesses do you want?” 

State Rep. Kevin Roberts, a Houston Republican and fellow member of the House panel studying opioids, said he did not know what went into Abbott’s decision making, so he couldn’t comment on the wisdom of the grant. But he agreed that the state should also consider wider issues when deciding which businesses are awarded grants from the enterprise fund.

“I do believe that there is some ethical responsibility in that process as well,” he said. “Just because things look profitable doesn’t mean you do them.”

The fact that McKesson got the state grant doesn’t shield it from liability if Texas ultimately files an opioid lawsuit, Roberts added. “If General Paxton goes forward, the fact that they got a TEF grant does not excuse them.”

Pressure to act

McKesson is also facing legal challenges outside of Texas.

In a recent report to the U.S. Securities and Exchange Commission, the company noted an opioid-related lawsuit brought by the State of West Virginia and nine similar complaints filed in state and federal courts in West Virginia against McKesson and other large distributors. McKesson also listed a federal lawsuit in which the Cherokee Nation alleges the company oversupplied drugs to its population.

In January, McKesson agreed to pay $150 million and revamp its compliance procedures to settle a lawsuit brought by the U.S. Department of Justice after prosecutors alleged the company failed to detect and report “suspicious orders” of opioids.

The company paid $13.25 million to settle a similar Justice Department suit in 2008. McKesson did not admit wrongdoing in either case.

Chasen, the spokeswoman, said McKesson is “really proud of our controlled substances monitoring program today,” and the recent scrutiny addresses conduct “that was really far in the past at this point.”

Chasen added that the company reports all orders “in real time” to the U.S. Drug Enforcement Agency, flagging suspicious ones. 

Mark Kinzly, a co-founder of the Texas Overdose Naloxone Initiative, which educates police officers and the public on overdose prevention, has been critical of the state’s mixed response to the opioid epidemic. In 2015, for example, Abbott drew the ire of Kinzly and other advocates when he vetoed a “Good Samaritan” bill that would have protected someone from prosecution, even if they possessed a small amount of drugs, when they called 911 to help a friend in the throes of overdose.

Abbott said at the time that the bill had an admirable goal but did not include “adequate protections to prevent its misuse by habitual drug abusers and drug dealers.”

Kinzly said Trump’s declaration of a national opioid emergency may lead more politicians to demonstrate support for expanding drug treatment programs. “That will put some pressure on Republican governors, I would imagine,” he said.

Trump, for his part, suggested Thursday that pharmaceutical companies remained in the federal government’s crosshairs.

“What they have and what they’re doing to our people is unheard of,” he said. “We will be bringing some very major lawsuits against people and against companies that are hurting our people.” 

Source: https://www.texastribune.org/2017/10/31/during-opioid-crisis-texas-subsidized-drug-company-its-now-investigati/

October 2017

By Christopher Ingraham

Drug overdose deaths surpassed 72,000 in 2017, according to provisional estimates recently released by the Centers for Disease Control and Prevention. That represents an increase of more than 6,000 deaths, or 9.5 percent, over the estimate for the previous 12-month period.

That staggering sum works out to about 200 drug overdose deaths every single day, or one every eight minutes.

The increase was driven primarily by a continued surge in deaths involving synthetic opioids, a category that includes fentanyl. There were nearly 30,000 deaths involving those drugs in 2017, according to the preliminary data, an increase of more than 9,000 over the prior year.

Deaths involving cocaine also shot up significantly, putting the stimulant on par with drugs such as heroin and the category of natural opiates that includes painkillers such as oxycodone and hydrocodone. One potential spot of good news is that deaths involving those latter two drug categories appear to have flattened out, suggesting the possibility that opiate mortality may be at or nearing its peak.


Overdose estimates for selected drug types in 2017.

The CDC cautions that these figures are early estimates based on monthly death records processed by the agency. The CDC adjusts these figures to correct for underreporting, because some recorded deaths are still pending full investigation. Final mortality figures are typically released at the end of the following calendar year.

The CDC updates these provisional numbers monthly. The recent inclusion of December 2017 means that a complete, albeit early look at 2017 overdose mortality is now available for the first time.

Geographically the deaths are distributed similarly to how they’ve been in prior years, with parts of Appalachia and New England showing the highest mortality rates. Once again, the highest rates were seen in West Virginia, with 58.7 overdose deaths for every 100,000 residents. The District of Columbia (50.4), Pennsylvania (44.1), Ohio (44.0) and Maryland (37.9) rounded out the top five.

At the other end of the spectrum, states in the Great Plains had some of the lowest death rates. Nebraska had the fewest with just 8.2 deaths per 100,000, a rate less than one-seventh the rate in West Virginia.

Despite the nationwide increase, the CDC’s preliminary data also shows overdose rates fell in a number of states, including North Dakota and Wyoming, compared with the prior year. Particularly significant were the decreases in Vermont and Massachusetts, two states with relatively high rates of overdose mortality.

Beyond that, the month-to-month data brings some potentially good news: Nationwide, deaths involving opioids have plateaued and even fallen slightly in recent months, from an estimated high of 49,552 deaths in the 12-month period ending in September 2017 down to 48,612 in the period ending January of this year. While it’s too early to say whether that trend will continue through 2018, those numbers are somewhat encouraging.


Opiate death estimates through January 2018.

A chief concern among substance abuse experts is the ubiquity of fentanyl, a synthetic opioid that’s roughly 50 times more potent than heroin. Because it’s cheap and relatively easy to make, it’s often mixed with other drugs such as heroin and cocaine.

Policymakers have struggled to come up with an adequate response to the opioid crisis. Overdose deaths initially ballooned during the Obama administration, which was criticized by experts for being slow to respond to the problem. Last year, the Trump administration declared the epidemic a “public health emergency” but allocated no new funding for states to address the issue. Former congressman Patrick Kennedy (D-R.I.), a member of the task force that the administration convened to tackle the epidemic, criticized President Trump late last year for being “all talk and no follow-through” on opioids.

https://www.washingtonpost.com/business/2018/08/15/fentanyl-use-drove-drug-overdose-deaths-record-high-cdc-estimates/?utm_term=.9c9d31666886

Abstract
Core deficits in social functioning are associated with various neuropsychiatric and neurodevelopmental disorders, yet biomarker identification and the development of effective pharmacological interventions has been limited. Recent data suggest the intriguing possibility that endogenous cannabinoids, a class of lipid neuromodulators generally implicated in the regulation of neurotransmitter release, may contribute to species-typical social functioning. Systematic study of the endogenous cannabinoid signaling could, therefore, yield novel approaches to understand the neurobiological underpinnings of atypical social functioning.

This article provides a critical review of the major components of the endogenous cannabinoid system (for example, primary receptors and effectors—Δ9-tetrahydrocannabinol, cannabidiol, anandamide and 2-arachidonoylglycerol) and the contributions of cannabinoid signaling to social functioning. Data are evaluated in the context of Research Domain Criteria constructs (for example, anxiety, chronic stress, reward learning, motivation, declarative and working memory, affiliation and attachment, and social communication) to enable interrogation of endogenous cannabinoid signaling in social functioning across diagnostic categories. The empirical evidence reviewed strongly supports the role for dysregulated cannabinoid signaling in the pathophysiology of social functioning deficits observed in brain disorders, such as autism spectrum disorder, schizophrenia, major depressive disorder, posttraumatic stress disorder and bipolar disorder. Moreover, these findings indicate that the endogenous cannabinoid system holds exceptional promise as a biological marker of, and potential treatment target for, neuropsychiatric and neurodevelopmental disorders characterized by impairments in social functioning.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5048207/

Introduction
Synaptic cell-adhesion molecules and their interactions with other molecular pathways affect both synapse formation and its function (Varoqueaux et al., 2006; Sudhof, 2008; Bemben et al., 2015a). Neurexins are presynaptic cell-adhesion molecules that interact with neuroligins and other postsynaptic partners. Neurexins are encoded by three genes, each of which encodes a long and short isoform, termed α- and β-neurexins, respectively (Sudhof, 2008). Interestingly, despite studies linking neurexins to autism and other neuropsychiatric disorders (Leone et al., 2010; Rabaneda et al., 2014), the precise cellular mechanisms underlying the role of neurexins in cognition remain poorly understood.

Since most biochemical studies of neurexins have focused on β-neurexins, investigating the synaptic actions of β-neurexins is particularly imperative. In their timely Cell article, Anderson et al. reported that β-neurexins selectively modulate synaptic strength at excitatory synapses by regulating postsynaptic endocannabinoid synthesis, describing an unexpected trans-synaptic mechanism for β-neurexins to control neural circuits via endocannabinoid signaling. 

Source: https://www.frontiersin.org/articles/10.3389/fnins.2016.00203/full

See also:

https://drugprevent.org.uk/ppp/2018/08/%CE%B2-neurexins-control-neural-circuits-by-regulating-synaptic-endocannabinoid-signaling/

Abstract
α- and β-neurexins are presynaptic cell-adhesion molecules implicated in autism and schizophrenia. We find that although β-neurexins are expressed at much lower levels than α-neurexins, conditional knockout of β-neurexins with continued expression of α-neurexins dramatically decreased neurotransmitter release at excitatory synapses in cultured cortical neurons. The β-neurexin knockout phenotype was attenuated by CB1-receptor inhibition which blocks presynaptic endocannabinoid signaling or by 2-arachidonoylglycerol synthesis inhibition which impairs postsynaptic endocannabinoid release. In synapses formed by CA1-region pyramidal neurons onto burst-firing subiculum neurons, presynaptic in vivo knockout of β-neurexins aggravated endocannabinoid-mediated inhibition of synaptic transmission and blocked LTP; presynaptic CB1-receptor antagonists or postsynaptic 2-arachidonoylglycerol synthesis inhibition again reversed this block. Moreover, conditional knockout of β-neurexins in CA1-region neurons impaired contextual fear memories. Thus, our data suggest that presynaptic β-neurexins control synaptic strength in excitatory synapses by regulating postsynaptic 2-arachidonoylglycerol synthesis, revealing an unexpected role for β-neurexins in the endocannabinoid-dependent regulation of neural circuits.

Source:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4709013/

See also:

https://drugprevent.org.uk/ppp/2018/08/endocannabinoid-mediates-excitatory-synaptic-function-of-%ce%b2-neurexins-commentary-%ce%b2-neurexins-control-neural-circuits-by-regulating-synaptic-endocannabinoid-signaling/

Introduction: This literature survey aims to extend the comprehensive survey performed by Bergamaschi et al. in 2011 on cannabidiol (CBD) safety and side effects. Apart from updating the literature, this article focuses on clinical studies and CBD potential interactions with other drugs.

Results: In general, the often described favorable safety profile of CBD in humans was confirmed and extended by the reviewed research. The majority of studies were performed for treatment of epilepsy and psychotic disorders. Here, the most commonly reported side effects were tiredness, diarrhea, and changes of appetite/weight. In comparison with other drugs, used for the treatment of these medical conditions, CBD has a better side effect profile. This could improve patients’ compliance and adherence to treatment. CBD is often used as adjunct therapy. Therefore, more clinical research is warranted on CBD action on hepatic enzymes, drug transporters, and interactions with other drugs and to see if this mainly leads to positive or negative effects, for example, reducing the needed clobazam doses in epilepsy and therefore clobazam’s side effects.

Conclusion: This review also illustrates that some important toxicological parameters are yet to be studied, for example, if CBD has an effect on hormones. Additionally, more clinical trials with a greater number of participants and longer chronic CBD administration are still lacking.

Keywords: : cannabidiol, cannabinoids, medical uses, safety, side effects, toxicity

Introduction

Since several years, other pharmacologically relevant constituents of the Cannabis plant, apart from Δ9-THC, have come into the focus of research and legislation. The most prominent of those is cannabidiol (CBD). In contrast to Δ9-THC, it is nonintoxicating, but exerts a number of beneficial pharmacological effects. For instance, it is anxiolytic, anti-inflammatory, antiemetic, and antipsychotic. Moreover, neuroprotective properties have been shown.1,2 Consequently, it could be used at high doses for the treatment of a variety of conditions ranging in psychiatric disorders such as schizophrenia and dementia, as well as diabetes and nausea.1,2

At lower doses, it has physiological effects that promote and maintain health, including antioxidative, anti-inflammatory, and neuroprotection effects. For instance, CBD is more effective than vitamin C and E as a neuroprotective antioxidant and can ameliorate skin conditions such as acne.3,4

The comprehensive review of 132 original studies by Bergamaschi et al. describes the safety profile of CBD, mentioning several properties: catalepsy is not induced and physiological parameters are not altered (heart rate, blood pressure, and body temperature). Moreover, psychological and psychomotor functions are not adversely affected. The same holds true for gastrointestinal transit, food intake, and absence of toxicity for nontransformed cells. Chronic use and high doses of up to 1500 mg per day have been repeatedly shown to be well tolerated by humans.1

Nonetheless, some side effects have been reported for CBD, but mainly in vitro or in animal studies. They include alterations of cell viability, reduced fertilization capacity, and inhibition of hepatic drug metabolism and drug transporters (e.g., p-glycoprotein).1Consequently, more human studies have to be conducted to see if these effects also occur in humans. In these studies, a large enough number of subjects have to be enrolled to analyze long-term safety aspects and CBD possible interactions with other substances.

This review will build on the clinical studies mentioned by Bergamaschi et al. and will update their survey with new studies published until September 2016.

Relevant Preclinical Studies

Before we discuss relevant animal research on CBD possible effects on various parameters, several important differences between route of administration and pharmacokinetics between human and animal studies have to be mentioned. First, CBD has been studied in humans using oral administration or inhalation. Administration in rodents often occures either via intraperitoneal injection or via the oral route. Second, the plasma levels reached via oral administration in rodents and humans can differ. Both these observations can lead to differing active blood concentrations of CBD.1,5,6

In addition, it is possible that CBD targets differ between humans and animals. Therefore, the same blood concentration might still lead to different effects. Even if the targets, to which CBD binds, are the same in both studied animals and humans, for example, the affinity or duration of CBD binding to its targets might differ and consequently alter its effects.

The following study, which showed a positive effect of CBD on obsessive compulsive behavior in mice and reported no side effects, exemplifies the existing pharmacokinetic differences.5 When mice and humans are given the same CBD dose, more of the compound becomes available in the mouse organism. This higher bioavailability, in turn, can cause larger CBD effects.

Deiana et al. administered 120 mg/kg CBD either orally or intraperitoneally and measured peak plasma levels.5 The group of mice, which received oral CBD, had plasma levels of 2.2 μg/ml CBD. In contrast, i.p. injections resulted in peak plasma levels of 14.3 μg/ml. Administering 10 mg/kg oral CBD to humans leads to blood levels of 0.01 μg/ml.6 This corresponds to human blood levels of 0.12 μg/ml, when 120 mg/kg CBD was given to humans. This calculation was performed assuming the pharmacokinetics of a hydrophilic compound, for simplicity’s sake. We are aware that the actual levels of the lipophilic CBD will vary.

A second caveat of preclinical studies is that supraphysiological concentrations of compounds are often used. This means that the observed effects, for instance, are not caused by a specific binding of CBD to one of its receptors but are due to unspecific binding following the high compound concentration, which can inactivate the receptor or transporter.

The following example and calculations will demonstrate this. In vitro studies have shown that CBD inhibits the ABC transporters P-gp (P glycoprotein also referred to as ATP-binding cassette subfamily B member 1=ABCB1; 3–100 μM CBD) and Bcrp (Breast Cancer Resistance Protein; also referred to as ABCG2=ATP-binding cassette subfamily G member 2).7 After 3 days, the P-gp protein expression was altered in leukemia cells. This can have several implications because various anticancer drugs also bind to these membrane-bound, energy-dependent efflux transporters.1 The used CBD concentrations are supraphysiological, however, 3 μM CBD approximately corresponds to plasma concentrations of 1 μg/ml. On the contrary, a 700 mg CBD oral dose reached a plasma level of 10 ng/ml.6 This means that to reach a 1 μg/ml plasma concentration, one would need to administer considerably higher doses of oral CBD. The highest ever applied CBD dose was 1500 mg.1Consequently, more research is warranted, where the CBD effect on ABC transporters is analyzed using CBD concentrations of, for example, 0.03–0.06 μM. The rationale behind suggesting these concentrations is that studies summarized by Bih et al. on CBD effect on ABCC1 and ABCG2 in SF9 human cells showed that a CBD concentration of 0.08 μM elicited the first effect.7

Using the pharmacokinetic relationships mentioned above, one would need to administer an oral CBD dose of 2100 mg CBD to affect ABCC1 and ABCG2. We used 10 ng/ml for these calculations and the ones in Table 1,6,8 based on a 6-week trial using a daily oral administration of 700 mg CBD, leading to mean plasma levels of 6–11 ng/ml, which reflects the most realistic scenario of CBD administration in patients.6 That these levels seem to be reproducible, and that chronic CBD administration does not lead to elevated mean blood concentrations, was shown by another study. A single dose of 600 mg led to reduced anxiety and mean CBD blood concentrations of 4.7–17 ng/ml.9

Table 1.

Inhibition of Human Metabolic Enzymes by Exogenous Cannabinoids In Vitro and the Extrapolated Levels of Oral Daily CBD Administration in Humans Needed to Reach These In Vitro Concentrations (Adapted)6,8

CYP-450 isoform 1A1 1A2 1B1 2A6 2B6 2C9 2D6 3A4 3A5 3A7
CBD (in μM) 0.2 2.7 3.6 55.0 0.7 0.9–9.9 1.2–2.7 1.0 0.2 12.3
aExtrapolated oral daily CBD doses to reach the levels above (in mg) 4900 63,000 84,000 1.28 Mio. Ca. 16,000 21,000–231,000 28,000–63,000 Ca. 23,000 4900 0.29 Mio.
aThe calculations made here are based on the assumption that the CBD distribution in the blood follows the pharmacokinetics of a hydrophilic substance such as alcohol. The reality is more complex, because CBD is lipophilic and, for example, will consequently accumulate in fat tissue. These calculations were made with the intention to give the reader an impression and an approximation of the supraphysiological levels used in in vitro studies.

It also seems warranted to assume that the mean plasma concentration exerts the total of observed CBD effects, compared to using peak plasma levels, which only prevail for a short amount of time. This is not withstanding, that a recent study measured Cmax values for CBD of 221 ng/ml, 3 h after administration of 1 mg/kg fentanyl concomitantly with a single oral dose of 800 mg CBD.10

CBD-drug interactions

Cytochrome P450-complex enzymes

This paragraph describes CBD interaction with general (drug)-metabolizing enzymes, such as those belonging to the cytochrome P450 family. This might have an effect for coadministration of CBD with other drugs.7 For instance, CBD is metabolized, among others, via the CYP3A4 enzyme. Various drugs such as ketoconazol, itraconazol, ritonavir, and clarithromycin inhibit this enzyme.11 This leads to slower CBD degradation and can consequently lead to higher CBD doses that are longer pharmaceutically active. In contrast, phenobarbital, rifampicin, carbamazepine, and phenytoin induce CYP3A4, causing reduced CBD bioavailability.11 Approximately 60% of clinically prescribed drugs are metabolized via CYP3A4.1 Table 1 shows an overview of the cytochrome inhibiting potential of CBD. It has to be pointed out though, that the in vitro studies used supraphysiological CBD concentrations.

Studies in mice have shown that CBD inactivates cytochrome P450 isozymes in the short term, but can induce them after repeated administration. This is similar to their induction by phenobarbital, thereby implying the 2b subfamily of isozymes.1 Another study showed this effect to be mediated by upregulation of mRNA for CYP3A, 2C, and 2B10, after repeated CBD administration.1

Hexobarbital is a CYP2C19 substrate, which is an enzyme that can be inhibited by CBD and can consequently increase hexobarbital availability in the organism.12,13 Studies also propose that this effect might be caused in vivo by one of CBD metabolites.14,15Generally, the metabolite 6a-OH-CBD was already demonstrated to be an inducer of CYP2B10. Recorcinol was also found to be involved in CYP450 induction. The enzymes CYP3A and CYP2B10 were induced after prolonged CBD administration in mice livers, as well as for human CYP1A1 in vitro.14,15 On the contrary, CBD induces CYP1A1, which is responsible for degradation of cancerogenic substances such as benzopyrene. CYP1A1 can be found in the intestine and CBD-induced higher activity could therefore prevent absorption of cancerogenic substances into the bloodstream and thereby help to protect DNA.2

Effects on P-glycoprotein activity and other drug transporters

A recent study with P-gp, Bcrp, and P-gp/Bcrp knockout mice, where 10 mg/kg was injected subcutaneously, showed that CBD is not a substrate of these transporters itself. This means that they do not reduce CBD transport to the brain.16 This phenomenon also occurs with paracetamol and haloperidol, which both inhibit P-gp, but are not actively transported substrates. The same goes for gefitinib inhibition of Bcrp.

These proteins are also expressed at the blood–brain barrier, where they can pump out drugs such as risperidone. This is hypothesized to be a cause of treatment resistance.16 In addition, polymorphisms in these genes, making transport more efficient, have been implied in interindividual differences in pharmacoresistance.10 Moreover, the CBD metabolite 7-COOH CBD might be a potent anticonvulsant itself.14 It will be interesting to see whether it is a P-gp substrate and alters pharmacokinetics of coadministered P-gp-substrate drugs.

An in vitro study using three types of trophoblast cell lines and ex vivo placenta, perfused with 15 μM CBD, found BCRP inhibition leading to accumulation of xenobiotics in the fetal compartment.17BCRP is expressed at the apical side of the syncytiotrophoblast and removes a wide variety of compounds forming a part of the placental barrier. Seventy-two hours of chronic incubation with 25 μM CBD also led to morphological changes in the cell lines, but not to a direct cytotoxic effect. In contrast, 1 μM CBD did not affect cell and placenta viability.17 The authors consider this effect cytostatic. Nicardipine was used as the BCRP substrate in the in vitro studies, where the Jar cell line showed the largest increase in BCRP expression correlating with the highest level of transport.17,and references therein

The ex vivo study used the antidiabetic drug and BCRP substrate glyburide.17 After 2 h of CBD perfusion, the largest difference between the CBD and the placebo placentas (n=8 each) was observed. CBD inhibition of the BCRP efflux function in the placental cotyledon warrants further research of coadministration of CBD with known BCRP substrates such as nitrofurantoin, cimetidine, and sulfasalazine. In this study, a dose–response curve should be established in male and female subjects (CBD absorption was shown to be higher in women) because the concentrations used here are usually not reached by oral or inhaled CBD administration. Nonetheless, CBD could accumulate in organs physiologically restricted via a blood barrier.17

Physiological effects

CBD treatment of up to 14 days (3–30 mg/kg b.w. i.p.) did not affect blood pressure, heart rate, body temperature, glucose levels, pH, pCO2, pO2, hematocrit, K+ or Na+ levels, gastrointestinal transit, emesis, or rectal temperature in a study with rodents.1

Mice treated with 60 mg/kg b.w. CBD i.p. for 12 weeks (three times per week) did not show ataxia, kyphosis, generalized tremor, swaying gait, tail stiffness, changes in vocalization behavior or open-field physiological activity (urination, defecation).1

Neurological and neurospychiatric effects

Anxiety and depression

Some studies indicate that under certain circumstances, CBD acute anxiolytic effects in rats were reversed after repeated 14-day administration of CBD.2 However, this finding might depend on the used animal model of anxiety or depression. This is supported by a study, where CBD was administered in an acute and “chronic” (2 weeks) regimen, which measured anxiolytic/antidepressant effects, using behavioral and operative models (OBX=olfactory bulbectomy as model for depression).18 The only observed side effects were reduced sucrose preference, reduced food consumption and body weight in the nonoperated animals treated with CBD (50 mg/kg). Nonetheless, the behavioral tests (for OBX-induced hyperactivity and anhedonia related to depression and open field test for anxiety) in the CBD-treated OBX animals showed an improved emotional response. Using microdialysis, the researchers could also show elevated 5-HT and glutamate levels in the prefrontal cortex of OBX animals only. This area was previously described to be involved in maladaptive behavioral regulation in depressed patients and is a feature of the OBX animal model of depression. The fact that serotonin levels were only elevated in the OBX mice is similar to CBD differential action under physiological and pathological conditions.

A similar effect was previously described in anxiety experiments, where CBD proved to be only anxiolytic in subjects where stress had been induced before CBD administration. Elevated glutamate levels have been proposed to be responsible for ketamine’s fast antidepressant function and its dysregulation has been described in OBX mice and depressed patients. Chronic CBD treatment did not elicit behavioral changes in the nonoperated mice. In contrast, CBD was able to alleviate the affected functionality of 5HT1A receptors in limbic brain areas of OBX mice.18 and references therein

Schiavon et al. cite three studies that used chronic CBD administration to demonstrate its anxiolytic effects in chronically stressed rats, which were mostly mediated via hippocampal neurogenesis.19 and references therein For instance, animals received daily i.p. injections of 5 mg/kg CBD. Applying a 5HT1A receptor antagonist in the DPAG (dorsal periaqueductal gray area), it was implied that CBD exerts its antipanic effects via these serotonin receptors. No adverse effects were reported in this study.

Psychosis and bipolar disorder

Various studies on CBD and psychosis have been conducted.20 For instance, an animal model of psychosis can be created in mice by using the NMDAR antagonist MK-801. The behavioral changes (tested with the prepulse inhibition [PPI] test) were concomitant with decreased mRNA expression of the NMDAR GluN1 subunit gene (GRN1) in the hippocampus, decreased parvalbumin expression (=a calcium-binding protein expressed in a subclass of GABAergic interneurons), and higher FosB/ΔFosB expression (=markers for neuronal activity). After 6 days of MK-801 treatment, various CBD doses were injected intraperitoneally (15, 30, 60 mg/kg) for 22 days. The two higher CBD doses had beneficial effects comparable to the atypical antipsychotic drug clozapine and also attenuated the MK-801 effects on the three markers mentioned above. The publication did not record any side effects.21

One of the theories trying to explain the etiology of bipolar disorder (BD) is that oxidative stress is crucial in its development. Valvassori et al. therefore used an animal model of amphetamine-induced hyperactivity to model one of the symptoms of mania. Rats were treated for 14 days with various CBD concentrations (15, 30, 60 mg/kg daily i.p.). Whereas CBD did not have an effect on locomotion, it did increase brain-derived neurotrophic factor (BDNF) levels and could protect against amphetamine-induced oxidative damage in proteins of the hippocampus and striatum. No adverse effects were recorded in this study.22

Another model for BD and schizophrenia is PPI of the startle reflex both in humans and animals, which is disrupted in these diseases. Peres et al., list five animal studies, where mostly 30 mg/kg CBD was administered and had a positive effect on PPI.20 Nonetheless, some inconsistencies in explaining CBD effects on PPI as model for BD exist. For example, CBD sometimes did not alter MK-801-induced PPI disruption, but disrupted PPI on its own.20 If this effect can be observed in future experiments, it could be considered to be a possible side effect.

Addiction

CBD, which is nonhedonic, can reduce heroin-seeking behavior after, for example, cue-induced reinstatement. This was shown in an animal heroin self-administration study, where mice received 5 mg/kg CBD i.p. injections. The observed effect lasted for 2 weeks after CBD administration and could normalize the changes seen after stimulus cue-induced heroin seeking (expression of AMPA, GluR1, and CB1R). In addition, the described study was able to replicate previous findings showing no CBD side effects on locomotor behavior.23

Neuroprotection and neurogenesis

There are various mechanisms underlying neuroprotection, for example, energy metabolism (whose alteration has been implied in several psychiatric disorders) and proper mitochondrial functioning.24 An early study from 1976 found no side effects and no effect of 0.3–300 μg/mg protein CBD after 1 h of incubation on mitochondrial monoamine oxidase activity in porcine brains.25 In hypoischemic newborn pigs, CBD elicited a neuroprotective effect, caused no side effects, and even led to beneficial effects on ventilatory, cardiac, and hemodynamic functions.26

A study comparing acute and chronic CBD administration in rats suggests an additional mechanism of CBD neuroprotection: Animals received i.p. CBD (15, 30, 60 mg/kg b.w.) or vehicle daily, for 14 days. Mitochondrial activity was measured in the striatum, hippocampus, and the prefrontal cortex.27 Acute and chronic CBD injections led to increased mitochondrial activity (complexes I-V) and creatine kinase, whereas no side effects were documented. Chronic CBD treatment and the higher CBD doses tended to affect more brain regions. The authors hypothesized that CBD changed the intracellular Ca2+ flux to cause these effects. Since the mitochondrial complexes I and II have been implied in various neurodegenerative diseases and also altered ROS (reactive oxygen species) levels, which have also been shown to be altered by CBD, this might be an additional mechanism of CBD-mediated neuroprotection.1,27

Interestingly, it has recently been shown that the higher ROS levels observed after CBD treatment were concomitant with higher mRNA and protein levels of heat shock proteins (HSPs). In healthy cells, this can be interpreted as a way to protect against the higher ROS levels resulting from more mitochondrial activity. In addition, it was shown that HSP inhibitors increase the CBD anticancer effect in vitro.28 This is in line with the studies described by Bergamaschi et al., which also imply ROS in CBD effect on (cancer) cell viability in addition to, for example, proapoptotic pathways such as via caspase-8/9 and inhibition of the procarcinogenic lipoxygenase pathway.1

Another publication studied the difference of acute and chronic administration of two doses of CBD in nonstressed mice on anxiety. Already an acute i.p. administration of 3 mg/kg was anxiolytic to a degree comparable to 20 mg/kg imipramine (an selective serotonin reuptake inhibitor [SSRI] commonly prescribed for anxiety and depression). Fifteen days of repeated i.p. administration of 3 mg/kg CBD also increased cell proliferation and neurogenesis (using three different markers) in the subventricular zone and the hippocampal dentate gyrus. Interestingly, the repeated administration of 30 mg/kg also led to anxiolytic effects. However, the higher dose caused a decrease in neurogenesis and cell proliferation, indicating dissociation of behavioral and proliferative effects of chronic CBD treatment. The study does not mention adverse effects.19

Immune system

Numerous studies show the CBD immunomodulatory role in various diseases such as multiple sclerosis, arthritis, and diabetes. These animal and human ex vivo studies have been reviewed extensively elsewhere, but studies with pure CBD are still lacking. Often combinations of THC and CBD were used. It would be especially interesting to study when CBD is proinflammatory and under which circumstances it is anti-inflammatory and whether this leads to side effects (Burstein, 2015: Table 1 shows a summary of its anti-inflammatory actions; McAllister et al. give an extensive overview in Table 1 of the interplay between CBD anticancer effects and inflammation signaling).29,30

In case of Alzheimer’s disease (AD), studies in mice and rats showed reduced amyloid beta neuroinflammation (linked to reduced interleukin [IL]-6 and microglial activation) after CBD treatment. This led to amelioration of learning effects in a pharmacological model of AD. The chronic study we want to describe in more detail here used a transgenic mouse model of AD, where 2.5-month-old mice were treated with either placebo or daily oral CBD doses of 20 mg/kg for 8 months (mice are relatively old at this point). CBD was able to prevent the development of a social recognition deficit in the AD transgenic mice.

Moreover, the elevated IL-1 beta and TNF alpha levels observed in the transgenic mice could be reduced to WT (wild-type) levels with CBD treatment. Using statistical analysis by analysis of variance, this was shown to be only a trend. This might have been caused by the high variation in the transgenic mouse group, though. Also, CBD increased cholesterol levels in WT mice but not in CBD-treated transgenic mice. This was probably due to already elevated cholesterol in the transgenic mice. The study observed no side effects.31 and references within

In nonobese diabetes-prone female mice (NOD), CBD was administered i.p. for 4 weeks (5 days a week) at a dose of 5 mg/kg per day. After CBD treatment was stopped, observation continued until the mice were 24 weeks old. CBD treatment lead to considerable reduction of diabetes development (32% developed glucosuria in the CBD group compared to 100% in untreated controls) and to more intact islet of Langerhans cells. CBD increased IL-10 levels, which is thought to act as an anti-inflammatory cytokine in this context. The IL-12 production of splenocytes was reduced in the CBD group and no side effects were recorded.32

After inducing arthritis in rats using Freund’s adjuvant, various CBD doses (0.6, 3.1, 6.2, or 62.3 mg/day) were applied daily in a gel for transdermal administration for 4 days. CBD reduced joint swelling, immune cell infiltration. thickening of the synovial membrane, and nociceptive sensitization/spontaneous pain in a dose-dependent manner, after four consecutive days of CBD treatment. Proinflammatory biomarkers were also reduced in a dose-dependent manner in the dorsal root ganglia (TNF alpha) and spinal cord (CGRP, OX42). No side effects were evident and exploratory behavior was not altered (in contrast to Δ9-THC, which caused hypolocomotion).33

Cell migration

Embryogenesis

CBD was shown to be able to influence migratory behavior in cancer, which is also an important aspect of embryogenesis.1 For instance, it was recently shown that CBD inhibits Id-1. Helix-loop-helix Id proteins play a role in embryogenesis and normal development via regulation of cell differentiation. High Id1-levels were also found in breast, prostate, brain, and head and neck tumor cells, which were highly aggressive. In contrast, Id1 expression was low in noninvasive tumor cells. Id1 seems to influence the tumor cell phenotype by regulation of invasion, epithelial to mesenchymal transition, angiogenesis, and cell proliferation.34

There only seems to exist one study that could not show an adverse CBD effect on embryogenesis. An in vitro study could show that the development of two-cell embryos was not arrested at CBD concentrations of 6.4, 32, and 160 nM.35

Cancer

Various studies have been performed to study CBD anticancer effects. CBD anti-invasive actions seem to be mediated by its TRPV1 stimulation and its action on the CB receptors. Intraperitoneal application of 5 mg/kg b.w. CBD every 3 days for a total of 28 weeks, almost completely reduced the development of metastatic nodules caused by injection of human lung carcinoma cells (A549) in nude mice.36 This effect was mediated by upregulation of ICAM1 and TIMP1. This, in turn, was caused by upstream regulation of p38 and p42/44 MAPK pathways. The typical side effects of traditional anticancer medication, emesis, and collateral toxicity were not described in these studies. Consequently, CBD could be an alternative to other MMP1 inhibitors such as marimastat and prinomastat, which have shown disappointing clinical results due to these drugs’ adverse muscoskeletal effects.37,38

Two studies showed in various cell lines and in tumor-bearing mice that CBD was able to reduce tumor metastasis.34,39 Unfortunately, the in vivo study was only described in a conference abstract and no route of administration or CBD doses were mentioned.36 However, an earlier study used 0.1, 1.0, or 1.5 μmol/L CBD for 3 days in the aggressive breast cancer cells MDA-MB231. CBD downregulated Id1 at promoter level and reduced tumor aggressiveness.40

Another study used xenografts to study the proapoptotic effect of CBD, this time in LNCaP prostate carcinoma cells.36 In this 5-week study, 100 mg/kg CBD was administered daily i.p. Tumor volume was reduced by 60% and no adverse effects of treatment were described in the study. The authors assumed that the observed antitumor effects were mediated via TRPM8 together with ROS release and p53 activation.41 It has to be pointed out though, that xenograft studies only have limited predictive validity to results with humans. Moreover, to carry out these experiments, animals are often immunologically compromised, to avoid immunogenic reactions as a result to implantation of human cells into the animals, which in turn can also affect the results.42

Another approach was chosen by Aviello et al.43 They used the carcinogen azoxymethane to induce colon cancer in mice. Treatment occurred using IP injections of 1 or 5 mg/kg CBD, three times a week for 3 weeks (including 1 week before carcinogen administration). After 3 months, the number of aberrant crypt foci, polyps, and tumors was analyzed. The high CBD concentration led to a significant decrease in polyps and a return to near-normal levels of phosphorylated Akt (elevation caused by the carcinogen).42 No adverse effects were mentioned in the described study.43

Food intake and glycemic effects

Animal studies summarized by Bergamaschi et al. showed inconclusive effects of CBD on food intake1: i.p. administration of 3–100 mg/kg b.w. had no effect on food intake in mice and rats. On the contrary, the induction of hyperphagia by CB1 and 5HT1A agonists in rats could be decreased with CBD (20 mg/kg b.w. i.p.). Chronic administration (14 days, 2.5 or 5 mg/kg i.p.) reduced the weight gain in rats. This effect could be inhibited by coadministration of a CB2R antagonist.1

The positive effects of CBD on hyperglycemia seem to be mainly mediated via CBD anti-inflammatory and antioxidant effects. For instance, in ob/ob mice (an animal model of obesity), 4-week treatment with 3 mg/kg (route of administration was not mentioned) increased the HDL-C concentration by 55% and reduced total cholesterol levels by more than 25%. In addition, treatment increased adiponectin and liver glycogen concentrations.44 and references therein

Endocrine effects

High CBD concentrations (1 mM) inhibited progesterone 17-hydroxylase, which creates precursors for sex steroid and glucocorticoid synthesis, whereas 100 μM CBD did not in an in vitro experiment with primary testis microsomes.45 Rats treated with 10 mg/kg i.p. b.w. CBD showed inhibition of testosterone oxidation in the liver.46

Genotoxicity and mutagenicity

Jones et al. mention that 120 mg/kg CBD delivered intraperetonially to Wistar Kyoto rats showed no mutagenicity and genotoxicity based on personal communication with GW Pharmaceuticals47,48These data are yet to be published. The 2012 study with an epilepsy mouse model could also show that CBD did not influence grip strength, which the study describes as a “putative test for functional neurotoxicity.”48

Motor function was also tested on a rotarod, which was also not affected by CBD administration. Static beam performance, as an indicator of sensorimotor coordination, showed more footslips in the CBD group, but CBD treatment did not interfere with the animals’ speed and ability to complete the test. Compared to other anticonvulsant drugs, this effect was minimal.48 Unfortunately, we could not find more studies solely focusing on genotoxicity by other research groups neither in animals nor in humans.

Acute Clinical Data

Bergamaschi et al. list an impressive number of acute and chronic studies in humans, showing CBD safety for a wide array of side effects.1 They also conclude from their survey, that none of the studies reported tolerance to CBD. Already in the 1970s, it was shown that oral CBD (15–160 mg), iv injection (5–30 mg), and inhalation of 0.15 mg/kg b.w. CBD did not lead to adverse effects. In addition, psychomotor function and psychological functions were not disturbed. Treatment with up to 600 mg CBD neither influenced physiological parameters (blood pressure, heart rate) nor performance on a verbal paired-associate learning test.1

Fasinu et al. created a table with an overview of clinical studies currently underway, registered in Clinical Trials. gov.49 In the following chapter, we highlight recent, acute clinical studies with CBD.

CBD-drug interactions

CBD can inhibit CYP2D6, which is also targeted by omeprazole and risperidone.2,14 There are also indications that CBD inhibits the hepatic enzyme CYP2C9, reducing the metabolization of warfarin and diclofenac.2,14 More clinical studies are needed, to check whether this interaction warrants an adaption of the used doses of the coadministered drugs.

The antibiotic rifampicin induces CYP3A4, leading to reduced CBD peak plasma concentrations.14 In contrast, the CYP3A4 inhibitor ketoconazole, an antifungal drug, almost doubles CBD peak plasma concentration. Interestingly, the CYP2C19 inhibitor omeprazole, used to treat gastroesophageal reflux, could not significantly affect the pharmacokinetics of CBD.14

A study, where a regimen of 6×100 mg CBD daily was coadministered with hexobarbital in 10 subjects, found that CBD increased the bioavailability and elimination half-time of the latter. Unfortunately, it was not mentioned whether this effect was mediated via the cytochrome P450 complex.16

Another aspect, which has not been thoroughly looked at, to our knowledge, is that several cytochrome isozymes are not only expressed in the liver but also in the brain. It might be interesting to research organ-specific differences in the level of CBD inhibition of various isozymes. Apart from altering the bioavailability in the overall plasma of the patient, this interaction might alter therapeutic outcomes on another level. Dopamine and tyramine are metabolized by CYP2D6, and neurosteroid metabolism also occurs via the isozymes of the CYP3A subgroup.50,51 Studying CBD interaction with neurovascular cytochrome P450 enzymes might also offer new mechanisms of action. It could be possible that CBD-mediated CYP2D6 inhibition increases dopamine levels in the brain, which could help to explain the positive CBD effects in addiction/withdrawal scenarios and might support its 5HT (=serotonin) elevating effect in depression.

Also, CBD can be a substrate of UDP glucuronosyltransferase.14Whether this enzyme is indeed involved in the glucuronidation of CBD and also causes clinically relevant drug interactions in humans is yet to be determined in clinical studies. Generally, more human studies, which monitor CBD-drug interactions, are needed.

Physiological effects

In a double-blind, placebo-controlled crossover study, CBD was coadministered with intravenous fentanyl to a total of 17 subjects.10Blood samples were obtained before and after 400 mg CBD (previously demonstrated to decrease blood flow to (para)limbic areas related to drug craving) or 800 mg CBD pretreatment. This was followed by a single 0.5 (Session 1) or 1.0μg/kg (Session 2, after 1 week of first administration to allow for sufficient drug washout) intravenous fentanyl dose. Adverse effects and safety were evaluated with both forms of the Systematic Assessment for Treatment Emergent Events (SAFTEE). This extensive tool tests, for example, 78 adverse effects divided into 23 categories corresponding to organ systems or body parts. The SAFTEE outcomes were similar between groups. No respiratory depression or cardiovascular complications were recorded during any test session.

The results of the evaluation of pharmacokinetics, to see if interaction between the drugs occurred, were as follows. Peak CBD plasma concentrations of the 400 and 800 mg group were measured after 4 h in the first session (CBD administration 2 h after light breakfast). Peak urinary CBD and its metabolite concentrations occurred after 6 h in the low CBD group and after 4 h in the high CBD group. No effect was evident for urinary CBD and metabolite excretion except at the higher fentanyl dose, in which CBD clearance was reduced. Importantly, fentanyl coadministration did not produce respiratory depression or cardiovascular complications during the test sessions and CBD did not potentiate fentanyl’s effects. No correlation was found between CBD dose and plasma cortisol levels.

Various vital signs were also measured (blood pressure, respiratory/heart rate, oxygen saturation, EKG, respiratory function): CBD did not worsen the adverse effects (e.g., cardiovascular compromise, respiratory depression) of iv fentanyl. Coadministration was safe and well tolerated, paving the way to use CBD as a potential treatment for opioid addiction. The validated subjective measures scales Anxiety (visual analog scale [VAS]), PANAS (positive and negative subscores), and OVAS (specific opiate VAS) were administered across eight time points for each session without any significant main effects for CBD for any of the subjective effects on mood.10

A Dutch study compared subjective adverse effects of three different strains of medicinal cannabis, distributed via pharmacies, using VAS. “Visual analog scale is one of the most frequently used psychometric instruments to measure the extent and nature of subjective effects and adverse effects. The 12 adjectives used for this study were as follows: alertness, tranquility, confidence, dejection, dizziness, confusion/disorientation, fatigue, anxiety, irritability, appetite, creative stimulation, and sociability.” The high CBD strain contained the following concentrations: 6% Δ9-THC/7.5% CBD (n=25). This strain showed significantly lower levels of anxiety and dejection. Moreover, appetite increased less in the high CBD strain. The biggest observed adverse effect was “fatigue” with a score of 7 (out of 10), which did not differ between the three strains.52

Neurological and neurospychiatric effects

Anxiety

Forty-eight participants received subanxiolytic levels (32 mg) of CBD, either before or after the extinction phase in a double-blind, placebo-controlled design of a Pavlovian fear-conditioning experiment (recall with conditioned stimulus and context after 48 h and exposure to unconditioned stimulus after reinstatement). Skin conductance (=autonomic response to conditioning) and shock expectancy measures (=explicit aspects) of conditioned responding were recorded throughout. Among other scales, the Mood Rating Scale (MRS) and the Bond and Bodily Symptoms Scale were used to assess anxiety, current mood, and physical symptoms. “CBD given postextinction (active after consolidation phase) enhanced consolidation of extinction learning as assessed by shock expectancy.” Apart from the extinction-enhancing effects of CBD in human aversive conditioned memory, CBD showed a trend toward some protection against reinstatement of contextual memory. No side/adverse effects were reported.53

Psychosis

The review by Bergamaschi et al. mentions three acute human studies that have demonstrated the CBD antipsychotic effect without any adverse effects being observed. This holds especially true for the extrapyramidal motor side effects elicited by classical antipsychotic medication.1

Fifteen male, healthy subjects with minimal prior Δ9-THC exposure (<15 times) were tested for CBD affecting Δ9-THC propsychotic effects using functional magnetic resonance imaging (fMRI) and various questionnaires on three occasions, at 1-month intervals, following administration of 10 mg delta-9-Δ9-THC, 600 mg CBD, or placebo. Order of drug administration was pseudorandomized across subjects, so that an equal number of subjects received any of the drugs during the first, second, or third session in a double-blind, repeated-measures, within-subject design.54 No CBD effect on psychotic symptoms as measured with PANSS positive symptoms subscale, anxiety as indexed by the State Trait Anxiety Inventory (STAI) state, and Visual Analogue Mood Scale (VAMS) tranquilization or calming subscale, compared to the placebo group, was observed. The same is true for a verbal learning task (=behavioral performance of the verbal memory).

Moreover, pretreatment with CBD and subsequent Δ9-THC administration could reduce the latter’s psychotic and anxiety symptoms, as measured using a standardized scale. This effect was caused by opposite neural activation of relevant brain areas. In addition, no effects on peripheral cardiovascular measures such as heart rate and blood pressure were measured.54

A randomized, double-blind, crossover, placebo-controlled trial was conducted in 16 healthy nonanxious subjects using a within-subject design. Oral Δ9-THC=10 mg, CBD=600 mg, or placebo was administered in three consecutive sessions at 1-month intervals. The doses were selected to only evoke neurocognitive effects without causing severe toxic, physical, or psychiatric reactions. The 600 mg CBD corresponded to mean (standard deviation) whole blood levels of 0.36 (0.64), 1.62 (2.98), and 3.4 (6.42) ng/mL, 1, 2, and 3 h after administration, respectively.

Physiological measures and symptomatic effects were assessed before, and at 1, 2, and 3 h postdrug administration using PANSS (a 30-item rating instrument used to assess psychotic symptoms, with ratings based on a semistructured clinical interview yielding subscores for positive, negative, and general psychopathology domains), the self-administered VAMS with 16 items (e.g., mental sedation or intellectual impairment, physical sedation or bodily impairments, anxiety effects and other types of feelings or attitudes), the ARCI (Addiction Research Center Inventory; containing empirically derived drug-induced euphoria; stimulant-like effects; intellectual efficiency and energy; sedation; dysphoria; and somatic effects) to assess drug effects and the STAI-T/S, where subjects were evaluated on their current mood and their feelings in general.

There were no significant differences between the effects of CBD and placebo on positive and negative psychotic symptoms, general psychopathology (PANSS), anxiety (STAI-S), dysphoria (ARCI), sedation (VAMS, ARCI), and the level of subjective intoxication (ASI, ARCI), where Δ9-THC did have a pronounced effect. The physiological parameters, heart rate and blood pressure, were also monitored and no significant difference between the placebo and the CBD group was observed.55

Addiction

A case study describes a patient treated for cannabis withdrawal according to the following CBD regimen: “treated with oral 300 mg on Day 1; CBD 600 mg on Days 2–10 (divided into two doses of 300 mg), and CBD 300 mg on Day 11.” CBD treatment resulted in a fast and progressive reduction in withdrawal, dissociative and anxiety symptoms, as measured with the Withdrawal Discomfort Score, the Marijuana Withdrawal Symptom Checklist, Beck Anxiety Inventory, and Beck Depression Inventory (BDI). Hepatic enzymes were also measured daily, but no effect was reported.56

Naturalistic studies with smokers inhaling cannabis with varying amounts of CBD showed that the CBD levels were not altering psychomimetic symptoms.1 Interestingly, CBD was able to reduce the “wanting/liking”=implicit attentional bias caused by exposure to cannabis and food-related stimuli. CBD might work to alleviate disorders of addiction, by altering the attentive salience of drug cues. The study did not further measure side effects.57

CBD can also reduce heroin-seeking behaviors (e.g., induced by a conditioned cue). This was shown in the preclinical data mentioned earlier and was also replicated in a small double-blind pilot study with individuals addicted to opioids, who have been abstinent for 7 days.52,53 They either received placebo or 400 or 800 mg oral CBD on three consecutive days. Craving was induced with a cue-induced reinstatement paradigm (1 h after CBD administration). One hour after the video session, subjective craving was already reduced after a single CBD administration. The effect persisted for 7 days after the last CBD treatment. Interestingly, anxiety measures were also reduced after treatment, whereas no adverse effects were described.23,58

A pilot study with 24 subjects was conducted in a randomized, double-blind, placebo-controlled design to evaluate the impact of the ad hoc use of CBD in smokers, who wished to stop smoking. Pre- and post-testing for mood and craving of the participants was executed. These tests included the Behaviour Impulsivity Scale, BDI, STAI, and the Severity of Dependence Scale. During the week of CBD inhalator use, subjects used a diary to log their craving (on a scale from 1 to 100=VAS measuring momentary subjective craving), the cigarettes smoked, and the number of times they used the inhaler. Craving was assessed using the Tiffany Craving Questionnaire (11). On day 1 and 7, exhaled CO was measured to test smoking status. Sedation, depression, and anxiety were evaluated with the MRS.

Over the course of 1 week, participants used the inhaler when they felt the urge to smoke and received a dose of 400 μg CBD via the inhaler (leading to >65% bioavailability); this significantly reduced the number of cigarettes smoked by ca. 40%, while craving was not significantly different in the groups post-test. At day 7, the anxiety levels for placebo and CBD group did not differ. CBD did not increase depression (in contract to the selective CB1 antagonist rimonabant). CBD might weaken the attentional bias to smoking cues or could have disrupted reconsolidation, thereby destabilizing drug-related memories.59

Cell migration

According to our literature survey, there currently are no studies about CBD role in embryogenesis/cell migration in humans, even though cell migration does play a role in embryogenesis and CBD was shown to be able to at least influence migratory behavior in cancer.1

Endocrine effects and glycemic (including appetite) effects

To the best of our knowledge, no acute studies were performed that solely concentrated on CBD glycemic effects. Moreover, the only acute study that also measured CBD effect on appetite was the study we described above, comparing different cannabis strains. In this study, the strain high in CBD elicited less appetite increase compared to the THC-only strain.52

Eleven healthy volunteers were treated with 300 mg (seven patients) and 600 mg (four patients) oral CBD in a double-blind, placebo-controlled study. Growth hormone and prolactin levels were unchanged. In contrast, the normal decrease of cortisol levels in the morning (basal measurement=11.0±3.7 μg/dl; 120 min after placebo=7.1±3.9 μg/dl) was inhibited by CBD treatment (basal measurement=10.5±4.9 μg/dl; 120 min after 300 mg CBD=9.9±6.2 μg/dl; 120 min after 600 mg CBD=11.6±11.6 μg/dl).60

A more recent study also used 600 mg oral CBD for a week and compared 24 healthy subjects to people at risk for psychosis (n=32; 16 received placebo and 16 CBD). Serum cortisol levels were taken before the TSST (Trier Social Stress Test), immediately after, as well as 10 and 20 min after the test. Compared to the healthy individuals, the cortisol levels increased less after TSST in the 32 at-risk individuals. The CBD group showed less reduced cortisol levels but differences were not significant.61 It has to be mentioned that these data were presented at a conference and are not yet published (to our knowledge) in a peer-reviewed journal.

Chronic CBD Studies in Humans

Truly chronic studies with CBD are still scarce. One can often argue that what the studies call “chronic” CBD administration only differs to acute treatment, because of repeated administration of CBD. Nonetheless, we also included these studies with repeated CBD treatment, because we think that compared to a one-time dose of CBD, repeated CBD regimens add value and knowledge to the field and therefore should be mentioned here.

CBD-drug interactions

An 8-week-long clinical study, including 13 children who were treated for epilepsy with clobazam (initial average dose of 1 mg/kg b.w.) and CBD (oral; starting dose of 5 mg/kg b.w. raised to maximum of 25 mg/kg b.w.), showed the following. The CBD interaction with isozymes CYP3A4 and CYP2C19 caused increased clobazam bioavailability, making it possible to reduce the dose of the antiepileptic drug, which in turn reduced its side effects.62

These results are supported by another study described in the review by Grotenhermen et al.63 In this study, 33 children were treated with a daily dose of 5 mg/kg CBD, which was increased every week by 5 mg/kg increments, up to a maximum level of 25 mg/kg. CBD was administered on average with three other drugs, including clobazam (54.5%), valproic acid (36.4%), levetiracetam (30.3%), felbamate (21.2%), lamotrigine (18.2%), and zonisamide (18.2%). The coadministration led to an alteration of blood levels of several antiepileptic drugs. In the case of clobazam this led to sedation, and its levels were subsequently lowered in the course of the study.

Physiological effects

A first pilot study in healthy volunteers in 1973 by Mincis et al. administering 10 mg oral CBD for 21 days did not find any neurological and clinical changes (EEG; EKG).64 The same holds true for psychiatry and blood and urine examinations. A similar testing battery was performed in 1980, at weekly intervals for 30 days with daily oral CBD administration of 3 mg/kg b.w., which had the same result.65

Neurological and neuropsychiatric effects

Anxiety

Clinical chronic (lasting longer than a couple of weeks) studies in humans are crucial here but were mostly still lacking at the time of writing this review. They hopefully will shed light on the inconsistencies observerd in animal studies. Chronic studies in humans may, for instance, help to test whether, for example, an anxiolytic effect always prevails after chronic CBD treatment or whether this was an artifact of using different animal models of anxiety or depression.2,18

Psychosis and bipolar disorder

In a 4-week open trial, CBD was tested on Parkinson’s patients with psychotic symptoms. Oral doses of 150–400 mg/day CBD (in the last week) were administered. This led to a reduction of their psychotic symptoms. Moreover, no serious side effects or cognitive and motor symptoms were reported.66

Bergamaschi et al. describe a chronic study, where a teenager with severe side effects of traditional antipsychotics was treated with up to 1500 mg/day of CBD for 4 weeks. No adverse effects were observed and her symptoms improved. The same positive outcome was registered in another study described by Bergamaschi et al., where three patients were treated with a starting dose of CBD of 40 mg, which was ramped up to 1280 mg/day for 4 weeks.1 A double-blind, randomized clinical trial of CBD versus amisulpride, a potent antipsychotic in acute schizophrenia, was performed on a total of 42 subjects, who were treated for 28 days starting with 200 mg CBD per day each.67 The dose was increased stepwise by 200 mg per day to 4×200 mg CBD daily (total 800 mg per day) within the first week. The respective treatment was maintained for three additional weeks. A reduction of each treatment to 600 mg per day was allowed for clinical reasons, such as unwanted side effects after week 2. This was the case for three patients in the CBD group and five patients in the amisulpride group. While both treatments were effective (no significant difference in PANSS total score), CBD showed the better side effect profile. Amisulpride, working as a dopamine D2/D3-receptor antagonist, is one of the most effective treatment options for schizophrenia. CBD treatment was accompanied by a substantial increase in serum anandamide levels, which was significantly associated with clinical improvement, suggesting inhibition of anandamide deactivation via reduced FAAH activity.

In addition, the FAAH substrates palmitoylethanolamide and linoleoyl-ethanolamide (both lipid mediators) were also elevated in the CBD group. CBD showed less serum prolactin increase (predictor of galactorrhoea and sexual dysfunction), fewer extrapyramidal symptoms measured with the Extrapyramidal Symptom Scale, and less weight gain. Moreover, electrocardiograms as well as routine blood parameters were other parameters whose effects were measured but not reported in the study. CBD better safety profile might improve acute compliance and long-term treatment adherence.67,68

A press release by GW Pharmaceuticals of September 15th, 2015, described 88 patients with treatment-resistant schizophrenic psychosis, treated either with CBD (in addition to their regular medication) or placebo. Important clinical parameters improved in the CBD group and the number of mild side effects was comparable to the placebo group.2 Table 2 shows an overview of studies with CBD for the treatment of psychotic symptoms and its positive effect on symptomatology and the absence of side effects.69

Table 2.

Studies with CBD with Patients with Psychotic Symptoms (Adapted)69

Assessment Oral CBD administration Total number of study participants Main findings
BPRS (brief psychiatric rating scale) Up to 1500 mg/day for 26 days 1 Improvement of symptomatology, no side effects
BPRS Up to 1280 mg/day for 4 weeks 3 Mild improvement of symptomatology of 1 patient, no side effects
BPRS, Parkinson Psychosis Questionnaire (PPQ) Up to 600 mg/day for 4 weeks 6 Improvement of symptomatology, no side effects
Stroop Color Word Test, BPRS, PANSS (positive and negative symptom scale) Single doses of 300 or 600 mg 28 Performance after placebo and CBD 300 mg compared to CBD 600 mg; no effects on symptomatology
BPRS, PANSS Up to 800 mg/day for 4 weeks 39 CBD as effective as amisulpride in terms of improvement of symptomatology; CBD displayed superior side effect profile

Treatment of two patients for 24 days with 600–1200 mg/day CBD, who were suffering from BD, did not lead to side effects.70 Apart from the study with two patients mentioned above, CBD has not been tested systematically in acute or chronic administration scenarios in humans for BD according to our own literature search.71

Epilepsy

Epileptic patients were treated for 135 days with 200–300 mg oral CBD daily and evaluated every week for changes in urine and blood. Moreover, neurological and physiological examinations were performed, which neither showed signs of CBD toxicity nor severe side effects. The study also illustrated that CBD was well tolerated.65

A review by Grotenhermen and Müller-Vahl describes several clinical studies with CBD2: 23 patients with therapy-resistant epilepsy (e.g., Dravet syndrome) were treated for 3 months with increasing doses of up to 25 mg/kg b.w. CBD in addition to their regular epilepsy medication. Apart from reducing the seizure frequency in 39% of the patients, the side effects were only mild to moderate and included reduced/increased appetite, weight gain/loss, and tiredness.

Another clinical study lasting at least 3 months with 137 children and young adults with various forms of epilepsy, who were treated with the CBD drug Epidiolex, was presented at the American Academy for Neurology in 2015. The patients were suffering from Dravet syndrome (16%), Lennox–Gastaut syndrome (16%), and 10 other forms of epilepsy (some among them were very rare conditions). In this study, almost 50% of the patients experienced a reduction of seizure frequency. The reported side effects were 21% experienced tiredness, 17% diarrhea, and 16% reduced appetite. In a few cases, severe side effects occurred, but it is not clear, if these were caused by Epidiolex. These were status epilepticus (n=10), diarrhea (n=3), weight loss (n=2), and liver damage in one case.

The largest CBD study conducted thus far was an open-label study with Epidiolex in 261 patients (mainly children, the average age of the participants was 11) suffering from severe epilepsy, who could not be treated sufficiently with standard medication. After 3 months of treatment, where patients received CBD together with their regular medication, a median reduction of seizure frequency of 45% was observed. Ten percent of the patients reported side effects (tiredness, diarrhea, and exhaustion).2

After extensive literature study of the available trials performed until September 2016, CBD side effects were generally mild and infrequent. The only exception seems to be a multicenter open-label study with a total of 162 patients aged 1–30 years, with treatment-resistant epilepsy. Subjects were treated for 1 year with a maximum of 25 mg/kg (in some clinics 50 mg/kg) oral CBD, in addition to their standard medication.

This led to a reduction in seizure frequency. In this study, 79% of the cohort experienced side effects. The three most common adverse effects were somnolence (n=41 [25%]), decreased appetite (n=31 [19%]), and diarrhea (n=31 [19%]).72 It has to be pointed out that no control group existed in this study (e.g., placebo or another drug). It is therefore difficult to put the side effect frequency into perspective. Attributing the side effects to CBD is also not straightforward in severely sick patients. Thus, it is not possible to draw reliable conclusions on the causation of the observed side effects in this study.

Parkinson’s disease

In a study with a total of 21 Parkinson’s patients (without comorbid psychiatric conditions or dementia) who were treated with either placebo, 75 mg/day CBD or 300 mg/day CBD in an exploratory double-blind trial for 6 weeks, the higher CBD dose showed significant improvement of quality of life, as measured with PDQ-39. This rating instrument comprised the following factors: mobility, activities of daily living, emotional well-being, stigma, social support, cognition, communication, and bodily discomfort. For the factor, “activities of daily living,” a possible dose-dependent relationship could exist between the low and high CBD group—the two CBD groups scored significantly different here. Side effects were evaluated with the UKU (Udvalg for Kliniske Undersøgelser). This assessment instrument analyzes adverse medication effects, including psychic, neurologic, autonomic, and other manifestations. Using the UKU and verbal reports, no significant side effects were recognized in any of the CBD groups.73

Huntington’s disease

Fifteen neuroleptic-free patients with Huntington’s disease were treated with either placebo or oral CBD (10 mg/kg b.w. per day) for 6 weeks in a double-blind, randomized, crossover study design. Using various safety outcome variables, clinical tests, and the cannabis side effect inventory, it was shown that there were no differences between the placebo group and the CBD group in the observed side effects.6

Immune system

Forty-eight patients were treated with 300 mg/kg oral CBD, 7 days before and until 30 days after the transplantation of allogeneic hematopoietic cells from an unrelated donor to treat acute leukemia or myelodysplastic syndrome in combination with standard measures to avoid GVHD (graft vs. host disease; cyclosporine and short course of MTX). The occurrence of various degrees of GVHD was compared with historical data from 108 patients, who had only received the standard treatment. Patients treated with CBD did not develop acute GVHD. In the 16 months after transplantation, the incidence of GHVD was significantly reduced in the CBD group. Side effects were graded using the Common Terminology Criteria for Adverse Events (CTCAE v4.0) classification, which did not detect severe adverse effects.74

Endocrine and glycemic (including appetite, weight gain) effects

In a placebo-controlled, randomized, double-blind study with 62 subjects with noninsulin-treated type 2 diabetes, 13 patients were treated with twice-daily oral doses of 100 mg CBD for 13 weeks. This resulted in lower resistin levels compared to baseline. The hormone resistin is associated with obesity and insulin resistance. Compared to baseline, glucose-dependent insulinotropic peptide levels were elevated after CBD treatment. This incretin hormone is produced in the proximal duodenum by K cells and has insulinotropic and pancreatic b cell preserving effects. CBD was well tolerated in the patients. However, with the comparatively low CBD concentrations used in this phase-2-trial, no overall improvement of glycemic control was observed.40

When weight and appetite were measured as part of a measurement battery for side effects, results were inconclusive. For instance, the study mentioned above, where 23 children with Dravet syndrome were treated, increases as well as decreases in appetite and weight were observed as side effects.2 An open-label trial with 214 patients suffering from treatment-resistant epilepsy showed decreased appetite in 32 cases. However, in the safety analysis group, consisting of 162 subjects, 10 showed decreased weight and 12 had gained weight.52 This could be either due to the fact that CBD only has a small effect on these factors, or appetite and weight are complex endpoints influenced by multiple factors such as diet and genetic predisposition. Both these factors were not controlled for in the reviewed studies.

Conclusion

This review could substantiate and expand the findings of Bergamaschi et al. about CBD favorable safety profile.1Nonetheless, various areas of CBD research should be extended. First, more studies researching CBD side effects after real chronic administration need to be conducted. Many so-called chronic administration studies, cited here were only a couple of weeks long. Second, many trials were conducted with a small number of individuals only. To perform a throrough general safety evaluation, more individuals have to be recruited into future clinical trials. Third, several aspects of a toxicological evaluation of a compound such as genotoxicity studies and research evaluating CBD effect on hormones are still scarce. Especially, chronic studies on CBD effect on, for example, genotoxicity and the immune system are still missing. Last, studies that evaluate whether CBD-drug interactions occur in clinical trials have to be performed.

In conclusion, CBD safety profile is already established in a plethora of ways. However, some knowledge gaps detailed above should be closed by additional clinical trials to have a completely well-tested pharmaceutical compound.

Abbreviations Used

AD Alzheimer’s disease
ARCI Addiction Research Center Inventory
BD bipolar disorder
BDI Beck Depression Inventory
CBD cannabidiol
HSP heat shock protein
IL interleukin
MRS Mood Rating Scale
PPI prepulse inhibition
ROS reactive oxygen species
SAFTEE Systematic Assessment for Treatment Emergent Events
STAI State Trait Anxiety Inventory
TSST Trier Social Stress Test
UKU Udvalg for Kliniske Undersøgelser
VAMS Visual Analogue Mood Scale
VAS Visual Analog Scales

Acknowledgments

The study was commissioned by the European Industrial Hemp Association. The authors thank Michal Carus, Executive Director of the EIHA, for making this review possible, for his encouragement, and helpful hints.

Author Disclosure Statement

EIHA paid nova-Institute for the review. F.G. is Executive Director of IACM.#

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June 2017

Researchers map out a cellular mechanism that offers a biological explanation for alcoholism, and could lead to treatments

Credit: Getty Images

You can lead a lab rat to sugar water, but you can’t make him drink—especially if there’s booze around.

New research published Thursday in Science may offer insights into why some humans who drink alcohol develop an addiction whereas most do not. After caffeine, alcohol is the most commonly consumed psychoactive substance in the world. For the majority of people the occasional happy hour beer or Bloody Mary brunch is where it stops. Yet we all know that others will drink compulsively, despite whatever consequence or darkness it brings.

The new research confirms earlier work showing this is true for rats; but it takes things a step further and supports a study design that could help scientists better understand addiction biology, and possibly develop more effective therapies for human addictive behaviors. Led by a team at Linköping University in Sweden, the researchers found that when given a choice between alcohol and a tastier, more biologically desirable sugar substitute, a subgroup of rats consistently preferred the alcohol. The authors further identified a specific brain region and molecular dysfunction most likely responsible for these addictive tendencies. They believe their findings and study design could be steps toward developing an effective pharmaceutical therapy for alcohol addiction, a kind of treatment that has eluded researchers for years.

A taste for sweetness is evolutionarily embedded in the mammalian brain; in the wild, sugar translates into fast calories and improved survival odds. For the new study, 32 rats were trained to sip a 20 percent alcohol solution for 10 weeks until it became habit. They were then presented with a daily choice between more alcohol or a solution of the noncaloric sweetener saccharine. (The artificial sweetener provides sugary-tasting enticement without the potential confounding variable of actual calories.) The majority of rats vastly preferred the faux sugar over the alcohol option.

But the fact that four rats—or 12.5 percent of the total—stuck with the alcohol was telling to senior author Markus Heilig, director of the Center for Social and Affective Neuroscience at Linköping, given the rate of alcohol misuse in humans is around 15 percent. So Heilig expanded the study. “There were four rats who went for alcohol despite the more natural reward of sweetness,” he says. “We built on that, and 600 animals later we found that a very stable proportion of the population chose alcohol.” What’s more, the “addicted” rats still chose alcohol even when it meant receiving an unpleasant foot shock.

To get a better sense of what was going on at a molecular level, Heilig and his colleagues analyzed which genes were expressed in the rodent subjects’ brains. The expression of one gene in particular—called GAT-3—was found to be greatly reduced in the brains of those who opted for alcohol rather than saccharine. GAT-3 codes for a protein that normally controls levels of a neurotransmitter called GABA, a common chemical in our brains and one known to be involved in alcohol dependence.

In collaboration with co-author and University of Texas at Austin research scientist Dayne Mayfield, Heilig’s team found that in brain samples from deceased humans who had suffered from alcohol addiction, GAT-3 levels were markedly lower in the amygdala—generally considered the brain’s emotional center. One might assume that any altered gene expression contributing to addictive behaviors would instead manifest in the brain’s reward circuitry—a network of centers involved in pleasurable responses to enticements like food, sex and gambling.

Yet the decrease in GAT-3 expression in both rats and humans was by far strongest in the amygdala. “Figuring out the reward circuitry has been a fantastic success story, but it’s probably of limited relevance to clinical addiction,” Heilig says. “The rewarding effect of drugs happens in everybody. It’s a completely different story in the minority of people who continue to take drugs despite adverse consequences.” He believes altered activity in the amygdala makes perfect sense, given that addiction—in both rats and humans—often brings with it negative emotions and anxiety.

Much previous addiction research has relied on models in which rodents learn to self-administer addictive substances, but without other options that could compete with drug use. It was French neuroscientist Serge Ahmed who recognized this as a major limitation to understanding addition biology given that, in reality, only a minority of humans develops addiction to a particular substance. By offering an alternative reward (that is, sweet water), his team showed only a minority of rats develop a harmful preference for drug use—a finding that has now been confirmed with several other commonly abused drugs.

Building on Ahmed’s concept, Heilig added the element of choice to his research. “You can’t determine the true reward of an addictive drug in isolation; it’s dependent on what other options are available—in our case a sugar substitute.” He says most models that have been used to study addiction, and to seek ways to treat it, were probably too limited in their design. “The availability of choice,” he adds, “is going to be fundamental to studying addiction and developing effective treatments for it.”

Paul Kenny, chair of neuroscience at Icahn School of Medicine at Mount Sinai, agrees. “In order to develop novel therapeutics for alcoholism it is critical to understand not just the actions of alcohol in the brain, but how those actions may differ between individuals who are vulnerable or resilient to the addictive properties of the drug,” he says. “This Herculean effort to impressively map out a cellular mechanism that likely contributes to alcohol dependence susceptibility will likely provide important new leads in the search for more effective therapeutics.” Kenny was not involved in the new research.

Heilig and his team believe they have already identified a promising addiction treatment based on their latest work,  and have teamed up with a pharmaceutical company in hopes of soon testing the compound in humans. The drug suppresses the release of GABA and thus could restore levels of the neurotransmitter to normal in people with a dangerous taste for alcohol. With any luck, one of civilization’s oldest  vices might soon loosen its grip.. Illumination.

Source:  www.scientificamerican.com/article/scientists-pinpoint-brain-region-that-may-be-center-of-alcohol-addiction/   June 21st 2018

TO ALL OUR READERS: THE NDPA WOULD URGE YOU TO READ THE REPORT MENTIONED IN THE ARTICLE BELOW, (Tracking the Money That’s Legalizing Marijuana and Why It Matters), WHICH GIVES A DETAILED DESCRIPTION OF HOW MARIJUANA BECAME THE NUMBER ONE DRUG OF CHOICE FOR MILLIONS OF PEOPLE WORLDWIDE, HOW IT BECAME ‘BIG BUSINESS’ IN THE USA AND WHY WE NEED TO DISSEMINATE THIS INFORMATION WIDELY.

Report by National Families in Action Rips the Veil Off the Medical Marijuana Industry
Research Traces the Money Trail and Reveals the Motivation Behind Marijuana as Medicine

Tracking the Money That’s Legalizing Marijuana and Why It Matters documents state-by-state financial data, exposing the groups and the amount of money used either to fund or oppose ballot initiatives legalizing medical or recreational marijuana in 16 U.S. states.

• NFIA report reveals three billionaires — George Soros, Peter Lewis and John Sperling — who contributed 80 percent of the money to medicalize marijuana through state ballot initiatives during a 13-year period, with the strategy to use medical marijuana as a runway to legalized recreational pot.
• Report shows how billionaires and marijuana legalizers manipulated the ballot initiative process, outspent the people who opposed marijuana and convinced voters that marijuana is medicine, even while most of the scientific and medical communities say marijuana is not medicine and should not be legal.

• Children in Colorado treated with unregulated cannabis oil have had severe dystonic reactions, other movement disorders, developmental regression, intractable vomiting and worsening seizures.

• A medical marijuana industry has emerged to join the billionaires in financing initiatives to legalize recreational pot.

ATLANTA, March 14, 2017 (GLOBE NEWSWIRE) — A new report by National Families in Action (NFIA) uncovers and documents how three billionaires, who favor legal recreational marijuana, manipulated the ballot initiative process in 16 U.S. states for more than a decade, convincing voters to legalize medical marijuana. NFIA is an Atlanta-based non-profit organization, founded in 1977, that has been helping parents prevent children from using alcohol, tobacco, and other drugs. NFIA researched and issued the paper to mark its 40th anniversary.

The NFIA study, Tracking the Money That’s Legalizing Marijuana and Why It Matters, exposes, for the first time, the money trail behind the marijuana legalization effort during a 13-year period. The report lays bare the strategy to use medical marijuana as a runway to legalized recreational pot, describing how financier George Soros, insurance magnate Peter Lewis, and for-profit education baron John Sperling (and groups they and their families fund) systematically chipped away at resistance to marijuana while denying that full legalization was their goal.

The report documents state-by-state financial data, identifying the groups and the amount of money used either to fund or oppose ballot initiatives legalizing medical or recreational marijuana in 16 states. The paper unearths how legalizers fleeced voters and outspent — sometimes by hundreds of times — the people who opposed marijuana.

Tracking the Money That’s Legalizing Marijuana and Why It Matters illustrates that legalizers lied about the health benefits of marijuana, preyed on the hopes of sick people, flouted scientific evidence and advice from the medical community and gutted consumer protections against unsafe, ineffective drugs. And, it proves that once the billionaires achieved their goal of legalizing recreational marijuana (in Colorado and Washington in 2012), they virtually stopped financing medical pot ballot initiatives and switched to financing recreational pot. In 2014 and 2016, they donated $44 million to legalize recreational pot in Alaska, Oregon, California, Arizona, Nevada, Massachusetts and Maine. Only Arizona defeated the onslaught (for recreational marijuana).

Unravelling the Legalization Strategy: Behind the Curtain

In 1992, financier George Soros contributed an estimated $15 million to several groups he advised to stop advocating for outright legalization and start working toward what he called more winnable issues such as medical marijuana. At a press conference in 1993, Richard Cowen, then-director of the National Organization for the Reform of Marijuana Laws, said, “The key to it [full legalization] is medical access. Because, once you have hundreds of thousands of people using marijuana medically, under medical supervision, the whole scam is going to be blown. The consensus here is that medical marijuana is our strongest suit. It is our point of leverage which will move us toward the legalization of marijuana for personal use.”

Between 1996 and 2009, Soros, Lewis and Sperling contributed 80 percent of the money to medicalize marijuana through state ballot initiatives. Their financial contributions, exceeding $15.7 million (of the $19.5 million total funding), enabled their groups to lie to voters in advertising campaigns, cover up marijuana’s harmful effects, and portray pot as medicine — leading people to believe that the drug is safe and should be legal for any use.
Today, polls show how successful the billionaires and their money have been. In 28 U.S. states and the District of Columbia, voters and, later, legislators have shown they believe marijuana is medicine, even though most of the scientific and medical communities say marijuana is not medicine and should not be legal. While the most recent report, issued by the National Academies of Sciences (NAS), finds that marijuana may alleviate certain kinds of pain, it also finds there is no rigorous, medically acceptable documentation that marijuana is effective in treating any other illness. At the same time, science offers irrefutable evidence that marijuana is addictive, harmful and can hinder brain development in adolescents. At the distribution level, there are no controls on the people who sell to consumers. Budtenders (marijuana bartenders) have no medical or pharmaceutical training or qualifications.

One tactic used by legalizers was taking advantage of voter empathy for sick people, along with the confusion about science and how the FDA approves drugs. A positive finding in a test tube or petri dish is merely a first step in a long, rigorous process leading to scientific consensus about the efficacy of a drug. Scientific proof comes after randomized, controlled clinical trials, and many drugs with promising early stage results never make it through the complex sets of hurdles that prove efficacy and safety. But marijuana legalizers use early promise and thin science to persuade and manipulate empathetic legislators and voters into buying the spin that marijuana is a cure-all.

People who are sick already have access to two FDA-approved drugs, dronabinol and nabilone, that are not marijuana, but contain identical copies of some of the components of marijuana. These drugs, available as pills, effectively treat chemotherapy-induced nausea and vomiting and AIDS wasting. The NAS reviewed 10,700 abstracts of marijuana studies conducted since 1999, finding that these two oral drugs are effective in adults for the conditions described above. An extract containing two marijuana chemicals that is approved in other countries, reduces spasticity caused by multiple sclerosis. But there is no evidence that marijuana treats other diseases, including epilepsy and most of the other medical conditions the states have legalized marijuana to treat. These conditions range from Amyotrophic lateral sclerosis (ALS) and Crohn’s disease to Hepatitis-C, post-traumatic stress disorder (PTSD) and even sickle cell disease.

Not So Fast — What about the Regulations?
Legalizers also have convinced Americans that unregulated cannabidiol, a marijuana component branded as cannabis oil, CBD, or Charlotte’s Web, cures intractable seizures in children with epilepsy, and polls show some 90 percent of Americans want medical marijuana legalized, particularly for these sick children. In Colorado, the American Epilepsy Society reports that children with epilepsy are receiving unregulated, highly variable artisanal preparations of cannabis oil recommended, in most cases, by doctors with no training in paediatrics, neurology or epilepsy. Young patients have had severe dystonic reactions and other movement disorders, developmental regression, intractable vomiting and worsening seizures that can be so severe that their physicians have to put the child into a coma to get the seizures to stop. Because of these dangerous side effects, not one paediatric neurologist in Colorado, where unregulated cannabidiol is legal, recommends it for these children.

Dr. Sanjay Gupta further clouded the issue when he produced Weed in 2013, a three-part documentary series for CNN on marijuana as medicine. In all three programs, Dr. Gupta promoted CBD oil, the kind the American Epilepsy Society calls artisanal. This is because not one CBD product sold in legal states has been purified to Food and Drug Administration (FDA) standards, tested, or proven safe and effective. The U.S. Congress and the FDA developed rigid processes to review drugs and prevent medical tragedies such as birth defects caused by thalidomide. These processes have facilitated the greatest advances in medicine in history.

“By end-running the FDA, three billionaires have been willing to wreck the drug approval process that has protected Americans from unsafe, ineffective drugs for more than a century,” said Sue Rusche, president and CEO of National Families in Action and author of the report. “Unsubstantiated claims for the curative powers of marijuana abound.” No one can be sure of the purity, content, side effects or potential of medical marijuana to cause cancer or any other disease. When people get sick from medical marijuana, there are no uniform mechanisms to recall products causing the harm. Some pot medicines contain no active ingredients. Others contain contaminants. “Sick people, especially children, suffer while marijuana medicine men make money at their expense,” added Ms. Rusche.

Marijuana Industry — Taking a Page from the Tobacco Industry
The paper draws a parallel between the marijuana and tobacco industries, both built with the knowledge that a certain percentage of users will become addicted and guaranteed lifetime customers. Like tobacco, legalized marijuana will produce an unprecedented array of new health, safety and financial consequences to Americans and their children.

“Americans learned the hard way about the tragic effects of tobacco and the deceptive practices of the tobacco industry. Making another addictive drug legal unleashes a commercial business that is unable to resist the opportunity to make billions of dollars on the back of human suffering, unattained life goals, disease, and death,” said Ms. Rusche. “If people genuinely understood that marijuana can cause cognitive, safety and mental health problems, is addictive, and that addiction rates may be three times higher than reported, neither voters nor legislators would legalize pot.”
The paper and the supporting data are available at www.nationalfamilies.org.
About National Families in Action

National Families in Action is a 501 (c) (3) nonprofit organization that was founded in Atlanta, Georgia in 1977. The organization helped lead a national parent movement credited with reducing drug use among U.S. adolescents and young adults by two-thirds between 1979 and 1992. For forty years, it has provided complex scientific information in understandable language to help parents and others protect children’s health. It tracks marijuana science and the marijuana legalization movement on its Marijuana Report website and its weekly e-newsletter of the same name.

Source: https://globenewswire.com/news-release/2017/03/14/936283/0/en/New-Report-by-National-Families-in-Action-Rips-the-Veil-Off-the-Medical-Marijuana-Industry.html

The following letter was submitted to the US government Food and Drug Adminstration by Australian Professor Dr. Stuart Reece as evidence against the suggested re-scheduling of cannabinoids in the USA. This item can be found online where a full list of carefully researched references is included. Professor Reece has produced an extraordinary article which should be widely read.

We cannot recommend this article highly enough.

NDPA April 2018

http://GordonDrugAbusePrevention.com

This website has been created as a public service to help address the problem of the use of marijuana and other mood- and mind-altering substances in the United States and around the world. A purpose is help inform the public, the media, and those in positions of public responsibility of the challenges facing the nation as a result of the widespread use of psychoactive and mood-altering substances, particularly marijuana and designer drugs. The harmful effects of these substances have not been well understood. In fact, there is great ignorance of the harmful effects of marijuana and other drugs that are being used for experimental or recreational purposes. The implications that the harmful effects that these drugs have for the health and wellbeing of individuals, families, and society are legion. * * * * * * *

Federal Register Submission
Food and Drug Administration,
10903 New Hampshire Ave.,
Silver Spring,
MD, 20993-0002, USA.

Re: Re-Scheduling of Cannabinoids in USA – Tetrahydrocannabinol and Cannabidiol Related Arteriopathy, Genotoxicity and Teratogenesis

I am very concerned about the potential for increased cannabis availability in USA implied by full drug legalization; however, a comprehensive and authoritative submission of the evidence would take weeks and months to prepare. Knowing what we know now and indeed, what has been available in the scientific literature for a growing number of years concerning a myriad of harmful effects of marijuana, marijuana containing THC should not be reclassified.

These effects that are now well documented in the scientific literature include, alarmingly, harm involving reproductive function and birth anomalies as a result of exposure to or use of marijuana with THC. In addition to all of the usual concerns which you will have heard from many sources including the following I have further particular concerns:

1) Effect on developing brains

2) Effect on driving

3) Effect as a Gateway drug to other drug use including the opioid epidemic

4) Effect on developmental trajectory and failure to attain normal adult goals(stable relationship, work, education)

5) Effect on IQ and IQ regression

6) Effect to increase numerous psychiatric and psychological disorders

7) Effect on respiratory system

8) Effect on reproductive system

9) Effect in relation to immunity and immunosuppression

10) Effect of now very concentrated forms of cannabis, THC and CBD which are widely available

11) Outdated epidemiological studies which apply only to the era before cannabis became so potent and so concentrated

12) Cannabis is now known to have an important arteriopathic effect and cardiovascular toxic effect .

These issues are all well covered by a rich recent literature including reviews from such major international authorities as Dr Nora Volkow Director of NIDA, Professor Wayne Hall and others .

Cannabinoid Therapeutics

In my view the therapeutic effects of cannabinoids have been wildly inflated by the press. Moreover, with over 1,000 studies listed for cannabinoids on clinicaltrials.gov, the chance of a type I experimental error, or studies being falsely reported to be positive when in fact they are not, is at last 25/1,000 at the 0.05 level.

THC as dronabinol is actually a failed drug from USA which has such a high incidence of side effects that it was rarely used as superior agents are readily available for virtually all of its touted and alleged therapeutic applications. My American liaisons advise that dronabinol sales have climbed in recent times as patients use it as a ruse to avoid detection of cannabinoid use at work in states where it is not yet legal. So when I call it a failed therapeutic I mean in a traditional sense, not in the novel way it is now applied for flagrantly flouting the law.

In considering the alleged benefits of cannabis one has to be particularly mindful of cannabis addiction in which cannabinoids will alleviate the effect of drug withdrawal as they do in any other addiction. Moreover, the fact that cannabis itself is known to cause both pain and nausea, greatly complicates the interpretation of many studies.

I also have the following concerns which relate in sum to the arteriopathy and vasculopathy and the genotoxicity of cannabis, tetrahydrocannabinol and likely including cannabidiol and various other cannabinoids:

Cannabinoid Arteriopathy

Particularly noteworthy amongst these various reports are two reports by Dr Nora Volkow in 2014, the Director of the National Institute of Drug Abuse at NIH to the New England Journal of Medicine which together document the adverse cardiovascular and cerebrovascular effects of cannabis at the epidemiological level ; a report from our own increase cardiovascular aging to BMJ Open ; a series of reports showing a fivefold

increase in the rate of heart attack within one hour after cannabis smoking ; several reports of cannabis related arteritis ; other reports of the cerebrovascular actions of cannabis ; documentation that cannabis exposure increases arterial stiffness and cardiovascular and organismal aging ; and a recent report showing that human endothelial vascular function – vasodilation – is substantially inhibited within just one minute of cannabis exposure .

It is also relevant that a synthetic cannabinoid was recently shown to directly induce both thromboxane synthase and lipoxygenase, and so be directly vasoconstrictive, prothrombotic and proinflammatory .

Vascular aging, including both macrovascular and microvascular aging is a major pathological feature not only because most adults in western nations die from myocardial infarction or cerebrovascular accidents, but also because local blood flow and microvascular function is a key determinant of stem cell niche activity in many stem cell beds. This has given rise to the vascular theory of aging which has been produced by some of the leading researchers at the National Health Lung and Blood Institute at NIH, amongst many others .

It can thus be said not only that “You are as old as your (macrovascular) arteries”, but also that “you are as old as your (microvascular) stem cells.” Hence the now compelling evidence for the little known arteriopathic complications of cannabis and cannabinoids, carry very far reaching implications indeed. This was confirmed directly in the clinical study of arterial stiffness from my clinic mentioned above .

Whilst aging, myocardial infarction and cerebrovascular accidents are all highly significant outcomes and major public health endpoints, these effects assume added significance in the context of congenital anomalies. Some congenital defects, such as gastroschisis, are thought to be due to a failure of vascular supply of part of the anterior abdominal wall . Hence in one recent study the unadjusted odds ratio of having a gastroschisis pregnancy amongst cannabis users (O.R.=8.03, 95%C.I. 5.63-11.46) was almost as high as that for heroin, cocaine and amphetamine users (O.R.= 9.35, 95%C.I.
6.64-13.15), and the adjusted odds ratio for any illicit drug use (of which was 84% cannabis) was O.R.=3.54 (95%C.I. 2.22-5.63) and for cannabis alone was said by these Canadian authors to be O.R.=3.0. Hence cannabis related vasculopathy – arteriopathy beyond its very serious implications in adults also carries implications for paediatric and congenital disorders and may also constitute a major teratogenic mechanism.

Cannabinoid Genotoxicity and Teratogenesis

Cannabis is associated with 11 cancers (lung, throat, bladder, airways, testes, prostate,

cervix, larynx) including;

Four congenital and thus inherited cancers (rhabdomyosarcoma, neuroblastoma,ALL,

AML and AMML);

Sativex product insert in many nations carries standard warning against its use by

males or females who might be having a baby.

Cannabis – and likely also CBD – is known to be associated with epigenetic changes

some of which are believed to be inheritable for at least four generations.

Cannabis is known to interfere with tubulin synthesis and binding and it also

acts via Stathmin so that microtubule function is impeded . This leads directly to

micronucleus formation. Cannabis has been known to test positive in the

micronucleus assay for over fifty years. This is a major and standard test for

genotoxicity. Micronucleus formation is known to lead directly to major chromosomal toxicity including chromosomal shattering – so-called chromothripsis –and is known to be associated with cell death, cancerogenesis and major foetal abnormalities.

Cannabis has also been linked definitively with congenital heart disease is a statement

by the American Heart Association and the American Academy of Pediatrics in 2007, on the basis of just three epidemiological studies, all done in the days before cannabis became so concentrated. Congenital heart defects have also been linked with

the father’s cannabis use . Indeed, one study showed that paternal cannabis use was

the strongest risk factor of all for preventable congenital cardiac defects.

Cannabis has also been linked with gastroschisis in at least seven cohort and case

control studies some of which are summarized in a Canadian Government

Report 200. In that report the geographic incidence of most major congenital anomalies

closely paralleled the use of cannabis as described in other major Canadian reports.

The overall adjusted odds ratio for cannabis induction of gastroschisis was

quoted by these authors as 3.0. Moreover, outbreaks of both congenital heart disease and gastroschisis in North Carolina also paralleled the local use of cannabis in that state as described by Department of Justice Reports . The incidence of gastroschisis was noted to double in North Carolina 1999-2001 in the same period the cannabis trade there was rising.

Figures of cannabis use in pregnant women in California by age were also

recently reported to JAMA 229, age group trend lines by age group which closely

approximate those reported by CDC for the age incidence of gastroschisis in the USA

Importantly much of the cannabis coming into both North Carolina and Florida is said to originate in Mexico. An eight-fold rise in the rate of gastroschisis has been reported from Mexico . Gastroschisis has also risen in Washington state. Cannabis has also been associated with 17 other major congenital defects by major Hawaiian epidemiological study reported by Forrester in 2007 when it was used alone

When considered in association with other drug use – which in many cases cannabis leads to – cannabis use was associated with a further 19 major congenital defects. In addition to the effect of cannabinoids on the epigenome and microtubules, cannabinoids have been firmly linked to a reduction of the ability of the cell to produce energy from their mitochondria. An extensive and robust evidence base now links cellular energy generation to the maintenance and care of cellular DNA .

Moreover, as the cellular energy charge falls so too DNA maintenance collapses, and indeed, the cell can spiral where its remaining energy resources, particularly as NAD+, are routed into failing and futile DNA repair, the cell slips into pseudohypoxic metabolism like the Warburg effect well known in cancerogenesis , NAD+ falls below the level required for further energy generation and cellular metabolism collapses. Hence this well-established collapse of the mitochondrial energy charge and transmembrane potential forms a potent engine of continuing and accelerating genotoxicity .

Moreover, the well documented decline in mitochondrial respiration induced by cannabinoids, including tetrahydrocannabinol, cannabidiol and anandamide achieves particular significance in the light of the robustly documented decline in cellular energetics including NAD+ which not only occurs with age but indeed, has now been shown to be one of the primary drivers of cellular and whole organismal aging. It follows therefore that cannabinoid administration (including THC andCBD) necessarily phenocopies cellular aging. This implies of course that cannabinoid dependent patients are old at the cellular level. Indeed, normal human aging is phenocopied in the clinical syndrome of cannabinoid dependence which includes:

1) Neurological deficits in:

i) attention,

ii) learning and

iii) memory;

iv) social withdrawal and disengagement and

v) academic and

vi) occupational underachievement

2) Psychiatric disorders including

i) Anxiety,

ii) Depression,

iii) Mixed Psychosis

iv) Bipolar Affective disorder and

v) Schizophrenia,

3) Respiratory disorders including:

i) Asthma

ii) Chronic Bronchitis (increased sputum production)

iii) Emphysema (Increased residual volume)

iv) Probably increased carcinomas of the aerodigestive tract

4) Immune suppression which generally implies

i) segmental immunostimulation in some parts of the immune system since the innate and adaptive immune systems exert profound homeostatic mechanisms in response to suppression of one of its parts. A Substantial literature on immunostimulation

5) Reproductive effects generally characterized by reduced

i) Male and

ii) Female fertility

6) Cardiovascular toxicity with elevated rates of

i) Myocardial infarction

ii) Cerebrovascular accident

iii) Arteritis

iv) Vascular age – vascular stiffness

7) Genotoxicity in

i) Respiratory epithelium and

ii) Gonadal tissues.

8) Osteoporosis

9) Cancers of the

i) Head and neck

ii) Larynx

iii) Lung

iv) Leukaemia

v) Prostate

vi) Cervix

vii) Testes

viii) Bladder

ix) Childhood neuroblastoma

x) Childhood acute lymphoblastic leukaemia

xi) Childhood Acuter Myeloid and myelomonocytic leukaemia

xii) Childhood rhabdomyosarcoma 201,202.

The issue here of course is that cannabinoid dependence therefore copies without exception all of the major disorders of old age, each of which is also faithfully phenocopied by cannabis dependence.

The most prominent disorders of older age include:

1) Alzheimer’s disease

2) Cardiovascular and cerebrovascular disease

3) Osteoporosis

4) Systemic inflammatory syndrome

5) Changes in lung volume and the mechanics of breathing

6) Cancers

Hence this provides one powerful pathway by which cannabinoid exposure can replicate and phenocopy the disorders of old age. This is not of course to suggest that this is the only such pathway. Obviously changes of the general level of immune activity, or alterations of the level of DNA repair occurring directly or indirectly associated with cannabis use can form similar such pathways: both are well documented in cannabis use and also in the aging literature as major pathways implicated in systemic aging.

Nevertheless, the decline in mitochondrial energetics together with its inherent genotoxic implications does seem to be a particularly well substantiated and robustly demonstrated pathway which must give serious pause to cannabinoid advocates if the sustainability of the health and welfare systems is to be factored in together with any consideration of individual patient, advocate and industrial-complex rights.

The genotoxicity of THC, CBD and CBN has been noted against sperm since at least 1999 (Zimmerman and Zimmerman in Nahas “Marijuana and Medicine” 1999, Springer). This is clearly highly significant as sperm go directly into the formation of the zygote and the new human individual. CB1R receptors are known to exist intracellularly on both the membranes of endoplasmic reticulum and mitochondria. In both locations they can induce organellar stress and major cell toxicity including disruption of DNA maintenance. Interestingly mitochondrial outer membrane CB1R’s signal via a complex signalling chain involving the G-protein transduction machinery, protein kinase A and cyclic-AMP across the intermembrane space to the inner membrane and cristae, in a fashion replicating much of the G-protein signalling occurring at the cell membrane. This machinery is also implicated in mitonuclear signalling, and the mitonuclear DNA balance between mitochondrial DNA and nuclear DNA transcriptional control, which has long been implicated in inducing the mitochondrial unfolded protein cellular stress response cell aging, stem cell behaviour and DNA genotoxic mechanisms.

You are no doubt aware that human sperm are structured like express outboard motors behind DNA packets with layers of mitochondria densely coiled around the rotating flagellum which powers their progress in the female reproductive tract. These mitochondria also carry CB1R’s and are significantly inhibited even at 100 nanomolar THC. The acrosome reaction is also inhibited .

Cannabidiol is known to act via the PPARγ system 101,302-308. PPARγ is known to have a major effect on gene expression, reproductive and embryonic and zygote function during development 309-332 so that significant genotoxic and / or teratogenic effects seem inevitable via this route. Drugs which act in this class, known as the thiazolidinediones, are classed as category B3 in pregnancy and caution is indicated in their use in pregnancy and lactation.

The Report of the Reproductive and Cancer Hazard Assessment Branch of the Office of Environmental Health Hazard Assessment of the Health Department of California was mentioned above in connection with the carcinogenicity of marijuana smoke . Since virtually all mutagens are also teratogens it follows therefore from the basic tenets of mutagenesis that if cannabis is unsafe as a known carcinogen it must also be at the very least a putative teratogen.

CBD has also been noted to be a genotoxic in other studies . All of which points to major teratogenic activity for both THC and CBD. Some of the quotations from Professor James Graham’s classical book on the effects of THC in hamsters and white rabbits, the best animal models for human genotoxicity, bear repeating:

a) “The concentration of THC was relatively low and the malignancy severe.”

b) “40-100μg resin/ml there occurred marked inhibition of cell division.

c) “large total dose, Hamsters, 25-300mg/kg …“oedema,phocomelia,omphalocoele, spina bifida, exencephaly, multiple malformations and myelocoele. This is a formidable list.”

d) “It is to this anti-mitotic action that the authors attribute the embryotoxic action of cannabis.”

e) “By such criteria resin or extract of cannabis would be forbidden to women

during the first three months of pregnancy.”

Indeed, even from the other side of the world I have heard many exceedingly adverse reports from US states in which cannabis has been legalized including Colorado, Washington, Oregon, Florida and California. Taken together the above evidence suggests that these negative reports stem directly from the now known actions of cannabis and cannabinoids, and are by no means incidental epiphenomena somehow related to social constructs surrounding cannabis use or the product forms, dosages, or routes of administration involved.

Cannabis that contains increasingly high levels of THC is now widely available, particularly in the jurisdictions where the use of cannabis has been legalized. This means that another major genotoxin, akin to Thalidomide, is being unleashed on the USA and the world. This is clearly a very grave, and. indeed, an entirely preventable occurrence.

Dr Frances Kelsey of FDA is said to have the public servant based at FDA who saved American from the thalidomide scandal which devastated so many other English-speaking nations including my own . This occurred because the genotoxicity section of the file application with FDA was blank. It was blank because thalidomide tested positive in various white rabbit and guinea pig assays. It is these same tests which cannabis is known to have failed. Dr Kelsey’s photograph has been published in the medical press with President Kennedy for her service to the nation. The challenge to FDA at this time seems whether Science can triumph over agenda driven populism, its primary vehicle, the mass media, and its primary proximate driver the burgeoning cannabis industry. Since FDA is the Federal agency par excellence where Health Science is weighed, commissioned and thoughtfully considered the challenge in our time would appear to be no less.

Evidence to date does not suggest that major congenital malformations are as common after prenatal cannabis exposure as they are after prenatal thalidomide exposure. Nevertheless the qualitative similarities remain and indeed are prominent. It is yet to be seen whether the rate of congenital anomalies after cannabis are quantitatively as common: epidemiological studies in a high potency era have not been undertaken; and even the birth defects rates from most birth defects registers in western nations including that held by CDC, Atlanta appear to be seriously out of date at the time of writing. Moreover the non-linear dose response curve in many cannabis genotoxicity studies which includes a sharp knee bend upwards beyond a certain threshold level which suggests that we could well be in for a very unpleasant quantitative surprise. At the time of writing this remains to be formally determined.

Dr Bertha Madras, Professor of Addiction Psychiatry at Harvard Medical School has recently argued against re-scheduling of cannabis. Her comments include the following:

“Why do nations schedule drugs? …… Nations schedule psychoactive drugs because we revere this three-pound organ (of our brain) differently than any other part of our body. It is the repository of our humanity. It is the place that enables us to write poetry and to do theater, to conjure up calculus and send rockets to Pluto three billion miles away, and to create I Phones and 3 D computer printing. And that is the magnificence of the human brain. Drugs can influence (the brain) adversely. So, this is not a war on drugs. This is a defense of our brains, the ultimate source of our humanity” .

I look forward to seeing the comments that you post concerning the reasons why the classification for marijuana should not be changed and that, indeed, the public should be alerted to the very harmful effects of marijuana with THC, especially in light of the wide range of marijuana’s harmful effects and the high potency of THC in today’s marijuana and in light of the idiosyncratic effects of marijuana of even low doses of THC and owing to the certain risk of harm to progeny and babies born to users of marijuana.

Please feel free to call on me if you would like further information concerning the research to which I have referred herein.

Yours sincerely,

Professor Dr. Stuart Reece, MBBS (Hons.), FRCS(Ed.), FRCS(Glas.), FRACGP, MD(UNSW). School of Psychiatry and Clinical Neurosciences Edith Cowan University and University of Western Australia, Perth, WA stuart.reece@uwa.edu.au

Source: http://GordonDrugAbusePrevention.com.

A small but vocal contingent of drug policy interpreters is attempting again to further the fallacious meme that ‘prohibition’ and ‘supply reduction’ are driving drug deaths in Australia, not poor policy interpretation and use which foster a permission model for the vulnerable and pop-culture informed community – particularly the young, Dalgarno Institute writes.

PRESS RELEASE FROM THE DALGARNO INSTITUTE…

The National Drug Strategy

The latest National Drug Strategy 2017-26, now puts Demand Reduction as the priority! The strategy states that “Harm Minimisation includes a range of approaches to help prevent and reduce drug related problems…including a focus on abstinence-oriented strategies… [Harm minimisation] policy approach does not condone drug use.” (page 6)“Prevention of uptake reduces personal, family and community harms, allow better use of health and law enforcement resources, generates substantial social and economic benefits and produces a healthier workforce. Demand Reduction strategies that prevent drug use are more cost effective than treating established drug-related problems…Strategies that delay the onset of use prevent longer term harms and costs to the community.” (page 8)

The National Drug Strategy segments the drug issue into three main categories:

Tobacco – Alcohol – Illicit drugs

A quick summary of the policy focus/emphasis on each drug can be encapsulated as follows:

Tobacco

QUIT! Cessation, and exit from tobacco use is the ONLY goal for this drug. There is no illusion about the journey to that destination being difficult, and the reality of failure clear, but the goal posts don’t move QUIT is the ONE message ONE focus and ONE voice in all sectors of the media, community, education and legislation arenas. (Remember this is a legal drug, and until about 20 years ago, utterly socially acceptable) We have reduced smoking rates of 75% of Australian Males (not including females) after World War II down to around 14% of total population. According to health data, approximately 100,000 people give up tobacco each year, but about the same take it up. No prizes for guessing that cohort make up? The 16-24-year-old demographic usually engage (research shows us) in tobacco use mostly when drinking alcohol. Of course, learning ‘smoking’ as a delivery mechanism also equips the tobacco user for ‘smoking’ of other drugs.

Alcohol

‘Moderate! Drink Responsibility!’ However, a growing educative and legislative push (due to the rising costs of alcohol harms to community) is seeing attitudes change, with now approx. 21 per cent of Australians of drinking age now abstinent! (Remember this is a legal and completely socially acceptable drug.)

Illicit drugs

The mantra? ‘Use is likely, so use carefully and don’t die!’ And we are perpetually informed by certain vested interests that for the 3.5 – 4% of illicit drug users in this country (Cannabis use excised from stats here) that cessation of, or exiting from, drug use is virtually impossible – well so the mantra educates, and that ‘learned behaviour’ of powerlessness and choice stripped victimhood is now parroted as reason enough to ‘validate’ the notion of intractability.

So, then it is touted, the only answer for this demographic is either legalisation or a suite of policies or policy interpretations that enables, empowers, endorses or equips on going drug use, because, it is believed any ‘prohibition’ messaging will not only fail, but be counterproductive. But apparently NOT so with Tobacco, where such prohibition messaging has worked brilliantly!!The cognitive dissonance in this space continues to be breathtaking!

So, what of Harm Reduction ONLY policy implementation of our three pillar National Drug Strategy?

Harm Reduction.

Let’s be clear – what we have now in Australia’s drug taking public psyche (learned/taught behaviour), is well educated and fully self-aware, (and product aware) young adults determining that any drug use risk is manageable. Why? These purported intelligent, sophisticated ‘buzz’ seeking and cashed up adult party goers, willingly and deliberately seek out illicit drugs, purchase them with disposable income, not because of the tyranny of addiction, but to ‘enhance the party experience’. They then take these substances to public events and consume these psychotropic toxins.

Of course, they are fully aware of the mantra they have been taught, as early as secondary school, that if something happens all you should do is call the ambulance. Not only will these remarkable and brave tax-payer funded public servants attend to your self-inflicted illegally induced harm, but will ferry you, at cost to the public purse, to an already overcrowded and strained public health facility. There they will be treated by caring professionals, who have more regard for their well-being than the hapless drug user does. Once they are discharged from the hospital, there (for the most part) is no cost to them, and complete impunity from the law. Little, if no legal action or facilitated diversion is taken and the illicit drug user goes on their way until next drug taking episode.

Whilst no one wants to see injury, let alone death from these reckless behaviours, the mechanisms to ‘save lives’ are already well in play and consequently risk/responsibility factors are disregarded. What must not happen, but clearly is happening, is this utter carelessness for wellbeing of self and others cannot, must not be endorsed or worse, enabled/empowered by poor policy or policy interpretation/use.

There is little or absolutely no accountability for this costly, dangerous, self-indulgent and illegal behaviour. And the cry from the pro-drug lobby is not to call for best practice demand reduction, prevention and/or recovery/exit from this activity/behaviour – No, it’s to declare ‘inevitability’ of behaviour and then, the careless equipping, enabling or empowering of mechanisms to assist the educated self-harmer to continue to use!

Again, it is this permission, NOT prohibition that is continuing to put young lives (and more of them) at risk. The no-longer tacit, but now abundantly clear message in the cultural market place, is that ‘you can take drugs anytime and anywhere and nothing will be done, other than assistance for you if things go pear shaped!’

It’s this message, and not demand and supply reduction vehicles which is empowering ongoing drug use.

It’s time to change the narrative around this ever-permissive drug culture – if not for the sake of people’s lives, then for the emerging generation who are watching this model set them up for engagement, not avoidance of illegal drug use.

Genuine compassion driven anti-drug Harm Reduction must always be about the cessation and/or exiting from drug use and any policy or policy interpretation that fosters a contrary outcome is not good drug policy. The drug policy/strategy interpretation narrative has meant that the term ‘harm reduction’ and ‘harm minimisation’ are now interchangeable terms. Essentially this ensures that Harm Reduction becomes the only pillar of the three-pillar strategy is in play.

This has worked marvellously at convincing even anti-drug citizens, that there is only one option available. Time will not permit to table every encounter we’ve had, but the following statement reflects numbers we have heard…

“Pity we can’t use your harm prevention education program, because it’s illegal. We are only allowed to teach harm reduction in schools!” Head of a State Government Regional Education group, Victoria.

Of course, this is patently false, as Demand Reduction and prevention are not only best practice models, but mandated in the NDS, particularly for the demographic with the developing brain – 12-28-year-old! The Key questions that must be asked about illicit drug policy, are the following;

* Does the policy (or interpretation – harm reduction only) lead to an exit from or cessation of drug use, or does it enable, endorse, empower or equip on going drug use?

* Does the policy (or interpretation) increase or reduce demand for illicit drugs?

* Does the policy (or interpretation) undermine or support the other two pillars? (i.e. increase or reduce Demand or Supply for drugs)

If the policy use/interpretation is creating cognitive dissonance in implementation and leads to a conflagration, rather than collaboration of all three pillars, then the strategy is going to have difficulty in effectively moving a culture away from drug use.

Well, perhaps that is exactly the agenda of the pro-drug lobbyists who have inordinate and disproportionate influence in drug policy implementation? I hear even genuine and compassionate harm reductionists, who actually want to stop drug use and see people recover, railing against supply reduction pillar as ‘waste of resources’. And staggeringly many of these same good people are silent on Demand Reduction, the key to seeing change. These two modes of thinking are the key elements of ensuring only one ‘pillar’ of the NDS is focused on, for genuine or disingenuous purposes. Again, one must ask, does the drug policy interpretation facilitate:

Reducing – Remediating – Recovery from drug use?

Or does the policy instead facilitate the:

Enabling – Empowering – Equipping of drug use?

This interpretative matrix needs to be applied to all drug categories and types – for example, do the following strategies lend themselves more to Enabling or Reducing on going drug use?

* Injecting rooms

* Needle Syringe Programs

* Pill Testing

* 12 Step Programs

* Therapeutic Communities

THE LOW-DOWN ON ‘DIRTY’ SYRINGES 29/5/17 (Anex)

People who inject drugs in Australia can appear to be well provided for with regard to sterile needles and syringes. Across the country there are 3500 needle and syringe programs (NSPs) which distribute almost 50 million pieces of equipment a year. But the international best practice for injecting drugs of a fresh needle for every injection is far from reality. People who inject drugs reuse syringes, share equipment like spoons, water and tourniquets, and a small proportion continue to share injecting equipment with others

. A 20-year survey by the Australian NSP Survey showed that…. Since 2011 the reuse had hovered around 21-25 per cent. The percentage of people who inject drugs who reported they shared syringes with others was also steady at 15-16 per cent from 2011-2015. And the sharing of equipment other than needles remained stable at 28-31 per cent.

This article in a recent ANEX update – notice the nonchalant manner that ‘best practice’ is used and the blithely mentioned MILLIONS of tax-payers funded syringes being unaccountably handed out, yet having 30% of injecting drug users STILL sharing equipment with 16% still sharing needles!

Of course, this proliferation of unaccountable injecting gear has been a key element in the rabid rise in street use and syringe/needle discarding. So, what may be the answer? Will we need to have 3500 injecting rooms open 24/7 for convenience of use and ease of access? Facilities too, with absolute zero accountability as there is absolutely NO potential ‘stigma bestowing’ process permitted that might challenge the behaviour of the self-harming drug taker!

If every injecting episode for every Intravenous drug user was to take place in an injecting room and a sunset clause on such behaviour, ensuring a transitioning to drug use exiting measures, then this might have some merit, as catastrophically expensive and unmanageable as that would be. However, the data tells us that for every single injecting episode that occurs ‘under supervision’, there are over 90 that happen elsewhere!

The appalling ‘health care’ logic, or lack of, is very concerning! It becomes even more so when policy caveats of ‘non-judgemental’ attitudes (whatever that this subjective descriptor can mean) are foisted upon, even the NSP staff – However, NO SUCH MORAL COMMENTARY can be levelled, what-so-ever, at the person who is the self-harming, law breaking, body destroying, and no doubt, family grieving drug taker! This at best is

‘moral’ hypocrisy – at worst unconsumable! (Of course, that last sentence itself is viewed as counterproductive and stigmatizing and thus not permitted in the discourse!)

“The perpetual permission of harm reduction only policies, NOT prohibition is putting lives at risk!” Dalgarno Institute.

Injecting Rooms

Gary Christian, Secretary for Drug Free Australia, has pointed to the lack of success by the Kings Cross Injecting Centre (MSIC) in reducing overdose deaths in the Kings Cross area. He said, “Tracking of overdose deaths in the Kings Cross area from 5 years before the injecting room opened compared with the 9 years after the injecting room was opened showed no change whatsoever in the percentage of deaths in the area as compared to the rest of NSW. The KPMG review showed that Kings Cross had 12% of NSW opiate deaths before the commencement of the MSIC, and in the 9 years after it remained at 12%, such has been its failure to make any difference.”

Evidence given to the NSW Parliament indicates that overdoses in the Kings Cross injecting room are 32 times higher than the overdose histories of those entering the injecting room, indicating that clients are experimenting with higher doses of opiates and cocktails of drugs knowing that if they should overdose in their experimentation, someone will bring them around. NSW Hansard records testimony from ex-clients of the injecting room who were rehabilitating from drugs that experimentation with higher doses of drugs is the reason for the inordinately high overdose rate in the room.

The question now appears to not be about ‘best practice’, but simply what emotive or socio-political drivers dictate when it comes to drug policy – So, where do you land? If you’re all for drug use, then another conversation and investigation in to the why of that is your priority. However, the disturbing reality for the tens of thousands of ex-users who already know the ultimate outcome of illicit drug use is. The reality is, those conversations and investigations are near impossible for a person using the substance in a culture that passively, no, actively permits it!

Any enterprise that inadvertently enables, empowers or equips ongoing illicit drug use has already breached best health care practice. Harm Reduction can never be about the support of on-going, health diminishing substance use. Caring, responsible and civic minded clinicians and policy makers will always be focused on movement toward exit from, and cessation of drug use. Mechanisms that enable any government agency to send a message to the community that we are not only supporting, but enabling tax payer funded illicit drug use, not only breaches care for the illegal drug user, but breaches international conventions. It also demonstrates a lack of concern for most of the non-drug using community.

I trust a thorough ‘best practice’ consideration of any drug policy ‘strategy’ will always seek to reduce demand for and use of any illicit drug, if not for the sake of the drug user, then for the wider community, who the vast majority of are illicit drug free. Our emerging generation need proactive and protective mechanisms to give them best chance to live drug free lives.

Let us be very clear, we are not conducting a ‘war against drugs’. We are however fighting for the brains, potentials, and in many instances, the very future of an entire emerging generation. (Dr Bertha Madras – Harvard) That for any caring civic minded human being is a fight worth having, and one worth joining!

Source: dbrecoveryresources.com/2018/04/permission-empowered-drug-policy-interpretations-drive-demand-for-drug-use/ Dalgarno Institute

July 2017 Revised January 2018

Injury Prevention Centre: Who we are

The Injury Prevention Centre (IPC) is a provincial organization that focuses on reducing catastrophic injury and death in Alberta. We act as a catalyst for action by supporting communities and decision-makers with knowledge and tools. We raise awareness about preventable injuries as an important component of lifelong health and wellness. We are funded by an operating grant from Alberta Health and we are housed at the School of Public Health, University of Alberta.

Injury in Alberta

Injuries are the leading cause of death for Albertans aged 1 to 44 years. In 2014, injuries resulted in 2,118 deaths, 63,913 hospital admissions and 572,653 emergency department visits. Of all age groups, young adults, 20 to 24 years old had the highest percentage of injury deaths with 84.9%. Youth, 15 to 19 years of age had the second highest percentage of injury deaths with 76.4%.

1. Alberta is spending an estimated $4 billion annually on injury – that amounts to $1,083.00 for every Albertan.

2. Potential impact of cannabis legalization on injury in Alberta In 2018, the Government of Canada will legalize the use of cannabis for recreational purposes. In the United States, some jurisdictions have similarly legalized cannabis for recreational use and have collected data on the changes in injuries due to cannabis use. Jurisdictions that have legalized the use of recreational as well as medical cannabis have experienced increases in injuries due to burns (100%), pediatric ingestion of cannabis (48%), drivers testing positive for cannabis and/or alcohol and drugs (9%), drivers testing positive for THC (6%) and drivers testing positive for the metabolite caboxy-THC (12%) when comparing pre- and post-legalization numbers.

3. (pg. 149) Of greatest concern are the traffic outcomes. “Fatalities substantially increased after legislation in Colorado and Washington, from 49 (in 2010) to 94 (in 2015) in Colorado, and from 40 to 85 in Washington. These outcomes suggest that after legislation, more people are driving while impaired by cannabis.”

4. (pg.155) Alberta can expect to see similar changes in injuries when the new laws take effect. The objective of this document is to recommend policies for inclusion in the Alberta Cannabis Framework that will minimize negative impacts of cannabis legalization on injuries to Albertans. Our focus is on:

* Preventing Cannabis-Impaired Driving

* Preventing Poisoning of Children by Cannabis

* Preventing Burns due to Combustible Solvent Hash Oil Extraction

* Preventing Other Injuries due to Cannabis Impairment

* Developing Surveillance to Identify Trends in Cannabis-Related injury

* Implementing a Comprehensive Public Education Plan

Injuries due to cannabis impairment in Alberta can be expected to rise following the legalization of recreational cannabis use. To mitigate the negative effects of legalization on injuries in Alberta, the Injury Prevention Centre recommends the Government of Alberta take the following actions for:

Preventing Cannabis-Impaired Driving

Impose administrative sanctions at a lower limit than Criminal Code impairment

Mandate a lower per se levels for THC/alcohol co-use

Increase sanctions for co-use of alcohol and cannabis

Separate cannabis and alcohol outlets by the creation of a public retail system for the distribution of cannabis products

Support Research to Improve Enforcement Tools

Apply sufficient resources to training and enforcement

Conduct public education regarding cannabis-impaired driving .

Preventing Poisoning of Children by Cannabis

Uphold federal legislation regarding packaging

Support public education on cannabis poisoning’

Preventing Burns due to Combustible Solvent Hash Oil Extraction

Prohibit the production of cannabis products using combustible solvents if it fails to appear in federal Bill C45.

Implement public education regarding the dangers of producing cannabis products using combustible solvents

Preventing Other Injuries due to Cannabis-Impairment

Inform the public about the risks of other activities when impaired

Develop Surveillance to Identify Trends in Cannabis-Related injury

Collect and analyze emergency department, hospital admission and death data for injuries involving cannabis impairment

Develop and implement a comprehensive public education campaign about the safe use of cannabis

Source: https://injurypreventioncentre.ca/downloads/positions/IPC%20-%20Cannabis%20Legalization Jan. 2018

EXECUTIVE SUMMARY

The objectives of this risk assessment were to:

· ascertain the state of the science in research into the potential health effects of low levels of tetrahydrocannabinol (THC) and other cannabinoids found in Cannabis sativa;

· identify key health hazards that may be associated with the presence of THC and other cannabinoids in consumer products made with industrial hemp (C. sativa cultivars with <0.3% (w/w) THC);

· assess the human health safety of the Canadian limit of 10 ug/g THC for raw materials and products made from industrial hemp; and

· to identify uncertainties and critical data gaps in the risk assessment.

Of the more than 60 cannabinoids identified in C. sativa, the toxicity of THC is the best characterized. Limited toxicity data have been reported for two other cannabinoids, cannabidiol (CBD) and cannabinol (CBN), but there are no toxicity data on the remaining cannabinoids.

Two key hazards of cannabinoid exposure are neuroendocrine disruption and neurological impairment. Neuroendocrine disruption by low levels of cannabinoids during developmental stages (perinatal, prepubertal, pubertal) leads to permanent adverse effects on brain and reproductive system development in animals. The lowest observed effect level (LOEL) for neuroendocrine disruption by THC was 1 ug/kg/d derived from a study in rats (no suitable human studies were available). Such effects could occur in humans. Similarities in the types of adverse effects, the cannabinoid receptor distribution in the brain, and the pharmacokinetics and metabolism of cannabinoids among humans and animal species support the extrapolation from animal data to humans for the purposes of risk assessment. Neurological impairment is manifested as deficits in performance with respect to cognitive and motor skills. The LOEL for neurological impairment by THC was 70 ug/kg based on data from a dose-response study in which human subjects who had a history of marihuana use received a single oral dose of THC, and cognitive and motor skills and perception of psychoactive effects were measured.

It was not deemed possible to develop a tolerable daily intake (TDI) due to the lack of a no observed effect level (NOEL), lack of data on chronic exposure and lack of data on the potential contribution of other cannabinoids to the adverse effects. Potential health risks of foods made with industrial hemp ingredients were characterized by estimating the amount of food from various food categories that would need to be eaten to reach a dose of THC equal to the LOELs for neurological impairment in humans and neuroendocrine effects in animals. Potential health risks from use of cosmetics and personal care products and nutraceuticals made with industrial hemp oil were characterized by comparing exposure to

THC through product use with the LOELs for neurological impairment in humans and neuroendocrine effects in animals. These exposure estimates were based on the assumption that the THC concentration in industrial hemp-based in ingredients was 10 ug/g, the current Canadian guideline.

The direct comparison of exposure results with the LOELs does not address:

· the bioaccumulative potential of THC with repeated dosing or consumer use;

· the lack of an identified NOELfor THC for neuroendocrine disruption or neurological impairment;

· the potential that some individuals may be more sensitive to THC than the adults with a history of marihuana use for which the LOEL of 70 ug/g for neurological impairment was observed;

· the possibility that humans could be more sensitive to THC than the rats in the study used to derive the LOEL of 1 ug/kg for neuroendocrine disruption; and,

· the potential for neuroendocrine disruption or neurological impairment by other cannabinoids (i.e. CBD, CBN and others) that would be present in industrial hemp-based products (concentrations of these have not been measured).

In consideration of the above uncertainties, the conclusions from the risk characterization were as follows:
Food: Risk of neuroendocrine disruption: Likely.

Risk of neurological impairment and psychoactivity: Likely, particularly for children.

With respect to neurological impairment, the amount of each food type that would need to be consumed to deliver a dose of THC equal to the LOEL exceeded the mean daily intake and "serving size" which may suggest an absence of risk. In the case of the child; however, some foods (dairy substitutes and candy) were identified that could be consumed in sufficient quantities on occasion in a single day or a single sitting to cause neurological impairment, or even psychoactive effects. For example 2.3 ice cream bars could deliver a dose of THC of 70 ug/kg (the LOEL for neurological impairment) and 4.6 ice cream bars could deliver a dose of 140 ug/kg (the LOEL for psychoactivity) for a 33.9 kg child.

Cosmetics: Risk of neuroendocrine disruption: Possible

Risk of neurological impairment: Unlikely

The risk of neurological impairment cannot be excluded entirely, particularly in the case of children without further information on the relative sensitivities of children vs adults, the relative sensitivities of marihuana users vs non users, the effects of repeated exposure over a long time period, the effects and concentrations of cannabinoids other than THC and the extent of dermal penetration and systemic exposure of topically applied cannabinoids under conditions of actual product use.

Nutraceuticals: Risk of neuroendocrine disruption: Likely

Risk of neurological impairment: Possible, particularly in children.

Major shortcomings related to key data gaps identified in the assessment that preclude the development of definitive conclusions regarding the degree of potential risk are:

· the inability to consider the potential contribution of cannabinoids other than THC (limited toxicity data for other cannabinoids indicate their ability to cause neuroendocrine disruption) to the overall health risks;

· the inability to consider the long term effects of bioaccumulation of THC over time from repeated low dose exposure due to lack of chronic low level toxicity studies and lack of data on the steady-state pharmacokinetics of THC;

· the inability to consider the effects of THC and other cannabinoids after multi-generation long term exposure;

· the inability to determine the degree of exposure to the developing fetus and nursing infant; and

· the lack of analytical data for THC and other cannabinoid concentrations, at detectable levels, in raw materials and finished products made from industrial hemp.

Abstract

Metabolic and behavioural effects of, and interactions between Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are influenced by dose and administration route.

Therefore we investigated, in Wistar rats, effects of pulmonary, oral and subcutaneous (sc.) THC, CBD and THC+CBD. Concentrations of THC, its metabolites 11-OH-THC and THC-COOH, and CBD in serum and brain were determined over 24h, locomotor activity (open field) and sensorimotor gating (prepulse inhibition, PPI) were also evaluated.

In line with recent knowledge we expected metabolic and behavioural interactions between THC and CBD. While cannabinoid serum and brain levels rapidly peaked and diminished after pulmonary administration, sc. and oral administration produced long-lasting levels of cannabinoids with oral reaching the highest brain levels.

Except pulmonary administration, CBD inhibited THC metabolism resulting in higher serum/brain levels of THC. Importantly, following sc. and oral CBD alone treatments, THC was also detected in serum and brain. S.c. cannabinoids caused hypolocomotion, oral treatments containing THC almost complete immobility.

In contrast, oral CBD produced mild hyperlocomotion. CBD disrupted, and THC tended to disrupt PPI, however their combination did not.

In conclusion, oral administration yielded the most pronounced behavioural effects which corresponded to the highest brain levels of cannabinoids. Even though CBD potently inhibited THC metabolism after oral and sc. administration, unexpectedly it had minimal impact on THC-induced behaviour.

Of central importance was the novel finding that THC can be detected in serum and brain after administration of CBD alone which, if confirmed in humans and given the increasing medical use of CBD-only products, might have important legal and forensic ramifications.

Source:  https://pubmed.ncbi.nlm.nih.gov/29129557/ Eur Neuropsychopharmacol. 2017 Dec;27(12):1223-1237. doi: 10.1016/j.euroneuro.2017.10.037. Epub 2017 Nov 10.

Behavioral Health Is Essential To Health • Prevention Works • Treatment Is Effective • People Recover In Brief

Fall 2014 • Volume 8 • Issue 3 An Introduction To Co-Occurring Borderline Personality Disorder And Substance Use Disorders

This In Brief is for health and human services professionals (e.g., social workers, vocational counselors, case managers, healthcare providers, probation officers). It is intended to introduce such professionals to borderline personality disorder (BPD)—a condition with very high rates of suicide and self-harm that often co-occurs with substance use disorders (SUDs).

This In Brief presents the signs and symptoms of BPD, with or without a co-occurring SUD, alerts professionals to the importance of monitoring clients with BPD for self-harm and suicidal behavior, and encourages professionals to refer such clients for appropriate treatment.

This In Brief is not meant to present detailed information about BPD or treatment guidelines for BPD or SUDs. How Common Is BPD?1 Estimates of BPD prevalence in the U.S. population range from 1.6 percent to 5.9 percent. BPD affects approximately 10 percent of all psychiatric outpatients and up to 20 percent of all inpatients.

What Is Borderline Personality Disorder?

BPD is one among several personality disorders (e.g., narcissistic personality disorder, paranoid personality disorder, antisocial personality disorder). According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5),1 personality disorders are generally characterized by:

■ Entrenched patterns of behavior that deviate significantly from the usual expectations of behavior of the individual’s culture.

■ Behavior patterns that are pervasive, inflexible, and resistant to change.

■ Emergence of the disorder’s features no later than early adulthood (unlike depression, for example, which can begin at any age).

■ Lack of awareness that behavior patterns and personality characteristics are problematic or that they differ from those of other individuals.

■ Distress and impairment in one or more areas of a person’s life (often only after other people get upset about his or her behavior).

■ Behavior patterns that are not better accounted for by the effects of substance abuse, medication, or some other mental disorder or medical condition (e.g., head injury).

BPD is a complex and serious mental illness. Individuals with BPD are often misunderstood and misdiagnosed. A history of childhood trauma (e.g., physical or sexual abuse, neglect, early parental loss) is more common for individuals with BPD.1,2 In fact, many individuals with BPD may have developed BPD symptoms as a way to cope with childhood trauma. However, it is important to note that not all individuals with BPD have a history of childhood trauma. It is also important to note that some of the symptoms of BPD overlap with those of several other DSM-5 diagnoses, such as bipolar disorder and posttraumatic stress disorder (PTSD).

Therefore, a diagnosis of BPD should be made only by a licensed and experienced mental health professional (whose scope of practice includes diagnosing mental disorders) and then only after a thorough assessment over time. Individuals with BPD often require considerable attention from their therapists and are generally considered to be challenging clients to treat.3,4,5 However, BPD may not be the chronic disorder it was once thought to be.

In Brief BPD often respond to appropriate treatment and may have a good long-term prognosis,1,5 experiencing a remission of symptoms with a relatively low occurrence of relapse.6,7 The DSM-5 indicates that BPD is diagnosed more often in women than in men (75 percent and 25 percent, respectively).1 Other research, however, has suggested that there may be no gender difference in prevalence in the general population,5,6 but that BPD is associated with a significantly higher level of mental and physical disability for women than it is for men.6 In addition, the types of co-occurring conditions tend to be different for women than for men. In women, the most common co-occurring disorders are major depression, anxiety disorders, eating disorders, and PTSD. Men with BPD are more likely to have co-occurring SUDs and antisocial personality disorder, and they are more likely to experience episodes of intense or explosive anger.8,9

What Are the Symptoms of BPD?

The DSM-5 classifies mental disorders and includes specific diagnostic criteria for all currently recognized mental disorders. It is a tool for diagnosis and treatment, but it is also a tool for communication, providing a common language for clinicians and researchers to discuss symptoms and disorders. According to the DSM-5, the symptoms of BPD include:1

■ Intense fear of abandonment and efforts to avoid abandonment (real or imagined).

■ Turbulent, erratic, and intense relationships that often involve vacillating perceptions of others (from extremely positive to extremely negative).

■ Lack of a sense of self or an unstable sense of self

■ Impulsive acts that can be hurtful to oneself (e.g., excessive spending, reckless driving, risky sex).

■ Repeated suicidal behavior or gestures or self-mutilating behavior. (See the section below on suicide and nonsuicidal self-injury.)

■ Chronic feelings of emptiness

■ Episodes of intense (and sometimes inappropriate) anger or difficulty controlling anger (e.g., repeated physical fights, inappropriate displays of anger)

■ Temporary feelings of paranoia (often stress-related) or severe dissociative symptoms (e.g., feeling detached from oneself, trancelike).

Anyone with some of these symptoms may need to be referred to a licensed mental health professional for a complete assessment. Exhibit 1 presents some examples of how a person with BPD might behave. Suicide and nonsuicidal self-injury BPD is unique in that it is the only mental disorder diagnosis that includes suicide attempts or self-harming behaviors among its diagnostic criteria.3 The risk of suicide is high among individuals with BPD, with as many as 79 percent reporting a history of suicide attempts10 and 8 percent to 10 percent dying by suicide—a rate that may be 50 times greater than the rate among the general population.11 More than 75 percent of individuals with BPD engage in deliberate self-harming behaviors known as nonsuicidal self-injury (NSSI) (e.g., cutting or burning themselves).12 Unlike suicide attempts, NSSI does not usually involve a desire or intent to die. Sometimes the person with BPD does not consider these behaviors harmful.4 One study involving 290 patients with BPD found that 90 percent of patients reported a history of NSSI, and over 70 percent reported the use of multiple methods of NSSI.10 Reasons for NSSI vary from person to person and, for some individuals, there may be more than one reason. The behaviors may be: 4,13,14

■ A way to express anger or pain

■ A way to relieve pain (i.e., shifting from psychic pain to physical pain)

■ A way to “feel” something.

■ A way to “feel real.”

■ An attempt to regulate emotions.

■ A form of self-punishment.

■ An effort to get attention or care from others. NSSI may include: 4,13,14

■ Cutting.

■ Burning.

■ Skin picking or excoriation.

■ Head banging.

■ Hitting.

■ Hair pulling

Exhibit 1. Examples of Symptomatic Behavior (BPD)

■ Patterns of intense and unstable relationships

John comes in to see his case manager, George, and announces that he plans to marry a woman he met at a speed-dating event the night before. George has heard this same story from John at least once a month for the past 4 months.

■ Emotions that seem to change quickly from one extreme to another

Suzie has been working with a vocational rehabilitation counselor, Tony, for 2 weeks to prepare for job retraining. One day, just after Tony gets everything set up for Suzie to begin her training, Suzie storms out of the office screaming at him, “You’re just trying to get rid of me! You don’t understand me at all! I hate you!” Later, when Tony calls to suggest that maybe Suzie would prefer to work with another counselor, Suzie begins to cry and says, “Please don’t drop me, Tony! I need you!”

■ Evidence of self-harm or self-mutilation

José is a probation officer. During his weekly appointment with his client, Annie, José notices a pattern of recent cuts across her left forearm. José asks her about them, and Annie becomes defensive and says, “Okay, I cut myself sometimes, so what? It’s none of your business. I’m not hurting anybody!”

■ Pattern of suicidal thoughts, gestures,* or attempts

Maria is a nurse. As she looks over the health history of her new patient, Sally, she notices that Sally has been hospitalized three times in the past 4 years after suicide attempts, and that she has seen six different therapists. Sally tells her, “Yeah, I get suicidal sometimes. I just can’t seem to find the right therapist who can help me.”

■ Intense displays of emotion that often seem inappropriate or out of proportion to the situation

Regina is a social worker at a domestic violence shelter. She notices one of her clients, Elena, sitting in the living room with a sketchpad in her lap. Regina asks if she can see what Elena is drawing. Elena turns the sketchpad around to reveal a beautiful, detailed drawing of the shelter house. Regina admires it and says how beautiful it is, then says, “That’s funny, I thought that the house number was on the right side of the door.” Elena, who had been smiling, takes the sketchpad from Regina, looks at the drawing, then rips it from the pad and begins tearing it up, saying, “You’re right, it’s all wrong! I’ll have to start all over again!”

*Regarding the word gestures: It is dangerous to dismiss or label any suicidal behavior as a gesture. Anyone who exhibits suicidal thoughts or behaviors of any kind needs to be assessed by a licensed mental health professional.

What Are the Symptoms of SUDs?

SUDs involve patterns of recurrent substance use that result in significant problems, which fall into the following categories:1

■ Impaired control—taking more of the substance than intended, trying unsuccessfully to cut down on use, spending an increasing amount of time obtaining and using the substance, craving or having a strong desire for substance use

■ Social impairment—failing to fulfill obligations at work, school, or home; continuing substance use in spite of the problems it causes; giving up or reducing other activities because of substance use

■ Risky use—using the substance(s) in situations in which it may be physically dangerous to do so (e.g., driving) or in spite of physical or psychological problems that may have been caused or may be made worse by substance use (e.g., liver problems, depression)

■ Pharmacological criteria—displaying symptoms of tolerance (need for increased amounts of the substance to achieve the desired effect) or withdrawal (a constellation of physical symptoms that occurs when the use of the substance has ceased)

What Is the Relationship Between BPD and SUDs?

One study15 found that the prevalence of BPD among individuals seeking buprenorphine treatment for opioid addiction exceeded 40 percent, and another16 found that nearly 50 percent of individuals with BPD were likely to report a history of prescription drug abuse. A large survey6 found that 50.7 percent of individuals with a lifetime diagnosis (i.e., meeting the criteria for a diagnosis at some point during the individual’s life) of BPD also had a diagnosis of an SUD over the previous 12 months. This same survey found that for individuals with a lifetime diagnosis of an SUD, 9.5 percent also had a lifetime diagnosis of BPD. This is a significantly higher incidence of BPD than that in the general public, which ranges from 1.6 percent to 5.9 percent.1

One longitudinal study17 found that 62 percent of patients with BPD met criteria for an SUD at the beginning of the study. However, over 90 percent of patients with BPD and a co-occurring SUD experienced a remission of the SUD by the time of the study’s 10-year follow-up. (Remission was defined as any 2-year period during which the person did not meet criteria for an SUD.) The authors also looked at whether there were recurrences of SUDs after periods of remission and found that the rate of recurrence was 40 percent for alcohol and 35 percent for drugs. The rate of new onsets of SUDs, while lower than expected, was still 21 percent for drugs and 23 percent for alcohol.

Another study18 found that individuals with BPD had higher rates of new SUD onsets even when their BPD symptoms improved (compared with new SUD onsets for individuals with other personality disorders). A client with BPD and a co-occurring SUD presents some particular challenges. BPD is difficult to treat, partly because of the pervasive, intractable nature of personality disorders and partly because clients with BPD often do not adhere to treatment and often drop out of treatment. The impulsivity, suicidality, and self-harm risks associated with BPD may all be exacerbated by the use of alcohol or drugs.19 In addition, the presence of BPD may contribute to the severity of SUD symptoms,20 and the course of SUD treatment may be more complicated for clients who also have BPD.21

Who Can Best Provide Treatment for People With BPD and SUDs?

Individuals who display some of the symptoms of BPD (as described above) should be referred to an experienced licensed mental health professional for a thorough mental health assessment and possible referral to treatment. It is important to know whether referral sources have experience treating clients with BPD. If individuals display symptoms of substance misuse, they should also be assessed for a co-occurring SUD. Individuals with BPD sometimes trigger intense feelings of frustration and even anger in their therapists and other providers.12

Clients with BPD often have difficulty developing good relationships, including productive working relationships with therapists and other providers (e.g., healthcare workers, case managers, vocational counselors). Some individuals with BPD may move from therapist to therapist (or other professionals) in an effort to find “just the right person.” Individuals who have an SUD may receive treatment from an individual counselor or therapist or from an outpatient treatment program. However, a co-occurring diagnosis of BPD may complicate SUD treatment. It is important for the professionals treating the person for either diagnosis to work in consultation with each other.

Treatment for BPD—especially with a co-occurring SUD— sometimes involves a team approach. Depending on the treatment plan, a person may have an individual therapist, a group therapist, a substance abuse counselor, a psychiatrist, and a primary care provider; treatment may need to be planned and managed through the coordinated efforts of all providers. Regular consultation among all providers can ensure that everyone is working toward the same goals from each of their professional perspectives. For example:

■ In individual therapy sessions, a therapist may help the client learn to tolerate gradually increasing levels of uncomfortable emotions (e.g., stress, anxiety) so that the client may begin to have more control over those emotions.

■ A psychiatrist may consider the use of medication for the client or evaluate currently prescribed medications to determine adherence and their effect on the client’s ability to engage in the emotional work of therapy.

■ A substance abuse counselor may work with the client to achieve abstinence, identify relapse triggers that may come up as the client does emotional work in therapy, and identify coping strategies for remaining abstinent.

■ A vocational counselor may need to work with the client on distress tolerance as it relates to employment issues, such as applying for jobs or beginning a new job. This may mean helping the client understand the importance of being at interviews, vocational training classes, or work on time (even if emotional problems make that difficult) and helping the client develop strategies to achieve a pattern of good work habits. Some people with BPD may consciously or unconsciously attempt to sabotage treatment by providing conflicting information to providers or by trying to turn one provider against another. Consultation among all providers can help deter this.

What Treatments Are Available for Individuals With BPD and SUDs?

Many studies have been done on treatment approaches for BPD or SUDs, but very few have involved participants with co-occurring BPD and SUDs.22,23,24 However, based on the studies that have been done on co-occurring BPD and SUDs, a few approaches seem to show promise.

Perhaps the most researched approach is Dialectical Behavior Therapy, which has been adapted for treatment of co-occurring BPD and SUDs (Dialectical Behavior Therapy-S [DBT-S]). It is important to note, however, that DBT-S and other promising approaches involve structured, manualized treatments that are quite intensive and require a significant amount of training and resources (e.g., staffing, space, finances) that may not be available in all areas.25 Many therapists work on their own with individuals who have BPD, using the best techniques that their training and experience have to offer—hopefully in regular consultation with an experienced clinical supervisor. Therapists often adapt psychotherapy to better meet the needs of an individual client, sometimes combining different therapeutic approaches or mixing techniques.4

However, for clients with both BPD and SUDs, the therapist may need to work with an SUD treatment provider to provide comprehensive care. Pharmacotherapy for BPD and SUDs The Food and Drug Administration (FDA) has not approved any medications for the treatment of BPD. However, individuals with BPD may take medications to alleviate some of their symptoms.11,22 For example, selective serotonin reuptake inhibitors may be prescribed for depressed mood, irritability, anger, and impulsivity.11 There are several FDA-approved medications for SUD treatment. For alcohol use disorder, these include acamprosate, disulfiram, and naltrexone.26

For opioid use disorder, approved medications include buprenorphine, a combination of buprenorphine and naloxone, methadone, and naltrexone.27 Some of these medications may be prescribed on a short-term basis (e.g., to ease withdrawal symptoms, lessen cravings), and others may be prescribed for long-term use (e.g., to facilitate longer periods of abstinence).26,27 Individuals may receive their prescriptions and medication management from a psychiatrist, from other types of healthcare providers, or from both (or, in the case of methadone, from an opioid treatment program). Individuals may take medication as one part of a treatment plan that also includes attending individual therapy, group therapy, group skill-building sessions, or a mutual-help group (e.g., 12-step program), or some combination of these.

What Are Some Things To Remember When Working With Someone Who Has Co-Occurring BPD and SUDs?

Some of the same guidelines that have been identified as necessary for mental health professionals who work with clients who have these two diagnoses may also be helpful for all human services professionals. Working with a client who has co-occurring BPD and SUDs requires:

■ Strong (but not rigid) professional boundaries—Be clear with the person about the expectations in the working relationship (e.g., length of appointments, level of support, contact outside regular appointments). Be aware of special requests to make exceptions to the usual rules for working with clients. These requests sometimes escalate over time. If in doubt about making an exception to the rules, discuss the situation with a supervisor who is knowledgeable about working with individuals who have BPD (within applicable confidentiality requirements).11

■ A commitment to self-care—If possible, schedule appointments with someone who has BPD right before lunch or before a break. Avoid scheduling back-to-back appointments with two individuals who have BPD. It is important to have some time between them to see clients with other diagnoses, to work on other tasks, or simply to take a break. Develop the habit of leaving work at work (i.e., don’t “replay” interactions with individuals who have BPD).

■ An awareness of how BPD may affect any kind of work with the individual—For example, fearing abandonment and avoiding abandonment are characteristics of BPD and may manifest in some unexpected ways. For example, if the professional relationship has focused on the person with BPD completing certain goals, that person may thwart his or her own progress to avoid the feelings of abandonment that would result from ending the working relationship.

■ Knowledge about what skills the individual who has BPD is learning in therapy—The person may need assistance applying those new skills to broader life situations. For example, perhaps one skill the person has learned is how to break down a seemingly overwhelming task into a series of small steps. Work with the person to apply that particular skill to the situation at hand.

Conclusions

It is important to remember that:

■ Most human services professionals will encounter clients with BPD in the course of their work.

■ Individuals with BPD often have co-occurring diagnoses (e.g., depression, SUDs). ■ BPD is often characterized by intense emotional displays and impulsive acts (e.g., self-harm, suicide attempts).

■ Working with an individual with BPD (with or without a co-occurring SUD) can be challenging.

■ Individuals with BPD (with or without a co-occurring SUD) deserve to receive appropriate treatment and deserve to be treated with compassion and respect.

■ Individuals with BPD often respond to appropriate treatment and experience a remission of symptoms with a relatively low occurrence of relapse.

■ Individuals with BPD (with or without a co-occurring SUD) may have a team of professionals who provide different aspects of care (e.g., therapist, psychiatrist).

■ It is important for all professionals involved in the care of an individual with BPD to communicate and work together.

Resources

SAMHSA resources

National Registry of Evidence-based Programs and Practices http://nrepp.samhsa.gov

Treatment Improvement Protocols (TIPs) (see back page for electronic access and ordering information)

TIP 36: Substance Abuse Treatment for Persons With Child Abuse and Neglect Issues

TIP 42: Substance Abuse Treatment for Persons With Co-Occurring Disorders

TIP 44: Substance Abuse Treatment for Adults in the Criminal Justice System

TIP 50: Addressing Suicidal Thoughts and Behaviors in Substance Abuse Treatment Web resources

American Psychiatric Association http://www.psych.org

American Psychological Association http://www.apa.org

Borderline Personality Disorder Resource Center http://bpdresourcecenter.org

Behavioral Health Is Essential To Health • Prevention Works • Treatment Is Effective • People Recover 7 An Introduction to Co-Occurring Borderline Personality Disorder and Substance Use Disorders Fall 2014, Volume 8, Issue 3

National Education Alliance for Borderline Personality Disorder http://www.borderlinepersonalitydisorder.com

National Institute of Mental Health http://www.nimh.nih.gov

National Institute on Drug Abuse http://www.drugabuse.gov

Notes

1 American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.

2 Battle, C. L., Shea, M. T., Johnson, D. M., Yen, S., Zlotnick, C., Zanarini, M. C., et al. (2004). Childhood maltreatment associated with adult personality disorders: Findings from the Collaborative Longitudinal Personality Disorders Study. Journal of Personality Disorders, 18(2), 193–211.

3 Dimeff, L. A., Comtois, K. A., & Linehan, M. M. (2009). Cooccurring addiction and borderline personality disorder. In R. K. Ries, D. A. Fiellin, S. C. Miller, & R. Saitz (Eds.), Principles of addiction medicine (4th ed., pp. 1227–1237). Philadelphia: Lippincott Williams & Wilkins.

4 National Institute of Mental Health. (2011). Borderline personality disorder. NIH Publication No. 11‑4928. Bethesda, MD: Author.

5 Substance Abuse and Mental Health Services Administration. (2011). Report to Congress on borderline personality disorder. HHS Publication No. (SMA) 11‑4644. Rockville, MD: Substance Abuse and Mental Health Services Administration.

6 Grant, B. F., Chou, S. P., Goldstein, R. B., Huang, B., Stinson, F. S., Saha, T. D., et al. (2008). Prevalence, correlates, disability, and comorbidity of DSM-IV borderline personality disorder: Results from the Wave 2 National Epidemiologic Survey on Alcohol and Related Conditions. Journal of Clinical Psychiatry, 69, 533–545.

7 Zanarini, M. C., Frankenburg, F. R., Hennen, J., Reich, D. B., & Silk, K. R. (2005). The McLean Study of Adult Development (MSAD): Overview and implications of the first six years of prospective follow-up. Journal of Personality Disorders, 19(5), 505–523.

8 Sansone, R. A., & Sansone, L. A. (2011). Gender patterns in borderline personality disorder. Innovations in Clinical Neuroscience, 8(5), 16–20.

9 Tadíc, A., Wagner, S., Hoch, J., Başkaya, Ö., von Cube, R., Skaletz, C., et al. (2009). Gender differences in axis I and axis II comorbidity in patients with borderline personality disorder. Psychopathology, 42, 257–263.

10 Zanarini, M. C., Frankenburg, F. R., Reich, D. B., Fitzmaurice, G., Weinberg, I., & Gunderson, J. G. (2008). The 10-year course of physically self-destructive acts reported by borderline patients and axis II comparison subjects. Acta Psychiatrica Scandinavica, 117, 177–184.

11 American Psychiatric Association. (2001). Practice guideline for the treatment of patients with borderline personality disorder. American Journal of Psychiatry, 158, 1–52.

12 Black, D. W., & Andreasen, N. C. (2011). Introductory textbook of psychiatry (5th ed.). Washington, DC: American Psychiatric Publishing.

13 Brown, M. Z., Comtois, K. A., & Linehan, M. M. (2002). Reasons for suicide attempts and nonsuicidal self-injury in women with borderline personality disorder. Journal of Abnormal Psychology, 111(1), 198–202.

14 Kleindienst, N., Bohus, M., Ludäscher, P., Limberger, M. F., Kuenkele, K., Ebner-Priemer, U. W., et al. (2008). Motives for nonsuicidal self-injury among women with borderline personality disorder. Journal of Nervous and Mental Disease, 196(3), 230–236.

15 Sansone, R. A., Whitecar, P., & Wiederman, M. W. (2008). The prevalence of borderline personality among buprenorphine patients. International Journal of Psychiatry in Medicine, 38(2), 217–226.

16 Sansone, R. A., & Wiederman, M. W. (2009). The abuse of prescription medications: Borderline personality patients in psychiatric versus non-psychiatric settings. International Journal of Psychiatry in Medicine, 39(2), 147–154.

17 Zanarini, M. C., Frankenburg, F. R., Weingeroff, J. L., Reich, D. B., Fitzmaurice, G. M., & Weiss, R. D. (2011). The course of substance use disorders in patients with borderline personality disorder and axis II comparison subjects: A 10-year follow-up study. Addiction, 106(2), 342–348.

18 Walter, M., Gunderson, J. G., Zanarini, M. C., Sanislow, C. A., Grilo, C. M., McGlashan, T. H., et al. (2009). New onsets of substance use disorders in borderline personality disorder over 7 years of follow-ups: Findings from the Collaborative Longitudinal Personality Disorders Study. Addiction, 104, 97–103.

19 van den Bosch, L. M. C., Verheul, R., & van den Brink, W. (2001). Substance abuse in borderline personality disorder: Clinical and etiological correlates. Journal of Personality Disorders, 15, 416–424.

20 Morgenstern, J., Langenbucher, J., Labouvie, E., & Miller, K. J. (1997). The comorbidity of alcoholism and personality disorders in a clinical population: Prevalence rates and relation to alcohol typology variables. Journal of Abnormal Psychology, 106(1), 74–84.

21 Center for Substance Abuse Treatment. (2005). Substance abuse treatment for persons with co-occurring disorders. Treatment Improvement Protocol (TIP) Series 42. HHS Publication No. (SMA) 13‑3992. Rockville, MD: Substance Abuse and Mental Health Services Administration.

22 Gianoli, M. O., Jane, J. S., O’Brien, E., & Ralevski, E. (2012). Treatment for comorbid borderline personality disorder and alcohol use disorders: A review of the evidence and future recommendations. Experimental and Clinical Psychopharmacology, 20(4), 333–344.In Brief In Brief, An Introduction to Co-Occurring Borderline Personality Disorder and Substance Use Disorders

23 Kienast, T., & Foerster, J. (2008). Psychotherapy of personality disorders and concomitant substance dependence. Current Opinion in Psychiatry, 21, 619–624.

24 Pennay, A., Cameron, J., Reichert, T., Strickland, H., Lee, N. K., Hall, K., et al. (2011). A systematic review of interventions for co-occurring substance use disorder and borderline personality disorder. Journal of Substance Abuse Treatment, 41(4), 363–373.

25 Zanarini, M. C. (2009). Psychotherapy of borderline personality disorder. Acta Psychiatrica Scandinavica, 120, 373–377.

26 Center for Substance Abuse Treatment. (2009). Incorporating alcohol pharmacotherapies into medical practice. Treatment Improvement Protocol (TIP) Series 49. HHS Publication No. (SMA) 13‑4380. Rockville, MD: Substance Abuse and Mental Health Services Administration.

27 Center for Substance Abuse Treatment. (2005). Medication-assisted treatment for opioid addiction in opioid treatment programs.

Treatment Improvement Protocol (TIP) Series 43. HHS Publication No. (SMA) 12‑4214. Rockville, MD: Substance Abuse and Mental Health Services Administration.

In Brief

This In Brief was written and produced under contract numbers 270-09-0307 and 270-14-0445 by the Knowledge Application Program, a Joint Venture of JBS International, Inc., and The CDM Group, Inc., for the Substance Abuse and Mental Health Services Administration (SAMHSA), U.S. Department of Health and Human Services (HHS). Christina Currier served as the Contracting Officer’s Representative.

Disclaimer: The views, opinions, and content of this publication are those of the authors and do not necessarily reflect the views, opinions, or policies of SAMHSA or HHS.

Public Domain Notice: All materials appearing in this document except those taken from copyrighted sources are in the public domain and may be reproduced or copied without permission from SAMHSA or the authors. Citation of the source is appreciated. However, this publication may not be reproduced or distributed for a fee without the specific, written authorization of the Office of Communications, SAMHSA, HHS. Electronic Access and Copies of Publication: This publication may be ordered or downloaded from SAMHSA’s Publications Ordering Web page at http://store.samhsa.gov. Or, please call SAMHSA at 1-877-SAMHSA-7 (1-877-726-4727) (English and Español).

Recommended Citation: Substance Abuse and Mental Health Services Administration. (2014). An Introduction to Co-Occurring Borderline Personality Disorder and Substance Use Disorders. In Brief, Volume 8, Issue 3. Originating Office: Quality Improvement and Workforce Development Branch, Division of Services Improvement, Center for Substance Abuse Treatment, Substance Abuse and Mental Health Services Administration, 1 Choke Cherry Road, Rockville, MD 20857. HHS Publication No. (SMA) 14-4879 Printed 2014

Source:

https://store.samhsa.gov/product/An-Introduction-to-Co-Occurring-Borderline-Personality-Disorder-and-Substance-Use-Disorders/SMA14-4879

Interviewed by Mark Gold, MD

FEATURED ADDICTION EXPERT: Brian Fuehrlein, MD, PhD, Assistant Professor, Yale University Director, Psychiatric Emergency Room, VA Connecticut Healthcare System

If a patient has overdosed on opioid, can you describe your approach to the emergency including the exam, medications, observation and discharge-transfer?

As the director of a psychiatric emergency room at VA Connecticut and Yale, I assume the care of patients after medical stabilization. Medical stabilization often includes Narcan administration and other possible treatments. While I am not generally directly involved in the Narcan administration, I will frequently see patients soon after a Narcan reversal (days to weeks). I have a very clear approach to these patients. My approach to a patient post Narcan reversal is aggressive and assertive. In my mind, I may be the last physician that this patient sees alive. I am very aggressive when discussing the severity of the illness and the critical need for treatment. When developing a treatment plan, I am very assertive. I will spend as much time as I can with the patient attempting to motivate them for treatment. When a patient has already required a Narcan reversal (and hence nearly died) they are high risk for this to occur again. This is as critical of a patient that I care for.

We generally refer to opioid overdoses as accidental, but do you have an idea of what percentage of the patients are depressed, wanted to die, or had passive suicidal ideation? Do you formally evaluate them for concurrent psychiatric illness at some time after you save their lives?

All patients who present to the psychiatric emergency room receive a thorough psychiatric and substance use assessment. The prevalence of co-occurring psychiatric illness with opioid use disorder (OUD) is very high. By the time the OUD has progressed to the point of intravenous use leading to Narcan reversal, there are typically many psychosocial consequences and stressors. In addition, these patients are often young (<30). These severe consequences, which often occur quickly, may lead to feelings of hopelessness, helplessness and passive suicidal ideation (SI). While I do not know firm percentages, in my experience the majority of those with severe opioid use disorder suffer from comorbid anxiety and/or depression. A lower percentage, but still significant amount, experience passive SI and will report things like “I was not trying to kill myself, but if I were to never wake up the world would be better off without me”. I would say that a small but significant percentage is actively suicidal at the time of the overdose with intent to die.

Patients will often have a history of multiple overdoses. What is your approach and ideal post rescue plan? Do you transfer them to a locked unit or give them a follow-up appointment? What happens to a person who is given Narcan and rescued by an EMT?

I tend to be as aggressive and assertive as possible while discussing the severity of the illness and the dire need for intensive treatment, especially in a patient who has had multiple overdoses. I attempt to motivate every patient who has experienced an overdose to be initiated on medication-assisted treatment (MAT). If agreeable, I will start buprenorphine in the VA/Yale psychiatric emergency room. Initiating buprenorphine in an emergency room setting is difficult in practice. Given the resources available at the VA we are able to do it. This practice is based upon a recent study at Yale that showed that initiating buprenorphine in emergency setting results in patients more likely to be connected to treatment. I also educate every patient about the need for a psychosocial support structure. I am a proponent of AA/NA programs and I discuss with all patients the importance of meetings/sponsorship. The goal for all patients who present post overdose is to initiate them on buprenorphine, transfer them to our substance use treatment program (either inpatient or IOP level of care) and then to attend 90 meetings in 90 days.

Unfortunately, many patients request discharge without willingness to engage directly in treatment. While state laws differ, in CT it is often hard to commit patients involuntarily specifically for substance use. If the patient is actively or passively suicidal or manic/psychotic, etc., we can often commit them on a psychiatric commitment. But if the risk stems primarily from ongoing substance use, we are often unable to hold the patient and force treatment upon them. We try very hard to motivate them for treatment. We will also engage their family to help with the motivation. But many patients are discharged home with outpatient follow-up only. We will prescribe a Narcan rescue kit, educate about harm reduction strategies, provide an appointment to see mental health within 7 days and place a follow-up phone call the day after discharge. But we are often unable to do more unless the patient is willing.

What is your suggestion for the role of Vivitrol post Narcan care?

I attempt to motivate all patients with opioid use disorder, particularly those post overdose, to initiate buprenorphine in the psychiatric emergency room. The first line treatment is buprenorphine, unless there is a reason/contraindication. For example, if adequate trials of buprenorphine have demonstrated its lack of efficacy in that patient, or if there was an intolerable side effect or adverse reaction. Methadone is generally the second line agent that is used following a buprenorphine failure. Following a Methadone treatment failure (side effect, etc), then Vivitrol the third line agent. Veterans at the VA will have an assigned outpatient treatment coordinator. We will collaborate with the outpatient team to determine the appropriate management of the opioid use disorder. We are able to initiate buprenorphine or Vivitrol the PER but Methadone initiation is deferred to the opioid treatment program. It is critical that patients with OUD are initiated on maintenance medication (one of the 3 mentioned) AND referred to a treatment program AND AA/NA.

Can you compare patients that you would suggest for Methadone vs. Suboxone vs. Vivitrol? How do you decide the doses? How long do you suggest MAT plus therapy and when to stop?

In general, buprenorphine is the first line, Methadone is second line and Vivitrol is third line, though this depends greatly on the individual patient. At times, Methadone is the first line agent if the patient requires the structure of the opioid treatment program or if the severity of the addiction is such that high dose Methadone is preferred. In general, buprenorphine is appropriate for the majority of the patients that I see in the psychiatric emergency room. Duration of MAT therapy remains debated. It depends on many factors and is an individual decision between the physician and the patient. In my opinion, a very important consideration when deciding whether to stop MAT is the patient’s commitment to a recovery program. If the patient is going to daily meetings, has a sponsor and is completing step work, I am more likely to endorse a plan of tapering down the buprenorphine than the same patient who is relying solely on the buprenorphine for sobriety.

Other considerations include IV use, previous OD with Narcan administration and other high risk behaviors. These would make me more likely to recommend longer term use of buprenorphine. In addition, the decision to stop MAT would depend on factors like cost, side effects, etc. Opioid use disorder is a deadly illness that requires long term treatment. When the illness is severe, high risk behaviors are present and the buprenorphine is not causing problems, I am unlikely to recommend tapering it off.

Are you seeing opioid overdose and addicts concurrently using marijuana, alcohol, cocaine, methamphetamine, other? Can you give us a sense of how many patients just use one drug or are just addicted to one drug? Do you do drug testing on all patients in the ED?

Yes, we perform urine drug screens on all patients who present to the psychiatric emergency room (PER). In my experience there are several groups of patients with opioid use disorder.

The most common group of patients with OUD also have a history of other substance use disorders. Most common would be marijuana, alcohol, cocaine and sedatives. While this group has struggled with an addiction to multiple substances, the opioids are the clear drug of choice. Many patients in this group will set all other drugs aside and only use them occasionally once opioids are discovered.

The second most common group with OUD continues to use other drugs concomitantly with the opioids. They may not identify opioids (or any of the others) as a clear drug of choice. This group will often speedball (mix opioids and cocaine). They also may unfortunately mix alcohol or sedatives with opioids, which is an unfortunate combination.

The least common group has OUD with no other history of substance use.

Methamphetamine is not as common in the northeast and hence for regional considerations I do not see it commonly. As a resident in Dallas, TX, methamphetamine use, with or without opioids, was common.

Do you have a protocol for switching someone from Suboxone to Naltrexone?

In the PER we do not generally complete an opioid detox and hence do not generally switch from buprenorphine to Naltrexone. We either initiate and titrate buprenorphine for maintenance or transfer to a local rehab or detox facility for completing detox.

Do you have an opioid detox protocol that you’d use in the hospital or ED?

First, we try hard to not detox OUD patients. Patients with OUD should be on MAT and we use the psychiatric emergency room (PER) visit as a means to initiate buprenorphine. We aggressively recommend buprenorphine initiation. If agreeable, we generally will start buprenorphine 4mg in the PER once withdrawal symptoms are moderate (COWS >8). We will then repeat the 4mg dose if indicated for a maximum dose of 8mg on day 1. The patient will then spend the night in the PER for observation.

On day 2, we titrate up to a maximum dose of 16mg if indicated. At that point the patient is ready for movement to the next level of care. Occasionally, patients will require a second night in the PER to titrate the buprenorphine up and for complete stabilization of withdrawal symptoms.

Once at a stabilizing dose the patients will generally move to our 21-day substance use treatment program. While in the program the buprenorphine is titrated as necessary. Upon completion of the program the patient is referred to the buprenorphine clinic in conjunction with a psychosocial program.

If the patient is unwilling to attend the 21-day program, and buprenorphine is initiated in the PER, the patient is discharged from the PER and seen daily in the outpatient detox/stabilization clinic until an appointment is available in the buprenorphine clinic. Given the resources at the VA we are able to initiate buprenorphine in the PER with confidence that a plan on the backend is achievable.

If the patient is unwilling to be on maintenance therapy then an opioid detox is completed. This is done with either buprenorphine or symptom-driven. Typically for detox, the patient is transferred to a local detox facility that the VA contracts with.

You have worked in both the inpatient and residential drug free drug programs and now Yale in ED and MAT, can you give me a sense of what lessons you have learned from each and how each might have a role and limitations?

Residential programs are a very important part of the recovery process but are not a cure for addiction. I often encounter patients who have completed our 21-day treatment program multiple times, each time having relapsed almost immediately after completion. When patients and/or families expect that years or decades of use will be cured after 21 days in a program they will naturally be disappointed. “Treatment begins when you leave the program” is a very important tenet of recovery. A good residential program will introduce/reinforce recovery principles and motivate the patient to continue this process after completion of the program. Without a solid aftercare program, residential programs are destined to fail.

Regarding the emergency room, many providers may not see the emergency room as an ideal environment for a discussion about recovery. Every patient that I see in the PER will hear about the importance for long term treatment and the need for a solid recovery program. I will discuss long term strategies including MAT, NA and other treatment options. Even with patients who present to the PER frequently, I always spend time discussing the importance of a solid foundation of recovery and the need for MAT. Even in the context of a busy emergency room, there is always time for a brief motivational interaction which may make a real difference and save a life.

Are you seeing meth or cocaine emergencies and/or overdoses? What is your approach?

Methamphetamine is not a common drug of abuse in this region of the country. Cocaine is incredibly common and it is commonly abused in the powder form or in the form of crack. It is often used in conjunction with opioids (speedballs). When cocaine overdoses occur (rarer than opioid overdoses), the patient is seen and stabilized in the medical ER prior to transfer to the PER. With patients who are using cocaine at levels so dangerous that it leads to overdose, I am aggressive and assertive the way I am with opioids. The difference with stimulants is the lack of MAT. Hence the reliance on a psychosocial treatment becomes more important. Patients are referred to the substance use treatment program to begin the recovery process. They are then referred to AA/NA, contingency management, CBT for addiction or other psychosocial support programs.

Source: https://www.rivermendhealth.com/resources/q-a-with-brian-fuehrlein-md-phd-the-opioid-epidemic-and-emergency-room-visits November 2017

By Christopher Glazek

You’re aware America is under siege, fighting an opioid crisis that has exploded into a public-health emergency. You’ve heard of OxyContin, the pain medication to which countless patients have become addicted. But do you know that the company that makes Oxy and reaps the billions of dollars in profits it generates is owned by one family?

The newly installed Sackler Courtyard at London’s Victoria and Albert Museum is one of the most glittering places in the developed world. Eleven thousand white porcelain tiles, inlaid like a shattered backgammon board, cover a surface the size of six tennis courts. According to the V&A’s director, the regal setting is intended to serve as a “living room for London,” by which he presumably means a living room for Kensington, the museum’s neighborhood, which is among the world’s wealthiest. In late June, Kate Middleton, the Duchess of Cambridge, was summoned to consecrate the courtyard, said to be the earth’s first outdoor space made of porcelain; stepping onto the ceramic expanse, she silently mouthed, “Wow.”

The Sackler Courtyard is the latest addition to an impressive portfolio. There’s the Sackler Wing at New York’s Metropolitan Museum of Art, which houses the majestic Temple of Dendur, a sandstone shrine from ancient Egypt; additional Sackler wings at the Louvre and the Royal Academy; stand-alone Sackler museums at Harvard and Peking Universities; and named Sackler galleries at the Smithsonian, the Serpentine, and Oxford’s Ashmolean. The Guggenheim in New York has a Sackler Center, and the American Museum of Natural History has a Sackler Educational Lab. Members of the family, legendary in museum circles for their pursuit of naming rights, have also underwritten projects of a more modest caliber—a Sackler Staircase at Berlin’s Jewish Museum; a Sackler Escalator at the Tate Modern; a Sackler Crossing in Kew Gardens. A popular species of pink rose is named after a Sackler. So is an asteroid.

The Sackler name is no less prominent among the emerald quads of higher education, where it’s possible to receive degrees from Sackler schools, participate in Sackler colloquiums, take courses from professors with endowed Sackler chairs, and attend annual Sackler lectures on topics such as theoretical astrophysics and human rights. The Sackler Institute for Nutrition Science supports research on obesity and micronutrient deficiencies. Meanwhile, the Sackler institutes at Cornell, Columbia, McGill, Edinburgh, Glasgow, Sussex, and King’s College London tackle psychobiology, with an emphasis on early childhood development.

The Sacklers’ philanthropy differs from that of civic populists like Andrew Carnegie, who built hundreds of libraries in small towns, and Bill Gates, whose foundation ministers to global masses. Instead, the family has donated its fortune to blue-chip brands, braiding the family name into the patronage network of the world’s most prestigious, well-endowed institutions. The Sackler name is everywhere, evoking automatic reverence; the Sacklers themselves, however, are rarely seen. [In 1974, when the Sackler brothers made a large gift to the Met—$3.5 million, to erect the Temple of Dendur—they stipulated that all museum signage, catalog entries, and bulletins referring to objects in the newly opened Sackler Wing had to include the names of all three brothers, each followed by “M.D.”]

The descendants of Mortimer and Raymond Sackler, a pair of psychiatrist brothers from Brooklyn, are members of a billionaire clan with homes scattered across Connecticut, London, Utah, Gstaad, the Hamptons, and, especially, New York City. It was not until 2015 that they were noticed by Forbes, which added them to the list of America’s richest families.

The magazine pegged their wealth, shared among twenty heirs, at a conservative $14 billion. (Descendants of Arthur Sackler, Mortimer and Raymond’s older brother, split off decades ago and are mere multi-millionaires.) To a remarkable degree, those who share in the billions appear to have abided by an oath of omertà: Never comment publicly on the source of the family’s wealth.

That may be because the greatest part of that $14 billion fortune tallied by Forbes came from OxyContin, the narcotic painkiller regarded by many public-health experts as among the most dangerous products ever sold on a mass scale. Since 1996, when the drug was brought to market by Purdue Pharma, the American branch of the Sacklers’ pharmaceutical empire, more than two hundred thousand people in the United States have died from overdoses of OxyContin and other prescription painkillers. Thousands more have died after starting on a prescription opioid and then switching to a drug with a cheaper street price, such as heroin. Not all of these deaths are related to OxyContin—dozens of other painkillers, including generics, have flooded the market in the past thirty years. Nevertheless, Purdue Pharma was the first to achieve a dominant share of the market for long-acting opioids, accounting for more than half of prescriptions by 2001.

According to the Centers for Disease Control, fifty-three thousand Americans died from opioid overdoses in 2016, more than the thirty-six thousand who died in car crashes in 2015 or the thirty-five thousand who died from gun violence that year. This past July, Donald Trump’s Commission on Combating Drug Addiction and the Opioid Crisis, led by New Jersey governor Chris Christie, declared that opioids were killing roughly 142 Americans each day, a tally vividly described as “September 11th every three weeks.” The epidemic has also exacted a crushing financial toll: According to a study published by the American Public Health Association, using data from 2013—before the epidemic entered its current, more virulent phase—the total economic burden from opioid use stood at about $80 billion, adding together health costs, criminal-justice costs, and GDP loss from drug-dependent Americans leaving the workforce. Tobacco remains, by a significant multiple, the country’s most lethal product, responsible for some 480,000 deaths per year. But although billions have been made from tobacco, cars, and firearms, it’s not clear that any of those enterprises has generated a family fortune from a single product that approaches the Sacklers’ haul from OxyContin.

Even so, hardly anyone associates the Sackler name with their company’s lone blockbuster drug. “The Fords, Hewletts, Packards, Johnsons—all those families put their name on their product because they were proud,” said Keith Humphreys, a professor of psychiatry at Stanford University School of Medicine who has written extensively about the opioid crisis. “The Sacklers have hidden their connection to their product. They don’t call it ‘Sackler Pharma.’ They don’t call their pills ‘Sackler pills.’ And when they’re questioned, they say, ‘Well, it’s a privately held firm, we’re a family, we like to keep our privacy, you understand.’ ”

To the extent that the Sacklers have cultivated a reputation, it’s for being earnest healers, judicious stewards of scientific progress, and connoisseurs of old and beautiful things. Few are aware that during the crucial period of OxyContin’s development and promotion, Sackler family members actively led Purdue’s day-to-day affairs, filling the majority of its board slots and supplying top executives. By any assessment, the family’s leaders have pulled off three of the great marketing triumphs of the modern era: The first is selling OxyContin; the second is promoting the Sackler name; and the third is ensuring that, as far as the public is aware, the first and the second have nothing to do with one another.

If you head north on I-95 through Stamford, Connecticut, you will spot, on the left, a giant misshapen glass cube. Along the building’s top edge, white lettering spells out ONE STAMFORD FORUM. No markings visible from the highway indicate the presence of the building’s owner and chief occupant, Purdue Pharma. Originally known as Purdue Frederick, the first iteration of the company was founded in 1892 on New York’s Lower East Side as a peddler of patent medicines. For decades, it sustained itself with sales of Gray’s Glycerine Tonic, a sherry-based liquid of “broad application” marketed as a remedy for everything from anemia to tuberculosis. The company was purchased in 1952 by Arthur Sackler, thirty-nine, and was run by his brothers, Mortimer, thirty- six, and Raymond, thirty-two. The Sackler brothers came from a family of Jewish immigrants in Flatbush, Brooklyn. Arthur was a headstrong and ambitious provider, setting the tone—and often choosing the path—for his younger brothers. After attending medical school on Arthur’s dime, Mortimer and Raymond followed him to jobs at the Creedmoor psychiatric hospital in Queens. There, they coauthored more than one hundred studies on the biochemical roots of mental illness. The brothers’ research was promising—they were among the first to identify a link between psychosis and the hormone cortisone—but their findings were mostly ignored by their professional peers, who, in keeping with the era, favored a Freudian model of mental illness.

Concurrent with his psychiatric work, Arthur Sackler made his name in pharmaceutical advertising, which at the time consisted almost exclusively of pitches from so-called “detail men” who sold drugs to doctors door-to-door. Arthur intuited that print ads in medical journals could have a revolutionary effect on pharmaceutical sales, especially given the excitement surrounding the “miracle drugs” of the 1950s—steroids, antibiotics, antihistamines, and psychotropics. In 1952, the same year that he and his brothers acquired Purdue, Arthur became the first adman to convince The Journal of the American Medical Association, one of the profession’s most august publications, to include a color advertorial brochure.

In the 1960s, Arthur was contracted by Roche to develop an advertising strategy for a new antianxiety medication called Valium. This posed a challenge, because the effects of the medication were nearly indistinguishable from those of Librium, another Roche tranquilizer that was already on the market. Arthur differentiated Valium by audaciously inflating its range of indications. Whereas Librium was sold as a treatment for garden- variety anxiety, Valium was positioned as an elixir for a problem Arthur christened “psychic tension.” According to his ads, psychic tension, the forebear of today’s “stress,” was the secret culprit behind a host of somatic conditions, including heartburn, gastrointestinal issues, insomnia, and restless-leg syndrome. The campaign was such a success that for a time Valium became America’s most widely prescribed medication—the first to reach more than $100 million in sales. Arthur, whose compensation depended on the volume of pills sold, was richly rewarded, and he later became one of the first inductees into the Medical Advertising Hall of Fame.

As Arthur’s fortune grew, he turned his acquisitive instincts to the art market, quickly amassing the world’s largest private collection of ancient Chinese artifacts. According to a memoir by Marietta Lutze, his second wife, collecting, exhibiting, owning, and donating art fed Arthur’s “driving necessity for prestige and recognition.” Rewarding at first, collecting soon became a mania that took over his life. “Boxes of artifacts of tremendous value piled up in numerous storage locations,” she wrote, “there was too much to open, too much to appreciate; some objects known only by a packing list.” Under an avalanche of “ritual bronzes and weapons, mirrors and ceramics, inscribed bones and archaic jades,” their lives were “often in chaos.” “Addiction is a curse,” Lutze noted, “be it drugs, women, or collecting.”

When Arthur donated his art and money to museums, he often imposed onerous terms. According to a memoir written by Thomas Hoving, the Met director from 1967 to 1977, when Arthur established the Sackler Gallery at the Metropolitan Museum of Art to house Chinese antiquities, in 1963, he required the museum to collaborate on a byzantine tax-avoidance maneuver. In accordance with the scheme, the museum first sold Arthur a large quantity of ancient artifacts at the deflated 1920s prices for which they had originally been acquired. Arthur then donated back the artifacts at 1960s prices, in the process taking a tax deduction so hefty that it likely exceeded the value of his initial donation. Three years later, in connection with another donation, Arthur negotiated an even more unusual arrangement. This time, the Met opened a secret chamber above the museum’s auditorium to provide Arthur with free storage for some five thousand objects from his private collection, relieving him of the substantial burden of fire protection and other insurance costs. (In an email exchange, Jillian Sackler, Arthur’s third wife, called Hoving’s tax-deduction story “fake news.” She also noted that New York’s attorney general conducted an investigation into Arthur’s dealings with the Met and cleared him of wrongdoing.)

In 1974, when Arthur and his brothers made a large gift to the Met—$3.5 million, to erect the Temple of Dendur—they stipulated that all museum signage, catalog entries, and bulletins referring to objects in the newly opened Sackler Wing had to include the names of all three brothers, each followed by “M.D.” (One museum official quipped, “All that was missing was a note of their office hours.”)

Hoving said that the Met hoped that Arthur would eventually donate his collection to the museum, but over time Arthur grew disgruntled over a series of rankling slights. For one, the Temple of Dendur was being rented out for parties, including a dinner for the designer Valentino, which Arthur called “disgusting.” According to Met chronicler Michael Gross, he was also denied that coveted ticket of arrival, a board seat. (Jillian Sackler said it was Arthur who rejected the board seat, after repeated offers by the museum.) In 1982, in a bad breakup with the Met, Arthur donated the best parts of his collection, plus $4 million, to the Smithsonian in Washington, D. C.

Arthur’s younger brothers, Mortimer and Raymond, looked so much alike that when they worked together at Creedmoor, they fooled the staff by pretending to be one another. Their physical similarities did not extend to their personalities, however. Tage Honore, Purdue’s vice-president of discovery of research from 2000 to 2005, described them as “like day and night.” Mortimer, said Honore, was “extroverted—a ‘world man,’ I would call it.” He acquired a reputation as a big-spending, transatlantic playboy, living most of the year in opulent homes in England, Switzerland, and France. (In 1974, he renounced his U. S. citizenship to become a citizen of Austria, which infuriated his patriotic older brother.) Like Arthur, Mortimer became a major museum donor and married three wives over the course of his life.

Mortimer had his own feuds with the Met. On his seventieth birthday, in 1986, the museum agreed to make the Temple of Dendur available to him for a party but refused to allow him to redecorate the ancient shrine: Together with other improvements, Mortimer and his interior designer, flown in from Europe, had hoped to spiff up the temple by adding extra pillars. Also galling to Mortimer was the sale of naming rights for one of the Sackler Wing’s balconies to a donor from Japan. “They sold it twice,” Mortimer fumed to a reporter from New York magazine. Raymond, the youngest brother, cut a different figure—“a family man,” said Honore. Kind and mild-mannered, he stayed with the same woman his entire life. Lutze concluded that Raymond owed his comparatively serene nature to having missed the worst years of the Depression. “He had summer vacations in camp, which Arthur never had,” she

wrote. “The feeling of the two older brothers about the youngest was, ‘Let the kid enjoy himself.’ ”

Raymond led Purdue Frederick as its top executive for several decades, while Mortimer led Napp Pharmaceuticals, the family’s drug company in the UK. (In practice, a family spokesperson said, “the brothers worked closely together leading both companies.”) Arthur, the adman, had no official role in the family’s pharmaceutical operations. According to Barry Meier’s Pain Killer, a prescient account of the rise of OxyContin published in 2003, Raymond and Mortimer bought Arthur’s share in Purdue from his estate for $22.4 million after he died in 1987. In an email exchange, Arthur’s daughter Elizabeth Sackler, a historian of feminist art who sits on the board of the Brooklyn Museum and supports a variety of progressive causes, emphatically distanced her branch of the family from her cousins’ businesses. “Neither I, nor my siblings, nor my children have ever had ownership in or any benefit whatsoever from Purdue Pharma or OxyContin,” she wrote, while also praising “the breadth of my father’s brilliance and important works.” Jillian, Arthur’s widow, said her husband had died too soon: “His enemies have gotten the last word.”

The Sacklers have been millionaires for decades, but their real money—the painkiller money—is of comparatively recent vintage. The vehicle of that fortune was OxyContin, but its engine, the driving power that made them so many billions, was not so much the drug itself as it was Arthur’s original marketing insight, rehabbed for the era of chronic-pain management. That simple but profitable idea was to take a substance with addictive properties—in Arthur’s case, a benzo; in Raymond and Mortimer’s case, an opioid—and market it as a salve for a vast range of indications.

In the years before it swooped into the pain-management business, Purdue had been a small industry player, specializing in over-the-counter remedies like ear-wax remover and laxatives. Its most successful product, acquired in 1966, was Betadine, a powerful antiseptic purchased in industrial quantities by the U. S. government to prevent infection among wounded soldiers in Vietnam. The turning point, according to company lore, came in 1972, when a London doctor working for Cicely Saunders, the Florence Nightingale of the modern hospice movement, approached Napp with the idea of creating a timed-release morphine pill. A long-acting morphine pill, the doctor reasoned, would allow dying cancer patients to sleep through the night without an IV. At the time, treatment with opioids was stigmatized in the United States, owing in part to a heroin epidemic fueled by returning Vietnam veterans. “Opiophobia,” as it came to be called, prevented skittish doctors from treating most patients, including nearly all infants, with strong pain medication of any kind. In hospice care, though, addiction was not a concern: It didn’t matter whether terminal patients became hooked in their final days. Over the course of the seventies, building on a slow-release technology the company had already developed for an asthma medication, Napp created what came to be known as the “Contin” system. In 1981, Napp introduced a timed-release morphine pill in the UK; six years later, Purdue brought the same drug to market in the U. S. as MS Contin.

MS Contin quickly became the gold standard for pain relief in cancer care. At the same time, a number of clinicians associated with the burgeoning chronic-pain movement started advocating the use of powerful opioids for noncancer conditions like back pain and neuropathic pain, afflictions that at their worst could be debilitating. In 1986, two doctors from Memorial Sloan Kettering hospital in New York published a fateful article in a medical journal that purported to show, based on a study of thirty-eight patients, that long-term opioid treatment was safe and

effective so long as patients had no history of drug abuse. Soon enough, opioid advocates dredged up a letter to the editor published in The New England Journal of Medicine in 1980 that suggested, based on a highly unrepresentative cohort, that the risk of addiction from long-term opioid use was less than 1 percent. Though ultimately disavowed by its author, the letter ended up getting cited in medical journals more than six hundred times.

As the country was reexamining pain, Raymond’s eldest son, Richard Sackler, was searching for new applications for Purdue’s timed-release Contin system. “At all the meetings, that was a constant source of discussion—‘What else can we use the Contin system for?’ ” said Peter Lacouture, a senior director of clinical research at Purdue from 1991 to 2001. “And that’s where Richard would fire some ideas—maybe antibiotics, maybe chemotherapy—he was always out there digging.” Richard’s spitballing wasn’t idle blather. A trained physician, he treasured his role as a research scientist and appeared as an inventor on dozens of the company’s patents (though not on the patents for OxyContin). In the tradition of his uncle Arthur, Richard was also fascinated by sales messaging. “He was very interested in the commercial side and also very interested in marketing approaches,” said Sally Allen Riddle, Purdue’s former executive director for product management. “He didn’t always wait for the research results.” (A Purdue spokesperson said that Richard “always considered relevant scientific information when making decisions.”)

Perhaps the most private member of a generally secretive family, Richard appears nowhere on Purdue’s website. From public records and conversations with former employees, though, a rough portrait emerges of a testy eccentric with ardent, relentless ambitions. Born in 1945, he holds degrees from Columbia University and NYU Medical School. According to a bio on the website of the Koch Institute for Integrative Cancer Research at MIT, where Richard serves on the advisory board, he started working at Purdue as his father’s assistant at age twenty-six before eventually leading the firm’s R&D division and, separately, its sales and marketing division. In 1999, while Mortimer and Raymond remained Purdue’s co-CEOs, Richard joined them at the top of the company as president, a position he relinquished in 2003 to become cochairman of the board. The few publicly available pictures of him are generic and sphinxlike—a white guy with a receding hairline. He is one of the few Sacklers to consistently smile for the camera. In a photo on what appears to be his Facebook profile, Richard is wearing a tan suit and a pink tie, his right hand casually scrunched into his pocket, projecting a jaunty charm. Divorced in 2013, he lists his relationship status on the profile as “It’s complicated.” WHEN PURDUE EVENTUALLY PLEADED GUILTY TO FELONY CHARGES IN 2007 FOR CRIMINALLY “MISBRANDING” OXYCONTIN, IT ACKNOWLEDGED EXPLOITING DOCTORS’ MISCONCEPTIONS ABOUT OXYCODONE’S STRENGTH.

Richard’s political contributions have gone mostly to Republicans—including Strom Thurmond and Herman Cain—though at times he has also given to Democrats. (His ex-wife, Beth Sackler, has given almost exclusively to Democrats.) In 2008, he wrote a letter to the editor of The Wall Street Journal denouncing Muslim support for suicide bombing, a concern that seems to persist: Since 2014, his charitable organization, the Richard and Beth Sackler Foundation, has donated to several anti-Muslim groups, including three organizations classified as hate groups by the Southern Poverty Law Center. (The family spokesperson said, “It was never Richard Sackler’s intention to donate to an anti-Muslim or hate group.”) The foundation has also donated to True the Vote, the “voter-fraud watchdog” that was the original source for Donald Trump’s inaccurate claim that three million illegal immigrants voted in the 2016 election.

Former employees describe Richard as a man with an unnerving intelligence, alternately detached and pouncing. In meetings, his face was often glued to his laptop. “This was pre-

smartphone days,” said Riddle. “He’d be typing away and you would think he wasn’t even listening, and then all of the sudden his head would pop up and he’d be asking a very pointed question.” He was notorious for peppering subordinates with unexpected, rapid-fire queries, sometimes in the middle of the night. “Richard had the mind of someone who’s going two hundred miles an hour,” said Lacouture. “He could be a little bit disconnected in the way he would communicate. Whether it was on the weekend or a holiday or a Christmas party, you could always expect the unexpected.”

Richard also had an appetite for micromanagement. “I remember one time he mailed out a rambling sales bulletin,” said Shelby Sherman, a Purdue sales rep from 1974 to 1998. “And right in the middle, he put in, ‘If you’re reading this, then you must call my secretary at this number and give her this secret password.’ He wanted to check and see if the reps were reading this shit. We called it ‘Playin’ Passwords.’ ” According to Sherman, Richard started taking a more prominent role in the company during the early 1980s. “The shift was abrupt,” he said. “Raymond was just so nice and down-to-earth and calm and gentle.” When Richard came, “things got a lot harder. Richard really wanted Purdue to be big—I mean really big.”

To effectively capitalize on the chronic-pain movement, Purdue knew it needed to move beyond MS Contin. “Morphine had a stigma,” said Riddle. “People hear the word and say, ‘Wait a minute, I’m not dying or anything.’ ” Aside from its terminal aura, MS Contin had a further handicap: Its patent was set to expire in the late nineties. In a 1990 memo addressed to Richard and other executives, Purdue’s VP of clinical research, Robert Kaiko, suggested that the company work on a pill containing oxycodone, a chemical similar to morphine that was also derived from the opium poppy. When it came to branding, oxycodone had a key advantage: Although it was 50 percent stronger than morphine, many doctors believed—wrongly—that it was substantially less powerful. They were deceived about its potency in part because oxycodone was widely known as one of the active ingredients in Percocet, a relatively weak opioid- acetaminophen combination that doctors often prescribed for painful injuries. “It really didn’t have the same connotation that morphine did in people’s minds,” said Riddle.

A common malapropism led to further advantage for Purdue. “Some people would call it oxy-codeine” instead of oxycodone, recalled Lacouture. “Codeine is very weak.” When Purdue eventually pleaded guilty to felony charges in 2007 for criminally “misbranding” OxyContin, it acknowledged exploiting doctors’ misconceptions about oxycodone’s strength. In court documents, the company said it was “well aware of the incorrect view held by many physicians that oxycodone was weaker than morphine” and “did not want to do anything ‘to make physicians think that oxycodone was stronger or equal to morphine’ or to ‘take any steps . . . that would affect the unique position that OxyContin’ ” held among physicians.

Purdue did not merely neglect to clear up confusion about the strength of OxyContin. As the company later admitted, it misleadingly promoted OxyContin as less addictive than older opioids on the market. In this deception, Purdue had a big assist from the FDA, which allowed the company to include an astonishing labeling claim in OxyContin’s package insert: “Delayed absorption, as provided by OxyContin tablets, is believed to reduce the abuse liability of a drug.”

The theory was that addicts would shy away from timed-released drugs, preferring an immediate rush. In practice, OxyContin, which crammed a huge amount of pure narcotic into a single pill, became a lusted-after target for addicts, who quickly discovered that the timed-release mechanism in OxyContin was easy

to circumvent—you could simply crush a pill and snort it to get most of the narcotic payload in a single inhalation. This wasn’t exactly news to the manufacturer: OxyContin’s own packaging warned that consuming broken pills would thwart the timed-release system and subject patients to a potentially fatal overdose. MS Contin had contended with similar vulnerabilities, and as a result commanded a hefty premium on the street. But the “reduced abuse liability” claim that added wings to the sales of OxyContin had not been approved for MS Contin. It was removed from OxyContin in 2001 and would never be approved again for any other opioid.

The year after OxyContin’s release, Curtis Wright, the FDA examiner who approved the pharmaceutical’s original application, quit. After a stint at another pharmaceutical company, he began working for Purdue. In an interview with Esquire, Wright defended his work at the FDA and at Purdue. “At the time, it was believed that extended-release formulations were intrinsically less abusable,” he insisted. “It came as a rather big shock to everybody—the government and Purdue—that people found ways to grind up, chew up, snort, dissolve, and inject the pills.” Preventing abuse, he said, had to be balanced against providing relief to chronic-pain sufferers. “In the mid-nineties,” he recalled, “the very best pain specialists told the medical community they were not prescribing opioids enough. That was not something generated by Purdue—that was not a secret plan, that was not a plot,that was not a clever marketing ploy. Chronic pain is horrible. In the right circumstances, opioid therapy is nothing short of miraculous; you give people their lives back.” In Wright’s account, the Sacklers were not just great employers, they were great people. “No company in the history of pharmaceuticals,” he said, “has worked harder to try to prevent abuse of their product than Purdue.”

Purdue did not invent the chronic-pain movement, but it used that movement to engineer a crucial shift. Wright is correct that in the nineties patients suffering from chronic pain often received inadequate treatment. But the call for clinical reforms also became a flexible alibi for overly aggressive prescribing practices. By the end of the decade, clinical proponents of opioid treatment, supported by millions in funding from Purdue and other pharmaceutical companies, had organized themselves into advocacy groups with names like the American Pain Society and the American Academy of Pain Medicine. (Purdue also launched its own group, called Partners Against Pain.) As the decade wore on, these organizations, which critics have characterized as front groups for the pharmaceutical industry, began pressuring health regulators to make pain “the fifth vital sign”—a number, measured on a subjective ten-point scale, to be asked and recorded at every doctor’s visit. As an internal strategy document put it, Purdue’s ambition was to “attach an emotional aspect to non cancer pain” so that doctors would feel pressure to “treat it more seriously and aggressively.” The company rebranded pain relief as a sacred right: a universal narcotic entitlement available not only to the terminally ill but to every American.

The company rebranded pain relief as a sacred right: a universal narcotic entitlement available not only to the terminally ill but to every American. By 2001, annual OxyContin sales had surged past $1 billion.

OxyContin’s sales started out small in 1996, in part because Purdue first focused on the cancer market to gain formulary acceptance from HMOs and state Medicaid programs. Over the next several years, though, the company doubled its sales force to six hundred—equal to the total number of DEA diversion agents employed to combat the sale of prescription drugs on the black market—and began targeting general practitioners, dentists, OB/GYNs, physician assistants, nurses, and residents. By 2001, annual OxyContin sales had surged past $1 billion. Sales reps were encouraged to downplay addiction risks. “It was sell, sell,

sell,” recalled Sherman. “We were directed to lie. Why mince words about it? Greed took hold and overruled everything. They saw that potential for billions of dollars and just went after it.” Flush with cash, Purdue pioneered a high-cost promotion strategy, effectively providing kickbacks—which were legal under American law—to each part of the distribution chain. Wholesalers got rebates in exchange for keeping OxyContin off prior authorization lists. Pharmacists got refunds on their initial orders. Patients got coupons for thirty- day starter supplies. Academics got grants. Medical journals got millions in advertising. Senators and members of Congress on key committees got donations from Purdue and from members of the Sackler family.

It was doctors, though, who received the most attention. “We used to fly doctors to these ‘seminars,’ ” said Sherman, which were, in practice, “just golf trips to Pebble Beach. It was graft.” Though offering perks and freebies to doctors was hardly uncommon in the industry, it was unprecedented in the marketing of a Schedule II narcotic. For some physicians, the junkets to sunny locales weren’t enough to persuade them to prescribe. To entice the holdouts—a group the company referred to internally as “problem doctors”—the reps would dangle the lure of Purdue’s lucrative speakers’ bureau. “Everybody was automatically approved,” said Sherman. “We would set up these little dinners, and they’d make their little fifteen-minute talk, and they’d get $500.”

Between 1996 and 2001, the number of OxyContin prescriptions in the United States surged from about three hundred thousand to nearly six million, and reports of abuse started to bubble up in places like West Virginia, Florida, and Maine. (Research would later show a direct correlation between prescription volume in an area and rates of abuse and overdose.) Hundreds of doctors were eventually arrested for running pill mills. According to an investigation in the Los Angeles Times, even though Purdue kept an internal list of doctors it suspected of criminal diversion, it didn’t volunteer this information to law enforcement until years later. As criticism of OxyContin mounted through the aughts, Purdue responded with symbolic concessions while retaining its volume-driven business model. To prevent addicts from forging prescriptions, the company gave doctors tamper-resistant prescription pads; to mollify pharmacists worried about robberies, Purdue offered to replace, free of charge, any stolen drugs; to gather data on drug abuse and diversion, the company launched a national monitoring program called RADARS.

Critics were not impressed. In a letter to Richard Sackler in July 2001, Richard Blumenthal, then Connecticut’s attorney general and now a U. S. senator, called the company’s efforts “cosmetic.” As Blumenthal had deduced, the root problem of the prescription-opioid epidemic was the high volume of prescriptions written for powerful opioids. “It is time for Purdue Pharma to change its practices,” Blumenthal warned Richard, “not just its public-relations strategy.”

It wasn’t just that doctors were writing huge numbers of prescriptions; it was also that the prescriptions were often for extraordinarily high doses. A single dose of Percocet contains between 2.5 and 10mg of oxycodone. OxyContin came in 10-, 20-, 30-, 40-, and 80mg formulations and, for a time, even 160mg. Purdue’s greatest competitive advantage in dominating the pain market, it had determined early on, was that OxyContin lasted twelve hours, enough to sleep through the night. But for many patients, the drug lasted only six or eight hours, creating a cycle of crash and euphoria that one academic called “a perfect recipe for addiction.” When confronted with complaints about “breakthrough pain”—meaning that the pills weren’t working as long as advertised—Purdue’s sales reps were given strict instructions to tell doctors to strengthen the dose rather than increase dosing frequency.

Sales reps were encouraged to downplay addiction risks. “It was sell, sell, sell,” recalled Sherman. “We were directed to lie. Why mince words about it?”

Over the next several years, dozens of class-action lawsuits were brought against Purdue. Many were dismissed, but in some cases Purdue wrote big checks to avoid going to trial. Several plaintiffs’ lawyers found that the company was willing to go to great lengths to prevent Richard Sackler from having to testify under oath. “They didn’t want him deposed, I can tell you that much,” recalled Marvin Masters, a lawyer who brought a class-action suit against Purdue in the early 2000s in West Virginia. “They were willing to sit down and settle the case to keep from doing that.” Purdue tried to get Richard removed from the suit, but when that didn’t work, the company settled with the plaintiffs for more than $20 million. Paul Hanly, a New York class-action lawyer who won a large settlement from Purdue in 2007, had a similar recollection. “We were attempting to take Richard Sackler’s deposition,” he said, “around the time that they agreed to a settlement.” (A spokesperson for the company said, “Purdue did not settle any cases to avoid the deposition of Dr. Richard Sackler, or any other individual.”)

When the federal government finally stepped in, in 2007, it extracted historic terms of surrender from the company. Purdue pleaded guilty to felony charges, admitting that it had lied to doctors about OxyContin’s abuse potential. (The technical charge was “misbranding a drug with intent to defraud or mislead.”) Under the agreement, the company paid $600 million in fines and its three top executives at the time—its medical director, general counsel, and Richard’s successor as president—pleaded guilty to misdemeanor charges. The executives paid $34.5 million out of their own pockets and performed four hundred hours of community service. It was one of the harshest penalties ever imposed on a pharmaceutical company. (In a statement to Esquire, Purdue said that it “abides by the highest ethical standards and legal requirements.” The statement went on: “We want physicians to use their professional judgment, and we were not trying to pressure them.”)

Fifty-three thousand Americans died from opioid overdoses in 2016, more than the thirty-six thousand who died in car crashes in 2015 or the thirty-five thousand who died from gun violence that year.

No Sacklers were named in the 2007 suit. Indeed, the Sackler name appeared nowhere in the plea agreement, even though Richard had been one of the company’s top executives during most of the period covered by the settlement. He did eventually have to give a deposition in 2015, in a case brought by Kentucky’s attorney general. Richard’s testimony—the only known record of a Sackler speaking about the crisis the family’s company helped create—was promptly sealed. (In 2016, STAT, an online magazine owned by Boston Globe Media that covers health and medicine, asked a court in Kentucky to unseal the deposition, which is said to have lasted several hours. STAT won a lower-court ruling in May 2016. As of press time, the matter was before an appeals court.)

In 2010, Purdue executed a breathtaking pivot: Embracing the arguments critics had been making for years about OxyContin’s susceptibility to abuse, the company released a new formulation of the medication that was harder to snort or inject. Purdue seized the occasion to rebrand itself as an industry leader in abuse-deterrent technology. The change of heart coincided with two developments: First, an increasing number of addicts, unable to afford OxyContin’s high street price, were turning to cheaper alternatives like heroin; second, OxyContin was nearing the end of its patents. Purdue suddenly argued that the drug it had been selling for nearly fifteen years was so prone to abuse that generic manufacturers should not be allowed to copy it.

On April 16, 2013, the day some of the key patents for OxyContin were scheduled to expire, the FDA followed Purdue’s lead, declaring that no generic versions of the original OxyContin formulation could be sold. The company had effectively won several additional years of patent protection for its golden goose.

Opioid withdrawal, which causes aches, vomiting, and restless anxiety, is a gruesome process to experience as an adult. It’s considerably worse for the twenty thousand or so American babies who emerge each year from opioid-soaked wombs. These infants, suddenly cut off from their supply, cry uncontrollably. Their skin is mottled. They cannot fall asleep. Their bodies are shaken by tremors and, in the worst cases, seizures. Bottles of milk leave them distraught, because they cannot maneuver their lips with enough precision to create suction. Treatment comes in the form of drops of morphine pushed from a syringe into the babies’ mouths. Weaning sometimes takes a week but can last as long as twelve. It’s a heartrending, expensive process, typically carried out in the neonatal ICU, where newborns have limited access to their mothers.

But the children of OxyContin, its heirs and legatees, are many and various. The second- and third-generation descendants of Raymond and Mortimer Sackler spend their money in the ways we have come to expect from the not-so-idle rich. Notably, several have made children a focus of their business and philanthropic endeavors. One Sackler heir helped start an iPhone app called Red Rover, which generates ideas for child-friendly activities for urban parents; another runs a child- development center near Central Park; another is a donor to charter-school causes, as well as an investor in an education start-up called AltSchool. Yet another is the founder of Beespace, an “incubator for emerging nonprofits,” which provides resources and mentoring for initiatives like the Malala Fund, which invests in education programs for women in the developing world, and Yoga Foster, whose objective is to bring “accessible, sustainable yoga programs into schools across the country.” Other Sackler heirs get to do the fun stuff: One helps finance small, interesting films like The Witch; a second married a famous cricket player; a third is a sound artist; a fourth started a production company with Boyd Holbrook, star of the Netflix series Narcos; a fifth founded a small chain of gastropubs in New York called the Smith.

Holding fast to family tradition, Raymond’s and Mortimer’s heirs declined to be interviewed for this article. Instead, through a spokesperson, they put forward two decorated academics who have been on the receiving end of the family’s largesse: Phillip Sharp, the Nobel-prize-winning MIT geneticist, and Herbert Pardes, formerly the dean of faculty at Columbia University’s medical school and CEO of New York-Presbyterian Hospital. Both men effusively praised the Sacklers’ donations to the arts and sciences, marveling at their loyalty to academic excellence. “Once you were on that exalted list of philanthropic projects,” Pardes told Esquire, “you were there and you were in a position to secure additional philanthropy. It was like a family acquisition.” Pardes called the Sacklers “the nicest, most gentle people you could imagine.” As for the family’s connection to OxyContin, he said that it had never come up as an issue in the faculty lounge or the hospital break room. “I have never heard one inch about that,” he said.

Pardes’s ostrich like avoidance is not unusual. In 2008, Raymond and his wife donated an undisclosed amount to Yale to start the Raymond and Beverly Sackler Institute for Biological, Physical and Engineering Sciences. Lynne Regan, its current director, told me that neither students nor faculty have ever brought up the OxyContin connection. “Most people don’t know about that,” she said. “I think people are mainly oblivious.” A spokesperson for the university added, “Yale does not vet donors for controversies that may or may not arise.”

In May, a dozen lawmakers in Congress sent a bipartisan letter to the World Health Organization warning that Sackler-owned companies were preparing to flood foreign countries with legal narcotics.

The controversy surrounding OxyContin shows little sign of receding. In 2016, the CDC issued a startling warning: There was no good evidence that opioids were an effective treatment for chronic pain beyond six weeks. There was, on the other hand, an abundance of evidence that long-term treatment with opioids had harmful effects. (A recent paper by Princeton economist Alan Krueger suggests that chronic opioid use may account for more than 20 percent of the decline in American labor-force participation from 1999 to 2015.) Millions of opioid prescriptions for chronic pain had been written in the preceding two decades, and the CDC was calling into question whether many of them should have been written at all. At least twenty-five government entities, ranging from states to small cities, have recently filed lawsuits against Purdue to recover damages associated with the opioid epidemic.

The Sacklers, though, will likely emerge untouched: Because of a sweeping non-prosecution agreement negotiated during the 2007 settlement, most new criminal litigation against Purdue can only address activity that occurred after that date. Neither Richard nor any other family members have occupied an executive position at the company since 2003.

The American market for OxyContin is dwindling. According to Purdue, prescriptions fell 33 percent between 2012 and 2016. But while the company’s primary product may be in eclipse in the United States, international markets for pain medications are expanding. According to an investigation last year in the Los Angeles Times, Mundipharma, the Sackler-owned company charged with developing new markets, is employing a suite of familiar tactics in countries like Mexico, Brazil, and China to stoke concern for as-yet-unheralded “silent epidemics” of untreated pain. In Colombia, according to the L.A. Times, the company went so far as to circulate a press release suggesting that 47 percent of the population suffered from chronic pain. [Napp is the family’s drug company in the UK. Mundipharma is their company charged with developing new markets.]

In May, a dozen lawmakers in Congress, inspired by the L.A. Times investigation, sent a bipartisan letter to the World Health Organization warning that Sackler-owned companies were preparing to flood foreign countries with legal narcotics. “Purdue began the opioid crisis that has devastated American communities,” the letter reads. “Today, Mundipharma is using many of the same deceptive and reckless practices to sell OxyContin abroad.” Significantly, the letter calls out the Sackler family by name, leaving no room for the public to wonder about the identities of the people who stood behind Mundipharma.

The final assessment of the Sacklers’ global impact will take years to work out. In some places, though, they have already left their mark. In July, Raymond, the last remaining of the original Sackler brothers, died at ninety-seven. Over the years, he had won a British knighthood, been made an Officer of France’s Légion d’Honneur, and received one of the highest possible honors from the royal house of the Netherlands. One of his final accolades came in June 2013, when Anthony Monaco, the president of Tufts University, traveled to Purdue Pharma’s headquarters in Stamford to bestow an honorary doctorate. The Sacklers had made a number of transformational donations to the university over the years—endowing, among other things, the Sackler School of Graduate Biomedical Sciences. At

Tufts, as at most schools, honorary degrees are traditionally awarded on campus during commencement, but in consideration of Raymond’s advanced age, Monaco trekked to Purdue for a special ceremony. The audience that day was limited to family members, select university officials, and a scrum of employees. Addressing the crowd of intimates, Monaco praised his benefactor. “It would be impossible to calculate how many lives you have saved, how many scientific fields you have redefined, and how many new physicians, scientists, mathematicians, and engineers are doing important work as a result of your entrepreneurial spirit.” He concluded, “You are a world changer.”

Source: This article appears in the November ’17 issue of Esquire.

Executive Summary

Purpose

Rocky Mountain High Intensity Drug Trafficking Area (RMHIDTA) is tracking the impact of marijuana legalization in the state of Colorado. This report will utilize, whenever possible, a comparison of three different eras in Colorado’s legalization history:

· 2006 – 2008: Medical marijuana pre-commercialization era

· 2009 – Present: Medical marijuana commercialization and expansion era

· 2013 – Present: Recreational marijuana era

Rocky Mountain HIDTA will collect and report comparative data in a variety of areas, including but not limited to:

· Impaired driving and fatalities

· Youth marijuana use

· Adult marijuana use

· Emergency room admissions

· Marijuana-related exposure cases

· Diversion of Colorado marijuana

This is the fifth annual report on the impact of legalized marijuana in Colorado. It is divided into ten sections, each providing information on the impact of marijuana legalization. The sections are as follows:

Section 1 – Impaired Driving and Fatalities:

· Marijuana-related traffic deaths when a driver was positive for marijuana more than doubled from 55 deaths in 2013 to 123 deaths in 2016.

· Marijuana-related traffic deaths increased 66 percent in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

o During the same time period, all traffic deaths increased 16 percent.

· In 2009, Colorado marijuana-related traffic deaths involving drivers testing positive for marijuana represented 9 percent of all traffic deaths. By 2016, that number has more than doubled to 20 percent.

Section 2 – Youth Marijuana Use:

· Youth past month marijuana use increased 12 percent in the three-year average (2013-2015) since Colorado legalized recreational marijuana compared to the three-year average prior to legalization (2010-2012).

· The latest 2014/2015 results show Colorado youth ranked #1 in the nation for past month marijuana use, up from #4 in 2011/2012 and #14 in 2005/2006.

· Colorado youth past month marijuana use for 2014/2015 was 55 percent higher than the national average compared to 39 percent higher in 2011/2012.

Section 3 – Adult Marijuana Use:

· College age past month marijuana use increased 16 percent in the three-year average (2013-2015) since Colorado legalized recreational marijuana compared to the three-year average prior to legalization (2010-2012).

· The latest 2014/2015 results show Colorado college-age adults ranked #2 in the nation for past-month marijuana use, up from #3 in 2011/2012 and #8 in 2005/2006.

· Colorado college age past month marijuana use for 2014/2015 was 61 percent higher than the national average compared to 42 percent higher in 2011/2012.

· Adult past-month marijuana use increased 71 percent in the three-year average (2013-2015) since Colorado legalized recreational marijuana compared to the three-year average prior to legalization (2010-2012).

· The latest 2014/2015 results show Colorado adults ranked #1 in the nation for past month marijuana use, up from #7 in 2011/2012 and #8 in 2005/2006.

· Colorado adult past month marijuana use for 2014/2015 was 124 percent higher than the national average compared to 51 percent higher in 2011/2012.

Section 4 – Emergency Department and Hospital Marijuana-Related Admissions:

· The yearly rate of emergency department visits related to marijuana increased 35 percent after the legalization of recreational marijuana (2011-2012 vs. 2013-2015).

· Number of hospitalizations related to marijuana:

o 2011 – 6,305

o 2012 – 6,715

o 2013 – 8,272

o 2014 – 11,439

o Jan-Sept 2015 – 10,901

· The yearly number of marijuana-related hospitalizations increased 72 percent after the legalization of recreational marijuana (2009-2012 vs. 2013-2015).

Section 5 – Marijuana-Related Exposure:

· Marijuana-related exposures increased 139 percent in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

· Marijuana-Only exposures more than doubled (increased 210 percent) in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

Section 6 – Treatment:

· Marijuana treatment data from Colorado in years 2006 – 2016 does not appear to demonstrate a definitive trend. Colorado averages 6,683 treatment admissions annually for marijuana abuse.

· Over the last ten years, the top four drugs involved in treatment admissions were alcohol (average 13,551), marijuana (average 6,712), methamphetamine (average 5,578), and heroin (average 3,024).

Section 7 – Diversion of Colorado Marijuana:

· In 2016, RMHIDTA Colorado drug task forces completed 163 investigations of individuals or organizations involved in illegally selling Colorado marijuana both in and out of state.

o These cases led to:

§ 252 felony arrests

§ 7,116 (3.5 tons) pounds of marijuana seized

§ 47,108 marijuana plants seized

§ 2,111 marijuana edibles seized

§ 232 pounds of concentrate seized

§ 29 different states to which marijuana was destined

· Highway interdiction seizures of Colorado marijuana increased 43 percent in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

· Of the 346 highway interdiction seizures in 2016, there were 36 different states destined to receive marijuana from Colorado.

o The most common destinations identified were Illinois, Missouri, Texas, Kansas and Florida.

Section 8 – Diversion by Parcel:

· Seizures of Colorado marijuana in the U.S. mail has increased 844 percent from an average of 52 parcels (2009-2012) to 491 parcels (2013-2016) in the four-year average that recreational marijuana has been legal.

· Seizures of Colorado marijuana in the U.S. mail has increased 914 percent from an average of 97 pounds (2009-2012) to 984 pounds (2013-2016) in the four-year average that recreational marijuana has been legal.

Section 9 – Related Data:

· Crime in Denver increased 17 percent and crime in Colorado increased 11 percent from 2013 to 2016.

· Colorado annual tax revenue from the sale of recreational and medical marijuana was 0.8 percent of Colorado’s total statewide budget (FY 2016).

· As of June 2017, there were 491 retail marijuana stores in the state of Colorado compared to 392 Starbucks and 208 McDonald’s.

· 66 percent of local jurisdictions have banned medical and recreational marijuana businesses.

Section 10 – Reference Materials:

This section lists various studies and reports regarding marijuana.

THERE IS MUCH MORE DATA IN EACH OF THE TEN SECTIONS. THIS PUBLICATION MAY BE FOUND ON THE ROCKY MOUNTAIN HIDTA WEBSITE; GO TO WWW.RMHIDTA.ORG AND SELECT REPORTS.

Source: WWW.RMHIDTA.ORG October 2017

Drug trafficking is now the most murderous criminal activity in American history. Overdose deaths from illegal drugs passed 50,000 in 2015 — many times the number of Americans killed by all Islamic terrorists over almost 20 years. Yet stopping the skyrocketing body count will require overcoming a pervasive misunderstanding of how drug abuse and addiction are caused.

Blaming the victim has created confusion and policy failure. No one starts using drugs intending to become an addict. While addiction may seem like slow-motion suicide, most addicts do not want to die — the poison hooks them, taking over their life. Media reports of addiction are mixed with entertainment and social media that present drug use as commonplace. More and more Americans are drawn to the flame, many introduced to substance abuse by a friend or family member. “Just say no” is dead. Yes, encouraging young people not to use drugs can save individual lives, but personal morality is not the right battleground.

There are multiple factors that may be contributing to this crisis. Does expanding supply trigger drug experimentation? Does human biology simply include a dangerous susceptibly to runaway addiction? Or is cultural confusion about freedom and self-destruction enabling and normalizing drug addiction? All these factors (and possibly more) likely play a part. But what causes an epidemic is the addictive poison itself, spread in sufficient quantities. Ultimately, America’s addiction catastrophe is properly understood as a mass poisoning.

As a result, cutting the drug supply — and only cutting supply — will reduce deaths and addiction. The evidence for this conclusion is manifest; ignoring it will cost countless more lives.

Curtailing Supply

There was no demand for crack before it was created and distributed by Colombian traffickers. There was no demand for meth before it was created by criminal gangs and then “cooked” by users. Similarly, there was no massive abuse of prescription opioids until they were irresponsibly marketed by some manufacturers and prescribed by physicians contrary to sound medical practice.

The increase in heroin and fentanyl use, addiction, and deaths followed the increase in the supply from Mexico and China. Conversely, during the George W. Bush Administration, when the supply of cocaine, crack, and meth began declining, use declined. Now, as cocaine production in Colombia has grown again, use and overdose deaths are climbing. Finally, the leveling trend in the abuse of prescription opioids has followed enforcement actions against pill mills and criminal physicians — that is, it follows an apparent reduction in supply. Americans have long accepted the claim that it is impossible to stop drug trafficking, even in the face of extensive evidence to the contrary. Anti-terrorism efforts must stop just a few dedicated individuals. This is a tough problem that Americans see solved every day. Yet the poisoning of millions is supposedly unstoppable. It isn’t.

Moreover, misunderstanding the cause of drug epidemics has shifted the policy debate away from the right goals: reducing the supply of drugs and returning addicts to sobriety. With deaths at historic levels, some still maintain that drug use is a right or otherwise not worth the cost of controlling. This harm reduction position is at odds with both supply control and all forms of prevention education — and increasingly at odds with treatment understood as having the goal of abstinence.

Many drug policy progressives now insist on medically supervised addiction. Such medication assisted treatment (MAT) amounts to government-supervised facilities for drug use (injection sites) or even government-supplied drugs for the addicted. The model here is the Netherlands, where endless, government-supported drug use is treated as a means of treating addiction. These addicts continue to be victimized by their own country, fostering a separate and profoundly dysfunctional underclass.

In the face of expanding supply, prevention and treatment efforts cannot be strategic — they can save individual lives, but new lives will be put at risk. This is merely squeezing an uncontained balloon. Moreover, if supply is reduced significantly, use and addiction will necessarily fall without respect to prevention and treatment efforts. The evidence of almost 50 years indicates that prevention and treatment efforts only contribute to strategic results when supply is reduced.

Prevention and treatment save lives, but their strategic effect is overwhelmed if supply and trafficking are not curtailed.

Policy proposals placing emphasis on reviving drug overdose victims mistake cause and effect. In the case of opioid addiction, the cause is the opioids themselves and increasingly, fentanyl. Revived addicts are still victims, and, sadly, many treated for opioid addiction will relapse in the face of burgeoning supply. Fentanyl and its variants are now driving the rapid rise in opioid deaths and drug overdoses in general. Information, albeit inadequate, suggests China is the source for these substances and the precursors to produce them. It seems there is no large-scale legitimate use for these chemicals outside of what is supposed to be controlled production for limited medical use — thus, industrial diversion is not a primary issue. Unfortunately, however, this means U.S. officials cannot attack fentanyl directly, but only via Chinese enforcement action.

China is likely to be sensitive to sustained pressure by authoritative American voices, whether from federal officials or prominent private individuals. America should ramp up this pressure soon. If executive branch officials cannot lead the charge, individuals from outside the executive, including members of Congress, should take the lead.

The Chinese are likely to act only in response to threats to their political or economic interests. Spurring them to act may require frequent confrontations over their performance in stopping fentanyl trafficking to the U.S. and Mexico. But sustained, genuine pressure works.

It is also possible that fentanyl and precursors are being trafficked from other Asian countries. Hence further — and swift — investigation is needed.

Bolstering Intelligence Resources

It is reasonable to anticipate that traffickers will seek to move production in response to pressure. If that happens, other Asian nations can be pressured by a range of escalating sanctions. Identification, especially public charging of foreign criminals, can be particularly helpful in disrupting trafficking operations, along with attacks on criminal funds and individuals through U.S. law.

An attack of sufficient power to collapse trafficking networks requires detailed intelligence. Such intelligence is also needed to prod foreign governments to act within their authority. Greater intelligence resources are also crucial for attacking trafficker finance, corruption operations, and measuring policy effectiveness. Attacking networks and responding to the drug epidemic requires comprehensive, real-time data. This data — from foreign intelligence services, domestic law enforcement agencies, and public health reports — should be fused into a strategic whole.

Fortunately, American intelligence has developed tools to attack such networked terrorist threats. At over 50,000 overdose deaths a year, the mass poisoning of drug trafficking is the most profound attack on America today. It is time to fully unleash intelligence tools on trafficking networks.

Without adequate intelligence, the magnitude of trafficking on the internet and “dark web” is unknown. Available information suggests it is significant, however. Federal drug enforcement has generally made electronic investigations a low priority, rejecting proposals to disrupt such markets by means of false sites, service denials, and cross-referencing data from multiple sources. All national security capacities are not yet deployed against opioid trafficking on the internet; this should change immediately. Past efforts to mount internet attacks by federal drug enforcement agencies have been crippled by ignorance, lack of experience, lack of vision, and complacency. The primary strategic goal should not just be to make future cases, but permanent market disruption; make it difficult to use the internet for trafficking by destroying the ability of buyers to connect with sellers.

Even the incomplete information on the opioid epidemic suggests that enforcement actions against pill mills and criminal physicians have reduced addiction and death driven by U.S. pharmaceutical sources. This has been a “supply control” success. Nonetheless, there is evidence of lower, but continued diversion. The pharmaceutical industry, the health insurance industry, and the federal government (the largest single health-care payer) all have information that should be brought together to identify and stop criminal diversion. The key point should be to focus attention on the biggest threat and its biggest components. There are regular reports of misuse of federal health-care funds to support addiction; some reports suggest areas where such practices are concentrated, which may serve as a starting point for enforcement actions.

Disrupting Networks Colombia is now back to producing more cocaine than it did prior to the dramatic drop in coca cultivation through Plan Colombia, which was largely due to the cooperation of former President Alvaro Uribe. Aside from a corresponding rise in cocaine overdose deaths, there are now reports of deaths resulting from cocaine-fentanyl mixtures. This deadly combination was seen about 10 years ago and may now be poised to cause harm on a greater scale. Much more fentanyl is available to Mexican traffickers carrying opioids and cocaine into the U.S. The Obama administration downplayed drug control in Colombia to pursue other goals. Colombian institutions are, again, put at risk by narcoterrorism. The previous security partnership needs reinvigoration, but the U.S. should make clear that the current trends are unacceptable for an ally and trading partner. A first step might be to have a government official or prominent private citizen warn the Colombian president that “if he doesn’t stop sending the cocaine, perhaps it is time to ask him to stop sending the coffee and the flowers.” Fortunately, former-president Uribe remains politically active and he knows how to attack the cocaine problem — Colombians would be wise to give him the job.

Contrary to the widespread belief that prescription diversion is driving the opioid crisis, available evidence indicates that most opioids and other illegal are produced outside the U.S. Further, these drugs seem to be arriving from Mexico. It is likely that most of them pass within six feet of a uniformed federal officer at our southern border. This is an unacceptable failure. Additional personnel will be useful, but the most important missing element is access to intelligence about trafficker operations. Enforcement agencies need to “see” into Mexico, and they need to see the structure of foreign and domestic trafficking networks.

Drug enforcement agencies and prosecutors need to treat individual cases as a means of network disruption, not as ends in themselves. In fact, it is likely that many smaller cases involving lesser charges that can be brought quickly will damage street-level trafficking networks more effectively than larger cases requiring longer investigations. In short, enforcement efforts need to become urgent and strategic.

Moreover, traffickers deserve stiff prison sentences. Such sentences are important leverage for turning traffickers against each other. Prison capacity for these death merchants must be made available to save lives. Enforcement pressure needs to be scaled to the threat.

Overall, drug enforcement management is insufficiently threat-based and seldom shifts resources rapidly to the greatest threats. While drug trafficking is killing more Americans than all other criminal activity combined, drug enforcement does not receive resources remotely proportional to the threat. The criminal-justice system is merely trying (and failing) to cope with the drug threat. It must come to see its mission as systematically destroying the threat — and plan, budget, and staff accordingly.

A Counter-Drug Strategy

An effective counter-drug strategy must attack at three points: source, distribution, and retail. If any one point of attack is particularly effective, it will substantially reduce use. It is probable, however, that the different points of attack will be effective in different degrees, while results will be cumulative and reinforcing.

At the retail level of street sales and use, the targets are whole communities, large geographic areas. Local and state efforts will be most important because there are insufficient federal resources to create the magnitude of the response required at the retail level. Local and state elements can be “enlisted” in a more unified national effort. That means encouraging and offering supplementary, strategic support with national personnel and resources.

Nevertheless, it may be critical to begin with willing state and local partners — those who commit their personnel and resources to the new strategy. These initial sites will also refine the elements of the strategy and demonstrate the effectiveness of more controversial components. Sites should be in priority areas and on as wide a scale as circumstances permit, but they should also be understood as points from which localized effort will flow outward — as ink spots on paper. Taking back individual communities in this way is an application of counterinsurgency concepts — it is also an established means of fighting epidemics.

At the retail level, the dealer and user are the center of gravity. Street-level enforcement needs to respond to opioid distribution as an immediate threat to life. Every sale can bring an overdose and every overdose can result in death. Each dealer is more like an active shooter than a house thief. Yet police response is frequently more focused on victim than on victimizer. The low-level dealer is also a low priority for enforcement personnel and prosecutors. This misguided policy is feeding the epidemic at the local level.

Accordingly, street-level enforcement should be reconceived in two ways. First, much greater urgency should be given to finding and incapacitating the dealer. Second, arresting users should be seen as a public health measure to screen for and treat addiction, as with the successful drug court model. Drug courts and diversion programs are already a major source of treatment admissions in the U.S. But this has been understood as a means of reducing the burden on the criminal-justice system. It should be seen as a necessary means of getting addicts who are in denial (as the vast majority are) into treatment and keeping them there through detoxification and stable sobriety. Street-level enforcement should be targeted to collapse dealer networks and should be tuned to become an intake channel for treatment.

All this will mean more arrests and more resources devoted to creating appropriate responses for users and dealers after arrest. Occasional, non-addicted users have a much lower probability of arrest at the point of drug sales because their purchases are infrequent. The risk to addicts is greater because they commonly need multiple doses per day. Thus, the normal pressure of street-level enforcement will tend to involve the larger dealers and the heavier users. Arrest and referral to treatment will save the lives of the addicted and even the arrest and warning of occasional users could be a potentially life-saving deterrent.

Such enforcement effort needs to be targeted, however. The obvious way to locate addicts and their dealers is to follow the reports of overdose victims. These reports provide a painful — but clear — geographic map of the epidemic. That map should be the basis for identifying priority areas nationally.

Currently, national information on overdose deaths lags by more than a year. This is unacceptable, and public health officials should be held accountable for creating a local, state, and national, real-time map of the epidemic. Preventing death means stopping traffickers and bringing effective outreach to the addicted in real time.

Finally, while attacking the source and border interdiction take the form of “outside-in” efforts, street enforcement and treatment involves an “inside-out” movement. Is this possible? Can individual communities make progress in the absence of full national success against the drug supply? Can a neighborhood-by-neighborhood strategy work?

Certainly, there is a risk of the epidemic moving back into improved areas from nearby trafficker enclaves. But, in fact, there are many law enforcement examples demonstrating that crime and drug trafficking is displaceable and containable with sustained, effective effort. The pace of the attack matters, and must run ahead of criminal replacement efforts. Local law enforcement agencies successfully contain certain crimes within specific geographic areas, and respond aggressively if criminals overstep boundaries. As in other matters, overwhelming the problem requires capable leadership with the authority, resources, and determination to prevail. For each part of the strategy above, it is important that one individual receive overall responsibility and that this individual understand that they will be removed in the absence of rapid progress. There is no accountability if there is no individual accountability.

The future of addiction in America rests on whether the supply of addictive drugs is dramatically reduced. The drug policy of the Trump administration will determine whether use and addiction are diminished or if they are more deeply embedded in American life — further expanding the underclass of addicted individuals living in misery and dying too young.

John P. Walters, chief operating officer of the Hudson Institute, was Director of National Drug Control Policy (2001–09).

Source: http://www.realclearpolicy.com/articles/2017/09/21/stopping_the_drug_epidemic_110362.html

Comment from Carla Lowe in the USA:

Hello from California,

A most informative article on the opioid epidemic from our friend John Walters. But I wonder how he would justify not addressing marijuana as a key link to this problem.

Perhaps he, like others far from California, is not aware of our 50,000 illegal marijuana grows, a 35 billion dollar business supplying 60% of the nation’s pot. And this is all in the name of so-called “medical” marijuana.

This situation will become significantly worse after January 1st when marijuana will be available just for fun for those over 21. Only Fools would think that kids’ use won’t rise in our formally golden state, now tragically turning green.

Please help us call on President Trump to enforce federal drug laws. It is absolutely our only hope in turning back this madness.

Carla Lowe CALMca.org

Comment from Dr. Stuart Reece in Australia

Yes John. The above is correct but only a partial analysis. Addiction is often based on the gateway drugs cannabis, alcohol and tobacco. Not only is this addictive basis not being addressed by current policies and practice but it is actively being sponsored by many US state Governments in the extremely false belief that reimbursement through taxation with compensate the community for the virtually endless destruction wrecked by drugs at all levels. Up till now the Feds have not addressed this issue either.

Worse still is what is being done to the next generation. It is not rocket science to observe that the children of these addicted patients are mostly not normal. This is very different to the rest of the community. Not only so but cannabis almost certainly underlies the international “gastroschisis epidemic” (where babies are born with their bowels hanging outside of their body) which no one is talking about, and is commonest in the youngest parents – because they smoke the most weed.

If we don’t start telling the truth about addiction in its totality the web of lies will engulf and enslave us all. The hardest hit will be the children and the poor. And, just as has happened in every single community across the globe in developed and developing nations, social decay and distress will become rampant and profligate.

Freedom begins with the truth – and showing a way out of our seductive mess – and breaking the spell of those who cannot wait to cash in on the collapse of the West.

[As illustrated in the Obituary of pioneering FDA scientist, Frances Oldham Kelsey in The Washington Post 8/8/15.]

THIS POST OBITUARY WAS A GODSEND, COMING JUST AS MANY POLITICAL LEADERS ARE BEGINNING A HEADLONG RUSH TO USURP FDA’S AUTHORITY TO APPROVE MARIJUANA-BASED MEDICINES IN FAVOR Of MONEY-CORRUPTED POLITICAL APPROVAL. THE ENDANGERED CITIZENRY, THEIR HEALTH PROFESSIONALS,POLITICAL LEADERS AND OBJECTIVE NEWS MEDIA JOURNALISTS , MUST STRONGLY RESIST THIS MISGUIDED ACTION BY POLTICIANS WHO ARE BLINDLY IGNORING THE HORRIFIC THALIDOMIDE PRECEDENT.

Edited excerpts with commentary follow: The full article is available at the following link:

http://www.washingtonpost.com/national/health-science/frances-oldham-kelsey-heroine-of-thalidomide-tragedy-dies-at-101/2015/08/07/ae57335e-c5da-11df-94e1-c5afa35a9e59_story.html

Frances Oldham Kelsey, FDA scientist who kept thalidomide off U.S. market, dies at 101

In the annals of modern medicine, it was a horror story of international scope: thousands of babies dead in the womb and at least 10,000 others in 46 countries born with severe deformities… The cause, scientists discovered by late 1961, was thalidomide, a drug that, during four years of commercial sales… was marketed to pregnant women as a miracle cure for morning sickness and insomnia.

The tragedy was largely averted in the United States, with much credit due to Frances Oldham Kelsey, a medical officer at the Food and Drug Administration in Washington, who raised concerns about thalidomide before its effects were conclusively known. For a critical 19-month period, she fastidiously blocked its approval while drug company officials maligned her as a bureaucratic nitpicker…

The global thalidomide calamity precipitated legislation…in October 1962 that substantially strengthened the FDA’s authority over drug testing. The new regulations, still in force, required pharmaceutical companies to conduct phased clinical trials, obtain informed consent from participants in drug testing, and warn the FDA of adverse effects, and granted the FDA with important controls over prescription-drug advertising…

In Washington, (Kelsey) joined a corps of reform-minded scientists who, although not yet empowered by the 1962 law that required affirmative FDA approval of any new drug, demanded strong evidence of effectiveness before giving their imprimatur.

At the time, a drug could go on the market 60 days after the manufacturer filed an application with the FDA… Meanwhile, pharmaceutical drug companies commonly supplied doctors with new drugs and encouraged them to test the product on patients, an uncontrolled and dangerous practice that relied almost entirely on anecdotal evidence. NICAP note: Much like today’s treatment of “medical marijuana.”

Thalidomide, which was widely marketed as a sedative as well as a treatment for pregnancy-related nausea during the first trimester of pregnancy, had proven wildly popular in Europe and a boon for its German manufacturer. NICAP note: Much like pro-pot propaganda today has created “wildly popular” support among a fact-deprived public, and boom-times for the Big Marijuana industry.

By the fall of 1960, a Cincinnati-based drug company, William S. Merrell, had licensed the drug and began to distribute it under the trade name Kevadon to 1,200 U.S. doctors in advance of what executives anticipated would be its quick approval by the FDA. NICAP note: Today, illegal drug companies produce and market hundreds of uncontrolled marijuana products and distribute them to corrupt doctors willing to “recommend” such unapproved marijuana “medicines.”

The Merrell application landed on Dr. Kelsey’s desk within weeks of her arrival at the agency…Immediately the application alarmed her. Despite what she called the company’s “quite fulsome” claims, the absorption and toxicity studies were so incomplete as to be almost meaningless. NICAP note: Much like the “quite fulsome claims” for pot medicines are legion today, as is the dearth of valid

studies verifying those claims. For the true documented scientific case against smoking weed as “medicine” see “The DEA Position on Marijuana” at link:

www.justice.gov/dea/docs/marijuana_position_2011.pdf

Dr. Kelsey rejected the application numerous times and requested more data. Merrell representatives, who had large potential profits riding on the application, began to complain to her bosses and show up at her office, with respected clinical investigators in tow, to protest the hold-up. NICAP note: Much as the Pot Legalization Lobbyists and ACLU show up at any attempts to limit sales and use of marijuana—and for the same reason: “large potential profits.”

Another reason for her concern was that the company had apparently done no studies on pregnant animals. At the time, a prevailing view among doctors held that the placental barrier protected the fetus from (harms from) what Dr. Kelsey once called “the indiscretions of the mother,” such as abuse of alcohol, tobacco or illegal drugs. Earlier in her career, however, she had investigated the ways in which drugs did in fact pass through the placenta from mother to baby… NICAP note: Today there are numerous valid studies showing that both mental and physical defects in children can be caused by a pregnant mother’s use of marijuana and other illegal drugs.

While Dr. Kelsey stood her ground on Kevadon, infant deaths and deformities were occurring at an alarming rate in places where thalidomide had been sold… NICAP note: Today, drug addiction, drug-related permanent disabilities and overdose deaths are “occurring at an alarming rate,” nearly all of which began with a shared joint of marijuana from a schoolmate or friend.

Dr. Kelsey might have remained an anonymous bureaucrat if not for a (previous) front-page story in The Post. The newspaper had received a tip about her from staffers working for Sen. Estes Kefauver, a Tennessee Democrat who had been stalled in his years-long battle with the pharmaceutical industry to bolster the country’s drug laws.

The coverage of Dr. Kelsey gave her — and Kefauver — a lift. As thousands of grateful letters flowed in to Dr. Kelsey from the public, the proposed legislation became hard to ignore or to water down. The new law was widely known as the Kefauver-Harris Amendments.

“She had a huge effect on the regulations adopted in the 1960s to help create the modern clinical trial system,” said Daniel Carpenter, a professor of government at Harvard University and the author of “Reputation and Power,” a definitive history of the FDA. “She may have had a bigger effect after thalidomide than before.”…

For decades, Dr. Kelsey played a critical role at the agency in enforcing federal regulations for drug development — protocols that were credited with forcing more rigorous standards around the world…

In Chicago, she helped Geiling investigate the 107 deaths that occurred nationwide in 1937 from the newly marketed liquid form of sulfanilamide, a synthetic antibacterial drug used to treat streptococcal infections. In tablet form, it had been heralded as a wonder-drug of the age, but it tasted unpleasant.

Because the drug was not soluble in water or alcohol, the chief chemist of its manufacturer, S.E. Massengill Co. of Bristol, Tenn., dissolved the sulfanilamide with an industrial substance that was a chemical relative of antifreeze. He then added cherry flavoring and pink coloring to remedy the taste and appearance.

Massengill rushed the new elixir to market without adequately testing its safety. Many who took the medicine — including a high number of children — suffered an agonizing death.

At the time, the FDA’s chief mandate, stemming from an obsolete 1906 law, was food safety. At the agency’s request, Geiling joined the Elixir Sulfanilamide investigation and put Dr. Kelsey to work on animal testing of the drug. She recalled observing rats as they “shriveled up and died.”

Amid national outrage over Elixir Sulfanilamide, Congress passed the Federal Food, Drug and Cosmetic Act of 1938, legislation that vastly expanded federal regulatory oversight over drugs and set a new benchmark for drug safety before marketing… NICAP note: Today, pro-pot politicians are rushing headlong into a massive campaign to block that objective FDA approval process for drugs and instead substitute a money-driven political process that will create a new “Thalidomide” out of marijuana and destroy many more American lives and futures.

Babies who suffered from the effects of thalidomide and survived grew up with a range of impairments. Some required lifelong home care… NICAP note: Is this to be the legacy of current politicians whose corrupt abandonment of the nation’s premier drug approval system will create generations of children “who suffered from the effects of POLITICAL APPROVED “medical” marijuana and survived with a range of impairments, some requiring lifelong home care?”

—————————————————————————————————————

Source: National Institute of Citizen Anti-drug Policy (NICAP)

NICAP COMMENTARY BY: DeForest Rathbone, Chairman.NICAP 8/9/15, Rev. 8/26/15

There is current research into the probable genotoxicity of marijuana and this has been likened to the harm to the foetus in the womb from the drug Thalidomide in the 1960’s.

In the annals of modern medicine, it was a horror story of international scope: thousands of babies dead in the womb and at least 10,000 others in 46 countries born with severe deformities. Some of the children were missing limbs. Others had arms and legs that resembled a seal’s flippers. In many cases, eyes, ears and other organs and tissues failed to develop properly. The cause, scientists discovered by late 1961, was thalidomide, a drug that, during four years of commercial sales in countries from Germany to Australia, was marketed to pregnant women as a miracle cure for morning sickness and insomnia.

The tragedy was largely averted in the United States, with much credit due to Frances Oldham Kelsey, a medical officer at the Food and Drug Administration in Washington, who raised concerns about thalidomide before its effects were conclusively known. For a critical 19-month period, she fastidiously blocked its approval while drug company officials maligned her as a bureaucratic nitpicker. Dr. Kelsey, a physician and pharmacologist later lauded as a heroine of the federal workforce, died Aug. 7 at her daughter’s home in London, Ontario. She was 101. Her daughter, Christine Kelsey, confirmed her death but did not cite a specific cause.

Dr. Kelsey did not single-handedly uncover thalidomide’s hazards. Clinical investigators and health authorities around the world played an important role, as did several of her FDA peers. But because of her tenacity and clinical training, she became the central figure in the thalidomide episode.

In July 1962, The Washington Post directed national attention on the matter — and on Dr. Kelsey — with a front-page article reporting that her “scepticism and stubbornness … prevented what could have been an appalling American tragedy.” [From 1962: ‘Heroine’ of FDA keeps bad drug off the market].

 

The global thalidomide calamity precipitated legislation signed by President John F. Kennedy in October 1962 that substantially strengthened the FDA’s authority over drug testing. The new regulations, still in force, required pharmaceutical companies to conduct phased clinical trials, obtain informed consent from participants in drug testing, and warn the FDA of adverse effects, and granted the FDA with important controls over prescription-drug advertising.

As the new federal law was being hammered out, Kennedy rushed to include Dr. Kelsey in a previously scheduled White House award ceremony honouring influential civil servants, including an architect of NASA’s manned spaceflight program.“In a way, they tied her to the moonshot in showing what government scientists were capable of,” said Stephen Fried, a journalist who investigated the drug industry in the book “Bitter Pills.” “It was an act of incredible daring and bravery to say we need to wait longer before we expose the American people to this drug.”

Dr. Kelsey became, Fried said, “the most famous government regulator in American history.”

‘I was the newest person there and pretty green’

Dr. Kelsey had landed at the FDA in August 1960, one of seven full-time medical officers hired to review about 300 human drug applications per year.The number of women pursuing careers in science was minuscule, but Dr. Kelsey had long been comfortable in male-dominated environments. Growing up in Canada, she spent part of her childhood in an otherwise all-boys private school. She had two daughters while shouldering the demands of medical school in the late 1940s.

In Washington, she joined a corps of reform-minded scientists who, although not yet empowered by the 1962 law that required affirmative FDA approval of any new drug, demanded strong evidence of effectiveness before giving their imprimatur.At the time, a drug could go on the market 60 days after the manufacturer filed an application with the FDA. If the medical officer determined that the submission was incomplete, the drug company could provide additional information, and the clock would start anew.

Meanwhile, pharmaceutical drug companies commonly supplied doctors with new drugs and encouraged them to test the product on patients, an uncontrolled and dangerous practice that relied almost entirely on anecdotal evidence. Thalidomide, which was widely marketed as a sedative as well as a treatment for pregnancy-related nausea during the first trimester of pregnancy, had proven wildly popular in Europe and a boon for its German manufacturer, Chemie Grünenthal.

By the fall of 1960, a Cincinnati-based drug company, William S. Merrell, had licensed the drug and began to distribute it under the trade name Kevadon to 1,200 U.S. doctors in advance of what executives anticipated would be its quick approval by the FDA.The government later estimated that more than 2.5 million tablets were given to about 20,000 patients, several hundred of whom were pregnant.

The Merrell application landed on Dr. Kelsey’s desk within weeks of her arrival at the agency. “I was the newest person there and pretty green,” she later said in an FDA oral history, “so my supervisors decided, ‘Well, this is a very easy one. There will be no problems with sleeping pills.’ ” Immediately the application alarmed her. Despite what she called the company’s “quite fulsome” claims, the absorption and toxicity studies were so incomplete as to be almost meaningless.

Dr. Kelsey rejected the application numerous times and requested more data. Merrell representatives, who had large potential profits riding on the application, began to complain to her bosses and show up at her office, with respected clinical investigators in tow, to protest the hold-up. Dr. Kelsey’s FDA superiors backed her as she conducted her research. By February 1961, she had found more evidence to support her suspicions, including a letter in the British Medical Journal by an English doctor who reported that his patients on thalidomide experienced a painful “tingling” in the arms and feet.

 

Dr. Kelsey also discovered that, despite warnings of side effects printed on British and German drug labels, Merrell had not notified the FDA of any adverse reactions.  Another reason for her concern was that the company had apparently done no studies on pregnant animals. At the time, a prevailing view among doctors held that the placental barrier protected the foetus from what Dr. Kelsey once called “the indiscretions of the mother,” such as abuse of alcohol, tobacco or illegal drugs. Earlier in her career, however, she had investigated the ways in which drugs did in fact pass through the placenta from mother to baby.

While Dr. Kelsey stood her ground on Kevadon, infant deaths and deformities were occurring at an alarming rate in places where thalidomide had been sold. The development of seal-like flippers, a condition known as phocomelia that previously affected an estimated 1 in 4 million infants, began to crop up by the dozens in many countries.

Clinical investigators, because of a variety of complications including spotty tracking systems, only belatedly made the link to thalidomide.  Grünenthal began pulling the drug from the market in Germany in late 1961. Health authorities in other countries issued warnings. Merrell waited until March 1962 to withdraw its U.S. application. By then, at least 17 babies were born in the United States with thalidomide-related defects, according to the FDA

Influence beyond thalidomide

Dr. Kelsey might have remained an anonymous bureaucrat if not for the front-page story in The Post. The newspaper had received a tip about her from staffers working for Sen. Estes Kefauver, a Tennessee Democrat who had been stalled in his years-long battle with the pharmaceutical industry to bolster the country’s drug laws. The coverage of Dr. Kelsey gave her — and Kefauver — a lift. As thousands of grateful letters flowed in to Dr. Kelsey from the public, the proposed legislation became hard to ignore or to water down. The new law was widely known as the Kefauver-Harris Amendments.

“She had a huge effect on the regulations adopted in the 1960s to help create the modern clinical trial system,” said Daniel Carpenter, a professor of government at Harvard University and the author of “Reputation and Power,” a definitive history of the FDA. “She may have had a bigger effect after thalidomide than before.”

In 1963, Dr. Kelsey was named chief of the FDA’s investigational drug branch. Four years later, she was named director of the new Office of Scientific Investigations, a position she held until 1995.  She spent another decade, until her retirement at 90, working at the FDA’s Center for Drug Evaluation and Research. In that role, she advised the director of its compliance office on scientific and medical issues and analyzed historical drug review issues.

According to historians of the FDA, she was instrumental in establishing the institutional review boards — a cornerstone of modern clinical drug development — that were created after abusive drug testing trials were exposed in prisons, hospitals and nursing homes. For decades, Dr. Kelsey played a critical role at the agency in enforcing federal regulations for drug development — protocols that were credited with forcing more rigorous standards around the world.

Name mistaken for a man’s

Frances Kathleen Oldham was born near Cobble Hill, on Vancouver Island, British Columbia, on July 24, 1914. Her father was a retired British army officer, and her mother came from a prosperous Scottish family.  The young “Frankie,” as she was called, grew up exploring the woods and shorelines, sometimes bringing home frogs for dissection. At McGill University in Montreal, she studied pharmacology — the effects of drugs on people — and received a bachelor’s degree in 1934 and a master’s degree in 1935.

A McGill professor urged her to apply for a research assistant job at the University of Chicago, where pharmacology professor Eugene Geiling accepted her without an interview. Geiling, who had mistaken the names Frances for the masculine Francis, addressed her by mail as “Mr. Oldham.”

“When a woman took a job in those days, she was made to feel as if she was depriving a man of the ability to support his wife and child,” Dr. Kelsey told the New York Times in 2010. “But my professor said: ‘Don’t be stupid. Accept the job, sign your name and put “Miss” in brackets afterward.’ ”

In Chicago, she helped Geiling investigate the 107 deaths that occurred nationwide in 1937 from the newly marketed liquid form of sulfanilamide, a synthetic antibacterial drug used to treat streptococcal infections. In tablet form, it had been heralded as a wonder-drug of the age, but it tasted unpleasant.Because the drug was not soluble in water or alcohol, the chief chemist of its manufacturer, S.E. Massengill Co. of Bristol, Tenn., dissolved the sulfanilamide with an industrial substance that was a chemical relative of antifreeze. He then added cherry flavouring and pink colouring to remedy the taste and appearance.

Massengill rushed the new elixir to market without adequately testing its safety. Many who took the medicine — including a high number of children — suffered an agonizing death.  At the time, the FDA’s chief mandate, stemming from an obsolete 1906 law, was food safety. At the agency’s request, Geiling joined the Elixir Sulfanilamide investigation and put Dr. Kelsey to work on animal testing of the drug. She recalled observing rats as they “shrivelled up and died.”

Amid national outrage over Elixir Sulfanilamide, Congress passed the Federal Food, Drug and Cosmetic Act of 1938, legislation that vastly expanded federal regulatory oversight over drugs and set a new benchmark for drug safety before marketing. Massengill’s owner ultimately was fined a maximum penalty of $26,000 for mislabelling and misbranding; by technical definition, an elixir contains alcohol.

‘We need to take precautions’

Dr. Kelsey received a doctorate from Chicago in 1938, then joined the faculty. In 1943, she wed a pharmacology colleague, Fremont Ellis Kelsey.  After graduating from Chicago’s medical school in 1950, Frances Kelsey taught pharmacology at the University of South Dakota medical school and was a fill-in doctor at practices throughout the state. She also became a U.S. citizen before arriving in Washington in 1960 when her husband was hired by the National Institutes of Health. He died in 1966 after a heart attack.

Survivors include their daughters, Susan Duffield of Shelton, Wash., and Christine Kelsey of London, Ontario; a sister; and two grandchildren. Dr. Kelsey moved to Ontario from suburban Maryland in 2014.

Babies who suffered from the effects of thalidomide and survived grew up with a range of impairment. Some required lifelong home care. Others held jobs and were not severely hindered by their disabilities. Many legal settlements were reached between drug companies and the victims of thalidomide, and new claims continue to surface. Grünenthal formally apologized to victims of thalidomide in 2012.

The drug, however, never disappeared entirely. Researchers have investigated thalidomide’s effects on H.I.V. and Crohn’s disease and have conducted clinical trials for on its use for rheumatoid arthritis and macular degeneration, a leading cause of blindness.

In 1998, the FDA approved the drug for the treatment of lesions from leprosy. In 2006, thalidomide was cleared for use with the medicine dexamethasone for certain cases of multiple myeloma, a cancer of the bone marrow.

The agency enforced strict safeguards, including pregnancy testing, for such new uses. “We need to take precautions,” Dr. Kelsey told an interviewer in in 2001, “because people forget very soon.”

Source:https://www.washingtonpost.com/national/health-science/frances-            oldham-kelsey-heroine-of-thalidomide-tragedy-dies-at-101/2015/08/07

Louise Stanger is a speaker, educator, licensed clinician, social worker, certified daring way facilitator and interventionist who uses an invitational intervention approach to work with complicated mental health, substance abuse, chronic pain and process addiction clients.

In the mid-to-late 2000s, Red Bull, an energy drink high on energy and low on nutritional value, made its North American debut with the famous “Red Bull gives you wings” campaign. The tag line, a nod to the “pick me up” qualities it gives to drinkers of the product, set the stage for the way in which teens and young adults relate to the nascent product category.

In essence, advertising birthed energy drinks as the way to find uplift, fight fatigue, and give that extra boost. Regrettably, no one was paying attention to the drinks’ negative side effects.

Red Bull has since spawned its own grocery store aisle of knock-offs – Monster, Rockstar, Full Throttle, Amp – to name a few. In 2016, U.S. retail sales of energy drinks topped $11 billion (Red Bull generated $5.1B in revenue in 2010). By comparison, that number is roughly how much Hollywood makes on movie tickets in a year.

Paradoxically, energy drinks’ meteoric rise in popularity and consumption has coincided with major health risks and the onslaught of addiction to other harmful substances. How did a drink that tastes like cough syrup land with such a huge impact?

Long before Red Bull “gave us wings,” Chaleo Yoovidhya, a Southeast Asian pharmacist, developed energy “tonics” aimed at labourers and truck drivers in the 1960s, according to The Dragonfly Effect, a book that looks at successful branding campaigns for products like energy drinks.

Then in the 1980s, an Austrian billionaire businessman named Dietrich Mateschitz discovered the tonics and married them with innovative guerrilla marketing to launch in North America. The aim was to put cans of Red Bull, the syrupy concoction of sugar and caffeine, in the hands of their target market: young adult males and teens who are oblivious to the drinks’ ingredients. The ad campaign struck like a lightning bolt and a multibillion dollar industry took ro

The key ingredient in energy drinks that gives the consumer energizing effects is caffeine. Though caffeine, found in commonly consumed drinks like coffee, tea and sodas, isn’t outright bad for you, the serving size, frequency and consumption patterns are cause for alarm.

Most energy drinks contain 70-200 milligrams of caffeine; for example, Rockstar 2X has 250 mg per 12 ounces, a 12 ounce can of Red Bull has 111 mg, and a 5-Hour Energy shot, a variation of the energy drink craze, is a whopping 207 mg of caffeine in just 2 ounces.

To put these concentration levels into perspective, the American Academy of Paediatrics maintains adolescents must not consume more than 100 mg of caffeine per day (it’s 500 mg for adults).

And more alarming than the serving sizes are the rates at which teens consume energy drinks. When young adults and teenagers get with their friends, they’ll consume 3-4 drinks in a short period of time or even chug (i.e. “shotgun”) whole cans in an instant. Despite this binge-style consumption, teens remain oblivious to the high caffeine content and unaware of the effects energy drinks have on the body. Other studies and researchers have observed energy drinks become the chaser for alcohol consumption in certain situations.

At these high levels of consumption, the Journal of the American Medical Association (JAMA) reports serious health risks associated with energy drinks. These include:

· Increased heart rate, irregularities and palpitations

· Increased blood pressure

· Sleep disturbances, insomnia

· Diuresis or increased urine production

· Hyperglycaemia (increased blood sugar), due to the high levels of sugar content, which may be harmful for people at risk for diabetes or already diabetic

Perhaps most dangerous are the serious side effects caused when energy drinks are consumed with alcohol. According to University Health News Daily, “the dangers of energy drinks mixed with alcohol are related to reduced sensation of intoxication and impaired judgment.”

Here’s how it goes: the user gets a burst of energy and alertness (increased heart rate and dilated blood vessels) from the high content of caffeine in the energy drink, prompting the person to feel less intoxicated and therefore drinking more alcohol and putting themselves at risk for alcohol poisoning and severely impaired judgment.

Teens, young adults and college-aged students who play drinking games or drink in high-risk environments such as parties, boating, swimming, beach days, etc. put themselves at greater risk of injury and bodily harm with these combinations.

In addition to high-risk environments and dangerous situations, energy drink and alcohol mixing lowers inhibitions, making room for engaging in high-risk behaviours such as unwanted sexual encounters, driving vehicles, boats and jet skis under the influence, and other behaviours that may lead to hospitalization or encounters with law enforcement.

We need look no further than the case of Four Loko, an energy drink that comes ready made with alcohol and caffeine for proof that mixing the two is dangerous. The drink gets its name from its four signature ingredients: alcohol, caffeine, taurine and guarana.

According to a report in The Week, the company that produced Four Loko, Phusion Projects of Chicago aka Drink Four Brewing Company, came under ethical fire for marketing to adolescents under the age of 21 (as most energy drink companies do – though this was the first to pre-mix alcohol and caffeine).

Four Loko also caught fire with college students and it didn’t take long for reports of blackouts and other alcohol overdose related incidents to take hold of its users. University campuses across the nation including the University of Rhode Island, Central Washington University and Worcester State University began to ban the beverage and companies with similar beverages have since reformulated its drinks and reduced its marketing toward underage students and young adults. In 2014, the company reached a settlement to stop production and distribution of Four Loko in the United States, according to a report in The Atlantic.

Moreover, the University of Maryland’s research on the topic has found a link between high energy drink consumption and developing addiction to other harmful substances later on. Researchers looked at the health and risk-taking habits of 1,099 college students over a four year period.

Their analysis of the study found that participants who consumed highly caffeinated drinks (energy drinks, sodas, etc.) are more likely to develop an addiction to cocaine, alcohol, or other substances when compared to students who did not consume such beverages. “The results suggest that energy drink users might be at heightened risk for other substance use, particularly stimulants,” says Amelia Arria, an associate professor and lead author of the study.

New research from Purdue University found that mixing alcohol and highly caffeinated drinks could significantly change the brain activity of a teenager. Dr. Richard van Rijn, the lead researcher, says “it seems the two substances (energy drinks and alcohol) together push [teenagers] over a limit that causes changes in their behaviour and changes the neurochemistry in their brains.”

Although energy drinks are regulated by the Food and Drug Administration, little oversight is given to labelling cans and packages with the risks related to consumption. As an educator, I believe the FDA must first do a better job of labelling. Just as cigarettes and alcohol have warning labels, so too must energy drinks.

Grocery stores should move energy drink products to areas where alcohol is sold – away from wandering young eyes. Public health discussions in high schools and middle schools need to take place. Youth and young adult sports teams must reconsider energy drink sponsorships and greater oversight concerning marketing practices toward under-aged youth.

As a young adult, if you do choose to consume these beverages, be sure to read the labels for serving sizes, caffeine content, and try to avoid mixing with alcohol. Parents, teachers, sports coaches, and community leaders must communicate to teenagers and young adults the harm energy drinks may cause. Together we must work together to be educated and informed against aggressive advertising to keep our teens and young adults healthy and engaged.

To learn more about Louise Stanger and her interventions and other resources, visit her website.

Source: http://www.huffingtonpost.com/entry/red-bull-monster-four-loko-rockstar-the-downside_us_59b021cce4b0bef3378cdcee    6th Sept.2017

 

 

 

Mathias B. Forrester and Ruth D. Merz

Hawaii Birth Defects Program, Honolulu, Hawaii, USA

Extracts from Study 

The literature on the association between prenatal illicit drug use and birth defects is inconsistent. The objective of this study was to determine the risk of a variety of birth defects with prenatal illicit drug use.

Data were derived from an active, population based adverse pregnancy outcome registry. Cases were all infants and foetuses with any of 54 selected birth defects delivered during 1986–2002.

The prenatal methamphetamine, cocaine, or marijuana use rates were calculated for each birth defect and compared to the prenatal use rates among all deliveries.

Among all deliveries, the prenatal use rate was 0.52% for methamphetamine,0.18% for cocaine, and 0.26% for marijuana.

Methamphetamine rates were significantly higher than expected for 14 (26%) of the birth defects.

Cocaine rates were significantly higher than expected for 13 (24%) of the birth defects.

Marijuana rates were significantly higher than expected for 21 (39%) of the birth defects. Increased risk for the three drugs occurred predominantly among birth defects associated with the central nervous system, cardiovascular system, oral clefts, and limbs. There was also increased risk of marijuana use among a variety of birth defects associated with the gastrointestinal system. Prenatal uses of methamphetamine, cocaine, and marijuana are all associated with increased risk of a variety of birth defects.

The affected birth defects are primarily associated with particular organ systems.

DISCUSSION

Using data from a Statewide, population-based registry that covered over 300,000 births and a 17-yr period, this investigation examined the association between over 50 selected birth defects and maternal use of methamphetamine, cocaine, or marijuana during pregnancy. Much of the literature on prenatal illicit drug use and birth defects involved case reports, involved a small number of cases, were not population-based, or focused on only one or a few particular birth defects.

There are various limitations to this investigation. The number of cases for many of the birth defects categories was relatively small, limiting the ability to identify statistically significant differences and resulting in large confidence intervals.

In spite of this, a number of statistically significant analyses were identified. Some statistically significant results might be expected to occur by chance. If 1 in every 20 analyses is expected to result in statistically significant differences solely by chance, then among the 162 analyses performed in this study, 8 would be expected to be statistically significant by chance. However, 48 statistically significant differences were identified. Thus, not all of the statistically significant results are likely to be due to chance.

This study included all pregnancies where methamphetamine, cocaine, or marijuana use was identified through either report in the medical record or positive toxicology test. This was done because neither self-report nor toxicology testing is likely to identify all instances of prenatal illicit drug use (Christmas et al., 1992).

In spite of using both methods for determining prenatal illicit drug use, all pregnancies involving methamphetamine, cocaine, or marijuana were not likely to have been identified. The degree of under ascertainment is unknown. A previous study examined the maternal drug use rate around the time of delivery in Hawaii during 1999 (Derauf et al., 2003). This study found 1.4% of the pregnancies involved methamphetamine use and 0.2% involved marijuana use. Among 1999 deliveries, the HBDP identified a prenatal methamphetamine use rate of 0.7% and a marijuana use rate of 0.4%. However, comparisons between the 2 studies should be made with caution because the previous study collected data from a single hospital during only a 2-mo period.

Another limitation is that the present study did not control for potential confounding factors such as maternal demographic characteristics, health behaviors, and prenatal care. Increased risk of birth defects has been associated with inadequate prenatal care (Carmichael et al., 2002), maternal smoking (Honein et al., 2001), and maternal alcohol use (Martinez-Frias et al., 2004).

These factors are also found with maternal illicit drug use (Cosden et al., 1997; Hutchins, 1997; Norton-Hawk, 1997). Thus the increased risk of selected birth defects with illicit drug use in this study might actually be due to one of these other underlying factors. Unfortunately, informationon some of the potential confounding factors such as socioeconomic status are not collected by the HBDP. Information collected on some other factors such as smoking and alcohol use is suspect because of negative attitudes toward their use during pregnancy. Moreover, the small number of cases among many of the birth defects groups would make controlling for these factors difficult.

Finally, this investigation included use of the illicit drugs at any time during the pregnancy. Most birth defects are believed to occur at 3–8 wk after conception (Makri et al., 2004; Sadler, 2000). In a portion of the cases, the drug use might have occurred at a time when it could not have caused the birth defect. Furthermore, this study does not include information on dose; however, teratogenicity of a substance may depend on its dose (Werler et al., 1990). In spite of the various potential concerns of the present study, data may suggest future areas of investigation where the limitations inherent in the present one are excluded.

This investigation found significantly higher than expected rates for prenatal use of methamphetamine, cocaine, and marijuana among a number of specific birth defects. Although not identical, there were general similarities between the three illicit drugs and the birth defects with which they were associated. Increased rates for methamphetamine, cocaine, and marijuana occurred predominantly among birth defects affecting the central nervous system, cardiovascular system, oral clefts, and limbs. There were also increased rates of marijuana use with a variety of birth defects associated with the gastrointestinal  system. With the exception of marijuana and encephalocele, none of illicit drugs were associated with neural-tube defects (anencephaly, spina bifida, encephalocele). The rates of use for the three illicit drugs were not significantly elevated with eye defects other than anophthalmia/microphthalmia, genitourinary defects, and musculoskeletal defects aside from limb defects.

In the majority of instances, the associations between particular illicit drugs and birth defects were found whether or not those cases involving use of multiple types of drugs were included.

Of the 14 significant associations between methamphetamine and specific birth defects, 10 (71.4%) remained once multiple drug cases were excluded. Corresponding rates were 61.5% (8 of 13) for cocaine and 81.0% (17 of 21) for marijuana.

The similarities in the patterns of birth defects with which methamphetamine, cocaine, and marijuana are associated might suggest that the three drugs exert similar effects on embryonic and foetal development. This might not be expected, considering that the three illicit drugs differ in their mechanisms of action and clinical effects (Leiken & Paloucek, 1998).

Some of the associations between methamphetamine, cocaine, and marijuana observed in the present investigation were previously reported. Other studies observed similar associations, or lack thereof, of methamphetamine or amphetamine with neural-tube defects (Shaw et al., 1996) and cardiovascular and musculoskeletal defects (McElhatton et al., 2000); cocaine with neural-tube defects (Shaw et al., 1996), cardiovascular defects (Lipshultz et al., 1991), ventricular septal defect and atrial septal defect (Ferencz et al., 1997c; Martin & Edmonds, 1991), tricuspid atresia (Ferencz et al., 1997d), craniosynostosis (Gardner et al., 1998), and situs inversus (Kuehl & Loffredo, 2002); and marijuana with neural-tube defects (Shaw et al., 1996), single ventricle (Steinberger et al., 2002), ventricular septal defect (Williams et al., 2004), tricuspid atresia (Ferencz et al., 1997d), and gastroschisis (Torfs et al., 1994).

In contrast, this study differed from other research with respect to their findings regarding methamphetamine or amphetamine and gastroschisis (Torfs et al., 1994); cocaine and microcephaly (Martin & Edmonds, 1991), conotruncal defects (Adams et al., 1989), endocardial cushion defect (Ferencz et al., 1997b), situs inversus (Ferencz et al., 1997a), oral clefts (Beatyet al., 2001), and genitourinary defects (Abe et al., 2003; Battin et al., 1995; Martin & Edmonds, 1991); and marijuana and conotruncal defects (Adams et al., 1989), Ebstein anomaly (Ferencz et al., 1997e; Correa-Villasenor et al., 1994), and oral clefts (Beaty et al., 2001).

The inconsistent findings between this and the other studies could be due to differences in study methodology, case classification, or number of cases. The mechanisms by which methamphetamine, cocaine, and marijuana might contribute to the rates for birth defects is currently unknown. Any potential explanation would have to take into account the observation that each of the illicit drugs was associated with a variety of specific birth defects affecting different organ systems. This might suggest that these three drugs would need to influence a basic, common factor involved in embryonic development.

Folic acid is involved in nucleic acid synthesis and cellular division (Scholl & Johnson, 2000) and thus would play an important role in the early growth and cellular proliferation of the embryo. Folic acid has been found to prevent a variety of birth defects (Forrester & Merz, 2005). Thus, anything that interferes with the activity of folic acid might be expected to increase the risk for these birth defects. Many of these birth defects were associated with methamphetamine, cocaine, and/or marijuana in the present study.

However, two of the birth defects most closely affected by folic acid—anencephaly and spina bifida—were not associated with any of the three illicit drugs. Vascular disruption has been suggested as a potential cause for a variety of different birth defects such as intestinal atresia/stenosis, limb reduction defects, and gastroschisis.

Since cocaine is a vasoconstrictor, it has been hypothesized that cocaine use could increase the risk of these vascular disruption defects (Hume et al., 1997; Martin et al., 1992; Hoyme et al., 1983; de Vries, 1980). Although this investigation found an association between cocaine and limb reduction deformities, no association was found with intestinal atresia/stenosis or gastroschisis.

In conclusion, this study found that prenatal use of methamphetamine, cocaine, or marijuana were associated with increased risk of a variety of birth defects. The affected birth defects were primarily associated with particular organ systems. Because of various limitations of the study, further research is recommended.

Source:  Journal of Toxicology and Environmental Health, Part A, 70: 7–18, 2007

MS Society says there is sufficient evidence of drug’s effectiveness to relax ban for patients with no other options

Ten thousand people with multiple sclerosis in the UK should be allowed to use cannabis legally in order to relieve their “relentless and exhausting” symptoms, experts in the disease have told ministers.

The MS Society claims the one in 10 sufferers of the condition whose pain and spasticity cannot be treated by medication available on the NHS should be able to take the drug without fear of prosecution.

The evidence on cannabis’s effectiveness, while not conclusive, is now strong enough that the government should relax the ban on the drug for MS patients who have no other treatment options, the society says in a report.

Doctors who treat MS patients have backed the society’s call, as have the Liberal Democrats and the Green party. Legalisation would ease “the extremely difficult situation in which many people with MS find themselves”, the charity said.

The society is calling for the first time for the 10,000 patients – one in 10 of the 100,000 people in Britain with MS – to be able to access cannabis without fear of arrest. It has changed its position after reviewing the evidence, consulting its medical advisers and seeking the views of 3,994 people who have the condition.

“We think cannabis should be legalised for medicinal use for people with MS to relieve their pain and muscle spasms when other treatments haven’t worked,” said Genevieve Edwards, the MS Society’s director of external affairs.

“The level of clinical evidence to support cannabis’s use for medicinal purposes is not conclusive. But there is sufficient evidence for our medical advisers to say that on the balance of probability, cannabis could benefit many people with MS experiencing pain and muscle spasms.” The charity is also urging NHS bosses to make Sativex, a cannabis-based drug used by some people with MS, available on prescription across the UK so that patients who can afford it no longer have to acquire it privately, at a cost of about £2,000 a year. Wales is the only home nation to provide the mouth spray through the NHS.

Patients’ inability to access Sativex on the NHS in England, Scotland and Northern Ireland “has resulted in many people with MS turning to illegal forms of cannabis as an alternative. It’s simply not right that some people are being driven to break the law to relieve their pain and spasticity. It’s also really risky when you’re not sure about the quality or dosage of what you’re buying,” Edwards said.

Norman Lamb, the Lib Dem health spokesman, said: “This is the strongest proof yet that the existing law on cannabis is a huge injustice that makes criminals of people whose only crime is to be in acute pain. This draconian law is potentially opening anything up to 10,000 MS sufferers to prosecution, and underlines why the Liberal Democrats have braved a tabloid backlash to campaign for the legalisation of cannabis. It is about time the government listened to the science.”

One in five (22%) MS patients who took part in a survey by the society said they had used cannabis to help manage their symptoms, but only 7% were still doing so. A quarter (26%) of those who had stopped taking it said they had done so out of fear of

prosecution. Another 26% of respondents had considered trying cannabis but had not done so for the same reason and also because they were concerned about the drug’s safety.

Doctors are divided over cannabis’s potential role in treating MS. Some are supportive while others are anxious about endorsing the use of a drug that can cause psychiatric problems. The Royal College of GPs said it was currently drawing up policy on the issue and could not comment. The Royal College of Physicians, which represents hospital doctors, said it had no policy on the issue.

Dr Willy Notcutt, a pain management specialist at the James Paget hospital in Norfolk, who has been treating MS patients for more than 20 years, said: “Every week I come across patients wishing to use cannabis to control their symptoms but who are unable to get proven drugs like Sativex from the NHS. Many patients seek illegal cannabis to get help. They can’t be sure of its origin but are being forced to commit a criminal act in order to obtain relief.”

Dr Waqar Rashid, a consultant neurologist at Brighton and Sussex University Hospitals NHS trust, said: “[Cannabis is] not a cure-all, and there are other treatments that should be tried first. But it makes sense for criminality not be a barrier to a treatment which could reduce the debilitating impact of symptoms and transform someone’s quality of life.”

Caroline Lucas, the Green party co-leader and its sole MP, said: “The MS Society’s new position is a big step forward, and recognises the fact that thousands of people with MS could benefit from the the use of medicinal cannabis. By rigidly sticking to criminalising cannabis the government drives MS sufferers to illegally acquire the drugs, thus putting themselves as risk of prosecution simply for searching for pain relief.” The National Institute for Health and Clinical Excellence (Nice), which advises the government, has told the NHS not to prescribe Sativex for spasticity because it is not cost-effective. The Home Office said: “This government has no plans to legalise cannabis. Cannabis is controlled as a Class B drug under the Misuse of Drugs Act 1971 and, in its raw form, currently has no recognised medicinal benefits in the UK.”

Case study: Steven Colborn, 55, from Seaham, County Durham

Imagine running a marathon while sharp pain darts up and down your legs. This is what multiple sclerosis feel like for me. When muscle spasticity kicks in my legs just twist and turn and bend back on themselves and it’s excruciatingly painful.

But three years ago I was offered a treatment that could help. During a regular appointment, a specialist nurse said they had managed to get a month’s supply of Sativex, a drug derived from cannabis, from the manufacturer.

The results were incredible. My muscle tension eased and I started to feel my legs moving better. I was able to get a good night’s sleep. I could exercise without getting as tired as quickly. For the first time in a long time I felt that I was managing my condition.

My month’s supply ran out and the drug wasn’t available free on the NHS. I was offered a muscle relaxer called Baclofen which hadn’t worked for me in the past.

I have been forced to pay for this drug myself. I can’t work any more so I rely on disability benefits. I have to save up a lot of money to be able to afford it – it costs £412 a month. Over the past four years I’ve only managed to buy about seven months’ worth.

I take Sativex but other people get similar relief from cannabis in its pure form. I don’t like taking this myself because of the narcotic effect, which you don’t get with Sativex. But for those it helps, it should be made legal.

I have had this illness for 36 years and every day I wake up and think ‘maybe there has been a breakthrough’. I know there will never be a cure, but I am just looking for a way to make things easier. Now I have been presented with something that offers me hope and the NHS say they cannot afford it. My question is: can you afford people like me getting worse?

Source:  https://www.theguardian.com/society/2017/jul/27/legalise-cannabis-as-treatment-of-last-resort-for-multiple-sclerosis-says-charity

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Comments by  NDPA:

UK  is 1st world nation with 1st world medicine approval system, even then we get things wrong e.g Thalidomide.

Cannabis based medicine is no problem if it goes through that system.

Sadly, ill people have been and are being exploited by the drug legalisation lobby, in furtherance of their nirvana of recreational cannabis for all.

Cannabis is a very harmful psychoactive drug, it induces dependency in around 1 in 9 or 10 users. It has numerous bad effects.

Smoking is obviously not a sensible delivery system for medication, yet a lot of those complaining want to smoke cannabis.

Cannabis based drugs like Sativex are in the pharmacopeia thanks to the wise licensing of the research on them by successive UK governments.

The mechanisms by which those cannabis based drugs are made available to  specific MS sufferers are a matter for the relevant authorities who deal with all pharmaceutical drugs. They must show efficacy and they must satisfy NICE.

There are no grounds at all for making cannabis any sort of special case, in fact the recreational user base and the legalisation lobby distort the arguments and would be better remaining silent.

Introduction  

On 31 July 2017 a court case commences in the Pretoria High Court about the constitutional legality of South Africa’s dagga legislation. The media is calling it the “Trial of the Plant”.

What is the “Trial of the Plant” about?

It is about the dagga plant and its prohibition in our society. Scientists have long since proven that the dagga plant is highly complex and dangerous and must be prohibited, but some believe it is not dangerous and even medicinal.

What does the law in SA say about dagga?

Except for medical and research exemptions, the possession, use, cultivation, transportation and distribution of dagga is criminalised in terms of the Drugs and drug trafficking act as well as the Medicines and related substances act.

Was the law not settled by the Constitutional court in 2002?

In 2002 a Rastafarian brought a case to the Constitutional Court about Dagga where he complained that the law prevented him smoking dagga as a religious observance and this violated his rights to religious freedom.

The court accepted that a Rastafarian’s religious rights were violated but dismissed the case as there is no objective way for law enforcement officials to distinguish between the possession or use of cannabis for religious or for recreational purposes.

The trial of the plant will in all likelihood be the final decider.

Why is that?

Because the Trial of the Plant will be the first and only case where there will be oral evidence given and tested, in the witness stand.

These other cases were fought and decided on affidavit evidence in a day or two.

The trial of the plant is very different and will take many days in court starting on 31 July and continuing through the month of August.

There are three legal teams comprising 6 attorneys, 11 advocates, 16 expert witnesses and as many as 12 other witnesses.  The trial will probably be recorded by the media and will also probably go all the way to the Constitutional Court to be finally decided.

DFL’s lead counsel is Adv Reg Willis instructed by the University of Pretoria Law Clinic.

How did this case start?

In 2010 a couple were arrested with approximately R500 000.00 worth of dagga in their home. They became known as the dagga couple.

To avoid prosecution they obtained an interdict in the Pretoria High Court against their prosecution, pending the outcome of a case to declare that all the SA dagga legislation is unconstitutional.

The case is against various government departments and against Doctors for Life International.

DFL joined this case to be of assistance to the State.

So for example DFL will lead the evidence of Harvard Professor Bertha Madras who is one of the foremost authorities on cannabis in the world. She contends that the legalisation of cannabis has to be resisted in the interests of the human brain.

Who is Doctors for Life and what does it do?

DFL is a non-profit relief and civil society organisation of doctors who care and give voluntarily of their own time and money to the many needs of the poor.

DFL serve the needs of the underprivileged communities they serve in South Africa and Southern Africa.  DFL also has an extensive track record of being involved in public interest cases predominantly as a friend of the court, especially to assist with scientific and similar evidence.

So then how is the dagga couple funding their case?

The dagga couple dragged the case out for some years, while they raised money.  They started an organisation called “Fields of Green for All” “FOGFA” which now has over 45000 supporters who are funding the case.

How important is this case for South Africa?

Given the role of dagga in crime, women and child abuse and the future of our youth, this trial is one of the most important to ever reach our courts.  If the dagga couple win their case as they want to, there will be no restriction on the possession, consumption, cultivation, transportation and distribution of cannabis.  A free for all.

Read our dagga court case press releases and more info on cannabis Media Release: High Court Blunders into Dagga Minefield

Source:  Letter from Johan Claassen  www.doctorsforlife.co.za) sent to Drugwatch International  27th July 2017

A new study provides credible evidence that marijuana legalization will lead to decreased academic success. (Elaine Thompson/AP)

The most rigorous study yet of the effects of marijuana legalization has identified a disturbing result: College students with access to recreational cannabis on average earn worse grades and fail classes at a higher rate. Economists Olivier Marie and Ulf Zölitz took advantage of a decision by Maastricht, a city in the Netherlands, to change the rules for “cannabis cafes,” which legally sell recreational marijuana. Because Maastricht is very close to the border of multiple European countries (Belgium, France and Germany), drug tourism was posing difficulties for the city. Hoping to address this, the city barred noncitizens of the Netherlands from buying from the cafes.

This policy change created an intriguing natural experiment at Maastricht University, because students there from neighboring countries suddenly were unable to access legal pot, while students from the Netherlands continued.

The research on more than 4,000 students, published in the Review of Economic Studies, found that those who lost access to legal marijuana showed substantial improvement in their grades. Specifically, those banned from cannabis cafes had a more than 5 percent increase in their odds of passing their courses. Low performing students benefited even more, which the researchers noted is particularly important because these students are at high-risk of dropping out. The researchers attribute their results to the students who were denied legal access to marijuana being less likely to use it and to suffer cognitive impairments (e.g., in concentration and memory) as a result.

Other studies have tried to estimate the impact of marijuana legalization by studying those U.S. states that legalized medicinal or recreational marijuana. But marijuana policy researcher Rosalie Pacula of RAND Corporation noted that the Maastricht study provide evidence that “is much better than anything done so far in the United States.”

States differ in countless ways that are hard for researchers to adjust for in their data analysis, but the Maastricht study examined similar people in the same location — some of them even side by side in the same classrooms — making it easier to isolate the effect of marijuana legalization. Also, Pacula pointed out that since voters in U.S. states are the ones who approve marijuana legalization, it creates a chicken and egg problem for researchers (i.e. does legalization make people smoke more pot, or do pot smokers tend to vote for legalization?). This methodological problem was resolved in the Maastricht study because the marijuana policy change was imposed without input from those whom it affected.

Although this is the strongest study to date on how people are affected by marijuana legalization, no research can ultimately tell us whether legalization is a good or bad decision: That’s a political question and not a scientific one. But what the Maastricht study can do is provides highly credible evidence that marijuana legalization will lead to decreased academic success — perhaps particularly so for struggling students — and that is a concern that both proponents and opponents of legalization should keep in mind.

Source:https://www.washingtonpost.com/news/wonk/wp/2017/07/25/these-       college-students-lost-access-to-legal-pot-and-started-getting-better-grades/?   

In his last article for Pro Talk, Renaming and Rethinking Drug Treatment, psychologist Robert Schwebel, Ph.D., author and developer of The Seven Challenges program, expressed his views about problems in typical drug and alcohol treatment. In this interview, he focuses on changes that he thinks would better meet the needs of individuals with substance problems.

The Seven Challenges Program

The Seven Challenges is described as “a comprehensive counselling program for teens and young adults that incorporates work on alcohol and other drug problems.” The program addresses much more than substance issues because it also helps young people develop better life skills, as well as manage their situational and psychological problems. Although there is an established structure for each session and a framework for decision-making (see website for the youth version of “The Seven Challenges”), it is not pre-scripted as in many traditional programs. Rather it is “exceptionally flexible, in response to the immediate needs of the clients.”

Independent studies funded by The Center for Substance Abuse Treatment and published in peer-reviewed journals have provided evidence that The Seven Challenges significantly decreases substance use of adolescents and greatly improves their overall mental health status. The program has been shown to be especially effective for the many young people with drug problems who also have trauma issues.

Just recently, a new version of The Seven Challenges program was introduced for adults and is being piloted in a research project. Soon, a book geared toward the general public by Dr. Schwebel that incorporates much of the philosophy of the program, as well as many of the decision-making and behavior change strategies, will be available.

Q&A: What Should Treatment Look Like?

Q: In your last article for Pro Talk, you argued strongly against the word “treatment” and suggested that we use the word “counselling” instead. Will you reiterate why you prefer using “counselling” when talking about professional help for people with substance problems?

Dr. S.: Counselling is an active and interactive process that’s responsive to the needs of individuals. It may include education, but it’s more than that because the information is personalized and offered in the context of a discussion about what’s happening in a person’s life. Effective counsellors help clients become aware of their options, expand those options, and make their own informed choices.

Treatment, on the other hand, sounds like something imposed and passive that an authority (say a doctor) does to someone else or tells them to do. It also implies recipients receive a standardized protocol or regime with a preconceived goal, usually abstinence when we’re talking about addiction. It doesn’t suggest autonomy of choice or collaboration.

 

Q: You stress the importance of choice and collaboration, suggesting both are important in addiction counselling. Please tell us more.

Dr. S.: In collaborative counselling that allows choices, clients get to identify the issues they want to work on. They make the decisions. We make it clear that we’re not there to make them quit using drugs…and couldn’t even if we tried. We tell them, “We’re here to support you in working on your issues, things that are important to you; things that are not going well in your life or as well you would like them to be going.”

We also support clients in decision-making about drugs. They set their own goals about using. One person might want to quit using, while another might want to set new limits. For those who want to change their drug use behavior, we check in with them about how they’re doing regarding their decision on a session-by-session basis. If they have setbacks, we’ll provide individualized support to help them figure out why, We’re not doubting them or trying to “catch” them. Rather, we’re helping them succeed with their own decisions to change. This type of check-in would not apply to individuals who have not yet decided to make changes.

 

Q: Many addiction programs feel that dealing with addiction should be the first priority and that other issues are secondary. What are your thoughts about this?

Dr. S.: I’ll start by saying that they have equal importance. Drug problems have everything to do with what is going on in a person’s life. And, a person’s life is very much affected by drug problems. I do want to say, however, that not everyone who winds up in an addiction program has an addiction. That’s a ridiculous generalization. They may be having problems with binge drinking, issues with family or jobs because of substance misuse, or legal problems because they were unlucky and got caught. (For instance they got arrested for another crime and tested positive for drugs.) They often wind up in places that require abstinence and wonder, “What am I doing here?” Then they’re told they’re “in denial.”

Traditional treatment tends to focus narrowly on drug problems, usually pushing an agenda of immediate abstinence. However, drug problems – whether or not they qualify as “addiction,” are very much connected to the rest of life. Therefore, clients need comprehensive counselling that addresses what’s happening in their overall lives and helps clients make their lives better. So it’s not all about use of substances and making the individual quit. The goal is to support clients and to help them make their own decisions about life and substance use.

We use the term “issues” – not “problems.” Whatever is most important to the individual that day is what we work on. A client might say, “I have an issue with my mother.” We don’t just want to have a discussion about the issue; we want to set a session goal so that a client gets practical help with an issue each time. Ideally we try to facilitate a next step, some sort of action that can be taken between sessions. We want to support our clients in making their own lives better. We like to reassure clients that we won’t be harping on drugs all the time: At least half of what we do is about everything else besides drugs. This means that counsellors need to know how to help people with their other problems. Unfortunately, many have a narrow background in drug treatment and don’t yet know how to do that.

 

Q: How do you address the issue of “powerlessness” which a number of young people have told me they struggled with in12-step treatment programs they’ve attended? Don’t adolescents by nature resist anything that threatens to take away their autonomy?

Dr. S.: One of our main messages is “You are powerful; people do take control over their drug use. You have that power within you.” We also say, “You don’t need to do it alone. You are entitled to support. We’re behind you. We’re not saying it’s easy and

there won’t be setbacks along the way. If there are, we’ll help you figure out why and how to handle it differently the next time. At the same time we’ll help you with other issues in your life so you’ll have less need for drugs.”

I think there is great harm in the all-or-nothing approach to drug and alcohol problems and that more people would come for help if they were not told that they’re powerless. Also, many more would come if they felt they could make a choice about drugs and did not expect to be coerced.

 

A New Version of The Seven Challenges

Following is the new adult version of Dr. Schwebel’s The Seven Challenges program:

· Challenging Yourself to Make Thoughtful Decisions About Your Life, Including Your Use of Alcohol and Other Drugs

· Challenging Yourself to Look at Your Responsibility and the Responsibility of Others for Your Problems

· Challenging Yourself to Look at What You Like About Alcohol and Other Drugs, and Why You Use Them

· Challenging Yourself to Honestly Look at Your Life, Including Your Use of Alcohol and Other Drugs

· Challenging Yourself to Look at Harm That Has Happened or Could Happen From Your Use of Alcohol and Other Drugs

· Challenging Yourself to Look at Where You Are Headed, Where You Would Like to Go, and What You Would Like to Accomplish

· Challenging Yourself to Take Action and Succeed With Your Decisions About Your Life and Use of Alcohol and Other Drugs

Source:  http://www.rehabs.com/pro-talk-articles/what-drug-and-alcohol-treatment-should-look-like-an-interview-with-dr-robert-schwebel/     17th July 2017

Medication-assisted treatment is often called the gold standard of addiction care. But much of the country has resisted it.

If you ask Jordan Hansen why he changed his mind on medication-assisted treatment for opioid addiction, this is the bottom line.

Several years ago, Hansen was against the form of treatment. If you asked him back then what he thought about it, he would have told you that it’s ineffective — and even harmful — for drug users. Like other critics, to Hansen, medication-assisted treatment was nothing more than substituting one drug (say, heroin) with another (methadone).

Today, not only does Hansen think this form of treatment is effective, but he readily argues — as the scientific evidence overwhelmingly shows — that it’s the best form of treatment for opioid addiction. He believes this so strongly, in fact, that he now often leads training sessions for medication-assisted treatment across the country.

“It almost hurts to say it out loud now, but it’s the truth,” Hansen told me, describing his previous beliefs. “I was kind of absorbing the collective fear and ignorance from the culture at large within the recovery community.” Hansen is far from alone. Over the past few years, America’s harrowing opioid epidemic — now the deadliest drug overdose crisis in the country’s history — has led to a lot of rethinking about how to deal with addiction. For addiction treatment providers, that’s led to new debates about the merits of the abstinence-only model — many of which essentially consider addiction a failure of willpower — so long supported in the US.

The case for prescription heroin

The Hazelden Betty Ford Foundation, which Hansen works for, exemplifies the debate. As one of the top drug treatment providers in the country, it used to subscribe almost exclusively to the abstinence-only model, based on an interpretation of the 12 steps of Alcoholics Anonymous and Narcotics Anonymous popularized in American addiction treatment in the past several decades. But in 2012, Hazelden announced a big switch: It would provide medication-assisted treatment.

“This is a huge shift for our culture and organization,” Marvin Seppala, chief medical officer of Hazelden, said at the time. “We believe it’s the responsible thing to do.”

From the outside, this might seem like a bizarre debate: Okay, so addiction treatment providers are supporting a form of treatment that has a lot of evidence behind it. So what?

But the growing embrace of medication-assisted treatment is demonstrative of how the opioid epidemic is forcing the country to take another look at its inadequate drug treatment system. With so many people dying from drug overdoses — tens of thousands a year — and hundreds of thousands more expected to die in the next decade, America is finally considering how its response to addiction can be better rooted in science instead of the moralistic stigmatization that’s existed for so long.

The problem is that the moralistic stigmatization is still fairly entrenched in how the US thinks about addiction. But the embrace of medication-assisted treatment shows that may be finally changing — and America may be finally looking at addiction as a medical condition instead of a moral failure.

The research is clear: Medication-assisted treatment works

One of the reasons opioid addiction is so powerful is that users feel like they must keep using the drugs in order to stave off withdrawal. Once a person’s body grows used to opioids but doesn’t get enough of the drugs to satisfy what it’s used to, withdrawal can pop up, causing, among other symptoms, severe nausea and full-body aches. So to avoid suffering through it, drug users often seek out drugs like heroin and opioid painkillers — not necessarily to get a euphoric high, but to feel normal and avoid withdrawal. (In the heroin world, this is often referred to as “getting straight.”)

Medications like methadone and buprenorphine (also known as Suboxone) can stop this cycle. Since they are opioids themselves, they can fulfil a person’s cravings and stop withdrawal symptoms. The key is that they do this in a safe medical setting, and when taken as prescribed do not produce the euphoric high that opioids do when they are misused. By doing this, an opioid user significantly reduces the risk of relapse, since he doesn’t have to worry about avoiding withdrawal anymore. Users can take this for the rest of their lives, or in some cases, doses may be reduced; it varies from patient to patient.

The research backs this up: Various studies, including systemic reviews of the research, have found that medication-assisted treatment can cut the all-cause mortality rate among addiction patients by half or more. Just imagine if a medication came out for any other disease — and, yes, health experts consider addiction a disease — that cuts mortality by half; it would be a momentous discovery.

“That is shown repeatedly,” Maia Szalavitz, a long time addiction journalist and author of Unbroken Brain: A Revolutionary New Way of Understanding Addiction, told me. “There’s so much data from so many different places that if you add methadone or Suboxone in, deaths go down, and if you take it away, deaths go up.” That’s why the biggest public health organizations — including the Centers for Disease Control and Prevention, the National Institute on Drug Abuse, and the World Health Organization — all acknowledge medication-assisted treatment’s medical value. And experts often describe it to me as “the gold standard” for opioid addiction care.

The data is what drove Hansen’s change in perspective. “If I wanted to view myself as an ethical practitioner and doing the best that I could for the people I served, I needed to make this change based on the overwhelming evidence,” he said. “And I needed to separate that from my personal recovery experience.”

Medication-assisted treatment is different from traditional forms of dealing with addiction in America, which tend to demand abstinence. The standards in this field are 12-step programs, which combine spiritual and moralistic ideals into a support group for people suffering from addiction. While some 12-step programs allow medication-assisted treatment, others prohibit it as part of their demand for total abstinence. The research shows this is a particularly bad idea for opioids, for which medications are considered the standard of care.

There are different kinds of medications for opioids, which will work better or worse depending on a patient’s circumstances. Methadone, for example, is only administered in a clinic, typically one to four times a day — but that means patients will have to make the trip to a clinic on a fairly regular basis. Buprenorphine is a take-home drug that’s taken once or twice a day, but the at-home access also means it might be easier to misuse and divert to the black market.

One rising medication, known as naltrexone or its brand name Vivitrol, isn’t an opioid — making it less prone to misuse — and only needs to be injected once a month. But it doesn’t work in the same way as methadone or buprenorphine. It requires full detoxification to use (usually three to 10 days of no opioid use), while buprenorphine, for example, only requires a partial detoxification process (usually 12 hours to two days). And instead of preventing withdrawal — indeed, the detox process requires going through withdrawal — it blocks the effects of opioids up to certain doses, making it much harder to get high or overdose on the drugs. It’s also relatively new, so there’s less evidence for its real-world effectiveness.

One catch is that even these medications, though the best forms of opioid treatment, do not work for as much as 40 percent of opioid users. Some patients may prefer not to take any medications because they see any drug use whatsoever as getting in the way of their recovery, in which case total abstinence may be the right answer for them. Others may not respond well physically to the medications, or the medications may for whatever reason fail to keep them from misusing drugs.

This isn’t atypical in medicine. What works for some people, even the majority, isn’t always going to work for everyone. So these are really first-line treatments, but in some cases patients may need alternative therapies if medication-assisted treatment doesn’t work. (That might even involve prescription heroin — which, while it’s perhaps counterintuitive, the research shows it works to mitigate the problems of addiction when provided in tightly controlled, supervised medical settings.)

Medication can also be paired with other kinds of treatment to better results. It can be used in tandem with cognitive behavioral therapy or similar approaches, which teach drug users how to deal with problems or settings that can lead to relapse. All of that can also be paired with 12-step programs like AA and NA or other support groups in which people work together and hold each other accountable in the fight against addiction. It all varies from patient to patient.

It is substituting one drug for another, but that’s okay

The main criticism of medication-assisted treatment is that it’s merely replacing one drug with another. Health and Human Services Secretary Tom Price recently echoed this criticism, saying, “If we’re just substituting one opioid for another, we’re not moving the dial much. Folks need to be cured so they can be productive members of society and realize their dreams.” (A spokesperson for Price later walked back the statement, saying Price supports all kinds of drug treatment.)

On its face, this argument is true. Medication-assisted treatment is replacing one drug, whether it’s opioid painkillers or heroin, with another, such as methadone or buprenorphine.

But this isn’t by itself a bad thing. Under the Diagnostic and Statistical Manual of Mental Disorders, it’s not enough for someone to be using or even physically dependent on drugs to qualify for a substance use disorder, the technical name for addiction. After all, most US adults use drugs — some every day or multiple times a day — without any problems whatsoever. Just think about that next time you sip a beer, glass of wine, coffee, tea, or any other beverage with alcohol or caffeine in it, or any time you use a drug to treat a medical condition.

The qualification for a substance use disorder is that someone is using drugs in a dangerous or risky manner, putting himself or others in danger. So someone with a substance use disorder would not just be using opioids but potentially using these drugs in a way that puts him in danger — perhaps by feeling the need to commit crimes to obtain the drugs or using the drugs so much that he puts himself at risk of overdose and inhibits his day-to-day functioning. Basically, the drug use has to hinder someone from being a healthy, functioning member of society to qualify as addiction.

The key with medication-assisted treatment is that while it does involve continued drug use, it turns that drug use into a much safer habit. So instead of stealing to get heroin or using painkillers so much that he puts his life at risk, a patient on medication-assisted treatment can simply use methadone or buprenorphine to meet his physical cravings and otherwise go about his day — going to school, work, or any other obligations.

Yet this myth of the dangers of medication-assisted treatment remains prevalent — to deadly results.

In 2013, Judge Frank Gulotta Jr. in New York ordered an opioid user arrested for drugs, Robert Lepolszki, off methadone treatment, which he began after his arrest. In January 2014, Lepolszki died of a drug overdose at 28 years old — a direct result, Lepolszki’s parents say, of failing to get the medicine he needed. In his defense,  Gulotta has continued to argue that methadone programs “are crutches — they are substitutes for drugs and drug cravings without enabling the participant to actually rid him or herself of the addiction.”

This is just one case, but it shows the real risk of denying opioid users medication: It can literally get them killed by depriving them of lifesaving medical care.

The myth is also a big reason why there are still restrictions on medication-assisted treatment. For example, the federal government still caps how many patients doctors can prescribe buprenorphine to, with strict rules about raising the cap. This limits how accessible the treatment is. A Huff Post analysis found that even if every doctor who can prescribe buprenorphine did so at the maximum rate in 2012, more than half of Americans with opioid use disorders could not get the medication. That’s on top of barriers to addiction treatment in general. According to a 2016 report by the surgeon general, just 10 percent of Americans with a drug use disorder obtain specialty treatment. The report attributed the low rate to severe shortages in the supply of care, with some areas of the country, particularly rural counties, lacking affordable options for treatment — which can lead to waiting periods of weeks or even months. Only recently has there been a broader push to fix this gap in care.

The medications used in treatment do carry some risks

None of this is to say that the medications used in these treatments are without any problems whatsoever. Methadone is tied to thousands of deadly overdoses a year, although almost entirely when it’s used for pain, not addiction, treatment — since it’s much more regulated in addiction care. Buprenorphine is safer in that, unlike common painkillers, heroin, and methadone, its effect has a ceiling — meaning it has no significant effect after a certain dose level. But it’s still possible to misuse, particularly for people with lower tolerance levels. And there are some reports of buprenorphine mills, where patients can get buprenorphine for misuse from unscrupulous doctors — similar to how pill mills popped up during the beginning of the opioid epidemic and provided patients easy access to painkillers.

Naltrexone, meanwhile, can heighten the risk of overdose and death in case of full relapse. Overdose and death are risks in any case of relapse, but they’re particularly acute for naltrexone because it requires a full detox process that eliminates prior tolerance. (Although this would typically require someone to stop taking naltrexone, since otherwise it blocks the effects of opioids up to certain doses.)

But when taken as prescribed, the medications are broadly safe and effective for addiction treatment. For regulators, it’s a matter of making sure the drugs aren’t diverted into misuse, while also providing good access to people who genuinely need them.

The fight over medication-assisted treatment is really about how we see addiction

Behind the arguments about medication-assisted treatment is a simple reality of how Americans view addiction: Many still don’t see it, as public health officials and experts do, as a disease.

With other diseases, there is no question that medication can be a legitimate answer. That medication is not viewed as a proper answer by many to addiction shows that people believe addiction is unique in some way — particularly, they view addiction as at least partly a moral failing instead of just a disease.

I get emails all the time to this effect. Here, for example, is a fairly representative reader message: “Darwin’s Theory says ‘survival of the fittest.’ Let these lost souls pay the price of their criminal choices and criminal actions. Society does not owe them multiple medical resuscitations from their own bad judgment, criminal activity, and self-inflicted wounds.”

This contradicts what addiction experts broadly agree on. As Stanford psychiatrist and Drug Dealer, MD author Anna Lembke put it, “If you see somebody who continues to use despite their lives being totally destroyed — losing their jobs, losing loved ones, ending up in jail — nobody would choose that. Nobody anywhere would ever choose that life. So clearly it is beyond this individual’s control on some level.”

Many Americans may understand this with, say, depression and anxiety. We know that people with these types of mental health problems are not in full control of their thoughts and emotions. But many don’t realize that addiction functions in a similar way — only that the thoughts and emotions drive someone to seek out drugs at just about any cost.

Some of the sentiment against medications, as Hansen can testify, is propagated by people suffering from addiction. Some of them believe that any drug use, even to treat addiction, goes against the goal of full sobriety. They may believe that if they got sober without medications, perhaps others should too. Many of them also don’t trust the health care system: If they got addicted to drugs because a doctor prescribed them opioid painkillers, they have a good reason to distrust doctors who are now trying to get them to take another medication — this time for their addiction.

The opioid epidemic, however, has gotten a lot of people in the addiction recovery world to reconsider their past beliefs. Funeral after funeral and awful statistic after awful statistic, there is a sense that there has to be a better way — and by looking at the evidence, many have come to support medication-assisted treatment.

“I remember sitting there,” Hansen said, speaking to his experience at a funeral, as a mother sang her dead son a lullaby, “thinking that we have to do better.”

Source:  German Lopez@germanrlopezgerman.lopez@vox.com  Jul 20, 2017

 

Medical Illness Model:

Near the end of the Second World War researchers and leaders in the recovery community jointly formulated the problem of uncontrolled drinking into what is now known as the Disease Model of alcoholism. This model postulates that, like medical illnesses, alcoholism–more specifically alcohol dependence, or addiction—can be diagnosed, its course observed, and its physical causes understood.

Further, scientific trials can be undertaken to identify the best treatments for those who suffer from it. The diagnosis of Alcohol Dependence, in this model, rested on four symptoms: 1) a tolerance to alcohol in which a person needs to drink ever greater amounts to reach a desired effect, 2) withdrawal symptoms, such as “the shakes” and others, on stopping use, 3) the Loss of Control phenomenon in which affected persons lose the ability to control how much they drink at a sitting and thereby can no longer predict how much they will drink from one episode to the next, and 4) social or physical impairment resulting from combinations of the first three symptom categories1.

This model pictures a condition from which many alcohol dependent people emerge every year, and into which many others return. View as a disease, alcoholism takes on the characteristics of a remitting-relapsing illness with primary symptoms that direct us to brain functioning. And, because ethyl alcohol is a very small molecule with easy access to most parts of the body, moderate to heavy alcohol use often injures other organs, such as the liver and heart among others.

Uncontrolled, or dependent, alcohol use also affects the social network setting of family as well as work activities, friendships, and legal involvement. Last, however, the Disease model brings with it the possibilities of treatment and of hope. At this date, effective medicinal agents against alcoholism are very few. But hope, that necessary ingredient for recovery, waxes strong in the illness model. In the words of the alcoholic patient quoted in the Part 2, “It is much easier to think of myself as an ill person working to become well, rather than a bad person trying to become good.”

Genetic Models:

From the Disease model has come another, that of genetic influence. The observation that alcoholism often runs in families for many years meant that family cultures or mores determined who would become alcoholic and who would not. While it is clear that cultural and family life influences are very powerful, more recent studies have noted that an underlying genetic disposition may be at play in some genealogical lines2. If so, the evidence suggests a confluence of many gene effects rather than the dominant/recessive results of inheritance in Mendelian models of genetic death, as for example, in Huntington’s Disease.

Instead, the gene effects seem to have more to do with the vulnerability towards alcoholism. One form appears in those who have a genetically-based insensitivity to alcohol—an “inborn tolerance,” and develop alcohol dependence at much higher rates than alcohol sensitive comparison groups. Another form may require a combination of

gene influences and environment conditions to come together to result in alcohol-plus-multiple drug dependence, sometimes referred to as Type 2 or Type B alcoholics.

Unexpectedly, the news of gene involvement was greeted with enthusiasm among some quarters of the actively drinking alcoholic public: “Since alcoholism is genetic, we can’t escape our genes and may as well keep drinking.” As with older models however, the element of choice remains present in the sober periods between drinking episodes. As some of the other models suggest, healing from alcoholism remains an individual process.

Psychological Adaptation Models in Illness and Recovery:

Further modern research asks that we look at individuals and their abilities to adapt to the stresses of life. Careful observation has established that individual humans have the ability to adapt creatively to the painful thoughts and feelings of living and to do so in ways that connect us together rather than drive us apart3. This model of Mature human psychological adaptation, however, emphasizes that the brain function at its healthy best. Heavy, continuous use of alcohol carries often subtle, if severe, effects on the brain that are as yet poorly understood.

But we know they exist because of their effects in driving down the ability to adapt, from psychological Maturity to much more rigid Primitive mechanisms of coping, such as when an alcoholic “denies” that an obvious problem exists at all. This kind of Denial can occur in the actively drinking alcoholic who understands that resolving his or her ambivalence toward drinking is too painful to contemplate; therefore, a failure to perceive the problem seems preferable than facing it.

So it is that the Adaptation model views the First of the Twelve Steps as addressing primitive Denial in coming to recognize that the individual’s alcoholism exists. Progressing along the continuum of the Steps leads finally to the Twelfth: helping others who have the same problem. In the Psychological Adaptation model, this exemplifies the Mature mechanism of Altruism: selflessly helping others. The occurrence of brain healing as abstinence continues—along with the progression towards psychological maturity, whether viewed in the Psychological Adaptation or the Twelve Step models—suggests that brain recovery process are at work. We can only recognize their existence at this point, and need to understand their biology if we are to improve treatments in the Disease model.

Many Models, More Questions:

With this overview of the different model formulations of the problem of alcoholism and what to do about it, we are now ready to look as specific questions from a scientific point of view. As this series unfolds, we will have recourse to use all of the models mentioned—now adding the crucial ingredient of evidence, systematically gathered. In future Updates, the discussion will focus on specific problems and what we can learn about them.

Source:  https://www.ncadd.org/blogs/research-update/models-of-alcoholism-medical-physiological-causes  14th Jan. 2014

Cannabis is the most widely used illicit drug in the United States, and trends show increasing use in the general population. As cannabis consumption rises, there has been significant emerging evidence for cannabis-related risks to health.1

Numerous lines of evidence suggest a correlation between cannabis consumption and a variety of psychiatric conditions, including cannabis-induced psychosis (CIP). While it can be difficult to differentiate CIP from other psychoses, CIP holds distinguishing characteristics, which may aid in its diagnosis. Given the increasing push toward cannabis legalization, assessing CIP and employing timely treatments is critical.

Specifically in youth, there is a direct relationship between cannabis use and its risks. The lack of knowledge surrounding its detrimental effects, combined with misunderstandings related to its therapeutic effects, has potential for catastrophic results.

CASE VIGNETTE

Ms. J, a 19-year-old college sophomore, was admitted to the Early Psychosis Unit at the Centre for Addiction and Mental Health (CAMH) displaying signs of agitation and acute psychosis. Her roommates had noted that her behavior had become increasingly bizarre, and she had isolated herself over the past month. She began smoking marijuana at the age of 17 and since starting college used it daily.

Ms. J exhibited signs of paranoia, believing other students in her dorm were stealing from her and trying to poison her. She remained adamant that all her problems were rooted in the competitive environment of the university and that smoking marijuana aided in keeping her sanity. In a sense, she was self-medicating. Her clinical presentation was consistent with a diagnosis of CIP.

After the hospitalization, she received outpatient case management services in the Early Psychosis Program at CAMH, which included motivational interviewing to raise her awareness about the importance of abstaining from cannabis use. She has been abstinent from cannabis for more than a year with no evidence of psychosis; she recently returned to school to finish her degree.

Epidemiology of CIP

Reports have shown a staggering increase in cannabis-related emergency department (ED) visits in recent years. In 2011, the Substance Abuse and Mental Health Services Administration (SAMHSA) and Drug Abuse Warning Network (DAWN) estimated a total of 1.25 million illicit-drug–related ED visits across the US, of which 455,668 were marijuana related.2 A similar report published in 2015 by the Washington Poison Center Toxic Trends Report showed a dramatic increase in cannabis-related ED visits.3 In states with recent legalization of recreational cannabis, similar trends were seen.4

States with medicinal marijuana have also shown a dramatic rise in cannabis-related ED visits. Moreover, states where marijuana is still illegal also showed increases.5 This widespread increase is postulated to be in part due to the easy accessibility of the drug, which contributes to over-intoxication and subsequent symptoms. Overall, from 2005 to 2011, there has been a dramatic rise in cannabis-related ED visits among all age groups and genders.

Neurobiology of CIP

Cannabis is considered an environmental risk factor that increases the odds of psychotic episodes, and longer exposure is associated with greater risk of psychosis in a dose-

dependent fashion. The drug acts as a stressor that leads to the emergence and persistence of psychosis. While a number of factors play a role in the mechanism by which consumption produces psychosis, the primary psychoactive ingredient is considered to be delta 9-tetrahydrocannabinol (delta9-THC). Properties of delta9-THC include a long half-life (up to 30 days to eliminate the long-acting THC metabolite carboxy-THC from urine) and high lipophilicity, which may contribute to CIP.

During acute consumption, cannabis causes an increase in the synthesis and release of dopamine as well as increased reuptake inhibition, similar to the process that occurs during stimulant use. Consequently, patients with CIP are found to have elevated peripheral dopamine metabolite products.

Findings from a study that examined presynaptic dopaminergic function in patients who have experienced CIP indicate that dopamine synthesis in the striatum has an inverse relationship with cannabis use. Long-term users had reduced dopamine synthesis, although no association was seen between dopaminergic function and CIP.6 This observation may provide insight into a future treatment hypothesis for CIP because it implies a different mechanism of psychosis compared with schizophrenia. As cannabis may not induce the same dopaminergic alterations seen in schizophrenia, CIP may require alternative approaches—most notably addressing associated cannabis use disorder.

Polymorphisms at several genes linked to dopamine metabolism may moderate the effects of CIP. The catechol-o-methyltransferase (COMT Val 158Met) genotype has been linked to increased hallucinations in cannabis users.7Homozygous and heterozygous genetic compositions (Met/Met, Val/Met, Val/Val) for COMT Val 158Met have been studied in patients with CIP and suggest that the presence of Val/Val and Val/Met genotypes produces a substantial increase in psychosis in relation to cannabis use. This suggests that carriers of the Val allele are most vulnerable to CIP attacks.

There has been much controversy surrounding the validity of a CIP diagnosis and whether it is a distinct clinical entity or an early manifestation of schizophrenia. In patients being treated for schizophrenia, those with a history of CIP had an earlier onset of schizophrenia than patients who never used cannabis.8Evidence suggests an association between patients who have received treatment for CIP and later development of schizophrenia spectrum disorder. However, it has been difficult to distinguish whether CIP is an early manifestation of schizophrenia or a catalyst. Nonetheless, there is a clear association between the 2 disorders.

Assessment of CIP

DSM-5 categorizes cannabis-induced psychotic disorder as a substance-induced psychotic disorder. However, there are distinguishing characteristics of CIP that differentiate it from other psychotic disorders such as schizophrenia. Clear features of CIP are sudden onset of mood lability and paranoid symptoms, within 1 week of use but as early as 24 hours after use. CIP is commonly precipitated by a sudden increase in potency (eg, percent of THC content or quantity of cannabis consumption; typically, heavy users of cannabis consume more than 2 g/d). Criteria for CIP must exclude primary psychosis, and symptoms should be in excess of expected intoxication and withdrawal effects. A comparison of the clinical features of idiopathic psychosis versus CIP is provided in the Table.

When assessing for CIP, careful history taking is critical. Time of last drug ingestion will indicate if a patient’s psychotic symptoms are closely related to cannabis intoxication/withdrawal effects. While acute cannabis intoxication presents with a range of transient positive symptoms (paranoia, grandiosity, perceptual alterations), mood symptoms (anxiety), and cognitive deficits (working memory, verbal recall, attention), symptoms that persist beyond the effects of intoxication and withdrawal are better categorized as CIP, regardless of the route of administration (smoke inhalation, oral, intravenous). CIP has historically been associated with fewer negative symptoms than schizophrenia; however, without a clear timeline of use, distinguishing schizophrenia from CIP may prove difficult.

A diagnosis of primary psychosis (eg, schizophrenia) is warranted in the absence of heavy cannabis use or withdrawal (for at least 4 weeks), or if symptoms preceded onset of heavy use. The age at which psychotic symptoms emerge has not proved to be a helpful indicator; different studies show a conflicting median age of onset.

Clinical features of schizophrenia and CIP share many overlapping characteristics. However, compared with primary psychoses with concurrent cannabis abuse, CIP has been established to show more mood symptoms than primary psychosis. The mood symptom profile includes obsessive ideation, interpersonal sensitivity, depression, and anxiety. Of significance is the presence of social phobia: 20% of patients with CIP demonstrate phobic anxiety compared with only 3.8% of patients with primary psychosis with cannabis abuse.

Hypomania and agitation have also been found to be more pronounced in cases of CIP.9 Visual hallucinations are more common and more distinct in CIP than in other psychoses such as schizophrenia. Perhaps the most discriminating characteristic of CIP is awareness of the clinical condition, greater disease insight, and the ability to identify symptoms as a manifestation of a mental disorder or substance use. The presence of much more rapidly declining positive symptoms is another distinctive factor of CIP.

Finally, family history may help distinguish CIP from primary psychosis. Primary psychosis has a strong association with schizophrenia and other psychotic disorders in first- or second-degree relatives, whereas CIP has a weaker family association with psychosis.

Treatment of CIP

As with all substance-induced psychotic states, abstinence from cannabis may be the definitive measure to prevent recurrence. With limited research surrounding CIP, achieving symptomatic treatment during acute phases of CIP has proved to be difficult. The Figure suggests possible treatment progression for CIP.

Pharmacotherapeutic interventions include the second-generation antipsychotic drug olanzapine and haloperidol. While both are equally effective, their different adverse- effect profiles should be taken into consideration when treating a patient; olanzapine is associated with significantly fewer extrapyramidal adverse effects.

One report indicates that antipsychotics worsened the condition in some patients.10 Conventional antipsychotics failed to abate the symptoms of CIP in one 20-year old man. Trials of olanzapine, lithium, and haloperidol had little to no effect on his psychosis. Risperidone was tried but elicited temporal lobe epilepsy with auditory, somatic, and olfactory hallucinations. However, the use of valproate sodium markedly improved his symptoms and cognition, returning him to baseline.

Carbamazepine has also been shown to have rapid effects when used as an adjunct to antipsychotics.11 Use of anti-seizure medication in CIP treatment has been hypothesized to reduce neuroleptic adverse effects, resulting in better tolerance of antipsychotics.10,11 These results suggest the use of adjunctive anti-epileptics should be considered in CIP treatment strategies, although further studies in a broad range of patients with CIP are needed.

Abstaining from cannabis is the most beneficial and effective measure for preventing future CIP events; however, it is likely to be the most difficult to implement.

Psychosocial intervention has a significant impact on early-phase psychosis, and when the intervention is initiated plays a role in disease outcomes. A delay in providing intensive psychosocial treatment has been associated with more negative symptoms compared with a delay in administrating antipsychotic medication.12 Employing cannabis- focused interventions with dependent patients who present with first-episode psychosis can decrease use in a clinically meaningful way and subjectively improve patient quality of life.

Compared with the standard of care, motivational interviewing significantly increases number of days abstinent from cannabis and aids in decreasing short-term consumption.13 Patients who are treated with motivational interviewing in addition to standard of care (combination of antipsychotic medication, regular office-based psychiatric contact, psychoeducation) are reported to also have more confidence and willingness to reduce cannabis use.

Patients with CIP who are unwilling or unable to decrease cannabis consumption may be protected from psychotic relapse with aripiprazole (10 mg/d). Its use suppresses the re-emergence of psychosis without altering cannabis levels. However, no direct comparison has been made with aripiprazole and other antipsychotics in treating CIP. Clearly, well-controlled large studies of putative treatments for CIP are needed.

Conclusions

As more countries and states approve legalization, and marijuana becomes more accessible, CIP and other cannabis-related disorders are expected to increase. Efforts should be made by physicians to educate patients and discourage cannabis use. Just as there was an era of ignorance concerning the damaging effects of tobacco, today’s conceptions about cannabis may in fact be judged similarly in the future. The onus is on psychiatrists to take an evidence-based approach to this increasing problem.

Source:  http://www.psychiatrictimes.com/substance-use-disorder/cannabis-induced-psychosis-review  14th July

New Hampshire has the second-highest rate of drug overdoses in the country. Eric Adams in Laconia (population 16,000) has been assigned one task to stop them.

Eric Adams is a handsome, clean-shaven man, almost 41, with a booming voice and hair clipped short enough for the military, which once was an ambition of his. After high school, he tried to join the Marines but was turned away because of his asthma. He needed three different inhalers then, plus injections. Today he has outgrown the problem. He is 5-foot-10, weighs 215 pounds and can dead lift 350.

Adams has worked in law enforcement for almost two decades.

He began as a guard at the New Hampshire state prison, where he asked to work in maximum security, then left to become a police officer in Tilton and was soon recommended for the Drug Task Force, a statewide operation against narcotics dealers. Adams grew his hair long and arranged undercover buys, a Glock 27 concealed in a holster beneath his jeans. Later he would return wearing a bulletproof vest, surrounded by fellow officers, to kick in the door with his pistol drawn.

Eric Adams in his office at the Laconia Police Department.
CreditNatalie Keyssar for The New York Times

Laconia, where Adams works today, is a former mill town in central New Hampshire surrounded by lakes. In midwinter, Laconia is home to 16,000 residents, though in summer that number swells to 30,000. Those are gleaming, sun-dappled days. Then winter falls on New England like a gavel.

A blight in the region is especially acute. Of the 13 states with the highest death rates from drug overdoses, five are in New England. New Hampshire in particular has more per capita overdose deaths than anywhere but West Virginia. In 2012, the state had 163 such deaths, a majority of them (as elsewhere in the country) from heroin and prescription opioids. In 2015, the state had nearly 500 deaths, the most in its history. In Manchester, its largest city, the police seized more than 27,000 grams of heroin that year, up from 1,314 grams a year earlier. In certain neighborhoods, a single dose of heroin can cost less than a six pack of Budweiser. Waiting lists for treatment programs stretch as long as eight weeks.

Those years spent guarding prisoners, and later kicking down doors, changed Adams’s thinking. So many of the drug users he saw had made one bad decision and then became chained to it, Adams realized. Or they had begun on a valid prescription for pain medication, after an injury, and then grew addicted. When refills grew scarce, they turned to alternatives. Many were no longer even using to get high, only to avoid the agony of withdrawal.

They were teenaged, middle-aged and elderly; they were students, bankers and grocery clerks. They were businesswomen with six-figure salaries and homeless men with shopping carts. Arresting a person like this did no good, because there was always another to replace him or her — and regardless, any jail sentence had limits. Afterward, Adams saw, everyone landed right back where they started.

‘‘We’re not getting anywhere,’’ he told his chief, Christopher Adams (the two men are not related), and his lieutenant. It turned out that they had already reached a similar conclusion. Until recently, Christopher Adams told me, he couldn’t recall ever hearing of a heroin case. ‘‘Now it’s every day,’’ he said. ‘‘It’s a majority. Not just in Laconia. It’s all over.’’ He and his lieutenant sat down to consider what their department might do. It seemed that there were three conceivable approaches to a drug problem: prevention, enforcement and treatment. To accomplish all three would mean regarding drug users, and misusers, as not only criminals. They were also customers who were being targeted and sold to; they were also victims who needed medical treatment. To coordinate all those approaches would require a particular sort of officer.

In September 2014, Eric Adams became the first person in New England — to his knowledge, the only person in the country — whose job title is prevention, enforcement and treatment coordinator. ‘‘I never thought I’d be doing something like this,’’ he told me. ‘‘I learned fast.’’ The department printed him new business cards: ‘‘The Laconia Police Department recognizes that substance misuse is a disease,’’ they read. ‘‘We understand you can’t fight this alone.’’ On the reverse, Adams’s cell phone number and email address were listed. He distributed these to every officer on patrol and answered his phone any time it rang, seven days a week. Strangers called him at 3 a.m., and Adams spoke with them for hours.

The department assigned him an unmarked Crown Victoria, and in it he followed the blips and squawks of a police scanner, driving to the scene of any overdose it reported and introducing himself to the victim, as well as any friends or family he could locate. Residents like these often shrank from the police or stiffened defensively. But when Adams told them that they weren’t under arrest, that he had only come to help, they seemed to sag in relief.

People who work with addicts generally agree that this moment, immediately after an overdose, offers the greatest chance to sway an addict, when he or she feels most vulnerable. ‘‘You’re at a crossroads right then and there,’’ a local paramedic told me. If an addict agreed to Adams’s help, Adams drove him to a treatment facility, sat beside him in waiting rooms, ferried his parents or siblings to visit him there or at the jail or hospital. He added the names of everyone he encountered to a spreadsheet, and he kept in touch even with those who relapsed. Were they feeling safe? Attending support meetings? Did they have a job? A place to sleep?

In the nearly three years since, as overdose rates have climbed across New Hampshire, those in Laconia have fallen. In 2014, the year Adams began, the town had 10 opioid fatalities. In 2016, the number was five. Fifty-one of its residents volunteered for treatment last year, up from 46 a year before and 14 a year before that. The county as a whole, Belknap, had fewer opioid-related emergency-room visits than any other New Hampshire county but one. Of the 204 addicts Adams has crossed paths with, 123 of them, or 60 percent, have agreed to keep in touch with him. Adams calls them at least weekly. Ninety-two have entered clinical treatment. Eighty-four, or just over 40 percent of all those he has met, are in recovery, having kept sober for two months or longer. Zero have died.

On most mornings, Adams arrives at his office well before 9 to answer email. By then, his phone is already chiming. ‘‘I thought when I got this position: Monday through Friday, day shifts, weekends off. I’m going to see my kids and wife more,’’ Adams said, laughing. ‘‘That’s not the case.’’ Pinned to the walls of his office, a windowless room on the second floor of the department, are pamphlets and resource guides for homelessness, peer-support groups and addiction hotlines, as well as a dry-erase board listing drug-treatment centers statewide. In December, when I visited one morning, the floor was cluttered with toys for local families in preparation for Christmas: doll sets, wireless headphones, a pillow the color of sorbet.

As soon as he began the job, Adams researched what social-service organizations the region had to offer and drove to their offices to introduce himself. A few employees at places like these knew one another from previous referrals, but many didn’t, so Adams went about acquainting them. At health conferences, he arrived to the quizzical frowns of social workers and realized that, of some 200 attendees, he was the only police officer. A network gradually sprouted around him. One morning in December, his first call was from Daisy Pierce, the director of a non-profit organization whose doors opened two weeks earlier; Adams is its chairman. Might Adams help her get a teenager into the Farnum Center, a treatment facility in Manchester, an hour south? Adams dialled a pastor he knew, who phoned a recovery coach. ‘‘For the first year and a half, I was the only transportation around here,’’ he told me when he hung up. ‘‘I would drive people down to Farnum all the time.’’

Next, Adams turned to a matter unresolved from the day before: a woman the county prosecutor had phoned about, asking if Adams could find her housing. Until recently, the woman had been staying at a homeless shelter, but that stay had ended and, because she was on probation, with nowhere else to sleep, Adams’s fellow officers had taken her to jail, though they could hold her for only one night. She would be released that day, still with nowhere else to stay. The next 48 hours would be critical, Adams felt. Here was a person who wanted to get sober but for whom the local authorities had little to offer.

From his desk, he dialled a treatment center, then various landlords and non-profit directors he knew. ‘‘Hi, this is Eric Adams over at the Laconia Police Department. I’m calling to see if you have anything. . . . ’’ Then he tried calling back the county prosecutor, tapping his fingers impatiently as the phone rang. When no one answered, he pulled a cellphone from his pocket and looked through it for numbers to dial on his office phone, while scribbling notes on two different legal pads. A cup from Dunkin’ Donuts sat on his desk, but he hadn’t had time to sip from it. After a half-dozen calls, he hung up the phone and sighed. ‘‘This is the biggest problem in the area,’’ he said. ‘‘It’s housing. There are only a handful of landlords that own so many properties.’’ Adams tried to be up front with landlords, and he didn’t blame them for sometimes rebuffing him, because they had to look out for their other tenants. But it meant limited options for a woman like the one he was trying to help.

He swivelled toward his computer and began scrolling through notes. Finding nothing, he rubbed his eyes with frustration, propped his elbows onto his desk and rested his chin on his hands to think. ‘‘Oh! Let me try — I haven’t talked with her in a while.’’ He dialled another number. ‘‘Hi, this is Eric Adams over at the Laconia Police Department. . . . ’’ A moment later, he hung up. ‘‘All right, this is the last one I can think of.’’ He dialled again. ‘‘I was wondering if you had any rentals available for a female. Oh, really? That’d be great.’’ He recited his email address. ‘‘Thank you!’’

Good news?  Adams shook his head. ‘‘Not for a couple weeks.’’ He stood, pushing back his chair, and cursed. Out of the office he strode to make a lap around the building to clear his head, then returned and looked at the clock — 9:40 a.m. He had a meeting at 10 at the local branch of the Bank of New Hampshire to help Pierce, the nonprofit director, apply for a new line of credit for their organization. Halfway to the door, he backtracked to pluck the Dunkin’ Donuts cup from his desk and sipped. ‘‘My coffee’s cold.’’

On a glass table in the bank lobby lay that morning’s copy of The Laconia Daily Sun. ‘‘Drug Sweep in Laconia Results in 17 Arrests,’’ its front page read. Headlines like that had become increasingly common, especially as the drugs themselves changed — first to opiates, then to opioids. They weren’t the same thing, Adams had learned. Opiates are derived from nature, and there are only so many, drugs like morphine, heroin and codeine. By contrast, opioids — though the word is now often used as an umbrella term for all these substances — technically means synthetic drugs like Vicodin, Percocet, fentanyl and OxyContin, all of which were invented in a laboratory.

This is why detectives sometimes encountered new opioids that were 20, 50, 100 times as potent as heroin. In a lab, you can do nearly anything. A dealer, even if he or she knows the difference, rarely bothers labelling, so a dose of so-called heroin might include fractions of nearly anything — meaning, of course, that the potency might be nearly anything. Overdoses happen not just when a person knowingly ingests a large dose but also when he or she ingests a dose of unknown composition.

After the meeting at the bank, Adams’s phone rang, and he vanished briefly. The call was from a woman whose son was arrested on charges of dealing meth. She wanted an intervention and hoped Adams might help. Steering toward the Belknap County jail, past homes spangled with Christmas lights, Adams admitted that he felt wary. He had already met this young man, who wanted nothing to do with him. Still, Adams would try. He never knew when an addict might begin saying ‘‘yes’’ to him. Sometimes this happened quickly: Adams’s phone would ring, and it was someone he met the previous day. ‘‘I’m exhausted,’’ the person would confess. Others waited a year or longer. All that time, they had hung onto his card. ‘‘I think I’m ready now,’’ they said.

Occasionally an addict used similar words even in rebuffing him — ‘‘I don’t think I’m ready yet’’ — a phrase that implicitly acknowledged a problem even as he or she denied one. It was the kind of sign Adams kept on the lookout for. Possibly this moment had come for the young man in jail.

When we arrived, Adams hustled through the drably carpeted lobby, hardly slowing before a receptionist and a guard waved him inside. A half-hour later, he returned, his face tight with frustration, and strode past me to the car without speaking. ‘‘He doesn’t have a problem,’’ he told me. ‘‘That’s what he said. He doesn’t have a problem.’’

Inside, he told me, guards had brought the young man from his cell into a windowed conference room, where he recognized Adams, as Adams predicted. ‘‘You know why I’m here,’’ Adams began gently.  ‘‘You’re trying to be nosy,’’ the man replied.

‘‘If you want to think of it that way, that’s fine.’’ Adams glanced at the young man’s file and explained that the man’s mother had called. ‘‘So I wanted to talk to you a little bit. This is an opportunity for you to get some help.’’ The young man went silent. ‘‘I mean, you got arrested,’’ Adams added, gesturing toward the file.  The man told him that he didn’t do the stuff, just sold it. He didn’t need help.

‘‘O.K.,’’ Adams told him, crossing his arms and leaning forward. Was the young man on any weight-loss program, then? ‘‘Because when I saw you before, to now, you’ve lost a lot of weight.’’ He nodded toward the young man, who was twitching uncomfortably in his chair. ‘‘And you’re all over the place, just sitting there.’’

When the man told Adams he was innocent, Adams reminded him that he was always available and slid him another one of his cards. Adams wished him well, then he asked guards to briefly fetch the woman they were holding overnight — the one for whom Adams was searching for housing — to check in and promise that he was trying.

Even as Adams nosed the Crown Vic out of the parking lot, he couldn’t get the episode out of his head. ‘‘Why won’t you just say, ‘I need this’?’’ he asked aloud, thinking of the young man. ‘‘Your life is going this way. You’ve been arrested. You’re homeless. It’s all drug-related.’’ He sighed. ‘‘The thing I had the hardest time learning was you’re not going to save everyone. That was very hard for me to accept.’’

A common sentiment among the police was that officers interacted with just 5 percent or so of the residents they served. In certain communities, that fraction was smaller. Laconia wasn’t a large town. ‘‘You think, mathematically,’’ Adams began, before pausing, ‘‘why can’t I? Why can’t I fix this?’’

For several miles he steered quietly, past muddied snowbanks. ‘‘It bothers me, but I’ve done what I can do right now. I can’t force him to want help.’’ He turned into the lot of the department and slowed into a parking spot.

‘‘Is there such a thing as an addict you have no sympathy for?’’ I wondered.  Adams considered this, letting the engine idle, and dropped his hands into his lap. Eleven seconds passed in silence. ‘‘I don’t think so,’’ he said finally. ‘‘There are reasons they are the way they are.’’

A kit with Narcan, a nasal spray that blocks the effect of opioids on the central nervous system. CreditNatalie Keyssar for The New York Times

Adams could list, from memory, addicts who had opened their lives to him, had volunteered for treatment, had wept in relief and gratitude. Already I had met two young adults who were newly in recovery and partly credited Adams for the lives they had regained. But those weren’t the names that tormented him.

Inside his office, he noticed two new voice-mail messages. The first was from a woman who read of Adams in the newspaper. ‘‘If you could tell me what to do? I’m more than willing to do whatever I need.’’ Adams scribbled something on a legal pad, then played the second voice mail. The same voice filled the room again, but now it broke into tears. Could Adams please tell her what to do?

Adams jotted another note, then checked his watch. Just past noon. Because he knew the work schedule of the mother of the young man he visited in jail, he knew she would be off soon and expecting his call. ‘‘She’s not going to be happy,’’ he said, mostly to himself. Rubbing his forehead, he sat down and dialed.

In so many towns all across the country, it is difficult to talk about an issue like heroin, not only because there is a stigma or because people worry about sounding impolite, but because everyone calibrates differently, based on neighbors and co-workers they see all day, how much of a problem it is or whether it is a problem at all. There were towns near Laconia — diplomatically, Adams declined to name them — that denied they had any drug crisis, even as the numbers they had showed otherwise. When presented with those numbers, some officials found alternative explanations.

Those were residents from other towns who just happened to cross the border, they argued. This reasoning just contributed to the problem, Adams said. Between 2004 and 2013, the number of New Hampshire residents receiving state-funded treatment for heroin addiction climbed by 90 percent. The number receiving treatment for prescription-opiate abuse climbed by 500 percent. But in terms of availability of beds, New Hampshire ranks second to last in New England in access to drug-treatment programs, ahead of only Vermont. The number who still need treatment is probably much higher. In October 2014, New Hampshire became the second-to-last state in the country to begin a prescription-drug-monitoring program, leaving only Missouri without one.

Engler, who was cautious and businesslike, with slicked hair and a graying goatee, had been mayor for three years, though he had lived in Laconia for almost 17 and owned The Laconia Daily Sun. Over his dress shirt he wore a fleece vest embroidered with the paper’s logo. Engler referred to what was happening in Laconia as ‘‘this so-called heroin epidemic,’’ his tone melodramatic, raising his hands defensively above his head.

‘‘We’re the county seat,’’ Engler told me. ‘‘We’re also the home of the regional hospital. Towns in New Hampshire are extremely close together. I think we tend to get credit for more things than are directly attributable to our residents.’’ Though he thought highly of Eric Adams, he also felt sceptical that heroin deserved to be considered an epidemic, regardless of the statistics. ‘‘When I go to a Rotary Club meeting, I don’t hear people sitting around talking about, ‘Woe is us, everybody’s dying of heroin.’ ’’

Might that be because, in a setting like the Rotary Club, heroin was not a topic of polite conversation?

‘‘There could be something to that,’’ Engler admitted. Still, an overdose death was an overdose death — it would appear in the news that way, and Engler would have heard of it. ‘‘I don’t believe there has been a huge, communitywide reaction to this. There’s not 100 people showing up at City Council meetings saying: ‘You have to do something about this. This is terrible.’ The papers aren’t full of letters to the editor. Not at all. And I think there’s a reason for that. The reason for that is’’ — Engler paused and crossed his arms — ‘‘since we have been in the so-called heroin epidemic in New Hampshire, I don’t believe there has been an instance in the Lakes Region, in Belknap County, where we have had a tragic story involving the son or daughter of someone from a prominent family. All it takes is one, usually. Somebody in Londonderry, some girl who was valedictorian of her class, her dad was a doctor or a lawyer or something like that, overdoses and dies, and suddenly it’s a crisis to everyone in town.’’

That very week, I told Engler, while tagging along with Adams for a meeting at the high school, I’d heard teachers mention a current student, a well-liked senior athlete, a team captain, whose sister had struggled with addiction and who had been open about the experience. Another member of the same graduating class, a girl whose grades ranked her in the top 10, had been walking with a friend in 2012 when a local mother, high while driving to pick up her own child from the middle school, swerved and struck them on the sidewalk. The girl survived. Her friend was killed.

The mayor was unmoved. ‘‘That was oxycodone,’’ Engler said dismissively. ‘‘Here, locally, the heroin epidemic, whatever you want to call it, has not crossed over in any obvious way from the underclass to the middle, middle–upper class.’’

Chadwick Boucher, a former addict and an early client of Eric Adams’s, with his work truck in his father’s yard. CreditNatalie Keyssar for The New York Times

Later that week, another prospective client phoned Adams. ‘‘I’m at wits’ end,’’ the man said. For the woman who needed housing, Adams helped track down a relative, at whose home she could stay until an apartment opened. On Friday evening, two more residents overdosed. Adams intended to visit them. Whether either one would accept Adams’s card, would call him, would enter treatment, would achieve recovery, would some day relapse, Adams couldn’t predict. There were no guarantees in this sort of work.

Early in his tenure, Adams made a presentation to ‘‘some prominent people in the community’’ — he didn’t want to name anyone — and afterward, as much of the room applauded, a man approached to shake Adams’s hand. As he reached out, the man said: ‘‘It’s a really good job you’re doing. I think it’s great. But my opinion is, if they stick a needle in their arm, they should die.’’

‘‘I’m sorry you feel that way,’’ Adams said, startled. ‘‘I’d hope you would feel differently if it was your own family member.’’  But the man shook his head. ‘‘That will never happen.’’

This sort of thing happened all the time when Adams began. Today it happened far less frequently. So many others had grown into Adams’s approach: fellow officers, downtown business owners, the captain at the Belknap County jail. Police officers from around New England and even farther away had phoned or travelled to Laconia to learn what Adams was doing, and whether the model could be replicated. Other towns, independently, had been pressed by the crisis to conceive approaches of their own. Manchester had turned its firehouses into safe stations. Gloucester, across the border in Massachusetts, had a network of community volunteers.

A city as large as Philadelphia or Boston could sensibly implement a PET approach too, Adams’s supervisors argued; a community like that would simply need more than one officer, with each assigned to a geographical area. But the shift this required would be profound, asking departments that for so long had thought mainly of enforcement to think differently. In Adams’s daily work, it was unavoidable that certain values competed. A client might divulge a crime to him, and he would be forced to interrupt her to give a Miranda warning. ‘‘If there is a crime, that individual needs to be held accountable,’’ he said. ‘‘But this is where our prosecutor, our judges, come into play.’’ Some attorneys had expressed discomfort with him and had insisted on being present when he met their clients. ‘‘I’m totally fine with that,’’ he said, ‘‘because it’s an opportunity for me to educate the attorney, to let them know what I do, how I do it, what the processes are.’’ In a role so complicated, with so much at stake, clearly it was vital that the right officer held the job.

In an empty conference room on the first floor of the department, I met a young man named Chadwick Boucher, an early client of Adams’s. The two men hugged when they saw each other, and then Adams disappeared upstairs to make calls while Boucher and I spoke. He was 27, though he had the calm demeanour of someone two or three times as old. As early as middle school, Boucher began sneaking his parents’ liquor, partly to fit in with older boys he admired, he told me. Soon he added marijuana. He played hockey then, and played well — invitations came from showcases in Boston and scouts from Division I colleges, including the University of New Hampshire, a national power. Instead, Boucher quit. It was too much pressure. He finished high school and moved in with a friend, who introduced him to OxyContin.

What followed was difficult to align into a neat chronology. He bounced from one friend’s apartment to another, from Oxy to Percocet and finally, when pills grew scarce, to heroin. There was a criminal distribution charge, probation, two treatment programs that he abandoned, feeling as though he didn’t belong. There were short-term jobs tending bar or waiting tables, collecting pay-checks before inevitably being fired. Suddenly he was high behind the wheel of his father’s Cutlass — not in the road, but in a driveway — startling awake to the police rapping on his window. Then he was at the Laconia police station, in a room with a plainclothes officer named Eric Adams.

‘‘He opened his arms to me,’’ Boucher recalled. It had felt bizarre, sharing the truth with a cop. But things had changed so quickly. Most of his family had stopped returning his calls, and all his friends had vanished. The only people around him now were strangers who shared his addiction, and he didn’t like or trust them. The difference in meeting someone like Adams was obvious. ‘‘He cares about my well-being,’’ Boucher said. ‘‘I needed that.’’

Adams wanted him to call every day, so Boucher called every day. Then every week. He entered another treatment program, and this time he graduated. He was now nearing a year sober. He owned a business and was caught up on his bills. He lived up the road in an apartment and had friends again, some of whom were in recovery, too. They made a point to talk openly about it, to keep an eye out for one another. Some he referred to Adams. He knew that recovery demanded his full attention, that it probably always would. If he lost anything else in his life — an apartment, a business — he lost that one thing only and could do without it. If he lost his recovery, he would lose everything, all at once.

I asked Boucher how he preferred to be named in this article — by only ‘‘Chad’’? Or would he prefer anonymity? But he shook his head. It was important to him to be honest about who he was. He hoped this would send a message to other addicts and to those who encountered them. ‘‘It’s important that people know there’s a way out.’’ Recovery from addiction was an achievable thing and, having discovered this fact, having discovered Eric Adams, Boucher intended to share it. The news might save lives. He knew it was possible that a business client might discover his unflattering past, that he might lose an account or two. ‘‘I’ve come way too far for that,’’ he said.

Source:  https://www.nytimes.com/2017/07/12/magazine/a-small-town-police-officers-war-on-drugs 

 

 

 

LOWELL, Mass. — They hide in weeds along hiking trails and in playground grass. They wash into rivers and float downstream to land on beaches. They pepper baseball dugouts, sidewalks and streets. Syringes left by drug users amid the heroin crisis are turning up everywhere.

In Portland, Maine, officials have collected more than 700 needles so far this year, putting them on track to handily exceed the nearly 900 gathered in all of 2016. In March alone, San Francisco collected more than 13,000 syringes, compared with only about 2,900 the same month in 2016. People, often children, risk getting stuck by discarded needles, raising the prospect they could contract blood-borne diseases such as hepatitis or HIV or be exposed to remnants of heroin or other drugs.

Activist Rocky Morrison, of the “Clean River Project,” holds up a fish bowl filled with hypodermic needles, that were recovered during 2016, on the Merrimack River. Charles Krupa / AP

It’s unclear whether anyone has gotten sick, but the reports of children finding the needles can be sickening in their own right. One 6-year-old girl in California mistook a discarded syringe for a thermometer and put it in her mouth; she was unharmed.

“I just want more awareness that this is happening,” said Nancy Holmes, whose 11-year-old daughter stepped on a needle in Santa Cruz, California, while swimming. “You would hear stories about finding needles at the beach or being poked at the beach. But you think that it wouldn’t happen to you. Sure enough.”

They are a growing problem in New Hampshire and Massachusetts — two states that have seen many overdose deaths in recent years.  “We would certainly characterize this as a health hazard,” said Tim Soucy, health director in Manchester, New Hampshire’s largest city, which collected 570 needles in 2016, the first year it began tracking the problem. It has found 247 needles so far this year.

Needles turn up in places like parks, baseball diamonds, trails and beaches — isolated spots where drug users can gather and attract little attention, and often the same spots used by the public for recreation. The needles are tossed out of carelessness or the fear of being prosecuted for possessing them.

One child was poked by a needle left on the grounds of a Utah elementary school. Another youngster stepped on one while playing on a beach in New Hampshire.

Even if adults or children don’t get sick, they still must endure an unsettling battery of tests to make sure they didn’t catch anything. The girl who put a syringe in her mouth was not poked but had to be tested for hepatitis B and C, her mother said.

Some community advocates are trying to sweep up the pollution. Rocky Morrison leads a clean-up effort along the Merrimack River, which winds through the old milling city of Lowell, and has recovered hundreds of needles in abandoned homeless camps that dot the banks, as well as in piles of debris that collect in floating booms he recently started setting.

He has a collection of several hundred needles in a fishbowl, a prop he uses to illustrate that the problem is real and that towns must do more to combat it.

“We started seeing it last year here and there. But now, it’s just raining needles everywhere we go,” said Morrison, a burly, tattooed construction worker whose Clean River Project has six boats working parts of the 117-mile river.

Among the oldest tracking programs is in Santa Cruz, California, where the community group Take Back Santa Cruz has reported finding more than 14,500 needles in the county over the past 4 1/2 years. It says it has gotten reports of 12 people getting stuck, half of them children.

“It’s become pretty commonplace to find them. We call it a rite of passage for a child to find their first needle,” said Gabrielle Korte, a member of the group’s needle team. “It’s very depressing. It’s infuriating. It’s just gross.”

Some experts say the problem will ease only when more users get treatment and more funding is directed to treatment programs.  Others are counting on needle exchange programs, now present in more than 30 states, or the creation of safe spaces to shoot up — already introduced in Canada and proposed by U.S. state and city officials from New York to Seattle.  Studies have found that needle exchange programs can reduce pollution, said Don Des Jarlais, a researcher at the Icahn School of Medicine at Mount Sinai hospital in New York.

But Morrison and Korte complain poor supervision at needle exchanges will simply put more syringes in the hands of people who may not dispose of them properly.

After complaints of discarded needles, Santa Cruz County took over its exchange from a non-profit in 2013 and implemented changes. It did away with mobile exchanges and stopped allowing drug users to get needles without turning in an equal number of used ones, said Jason Hoppin, a spokesman for the Santa Cruz County.

Along the Merrimack, nearly three dozen riverfront towns are debating how to stem the flow of needles. Two regional planning commissions are drafting a request for proposals for a clean-up plan. They hope to have it ready by the end of July.

“We are all trying to get a grip on the problem,” said Haverhill Mayor James Fiorentini. “The stuff comes from somewhere. If we can work together to stop it at the source, I am all for it.”

Source:  http://www.nbcnews.com/storyline/americas-heroin-epidemic/discarded-syringes-heroin-crisis-create-health-environmental-problems-n783671  July 2017

 

Blue Cross Blue Shield issued a report on the opioid crisis with their data from all members in their commercial plans.  Early in the document, they report a pair of striking numbers.

First, that 21% of members filled a prescription for an opioid in 2015. I’ve heard these kinds of numbers before, but I never get numb. That’s 1 in 5 members, despite growing attention to excessive prescribing of opioids.

Second, a 493% increase in diagnosis of opioid use disorders over 7 years. My reaction is that this has to reflect changes in coding or diagnostic practices rather than the population. It’s implausible that there was an increase this large in the number of people with an opioid use disorder.

The document then devotes a great deal of attention to opioid prescribing.

Toward the end, there are a couple of graphics that caught my attention.

First, a map showing rates of opioid use disorders.

 

Then, this:

Though critical to treating opioid use disorder, the use of medication-assisted treatments (e.g., methadone) does not always track with rates of opioid use disorder (compare Exhibits 10 and 11). For example, New England leads the nation in use of medication-assisted treatments but it has lower levels of opioid use disorder than other parts of the country

 

So . . . they note that New England has average rates of opioid use disorders, yet they have high rates of utilization of medication-assisted treatment. This caught my attention because New England has higher rates of overdose, as depicted in the CDC graphics below.

Number and age-adjusted rates of drug overdose deaths by state, US 2015

 

Statistically significant drug overdose death rate increase from 2014 to 2015, US states

(It’s worth noting that BCBS is not among the top 3 insurers in Maine or New Hampshire, but they are the biggest in Massachusetts and Vermont.)

It begs questions about what the story is, doesn’t it?

I don’t presume to know the answers.

§ What was the sequence of events for the high OD rates and the utilization of MAT? And, what impact, if any, has the expansion of MAT had on overdose rates?

§ Is the BCBS data representative? (This brand new SAMHSA report suggest that the data about use is representative.)

§ We know that opioid maintenance meds reduce risk of OD, but we also know that people stop taking these meds at high rates. Does this imply that, in the real world, these meds end up providing less OD protection than hoped?

§ What are the policies and practices of the other insurers in the state?  (For example, we know that Anthem [the largest insurer in Maine and Vermont] recently ended prior authorization requirements for MAT. It’s not clear how restrictive they had been. They also are attempting to institute reformsto address the fact that, “only about 16 to 19 percent of the members taking the medications for opioid use disorder also were getting the recommended in-person counseling.”)

§ Are there regional differences in drug potency that explain this?

Let’s hope that more insurers follow suit and share their data.

Source:   https://addictionandrecoverynews.wordpress.com/2017/07/16/blue-cross-blue-shield-publishes-major-opioid-report/

It is vital that physicians—particularly psychiatrists who are on the frontlines with patients who struggle with cannabis use—are able to identify and characterize cannabis use disorders; provide education; and offer effective, evidence-based treatments. This article provides a brief overview of each of these topics by walking through clinical decision-making with a case vignette that touches on common experiences in treating a patient with cannabis use disorder.

A separate and important issue is screening for emerging drugs of abuse, including synthetic “marijuana” products such as K2 and spice. Although these products are chemically distinct from the psychoactive compounds in the traditional cannabis plant, some cannabis users have tried synthetic “marijuana” products because of their gross physical similarity to cannabis plant matter.

CASE VIGNETTE

Mr. M is a 43-year-old legal clerk who has been working in the same office for 20 years. He presents as a referral from his primary care physician to your outpatient psychiatry office for an initial evaluation regarding “managing some mid-life issues.” He states that while he likes his job, it is the only job he has had since graduating college and he finds the work boring, noting that most of his co-workers have gone on to law school or more senior positions in the firm. When asked what factors have prevented him from seeking different career opportunities, he states that he would “fail a drug test.” Upon further inquiry, Mr. M says he has been smoking 2 or 3 “joints” or taking a few hits off of his “vaping pen” of cannabis daily for many years, for which he spends approximately $70 to $100 a week.

He first used cannabis in college and initially only smoked “a couple hits” in social settings. Over time, he has needed more cannabis to “take the edge off” and has strong cravings to use daily. He reports liking how cannabis decreases his anxiety and helps him fall asleep, although he thinks the cannabis sometimes makes him “paranoid,” which results in his avoidance of family and friends.

More recently, he identifies conflict and regular arguments with his wife over his cannabis use—she feels it prevents him from being present with his family and is a financial burden. He admits missing an important awards ceremony for her work and sporting events for his children, for which he had to “come up with excuses,” but the truth is that he ended up smoking more than he had intended and lost track of the time.

Mr. M reports multiple previous unsuccessful attempts to reduce his use and 2 days when he stopped completely, which resulted in “terrible dreams,” poor sleep, sweating, no appetite, anxiety, irritability, and strong cravings for cannabis. Resumption of his cannabis use relieved these symptoms. He denies tobacco or other drug use, including use of synthetic marijuana products such as K2 or spice, and reports having a glass of wine or champagne once or twice a year for special occasions.

The diagnosis

In the transition from DSM IV-TR to DSM-5, cannabis use disorders, along with all substance use disorders, have been redefined in line with characterizing a spectrum of

pathology and impairment. The criteria to qualify for a cannabis use disorder remain the same except for the following:

1. The criterion for recurrent legal problems has been removed.

2. A new criterion for craving or a strong desire or urge to use cannabis has been added, and the terms abuse and dependence were eliminated.

To qualify as having a cannabis use disorder, a threshold of 2 criteria must be met. Severity of the disorder is characterized as “mild” if 2 or 3 criteria are met, “moderate” if 4 or 5 criteria are met, and “severe” if 6 or more criteria are met. Mr. M demonstrates 3 symptoms of impaired control: using longer than intended, unsuccessful efforts to cut back, and craving; 3 symptoms of social impairment: failure to fulfil home obligations, persistent problems with his wife, and reduced pursuit of occupational opportunities; 1 symptom of risky use: continued use despite paranoia; and 2 symptoms of pharmacological properties: tolerance and withdrawal. As such, he meets 9 criteria, which qualify him for a diagnosis of severe cannabis use disorder.

You summarize Mr. M’s 9 symptoms and counsel him about severe cannabis use disorder. He becomes upset and states that he was not aware one could develop an “addiction” to cannabis. He expresses an interest in treatment and asks what options are available.

Treatment options

Psychotherapeutic treatments, including motivational enhancement treatment (MET), cognitive behavioral therapy (CBT), and contingency management (CM), have demonstrated effectiveness in reducing frequency and quantity of cannabis use, but abstinence rates remain modest and decline after treatment. Generally, MET is effective at engaging individuals who are ambivalent about treatment; CM can lead to longer periods of abstinence during treatment by incentivizing abstinence; and CBT can work to enhance abstinence following treatment (preventing relapse). Longer duration of psychotherapy is associated with better outcomes. However, access to evidence-based psychotherapy is frequently limited, and poor adherence to evidence-based psychotherapy is common.

In conjunction with psychotherapy, medication strategies should be considered. Because there are no FDA-approved pharmacological agents for cannabis use disorder, patients should understand during the informed consent process that all pharmacotherapies used to treat this disorder are off-label. A number of clinical trials provide evidence for the off-label use of medications in the treatment of cannabis use disorder. The current strategies for the off-label treatment of cannabis use disorder target withdrawal symptoms, aim to initiate abstinence and prevent relapse or reduce use depending on the patient’s goals, and treat psychiatric comorbidity and symptoms that may be driving cannabis use. Here we focus on the evidence supporting these key strategies.

Targeting withdrawal and craving

Cannabis withdrawal is defined by DSM-5 as having 3 or more of the following signs and symptoms that develop after the cessation of prolonged cannabis use:

• Irritability, anger, or aggression

• Nervousness or anxiety

• Sleep difficulty

• Decreased appetite or weight loss

• Restlessness

• Depressed mood

• At least one of the following physical symptoms that causes discomfort: abdominal pain, shakiness/tremors, sweating, fever, chills, or headache

Withdrawal symptoms may be present within the first 24 hours. Overall, they peak within the first week and persist up to 1 month following the last use of cannabis. In the case of Mr. M, insomnia, poor appetite, and irritability as well as sweating are identified, which meet DSM-5 criteria for cannabis withdrawal during the 2 days he abstained from use. He also identifies strong craving and vivid dreams, which are additional withdrawal symptoms included on marijuana withdrawal checklists in research studies, although not included in DSM-5 criteria. These and other symptoms should be considered in clinical treatment.

Medication treatment studies for cannabis withdrawal have hypothesized that if withdrawal symptoms can be reduced or alleviated during cessation from regular cannabis use, people will be less likely to resume cannabis use and will have better treatment outcomes. Studies have shown that dronabinol and nabilone improved multiple withdrawal symptoms, including craving; and quetiapine, zolpidem, and mirtazapine help with withdrawal-induced sleep disturbances.1-5

Combining dronabinol and lofexidine (an alpha-2 agonist) was superior to placebo in reducing craving, withdrawal, and self-administration during abstinence in a laboratory model. However, in a subsequent treatment trial, the combined medication treatment was not superior to placebo in reducing cannabis use or promoting abstinence.6

Six double-blind placebo-controlled pharmacotherapy trials in adults with cannabis use disorder have looked at withdrawal as an outcome.7 Of these studies, only dronabinol, bupropion, and gabapentin reduced withdrawal symptoms.8-10 In addition to reducing withdrawal symptoms, nabiximols/Sativex (a combination tetrahydrocannabinol [THC] and cannabidiol nasal spray not available in the US) increased retention (while actively on the medication in an inpatient setting) but did not reduce outpatient cannabis use at follow-up.11

All of the medications available for prescription in the US can be monitored reliably with urine drug screening to assess for illicit cannabis use except dronabinol, which will result in a positive screen for cannabis. When using urine drug screening, remember that for heavy cannabis users the qualitative urine drug screen can be positive for cannabis up to a month following cessation. When selecting a medication, take into account the cost of the medication, particularly since insurance will likely not cover THC agonists such as dronabinol for this indication, and possible misuse or diversion of scheduled substances (eg, dronabinol, nabilone). In addition, monitoring for reductions in substance use and withdrawal symptoms is key.

Abstinence initiation and relapse prevention

Other clinical trials have looked at medications to promote abstinence by reducing stress-induced relapse, craving (not as a component of withdrawal), and the reinforcing aspects of cannabis. Of these trials, the following results show potential promise with positive findings: gabapentin reduced quantitative THC urine levels and improved cognitive functioning (in addition to decreasing withdrawal), and buspirone led to more negative urine drug screens for cannabis (although the difference was not significant compared with placebo).10,12 However, in a follow-up larger study, no differences were seen compared with placebo and women had worse cannabis use outcomes on buspirone.13

N-acetylcysteine resulted in twice the odds of a negative urine drug screen in young adults and adolescents (although there was no difference between adolescent groups in self-report of cannabis use).14 Gray and colleagues15 reported that no differences were seen between N-acetylcysteine and placebo (results of the trial are soon to be published). Topiramate resulted in significantly decreased grams of cannabis used but no difference in percent days used or proportion of positive urine drug screens.16 In a recent small clinical trial, reductions in cannabis use were seen with oxytocin in combination with MET.17 Studies with nabilone and long-term naltrexone administration reduced relapse and cannabis self-administration and subjective effects, respectively, which suggests promising avenues yet to be explored by clinical trials.2,18

Treatment of psychiatric comorbidity

Other studies have looked at the effects of treating common comorbid psychiatric disorders in adults with cannabis use disorder, postulating that if the psychiatric disorder is treated, the individual may be more likely to abstain or reduce his or her cannabis use. For example, if a person is less depressed, he may better engage in CBT for relapse prevention.

Fluoxetine for depression and cannabis use disorder in adolescents decreased cannabis use and depression, although there was no difference compared with placebo.19 A trial of venlafaxine for adults with depression and cannabis use disorder demonstrated less abstinence with greater withdrawal-like symptoms compared with placebo.20,21 These findings suggest that this antidepressant might not be beneficial for treatment-seeking individuals with cannabis use disorder and may actually negatively affect outcomes.

CASE VIGNETTE CONT’D

After discussing and presenting the different psychotherapy and medication treatment options to Mr. M, you and he decide to start CBT to help with abstinence initiation. In addition, you prescribe 20 mg of dronabinol up to 2 times daily in combination with 50 mg of naltrexone daily, to help globally target Mr. M’s withdrawal symptoms and prevent relapse once abstinence is achieved. However, a few days later, Mr. M calls to say that his insurance will not cover the prescription for dronabinol and he cannot afford the high cost. Given his main concerns of cannabis withdrawal symptoms, you select gabapentin up to 400 mg 3 times daily and continue weekly individual CBT.

Mr. M calls back several days later and reports that he has made some improvements in reducing the frequency of his cannabis use, which he attributes to the medication, but he thinks he needs additional assistance. After reviewing the treatment options again, he gives informed consent to start 1200 mg of N-acetylcysteine twice daily. After 10 weeks of this medication, his urine screens are negative.

You continue to provide relapse prevention CBT. He reports to you that his anxiety and insomnia are almost resolved, and you suspect that withdrawal was the cause of these symptoms. He reports significant improvement in his relationship with his family and recently received a promotion at work for “going above and beyond” on a project he was given the lead.

Over the next 6 months, he has 2 relapses that in functional analysis with you are determined to be triggered by unsolicited contact from his former drug dealer. Together, you develop a plan to block any further contact from the drug dealer. After several months, both the gabapentin and N-acetylcysteine are tapered and discontinued. Mr. M continues to see you for biweekly therapy sessions with random drug screens every 4 to 6 weeks.

Conclusion

Based on the available evidence, gabapentin, THC agonists, naltrexone, and possibly N-acetylcysteine show the greatest promise in the off-label treatment of cannabis use disorders. System considerations, such as medication cost, need to be factored into the decision-making as well as combination medication and psychotherapy approaches, which—as demonstrated in the case of Mr. M—may ultimately work best. Until further research elucidates the standard of medication practices for cannabis use disorder, the best off-label medication strategy should target any co-occurring disorders as well as any identified problematic symptoms related to cannabis use and cessation of use. When available, referral for evidence-based psychotherapy should be made.

Source:  (http://www.psychiatrictimes.com)  30th June 201

Investigating the proposition that cannabis is worth bothering with, this hot topic looks at reports that stronger cannabis on the market is increasing harms to users, prospects of recovery from disorders and dependence, and the emerging response to synthetic forms of cannabis like ‘spice’.

CANNABIS IN THE LAW

A controlled ‘Class B’ substance, cannabis carries legal penalties for possession, supply, and production. Between 2004–2009 cannabis was reclassified as a ‘Class C’ substance, meaning for a brief period of time it carried lesser penalties for possession. In 2009, the Association of Chief Police Officers issued new guidance, advising officers to take an escalating approach to the policing of cannabis possession for personal use: • A warning • A penalty notice for disorder (PND) • Arrest

This three-tiered approach was designed to be “ethical and non-discriminatory”, but also reinforce the “national message that cannabis is harmful and remains illegal”.

In 1990s Britain a common reaction to allocating resources to treating cannabis users was, ‘Why bother? We have more than enough patients with problems with serious drugs like heroin.’ The typically calming use of the drug by adults was seen as preferable to the main alternative – alcohol and its associated violence and disorder. Calls for a treatment response were seen as pathologising what in many societies is both normal and in some ways desirable youth development: trying new experiences, challenging conventions, and exposing the hypocrisy of alcohol-drinking adults. In 1997 the Independent on Sunday launched a campaign to decriminalise cannabis, culminating in a mass ‘roll-up’, and 16,000-strong pro-cannabis march from Hyde Park to Trafalgar Square. Its Editor Rosie Boycott wrote in the paper about her own coming-of-age experience smoking cannabis, telling readers:

“I Rolled my first joint on a hot June day in Hyde Park. Summer of ’68. Just 17. Desperate to be grown-up. … My first smoke, a mildly giggly intoxication, was wholly anti-climatic. The soggy joint fell apart. I didn’t feel changed. But that act turned me – literally – into an outlaw. I was on the other side of the fence from the police – or the fuzz, as we used to call them. So were a great many of my generation.”

The campaign was explosive, but short-lived, apparently subsiding when Boycott left to take up her role as Editor of the Daily Express. A decade later, the Independent issued an apology for the campaign. ‘If only they had known then, what they knew now’, was the message of the article, referring to the reportedly damaging impact of the more potent strains of cannabis and its links to “mental health problems and psychosis for thousands of teenagers”.

Are stronger strains creating more problems?

There has been a long-standing, but controversial, association between cannabis strength and harm. Reading newspaper articles on the subject, it wouldn’t be unusual to see a headline drawing a straight line between ‘super-strength skunk’ and addiction, violence, deaths, or psychosis. In 2008, then Prime Minister Gordon Brown spoke in a similar vein, telling a breakfast-television viewing audience:

I have always been worried about cannabis, with this new skunk, this more lethal part of cannabis.

I don’t think that the previous studies took into account that so much of the cannabis on the streets is now of a lethal quality and we really have got to send out a message to young people – this is not acceptable.

Brown was warning of a dangerous new strain of cannabis on the market, that caused very severe harms to users – contrasting starkly with the common perception of cannabis as a ‘low harm’ or ‘no harm’ drug. The strength or potency of cannabis is determined by the amount of ‘THC’ it contains. THC produces the ‘high’ associated with cannabis, and another major component ‘CBD’ produces the sedative and anti-anxiety effects. As well as potency, the relative amounts of THC and CBD are important for understanding the effects of cannabis – something explored in a University College London study during the programme Drugs Live: Cannabis on Trial. The research team compared two different types of cannabis: the first had high levels of THC (approx. 13%) but virtually no CBD; and the second had a lower level of THC (approx. 6.5%) and substantial amounts of CBD (approx. 8%). They found that CBD had a moderating or protective effect on some of the negative effects of THC, and that “many of the effects that people enjoy are still present in low-potency varieties without some of the harms associated with the high-potency varieties”. At least in the US over the last two decades (between 1995–2014), potency has increased from around 4% to 12%, and the protective CBD content of cannabis has decreased, from around 28% to less than 15%, significantly affecting the ratio of THC to CBD, and with it, the nature and strength of the psychoactive effect of cannabis. Until the 1990s, herbal cannabis sold in the UK was predominantly imported from the Caribbean, West Africa, and Asia. After this time, it was increasingly produced in the UK, being grown indoors using intensive means (artificial lighting, heating, and control of day-length). A study funded by the Home Office analysed samples of cannabis confiscated by 23 police forces in England and Wales in 2008, and found that over 97% of herbal cannabis had been grown by intensive methods; its average potency of 16% compared with just 8% for traditional imported herbal cannabis. This matched other reports of home-grown cannabis being consistently (around 2–3 times) stronger than imported herbal cannabis and cannabis resin.

In 2015, observing a decrease in the use of cannabis in England and Wales, but parallel increase in demand for treatment, a UK study examined whether the trend could be explained by an increase in the availability of higher-potency cannabis. Over 2500 adults were surveyed about their use of different types of cannabis, severity of dependence, and cannabis-related concerns. The researchers found that higher potency cannabis was associated with a greater severity of dependence, especially in young people, and was rated by participants as causing more memory impairment and paranoia than lower potency types. However at the same time, it was reported to produce the best ‘high’, and to be the preferred type.

By definition cannabis is a psychoactive substance, which means it can change people’s perceptions, mood, and behaviour. Higher potency cannabis contains more of the psychoactive component, so it makes sense that higher potency cannabis could increase the risk of temporary or longer-term (adverse) problems with perceptions, mood, and behaviour. However, there is a particular concern that cannabis use could be linked to ‘psychosis’, a term describing a mental illness where a person perceives or interprets reality in a very different way to those around them, which can include hallucinations or delusions.

Whether cannabis causes psychosis, precipitates an existing predisposition, aggravates an existing condition, or has no impact at all on psychotic symptoms, has for decades been hotly contested. With our focus on evaluations of interventions, Drug and Alcohol Findings is in no position to pronounce on this issue, nor on the possibility that the drug might sometimes improve mental health, but some examples of research informing this debate are included below. A 2009 UK study examined whether daily use of high-potency cannabis was linked to an elevated risk of psychosis, comparing 280 patients in London presenting with a first episode of psychosis with a healthy control group. The patients were found to be more likely to smoke cannabis on a daily basis than the control group, and to have smoked for more than five years. Among those who used cannabis, 78% of the patients who had experienced psychosis used higher-potency cannabis, compared with 37% of those in the control group. The findings indicated that the risk of psychosis was indeed greater among the people who were using high potency cannabis on a frequent basis, but couldn’t show that the cannabis use caused the psychosis, or even that the cannabis use made the group more susceptible to psychosis. The wider literature on mental health and substance use would suggest that the association is more complex than this. A recently published paper from the University of York has demonstrated the complications of attributing any association between cannabis use and psychosis to a causal effect of cannabis use rather than other factors or a reverse causal effect. A calculation based on data from England and Wales helped to put this into perspective, indicating that even if cannabis did cause psychosis more than 20,000 people would need to be stopped using cannabis to prevent just one case of psychosis. The apparent steady increase in cannabis potency in the UK since the 1990s is important context for further research. Where higher potency cannabis is increasingly becoming the norm, and is the preference for cannabis users, it would be relevant to generate more evidence of the health-related problems with high potency cannabis, and the treatment and harm reduction solutions based around these health-related problems.

Cannabis accounts for half of all new drug treatment patients

The most widely used illegal drug in Europe, many seemingly enjoy cannabis without it leading to any significant negative social or health effects. However, numbers entering treatment for cannabis use problems have been on the rise (both in the UK, and the rest of Europe), while heroin treatment numbers have fallen  chart. According to Public Health England, this is not because more people are using cannabis, but perhaps because services relieved of some of the recent pressure of opiate user numbers are giving more priority to cannabis, because they are making themselves more amenable to cannabis users, and because of emerging issues with stronger strains of the drug. Whatever the causes, across the UK figures submitted to the European drug misuse monitoring centre show that the proportion of patients starting treatment for drug problems who did so primarily due to their cannabis use rose steadily from 11% in 2003/04 to 22% in 2011/12. With the caveat that data from 2013 onwards is not directly comparabledue to changes in methodology, in 2014 and 2015 the proportion of patients who entered treatment primarily because of a cannabis issue hovered above previous years at 26% (25,278 and 26,295 respectively). Among first ever treatment presentations, the increase from 2003/04 was more pronounced, from 19% to 37%. By 2013, cannabis use had become the main prompt for half the patients who sought treatment for the first time (at 49%), and stayed relatively constant at 47% in 2014, and 48% in 2015.

Showing that more users was not the reason for more starting treatment, over about the same period, in England and Wales the proportion of 16–59-year-olds who in a survey said they had used cannabis in the past year fell from about 11% to 7% in 2013/14, then stayed at that level in 2014/15 and 2015/16. The treatment figures largely reflect trends in England, where in 2013/14 the number of patients starting treatment with cannabis use problems had risen to 30,422, 21% of all treatment starters, up from 23,018 and 19% in 2005/06. Subsequently the number dropped to 27,965 in 2015/16, still around a fifth of all treatment starters. Among the total treatment population – starting or continuing in treatment – cannabis numbers rose from 40,240 in 2005/06 to peak at 64,407 in 2013/14 before falling back to 59,918 in 2015/16; corresponding proportions again hovered around a fifth. As a primary problem substance among under-18s cannabis dominated, accounting for three-quarters of all patients in treatment in 2015/16 and in numbers, 12,863. The dominance of cannabis increased from 2008/09 as numbers primarily in treatment for drinking problems fell.

‘All treatments appear to work’

According to the two main diagnostic manuals used in Europe and the USA, problem cannabis use can develop into a cannabis use disorder or cannabis dependence, identifiable by a cluster of symptoms including: loss of control; inability to cut down or stop; preoccupation with use; neglecting activities unrelated to use; continued use despite experiencing problems; and the development of tolerance and withdrawal. This level of clinical appreciation for cannabis use problems didn’t exist when researcher and writer William L. White entered the addictions field half a century ago:

“When I first entered the rising addiction treatment system in the United States nearly half a century ago, there existed no clinical concept of cannabis dependence and thus no concept of recovery from this condition. In early treatment settings, cannabis was not consider[ed] a “real” drug, the idea of cannabis addiction was scoffed at as remnants of “Reefer Madness,” and casual cannabis use was not uncommon among early staff working in addiction treatment programs of the 1960s. Many in the field remain sceptical of the idea of cannabis dependence, specifically whether problem users at the severe end experience physiological withdrawal. However, reviewing what they believe is mounting evidence, these authors suggest there can be confidence in the existence of a “true withdrawal syndrome” – albeit one that differs qualitatively from the “significant medical or psychiatric problems as observed in some cases of opioid, alcohol, or benzodiazepine withdrawals”. In the case of cannabis, the main symptoms are primarily emotional and behavioural, although appetite change, weight loss, and some physical discomfort are reported. A brief review aimed at practitioners in UK primary care provides guidance on how to manage symptoms of withdrawal among patients trying to stop or reduce their cannabis use.

Research has come a long way, says William L. White, with now “clear data supporting the dependency producing properties of cannabis, a clear conceptualization of cannabis use disorders (CUD) and cannabis dependence (CD)”, but until recently, very little evidence about the prospects of long-term recovery. Yet, key papers – found here and here – indicate that:

• Full remission from cannabis use disorders is not only possible, but probable.

• Stable remission takes time – an average of 33 months.

• Abstinence may not be initially realistic for heavy cannabis users – but those in  remission are usually able to reduce the intensity of their use and its  consequences.

At least in the United States, it seems dependence is more quickly overcome from cannabis than the main legal drugs. A survey of the US general adult population found that within a year of first becoming dependent, 3% each of smokers and drinkers were in remission and remained so until they were surveyed. For cannabis the figure was nearly 5% and for cocaine, nearly 9%. After ten years the proportions in remission had risen to 18% for nicotine, 37% for alcohol, 66% for cannabis and 76% for cocaine. About 26 years after first becoming dependent, half the people at some time dependent on nicotine were in remission, a milestone reached for alcohol after 14 years, for cannabis six years, and for cocaine, five.

Specialised treatment programmes for cannabis users in European countries

Generally for people with cannabis use problems, the European Monitoring Centre for Drugs and Drug Addiction concluded in 2015, and before that in 2008, that “all treatments appear to work”. For adults, effective treatments include motivational interviewing, motivational enhancement therapy and cognitive-behavioural therapy, and for younger people, family-based therapies seem most beneficial. Less important than the type of treatment is the treatment context and the individual’s determination to overcome their problems through treatment. And there is “no firm basis for a conclusion” that cannabis-specific interventions (designed around the risks and harms associated with cannabis) are more effective than general substance use treatment tailored to the individual needs of the cannabis user seeking treatment chart. In some studies brief interventions have been found to work just as well as more intensive treatment, but when the patients are heavily dependent, and the most difficult cases are not filtered out by the research, longer and more individualised therapies can have the advantage. When the World Health Organization trialled its ASSIST substance use screening and brief advice programme in Australia, India, the United States, and Brazil, just over half the identified patients (all had to be at moderate risk of harm but probably not dependent) were primarily problem cannabis users. Among these, risk reduction in relation to this drug was significantly greater among patients allocated to a brief advice session than among those placed on a three-month waiting list for advice. In each country too, risk reduction was greater among intervention patients, except for the USA, where the order was reversed. Suggesting that severity of use was not a barrier to reacting well to brief intervention, only patients at the higher end of the moderate risk spectrum further reduced their cannabis use/risk scores following intervention. The ASSIST study was confined to adults, but young people in secondary schools in the USA whose problem substance use focused mainly on cannabis also reacted well to brief advice.

The relative persistence of opiate use problems versus the transitory nature of those primarily related to cannabis seemed reflected in an analysis of treatment entrants in England from 1 April 2005 to the end of 2013/14, the last time this particular analysis was published. At the end of this period just 7% of primary cannabis users were still in or back in treatment compared to the 30% overall figure and 36% for primary opiate users. The figure peaked at 43% for users of opiates and crack. Over half – 53% – of primary cannabis users had left treatment as planned, apparently having overcome their cannabis problems, compared to 27% of primary opiate users and just 20% with dual opiates and crack use problems. Another 40% of cannabis users had left treatment in an unplanned manner, a slightly higher proportion than among opiate users. The figures tell a tale of relatively high level of success which enables cannabis users to leave treatment, though even in the absence of recorded success, few stay long-term.

However, the forms patients in England complete with their keyworkers while in treatment seem to tell a different story. Compared to how they started treatment, around six months later 45% of primary cannabis users were assessed as using just as often (including a few using more), compared to 30% of opiate users and 42% whose main problem drugs were both opiates and crack, suggesting more rapid and/or more complete remission for opiate users than for cannabis users. One interpretation is that the widespread use of substitute drugs like methadone more reliably reduced the illegal opiate use of opiate users and also helped retain them in treatment, while cannabis users tended quickly to leave treatment, having done well or not. However, these figures relate only to patients who completed the forms at their six-month review, which in practice could have happened anywhere from about one to six months after their assessment for treatment. What proportion of primary cannabis users were still in treatment at that point and available to complete the forms is not clear, but they may have been the patients whose problems were deep seated enough to require extended treatment.

Enjoyable and trouble-free for many, but not without harms Harm reduction – the “set of practical strategies and ideas aimed at reducing negative consequences associated with drug use” – is mostly associated with ‘harder’ drugs like heroin, for which blood-borne viruses and drug-related deaths are clear and severe risks. Yet while “many people experience cannabis as enjoyable and trouble free”, there are also varying degrees of harm with this drug depending on the characteristics of the person using, the type of the cannabis, and the way they consume it. Many formal cannabis harm reduction programmes borrow from the fields of alcohol and tobacco. Advice includes:

• safer modes of administration (eg, on the use of vaporisers, on rolling safer joints, on less risky modes of inhaling) Many people experience cannabis as enjoyable and trouble free … some people require help to reduce or stop

• skills to prevent confrontation with those who disapprove of use

• encouraging users to moderate their use

 

• discouraging mixing cannabis with other drugs

• drug driving prevention and controls

• reducing third-party exposure to second-hand smoke

• education about spotting signs of problematic use

• self-screening for problematic use

In some parts of the UK, National Health Service tobacco smoking cessation services incorporated cannabis into their interventions with adults; and Health Scotland, also addressing the risks of tobacco and cannabis smoking, published a booklet for young people titled Fags ‘n’ Hash: the essential guide to cutting down the risks of using tobacco and cannabis.

Vaporising or swallowing cannabis offers a way to avoid respiratory risks, but only a minority of cannabis do this, most choosing to smoke cannabis joints (or cannabis and tobacco joints). While not all will know about the different health risks, cannabis users may choose against safer consumption methods anyway for a range of reasons (including their own thoughts about safe use):

• Users may find it easier to control the effects (eg, severity, length of effect) of cannabis when inhaling in the form of a joint or spliff

• Preparing and sharing joints can be an enjoyable part of the routine, or part of a person’s social activities

• Alternative methods of smoking (eg, bongs and vaporisers) may be inconvenient to use, or expensive to buy

 

Most harm reduction advice is delivered informally long before users come into contact with drugs professionals – for example through cannabis magazines, websites, and headshops – highlighting the importance of official sources engaging with non-official sources to promote the delivery of accurate, evidence-based harm reduction messages.

A new high

In May 2016 the Psychoactive Substances Act placed a ‘blanket ban’ on new psychoactive substances (previously known as ‘legal highs’), including synthetic cannabinoids (synthetic forms of cannabis). Prior to this, in 2014, there had been 163 reported deaths from new psychoactive substances in the UK, and 204 the year after. The average age was around 28, younger than the average age for other drug misuse deaths of around 38. The fact that these psychoactive substances – which produced similar effects to illicit drugs like cannabis, cocaine, and ecstasy – could be bought so easily online or on the high street, appeared inconsistent; and each fatality prompted “an outcry for something to be done to prevent further tragedies”. This was the context (and arguably the political trigger) for the introduction of the Psychoactive Substances Act. While possession of a psychoactive substance as such wasn’t criminalised;, production, supply, offer to supply, possession with intent to supply, import or export were – with a maximum penalty of seven years’ imprisonment.

Just seven months after the Act came into effect, the Home Office labelled it a success, with a press release stating that nearly 500 people had been arrested, 332 shops around the UK had been stopped from selling the substances, and four people had been sent to prison. But did the Psychoactive Substances Act have the presumably desired effect of limiting access to psychoactive substances (and reducing deaths), or did it just push the drugs the way of dealers? It is perhaps too early to tell, but former chair of the Advisory Council on the Misuse of Drugs Professor Nutt had warned before the Act came into effect that the ‘blanket ban’ would make it harder (not easier) to control drugs. And while Chief executive of DrugWise Harry Shapiro had said the new law would make new psychoactive substances harder to obtain, he also agreed that sale of the drugs would not cease, but merely be diverted to the illicit market: “The same people selling heroin and crack will simply add this to their repertoire.” The paper “From niche to stigma” examined the changing face of the new psychoactive substance user between 2009 and 2016, focusing on people using the synthetic cannabis known as ‘spice’. It looked at the transition of (then) ‘legal highs’ from an “experimental and recreational” scene associated with a “niche middle class demographic”, to “those with degrees of stigma”, especially homeless, prison, and socially vulnerable youth populations (including looked after children, those involved in or at risk of offending, and those excluded or at risk of exclusion from mainstream education). In 2014, the DrugScope Street Drug Survey also observed a problem among these particular groups, recording a “rapid rise in the use of synthetic cannabinoids such as Black Mamba and Exodus Damnation by opiate users, the street homeless, socially excluded teenagers and by people in prison”.

‘SPICE’ AND OTHER SYNTHETICS

Cannabis contains two key components:

• ‘THC’ (tetrahydrocannabinol), which produces the ‘high’

• ‘CBD’ (cannabidiol), which produces the sedative and anti-anxiety effects

Synthetic forms of cannabis contain chemicals that aim to copy the effects of ‘THC’ in cannabis. But the effects of synthetic cannabis can be quite different (and often stronger): firstly, because synthetic production makes it easier to manipulate the amount of the THC-like chemical; and secondly, because of the absence of the moderating equivalent of ‘CBD’. Some synthetics are purposely designed to resemble herbal cannabis, and can be consumed in the same ways (eg, smoked or inhaled). The names also often have deliberate cannabis connotations. The risk of this is that people wishing to take cannabis may be initially unaware that they have been sold the synthetic form, or may believe from the look of it that it will produce similar sought-after effects. The greater intensity of synthetic cannabis at lower dose levels ( box) ensures that it has an appeal in terms of potency and affordability, but may put those with fewer resources at greater harm.

In 2014, the prison inspectorate for England and Wales raised concerns about the rise in the use of psychoactive substances in prisons, in particular synthetic cannabis. A study set in an English adult male prison found that the nature of the market was posing significant challenges to the management of offenders. There, the primary motivation for consumption was being able to take a substance without it being detected. Given this motivation, and the greater likelihood of harms from synthetic versus natural cannabis, the researchers concluded that it was imperative for mandatory drug-testing policies to be revised, and instead rooted in harm reduction – something which would also apply to people on probation subject to mandatory drug-testing.

Cannabis throws up a range of issues rather different from those associated with the drugs treatment in the UK has normally focused on. If current trends continue, understanding the findings will become yet more important to British treatment services.

Source:   http://findings.org.uk/PHP/dl.php?file=cannabis_treat.    Last revised 10 July 2017. 

Legalizing recreational marijuana use in Colorado, Oregon and Washington has resulted in collision claim frequencies that are about three percent higher overall than would have been expected without legalization, a new insurance report has found.

The Highway Loss Data Institute (HLDI) report says that more drivers admit to using marijuana, and the substance is showing up more frequently among people involved in crashes.

The HLDI report authors note that although there is evidence from simulator and on-road studies that marijuana can degrade some aspects of driving performance, researchers haven’t been able to definitively connect marijuana use with more frequent real-world crashes.

Some studies have found that using the drug could more than double crash risk, while others, including a large-scale federal case-control study, have failed to find a link between marijuana use and crashes. Studies on the effects of legalizing marijuana for medical use also have been inconclusive.

Colorado and Washington were the first states to legalize recreational marijuana for adults age 21 and older with voter approval in November 2012. Retail sales began in January 2014 in Colorado and in July 2014 in Washington. Oregon voters approved legalized recreational marijuana in November 2014, and sales started in October 2015.

HLDI conducted a combined analysis using neighbouring states as additional controls to examine the collision claims experience of Colorado, Oregon and Washington before and after law changes. Control states included Idaho, Montana, Nevada, Utah and Wyoming, plus Colorado, Oregon and Washington prior to legalization of recreational use.

During the study period, Nevada and Montana permitted medical use of marijuana, Wyoming and Utah allowed only limited use for medical purposes, and Idaho didn’t permit any use. Oregon and Washington authorized medical marijuana use in 1998, and Colorado authorized it in 2000.

HLDI also looked at loss results for each state individually compared with loss results for adjacent states without legalized recreational marijuana use prior to November 2016.  “The combined-state analysis shows that the first three states to legalize recreational marijuana have experienced more crashes,” says Matt Moore, senior vice president of HLDI. “The individual state analyses suggest that the size of the effect varies by state.”

Colorado saw the biggest estimated increase in claim frequency compared with its control states. After retail marijuana sales began in Colorado, the increase in collision claim frequency was 14 percent higher than in nearby Nebraska, Utah and Wyoming. Washington’s estimated increase in claim frequency was 6 percent higher than in Montana and Idaho, and Oregon’s estimated increase in claim frequency was 4 percent higher than in Idaho, Montana and Nevada.

“The combined effect for the three states was smaller but still significant at 3 percent,” Moore says. “The combined analysis uses a bigger control group and is a good representation of the effect of marijuana legalization overall. The single-state analyses show how the effect differs by state.”

Each of the individual state analyses also showed that the estimated effect of legalizing recreational use of marijuana varies depending on the comparison state examined. For example, results for Colorado vary from a 3 percent increase in claim frequency when compared with Wyoming to a 21 percent increase when compared with Utah.

Data spanned collision claims filed between January 2012 and October 2016 for 1981 to 2017 model vehicles. Analysts controlled for differences in the rated driver population, insured vehicle fleet, the mix of urban versus rural exposure, unemployment, weather and seasonality.

Collision claims are the most frequent kind of claims insurers receive. Collision coverage insures against physical damage to a driver’s vehicle in a crash with an object or other vehicle, generally when the driver is at fault. Collision claim frequency is the number of collision claims divided by the number of insured vehicle years.

HLDI said it will continue to examine insurance claims in states that allow recreational use of marijuana. Meanwhile, IIHS has begun a large-scale case-control study in Oregon to assess how legalized marijuana use may be changing the risk of crashes with injuries. Preliminary results are expected in 2020.

In addition to Colorado, Oregon and Washington, five other states and Washington, D.C., have legalized marijuana for all uses, and 21 states have comprehensive medical marijuana programs as of June. An additional 17 states permit limited access for medical use. Marijuana is still an illegal controlled substance under federal law.

“Worry that legalized marijuana is increasing crash rates isn’t misplaced,” says David Zuby, executive vice president and chief research officer of the Insurance Institute for Highway Safety. “HLDI’s findings on the early experience of Colorado, Oregon and Washington should give other states eyeing legalization pause.”

The Highway Loss Data Institute (HLDI) conducts studies of insurance data on vehicle losses and by publishes insurance loss results by vehicle make and model. Its sister research organization, the Insurance Institute for Highway Safety (IIHS), is focused reducing the losses from motor vehicle crashes. Both organizations are wholly supported by auto insurers and insurance associations.

State Efforts

The Governors Highway Safety Association (GHSA) has urged states to equip themselves with the latest research and recommends that they increase drug testing, bolster laboratory resources, track alcohol (DUI) and drugged (DUID) related driving data separately in state records, use surveys to gauge public attitudes, and evaluate the effects of any law or program changes.

The group has issued a guide, Drug Impaired Driving: A Guide for States, for states. Chief among the report’s recommendations is increased training for law enforcement officers to help them identify and arrest drugged drivers.

“As states across the country continue to struggle with drug-impaired driving, it’s critical that we help them understand the current landscape and provide examples of best practices so they can craft the most effective countermeasures,” said Jonathan Adkins, executive director of GHSA.

GHSA said this year five states are getting grants totalling $100,000 to implement Advanced Roadside Impaired Driving Enforcement (ARIDE) training and Drug Recognition Expert (DRE) programs. The states are Illinois, Montana, Washington, West Virginia and Wisconsin.

Related Research

The HLDI authors cite other research into drugs and driving including a 2016 IIHS survey that found that drivers in Colorado, Oregon and Washington were more likely to view marijuana as a highway safety problem than drivers in states without legalized use (Drivers say alcohol is bigger threat than pot).

A 2016 Columbia University study looked at traffic fatalities in 19 states before and after they enacted legalized medical marijuana laws. On average there was an 11 percent reduction in fatality rates, although the results varied across states. Seven states saw a reduction, while two had an increase, and the other 10 didn’t change.

Researchers using the National Advanced Driving Simulator found that while drivers under the influence of marijuana had trouble maintaining constant lane position, they drove more slowly and with more headway than drivers not under the influence.

About 1 in 5 weekend night-time drivers tested positive for at least one legal or illegal drug in the 2013-14 National Roadside Survey of Alcohol and Drug Use by Drivers conducted by the National Highway Traffic Safety Administration (NHTSA) (More drivers use marijuana, but link to crashes is murky).

A 2016 AAA Foundation study in Washington since legalization estimated that the prevalence of drivers in fatal crashes with marijuana in their blood roughly doubled from 8.3 percent in 2013 to 17 percent in 2014.

The National Highway and Traffic Safety Administration (NHTSA) examined the crash risk associated with driver drug use and found that drivers who tested positive for marijuana were overrepresented in the crash-involved population (More drivers use marijuana, but link to crashes is murky). However, they found no link between marijuana use and driver crash risk. The study, published in 2016, included 2011-12 data on police-reported crashes in Virginia Beach, Virginia, where it is illegal to use marijuana.

Source:  http://www.insurancejournal.com/news/

INTRODUCTION

Drug addiction is a chronic and relapsing disease that often begins during adolescence.

Epidemiological evidence documents an association between marijuana use during adolescence and subsequent abuse of drugs such as heroin and cocaine (1, 2). While many factors including societal pressures, family, culture, and drug availability can contribute to this apparent `gateway’ association, little is known about the neurobiological basis underlying such potential vulnerability.

Of the neural substrates that have been investigated, the enkephalinergic opioid system is  consistently altered by developmental marijuana exposure (3–5), perhaps reflecting neuroanatomical interactions between cannabinoid receptor type 1 and the enkephalinergic system (6, 7).

Debates exist, however, regarding the relationship between proenkephalin (Penk) dysregulation and opiate susceptibility. We previously reported that adult rats exposed to Δ9-tetrahydrocannabinol (THC; primary psychoactive component of marijuana) during adolescence exhibit increased heroin self administration (SA) as well as increased expression of Penk, the gene encoding the opioid neuropeptide enkephalin, in the nucleus accumbens shell (NAcsh), a mesolimbic structure critically involved in reward-related behaviors (3).

Although these data suggest that increased NAcsh Penk expression and heroin SA behavior are independent consequences of adolescent THC exposure, they do not address a possible causal relationship between THCinduced  Penk upregulation in NAcsh and enhanced behavioral susceptibility to opiates.

Moreover, insights regarding the neurobiological mechanisms by which adolescent THC exposure maintains upregulation of Penk into adulthood remain unknown.

Here, we take advantage of viral-mediated gene transfer strategies to show that adulthood addiction-like behaviors induced by adolescent THC exposure are dependent on discrete regulation of NAcsh Penk gene expression. A number of recent studies have demonstrated an important role for histone methylation in the regulation of drug-induced behaviors and transcriptional plasticity, particularly alteration of repressive histone H3 lysine 9 (H3K9) methylation at NAc gene promotors (8, 9).

We report here that one mechanism by which adolescent THC exposure may mediate Penk upregulation in adult NAcsh is through reduction of H3K9 di- and trimethylation, a functional consequence of which may be decreased transcriptional repression of Penk.

ABSTRACT

Background

Marijuana use by teenagers often predates the use of harder drugs, but the neurobiological underpinnings of such vulnerability are unknown. Animal studies suggest enhanced heroin self-administration (SA) and dysregulation of the endogenous opioid system in the nucleus accumbens shell (NAcsh) of adults following adolescent Δ9-tetrahydrocannabinol (THC) exposure. However, a causal link between Penk expression and vulnerability to heroin has yet to be established.

Methods

To investigate the functional significance of NAcsh  Penk tone, selective viral mediated knockdown and overexpression of Penk was performed, followed by analysis of subsequent heroin SA behavior. To determine whether adolescent THC exposure was associated with chromatin alteration, we analyzed levels of histone H3 methylation in the NAcsh via ChIP atfive sites flanking the Penk gene transcription start site.

Results

Here, we show that regulation of the proenkephalin (Penk) opioid neuropeptide gene in NAcsh directly regulates heroin SA behavior. Selective viral-mediated knockdown of Penk in striatopallidal neurons attenuates heroin SA in adolescent THC-exposed rats, whereas Penk overexpression potentiates heroin SA in THC-naïve rats. Furthermore, we report that adolescent THC exposure mediates Penk upregulation through reduction of histone H3 lysine 9 (H3K9) methylation in the NAcsh, thereby disrupting the normal developmental pattern of H3K9 methylation.

Conclusions

These data establish a direct association between THC-induced NAcsh Penk upregulation and heroin SA and indicate that epigenetic dysregulation of Penk underlies the long term effects of THC.

Source:  Biol Psychiatry. 2012 November 15; 72(10): 803–810. doi:10.1016/j.biopsych.2012.04.026.

Findings From A UK Birth Cohort

ABSTRACT

Background

Evidence on the role of cannabis as a gateway drug is inconsistent. We characterise patterns of cannabis use among UK teenagers aged 13–18 years, and assess their influence on problematic substance use at age 21 years.

Methods

We used longitudinal latent class analysis to derive trajectories of cannabis use from self-report measures in a UK birth cohort. We investigated (1) factors associated with latent class membership and (2) whether latent class membership predicted subsequent nicotine dependence, harmful alcohol use and recent use of other illicit drugs at age 21 years.

Results

5315 adolescents had three or more measures of cannabis use from age 13 to 18 years. Cannabis use patterns were captured as four latent classes corresponding to ‘non-users’ (80.1%), ‘late-onset occasional’ (14.2%), ‘early-onset occasional’ (2.3%) and ‘regular’ users (3.4%).

Sex, mother’s substance use, and child’s tobacco use, alcohol consumption and conduct problems were strongly associated with cannabis use.

At age 21 years, compared with the non-user class, late-onset occasional, early-onset occasional and regular cannabis user classes had higher odds of nicotine dependence (OR=3.5, 95% CI 0.7 to 17.9; OR=12.1, 95% CI 1.0 to 150.3; and OR=37.2, 95% CI 9.5 to 144.8, respectively); harmful alcohol consumption (OR=2.6, 95% CI 1.5 to 4.3; OR=5.0, 95% CI 2.1 to 12.1; and OR=2.6, 95% CI 1.0 to 7.1, respectively); and other illicit drug use (OR=22.7, 95% CI 11.3 to 45.7; OR=15.9, 95% CI 3.9 to 64.4; and OR=47.9, 95% CI 47.9 to 337.0, respectively).

Conclusions

One-fifth of the adolescents in our sample followed a pattern of occasional or regular cannabis use, and these young people were more likely to progress to harmful substance use behaviours in early adulthood.

Source:  http://dx.doi.org/10.1136/jech-2016-208503

ABSTRACT

PURPOSE:

Nationwide data have been lacking on drug abuse (DA)-associated mortality. We do not know the degree to which this excess mortality results from the characteristics of drug-abusing individuals or from the effects of DA itself.

METHOD:

DA was assessed from medical, criminal, and prescribed drug registries. Relative pairs discordant for DA were obtained from the Multi-Generation and Twin Registers. Mortality was obtained from the Swedish Mortality registry.

RESULTS:

We examined all individuals born in Sweden 1955-1980 (n = 2,696,253), 75,061 of whom developed DA. The mortality hazard ratio (mHR) (95% CIs) for DA was 11.36 (95% CIs, 11.07-11.66), substantially higher in non-medical (18.15, 17.51-18.82) than medical causes (8.05, 7.77-8.35) and stronger in women (12.13, 11.52-12.77) than in men (11.14, 10.82-11.47). Comorbid smoking and alcohol use disorder explained only a small proportion of the excess DA-associated mortality.

Co-relative analyses demonstrated substantial familial confounding in the DA-mortality association with the strongest direct effects seen in middle and late-middle ages. The mHR was highest for opiate abusers (24.57, 23.46-25.73), followed by sedatives (14.19, 13.11-15.36), cocaine/stimulants (12.01, 11.36-12.69), and cannabis (10.93, 9.94-12.03).

CONCLUSION:

The association between registry-ascertained DA and premature mortality is very strong and results from both non-medical and medical causes. This excess mortality arises both indirectly-from characteristics of drug-abusing persons-and directly from the effects of DA. Excess mortality of opiate abuse was substantially higher than that observed for all other drug classes. These results have implications for interventions seeking to reduce the large burden of DA-associated premature mortality.

Source:  https://www.ncbi.nlm.nih.gov/pubmed/28550519   May 2017

Ketamine Continues to Impress and Confound Researchers

A novel glutamatergic hypothesis of depression, using a 50-year-old anaesthesia medicine, has had a remarkable run as of late. First an anaesthetic, then a popular club drug in the 90s known as “Special K” (and currently still popular in Hong Kong as a “Rave Drug”), and now a novel, fast acting antidepressant, ketamine is a N-Methyl D-Aspartame (NMDA) receptor antagonist. Ketamine was FDA-approved in the U.S. as an anaesthetic nearly 50 years ago. It is used primarily by anaesthesiologists in both hospital and surgical settings. As an N-Methyl D-Aspartame (NMDA) receptor antagonist with dissociative properties, NMDA receptors possess high calcium permeability, which allows ketamine to reach its target quickly. Increasing clinical evidence has shown that a single sub-anaesthetic dose (0.5 mg/kg) of IV-infused ketamine exerts impressive antidepressant effects within hours of administration. These effects have stabilized suicidality in severely depressed, treatment-resistant individuals. The effects of low-dose ketamine infusion therapy can last up to seven days, although the dosing and patient characteristics regarding its optimal effectiveness have not been established.

In my book, “The Good News About Depression: Cures And Treatments In The New Age of Psychiatry”–Revised (1996), I said there was never a better time to be depressed, due in part to recent breakthroughs in understanding of the underlying biology of depression, plus the discovery of novel therapeutics e.g., the SSRIs. Today that book might be called the “Better News About Depression” as a result of the effectiveness of novel treatments such as Transcranial Magnetic Stimulation (TMS) and now ketamine, which has illuminated and broadened our understanding and view of treating depression.

Why Is This Better News?

New clinical and preclinical studies suggest that dysfunction of the glutamatergic system is perhaps more relevant and important than the current catecholamine hypothesis and therapy that targets serotonin, norepinephrine and sometimes dopamine. These medications often take four to six weeks to exert any therapeutic benefit, whereas rapid reductions in depressive symptoms have been observed in response to a single dose of ketamine. This is a vast departure from the SSRIs and SSNRIs that have occupied the mainstream of pharmacological therapy for depression and anxiety disorders for more than 30 years.

Lastly, the mechanism of action of NDMA antagonists are comparatively underexplored but vitally important to our understanding of depression, reversal of suicidality, as well as the debilitating, depressive symptoms induced by abuse of alcohol and other drugs. This review highlights the current evidence supporting the antidepressant effects of ketamine as well as other glutamatergic modulators, such as D-cycloserine, riluzole, CP-101,606, CERC-301 (previously known as MK-0657), basimglurant, JNJ-40411813, dextromethorphan, nitrous oxide, GLYX-13, and esketamine. This all adds up to some very good news for depressed persons and especially those who do not respond to previous SSRI or SSNRI treatments.

Source: http://www.rivermendhealth.com/resources/ketamine-fast-acting-antidepressant/  June2017

 

One in 5 adolescents at risk of tobacco dependency, harmful alcohol consumption and illicit drug use

Researchers from the University of Bristol have found regular and occasional cannabis use as a teen is associated with a greater risk of other illicit drug taking in early adulthood.   The study by Bristol’s Population Health Science Institute, published online in the Journal of Epidemiology & Community Health, also found cannabis use was associated with harmful drinking and smoking.

Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), the researchers looked at levels of cannabis use during adolescence to determine whether these might predict other problematic substance misuse in early adulthood — by the age of 21.

The researchers looked at data about cannabis use among 5,315 teens between the ages of 13 and 18. At five time points approximately one year apart cannabis use was categorised as none; occasional (typically less than once a week); or frequent (typically once a week or more).

When the teens reached the age of 21, they were asked to say whether and how much they smoked and drank, and whether they had taken other illicit drugs during the previous three months. Some 462 reported recent illicit drug use: 176 (38%) had used cocaine; 278 (60%) had used ‘speed’ (amphetamines); 136 (30%) had used inhalants; 72 (16%) had used sedatives; 105 (23%) had used hallucinogens; and 25 (6%) had used opioids.

The study’s lead author, Dr Michelle Taylor from the School of Social and Community Medicine said:

“We tend to see clusters of different forms of substance misuse in adolescents and young people, and it has been argued that cannabis acts as a gateway to other drug use. However, historically the evidence has been inconsistent.

“I think the most important findings from this study are that one in five adolescents follow a pattern of occasional or regular cannabis use and that those individuals are more likely to be tobacco dependant, have harmful levels of alcohol consumption or use other illicit drugs in early adulthood.”

In all, complete data were available for 1571 people. Male sex, mother’s substance misuse and the child’s smoking, drinking, and behavioural problems before the age of 13 were all strongly associated with cannabis use during adolescence. Other potentially influential factors were also considered: housing tenure; mum’s education and number of children she had; her drinking and drug use; behavioural problems when the child was 11 and whether s/he had started smoking and/or drinking before the age of 13.

After taking account of other influential factors, those who used cannabis in their teens were at greater risk of problematic substance misuse by the age of 21 than those who didn’t.

Teens who regularly used cannabis were 37 times more likely to be nicotine dependent and three times more likely to have a harmful drinking pattern than non-users by the time they were 21. And they were 26 times more likely to use other illicit drugs.

Both those who used cannabis occasionally early in adolescence and those who starting using it much later during the teenage years had a heightened risk of nicotine dependence, harmful drinking, and other illicit drug use. And the more cannabis they used the greater was the likelihood of nicotine dependence by the age of 21.

This study used observational methods and therefore presents evidence for correlation but not does not determine clear cause and effect — whether the results observed are because cannabis use actually causes the use of other illicit drugs. Furthermore, it does not identify what the underlying mechanisms for this might be. Nevertheless, clear categories of use emerged.

Dr Taylor concludes:

“We have added further evidence that suggests adolescent cannabis use does predict later problematic substance use in early adulthood. From our study, we cannot say why this might be, and it is important that future research focuses on this question, as this will enable us to identify groups of individuals that might as risk and develop policy to advise people of the harms.

“Our study does not support or refute arguments for altering the legal status of cannabis use — especially since two of the outcomes are legal in the UK. This study and others do, however, lend support to public health strategies and interventions that aim to reduce cannabis exposure in young people.”

Journal Reference:

1. Michelle Taylor, Simon M Collin, Marcus R Munafò, John MacLeod, Matthew Hickman, Jon Heron. Patterns of cannabis use during adolescence and their association with harmful substance use behaviour: findings from a UK birth cohort. Journal of Epidemiology and Community Health, 2017; jech-2016-208503 DOI: 10.1136/jech-2016-208503

Source:   www.sciencedaily.com/releases/2017/06/170607222448<.htm>. 7 June 2017.

Patterns of illicit drug use in each UK country analysed in annual report

An overview of illicit drug use across the whole of the UK in 2016 has been published by the Home Office.

The ‘United Kingdom Drug Situation: Focal Point Annual Report 2016’ has collated data across all four home nations and includes specific analysis of policy, prevention, treatment, drug-related deaths, infectious diseases and drug markets.

Key points relating to the UK as a whole:

· Prevalence in the general population is lower now than ten years ago, with cannabis being the main driver of that reduction. However, there has been little change in recent years.

· Seizures data suggests that herbal cannabis has come to dominate the market. While resin was involved in around two-thirds of cannabis seizures in 2000, it was involved in only five per cent in 2015/16.

· Using the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) definition, which refers to deaths caused directly by the consumption of at least one illicit drug, the total number of drug-related deaths in the UK during 2014 was 2,655; a five per cent increase from 2013 and the highest number reported to date.

· Over the last decade the average age of death has increased from 37.6 years in 2004 to 41.6 in 2014, with males being younger than females (40.3 years and 44.6 years respectively). The largest proportion of deaths in the UK in 2014 was in the 40–44 years age group.

· There were 124,234 treatment presentations in the UK in 2015. This total includes for the first time, data from individuals presenting to treatment services in prisons in England.

· Benzodiazepines were cited as a primary problem substance in far greater proportion of cases in Scotland and Northern Ireland than in England or Wales, whereas Wales had a far higher proportion of clients citing amphetamines/methamphetamines than in any of the other countries.

· National Take-Home Naloxone programmes continue to supply naloxone to those exiting prison in Scotland and Wales: there were 932 kits issued by NHS staff in prisons in Scotland, and 146 in Wales, in 2015/16.

· There were 50 new diagnoses of HIV among people who inject drugs reported from Scotland, compared with 17 in 2014. This increase was due to an outbreak of HIV in people who inject drugs in Glasgow.

Source:  http://www.sdf.org.uk/patterns-illicit-drug-use-uk-country-analysed-annual-report/

Sirs,

I believe that a state’s Attorney General and Secretary of State have the obligation to reject any petition that is obviously in violation of any law.

Whether a ballot initiative is properly worded or not, if it proposes, facilitates or allows the violation of any law – it is illegal.

EXCERPT:  “In an opinion dated Tuesday and released Wednesday, Rutledge said the ballot title of the proposal is ambiguous and “that a number of additions or changes” are needed “to more fully and correctly summarize” the proposal.

“The proposal [to legalize recreational marijuana use in the state] by Larry Morris of West Fork would allow for the cultivation, production, distribution, sale and possession of marijuana for recreational use in Arkansas.”:

As you can readily see, Mr. Morris’ proposal would violate federal law and place persons who engage in any of those activities at risk of federal prosecution or other liability.

I draw to your attention a  LEGAL PRIMER(BELOW) ON: ENFORCING THE CONTROLLED SUBSTANCE ACT IN STATES THAT HAVE COMMERCIALIZED MARIJUANA by Mr. David Evans, Esq. in which he concludes that: “Anyone who participates in the growing, possession, manufacturing, distribution, or sales of marijuana under state law or aids or facilitates or finances such actions is at risk of federal prosecution or other liability.”

I ask that you continue to reject these illegal proposals to legalize marijuana in any form in our state of Arkansas.

I reiterate, it is your job to UPHOLD the LAW, not facilitate LAWBREAKING.

Jeanette McDougal

Board Member, Drug Watch, Intl.

Director, NAHAS – National Alliance of Health and Safety dems8692@aol.com

HUNTINGTON, W.Va. — Officer Sean Brinegar arrived at the house first — “People are coming here and dying,” the 911 caller had said — and found a man and a woman panicking. Two people were dead inside, they told him.

Brinegar, 25, has been on the force in this Appalachian city for less than three years, but as heroin use has surged, he has seen more than his fair share of overdoses. So last Monday, he grabbed a double pack of naloxone from his gear bag and headed inside.

A man was on the dining room floor, his thin body bluish-purple and skin abscesses betraying a history of drug use. He was dead, Brinegar thought, so the officer turned his attention to the woman on a bed. He could see her chest rising but didn’t get a response when he dug his knuckle into her sternum.

Brinegar gave the woman a dose of injected naloxone, the antidote that can jumpstart the breathing of someone who has overdosed on opioids, and returned to the man. The man sat up in response to Brinegar’s knuckle in his sternum — he was alive after all — but started to pass out again. Brinegar gave him the second dose of naloxone.

Maybe on an average day, when this Ohio River city of about 50,000 people sees two or three overdoses, that would have been it. But on this day, the calls kept coming.

Two more heroin overdoses at that house, three people found in surrounding yards. Three overdoses at the nearby public housing complex, another two up the hill from the complex.

From about 3:30 p.m. to 7 p.m., 26 people overdosed in Huntington, half of them in and around the Marcum Terrace apartment complex. The barrage occupied all the ambulances in the city and more than a shift’s worth of police officers.

By the end of it, though, all 26 people were alive. Authorities attributed that success to the cooperation among local agencies and the sad reality that they are well-practiced at responding to overdoses. Many officials did not seem surprised by the concentrated spike.

“It was kind of like any other day, just more of it,” said Dr. Clay Young, an emergency medicine doctor at Cabell Huntington Hospital.

But tragic news was coming. Around 8 p.m., paramedics responded to a report of cardiac arrest. The man later died at the hospital, and only then were officials told he had overdosed. On Wednesday, authorities found a person dead of an overdose elsewhere in Cabell County and think the death could have happened Monday. They are investigating whether those overdoses are tied to the others, potentially making them Nos. 27 and 28.

It’s possible that the rash of overdoses was caused by a particularly powerful batch of heroin or that a dearth of the drug in the days beforehand weakened people’s tolerance. But police suspect the heroin here was mixed with fentanyl, a synthetic opioid that is many times more potent than heroin. A wave of fatal overdoses signaled fentanyl’s arrival in Huntington in early 2015, and now some stashes aren’t heroin laced with fentanyl, but “fentanyl laced with heroin,” said Police Chief Joe Ciccarelli. Another possibility is carfentanil, another synthetic opioid, this one used to sedate elephants. Police didn’t recover drugs from any of the overdoses, but toxicology tests from the deaths could provide answers.

A battle-scarred city

In some ways, what happened in Huntington was as unremarkable as the spurts in overdoses that have occurred in other cities. This year, fentanyl or carfentanil killed a dozen people in Sacramento, nine people in Florida, and 23 people in about a month in Akron, Ohio. The list of cities goes on: New Haven, Conn.; Columbus, Ohio; Barre, Vt.

But what happened in Huntington stands out in other ways. It underlines the potential of a mysterious substance to unleash wide-scale trauma and overwhelm a city’s emergency response. And it suggests that a community that is doing all the right things to combat a worsening scourge can still get knocked back by it.

“From a policy perspective, we’re throwing everything we know at the problem,” said Dr. James Becker, the vice dean for governmental affairs and health care policy at the medical school at Marshall University here. “And yet the problem is one of those that takes a long time to change, and probably isn’t going to change for quite a while.”

Surrounded by rolling hills packed with lush trees, Huntington is one of the many fronts in the fight against an opioid epidemic that is killing almost 30,000 Americans a year. But this city, state, and region are among the most battle-scarred. West Virginia has the highest rate of fatal drug overdoses of any state and the highest rate of babies born dependent on opioids among the 28 states that report data. But even compared with other communities in West Virginia, Huntington sees above-average rates of heroin use, overdose deaths, and drug-dependent newborns. Local officials estimate up to 10 percent of residents use opioids improperly.

The heroin problem emerged about five years ago when authorities around the country cracked down on “pill mills” that sent pain medications into communities; officials here specifically point to a 2011 Florida law that arrested the flow of pills into the Huntington area.

As the pills became harder to obtain and harder to abuse, people turned to heroin. It has devoured many communities in Appalachia and beyond.

In Huntington, law enforcement initially took the lead, with police arresting hundreds of people. They seized thousands of grams of heroin. But it wasn’t making a dent. So in November 2014, local leaders established an office of drug control policy.

“As far as numbers of arrests and seizures, we were ahead of the game, but our problem was getting worse,” said Jim Johnson, director of the office and a former Huntington police officer. “It became very obvious that if we did not work on the demand side just as hard as the supply side, we were never going to see any success.”

The office brought together law enforcement, health officials, community and faith leaders, and experts from Marshall to try to tackle the problem together.

Changes in state law have opened naloxone dissemination to the public and protected people who report overdoses. But the city and its partners have gone further, rolling out programs through the municipal court system to encourage people to seek treatment. One program is designed to help women who work as prostitutes to feed their addiction. Huntington has eight of the state’s 28 medically assisted detox beds, and they’re always full.

Also, in 2014, a center called Lily’s Place opened in Huntington to wean babies from drugs. Last year, the local health department launched this conservative state’s first syringe exchange. The county, health officials know, is at risk for outbreaks of HIV and hepatitis C because of shared needles, so they are trying to get ahead of crises seen in other communities afflicted by addiction.

“Huntington just happens to have taken ownership of the problem, and very courageously started some programs … that have been models for the rest of the state,” said Kenneth Burner, the West Virginia coordinator for the Appalachia High Intensity Drug Trafficking Areas program.

‘A revolving door’

While paramedics in the area have carried naloxone for years, it was this spring that Huntington police officers were equipped with it. Just a few officers have administered it, but Monday was Brinegar’s third time reviving overdose victims with naloxone.

Paramedics, who first try reviving victims by pumping air with a bag through a mask, had to administer another 10 doses of naloxone Monday. Three doses went to one person, said Gordon Merry, the director of Cabell County Emergency Services. During the response, ambulances from stations outside Huntington were called into the city to assist the eight or so response teams already deployed.

Merry was clearly proud of the response, but also frustrated. He was tired, he said, of people whom emergency crews revived going back to drugs. Because of the power of their disease, saving their lives didn’t get at the root of their addiction.

“It’s a revolving door. We’re not solving the problem past reviving them,” he said. “We gave 26 people another chance on life, and hopefully one of those 26 will seek help.”

In the part of town where half the overdoses happened, some homes are well-kept, with gardens, bird feeders, and American flags billowing. “Home Sweet Home,” read an engraved piece of wood above one front door; in another front yard, a wooden sculpture presented a bear holding a fish with “WELCOME” written across its body.

But many structures are decrepit and have their windows blacked out with cardboard and sheets. At one boarded-up house, the metal slats that once made up an overhang for the front porch split apart and warped as they collapsed, like gnarled teeth. On the plywood that covered a window frame was a message spelled out in green dots: GIRL SCOUTS RULE.

In and around the public housing complex, which is made up of squat two-story brick buildings sloping up a hill, people either said they did not know what had happened Monday, or that “lowlifes” in another part of the complex sparked the problem. Even as paramedics were responding to the overdoses, police started raiding residences as part of their investigation, including apartments at the complex, the chief said.

Just up the hill, a man named Bill was sitting on a recliner on his front porch with his cat. He said he saw the police out in the area Monday, but doesn’t pay much attention to overdoses anymore. They are so frequent.

Bill, who is retired, asked to be identified only by his first name because he said he has a son in law enforcement. He has lived in that house for five decades and started locking his door only in recent years. His neighbors’ house had been broken into, and he had seen people using drugs in cars across the street from his house. He called the police sometimes, he said, but the users were always gone by the time the police arrived.

“I hate to say this, but you know, I’d let them die,” Bill said. “If they knew that no one was going to revive them, maybe they wouldn’t overdose.”

Even here, where addiction had touched so many lives, it’s not an uncommon sentiment. Addiction is still viewed by some as a bad personal choice made by bad people.

“Some folks in the community just didn’t care” that 26 of their fellow residents almost died, said Matt Boggs, the executive director of Recovery Point.  Recovery Point is a long-term recovery program that teaches “clients” to live a life without drugs or alcohol. Boggs himself is a graduate of the program, funded by the state and donations and grants.

The clients live in bunk rooms at the facility for an average of more than seven months before graduating. The program says that about two-thirds of graduates stay sober in the first year after graduation, and about 85 percent of those people are sober after two years.

Local officials praise Recovery Point, but like many other recovery programs, it is limited in what it can do. It has 100 beds for men at its location in Huntington, and is expanding at other sites in the state, but Boggs said there’s a waiting list of a couple hundred people.

Mike Thomas, 30, graduated from the main part of the program a month ago and is working as a peer mentor there as he transitions out of the facility. Thomas has been clean since Oct. 15, 2015, but has dreams about getting high or catches himself thinking he could spare $100 from his bank account for drugs.

Thomas hopes to find a full-time job helping addicts. His own recovery will be a lifelong process, one that can be torn apart by a single bad decision, he said. He will always be in recovery, never recovered.    “I’m not cured,” he said.

 

A killer that doesn’t discriminate

As heroin has bled into communities across the country, it has spread beyond the regular drug hotbeds in cities. On a 2004 map of drug use in Huntington — back then, mostly crack cocaine — a few blocks of the city glow red. Almost the entire city glows in yellows and reds on the 2014 map.

In 2015, there were more than 700 drug overdose calls in Huntington, ranging from kids in their early teens to seniors in their late 70s. In 2014, it was 272 calls; in 2012, 146. One bright spot: fatal overdoses, which stood at 58 in 2015, have ticked down so far this year.

“I used to be able to say, ‘We need to focus here,’” said Scott Lemley, a criminal intelligence analyst at the police department. “I can’t do that anymore.”

Heroin hasn’t just dismantled geographic barriers. It has infiltrated every demographic “It doesn’t discriminate.   Prominent businessmen, their child. Police officers, their child. Doctors, their child,” Merry said. “The businessman and police officer do not have their child anymore.”

The businessman is Teddy Johnson. His son, Adam, died in 2007 when he was 22, one of a dozen people who died in a five-month period because of an influx of black-tar heroin. The drug hadn’t made its full resurgence into the region yet, but now, Johnson sees the drug that killed his son everywhere.

 

Teddy Johnson lost his son, Adam, in 2007 to a heroin overdose. He has several tattoos dedicated to Adam’s memory.  He runs a plumbing, heating, and kitchen fixture and remodelling business. From his storefront, he has witnessed deals across the street.

Adam, who was a student at Marshall, was a musician and artist who hosted radio shows. He was the life of any party, his dad said.

Johnson was describing Adam as he sat at the marble countertop of a model kitchen in his business last week. With the photos of his kids on the counter, it felt like a family’s home. Johnson explained how he still kept Adam’s bed made, how he kept his son’s room the same, and then he began to cry.

“The biggest star in the sky we say is Adam’s star,” he said. “When we’re in the car — and it can’t be this way — but it always seems to be in front of us, guiding us.”

Adam’s grave is at the top of a hill near the memorial to the 75 people — Marshall football players, staff, and fans — who died in a 1970 plane crash. It’s a beautiful spot that Johnson visits a few times each week, bringing flowers and cutting the grass around his son’s grave himself. Recently a note was left there from a couple Johnson knows who

just lost their son to an overdose; they were asking Adam to look out for their son in heaven.

But even here, at what should be a respite, Johnson can’t escape what took his son. He said he has seen deals happen in the cemetery, and he recently found a burnt spoon not more than 20 feet from his son’s grave.

Johnson keeps fresh flowers on his son’s grave and cuts the grass around the grave himself.

“I’ve just seen too much of it,” he said.

If Huntington doesn’t have a handle on heroin, at least the initiatives are helping officials understand the scale of the problem. More than 1,700 people have come through the syringe exchange since it opened, where they receive a medical assessment and learn about recovery options. The exchange is open one day a week, and in less than a year, it has distributed 150,000 clean syringes and received 125,000 used syringes.

But to grow and sustain its programs, Huntington needs money, officials say. The community has received federal grants, and state officials know they have a problem. But economic losses and the collapse of the coal industry that fueled the drug epidemic have also depleted state coffers.

“We have programs ready to launch, and we have no resources to launch them with,” said Dr. Michael Kilkenny, the physician director of the Cabell-Huntington Health Department. “We’re launching them without resources, because our people are dying, and we can’t tolerate that.”

In some ways, Huntington is fortunate. It has a university with medical and pharmacy schools enlisted to help, and a mayor’s office and police department collaborating with public health officials. But what does that herald then for other communities?

“If I feel anxious about what happens in Huntington and in Cabell County, I cannot imagine what it must be like to live in one of these other at-risk counties in the United States, where they don’t have all those resources, they don’t have people thinking about it,” said Dr. Kevin Yingling, the dean of the Marshall University School of Pharmacy.

Yingling, Kilkenny, and others were gathered on Friday afternoon to talk about the situation in Huntington, including the rash of overdoses. But by then, there was already a different incident to discuss.

A car had crashed into a tree earlier that afternoon in Huntington. A man in the driver seat and a woman in the passenger seat had both overdosed and needed naloxone to be revived. A preschool-age girl was in the back seat.

Source:    https://www.statnews.com/2016/08/22/heroin-huntington-west-virginia-overdoses/ 22.08.16

In this guest blog, Kate Fleming, Senior Lecturer, Public Health Institute, Liverpool John Moores University, and Raja Mukherjee, Consultant Psychiatrist, Lead Clinician UK National FASD clinic, Surrey and Borders Partnership NHS Foundation Trust consider the context and future for Foetal Alcohol Spectrum Disorders in the UK.

A recent opinion piece in The Guardian entitled Nothing prepared me for pregnancy- apart from the never ending hangover of my 20s took a, presumably, humorous take on the tiredness, vomiting, dehydration, and secrecy that so many women live through in early pregnancy, likening this to days spent hungover after excessive drinking in the author’s early 20s.

In an article that was entirely about alcohol and pregnancy there was reassuringly no mention of the author consuming alcohol during pregnancy, indeed quite the reverse “I don’t actually want booze in my body”.  But neither was there explicit reference to the harms that alcohol can cause in pregnancy.

The harms caused by consuming alcohol in pregnancy

Foetal Alcohol Spectrum Disorders (FASD) is an umbrella term that encompasses the broad range of conditions that are related to maternal alcohol consumption.  The most severe end of the spectrum is Foetal Alcohol Syndrome (FAS) associated with distinct facial characteristics, growth restriction and permanent brain damage.  However, the spectrum includes conditions displaying mental, behavioural and physical effects on a child which can be difficult to diagnose.  Confusingly, these conditions also go under several other names including Neuro-developmental Disorder associated with Prenatal Alcohol Exposure (ND-PAE) the preferred term by the American Psychiatric Association’s fifth version of its Diagnostic and Statistical Manual (APA DSM-V), alcohol-related birth defects, alcohol-related neuro-developmental disorder, and partial foetal alcohol syndrome.

How common is FASD? A recent study which brought together information from over 300 studies estimates the prevalence of drinking in pregnancy to be close to 10%, and around 1 in 4 women in Europe drinking during pregnancy. Their estimates of FAS (the most severe end of the spectrum) were 14.6 per 10000 people worldwide or 37.4 per 10000 people in Europe, corresponding to 1 child in every 67 women who drank being born with FAS.

Given the figure for alcohol consumption in pregnancy is even higher in the UK, with some studies suggesting up to 75% of women drink at some point in their pregnancy, conservatively in the UK we might expect a prevalence of FASD of at least 1%.  We also know that it is highly unlikely that anything close to this number of individuals have formally had a diagnosis.  This lack of knowledge of the prevalence in the UK is hampering efforts to ensure the required multi-sector support for those affected by FASD and their families.

Current policy

For some time a significant focus of alcohol in pregnancy research was to try and identify a safe threshold of consumption, without demonstrable success.  No evidence of harm at low levels does not however equate to evidence of no harm and as such in 2016 the Chief Medical Officer revised guidance on alcohol consumption in pregnancy to recommend that women should avoid alcohol when trying to conceive or when pregnant.  Though this clarity of guidelines has been well received by the overwhelming majority of health professionals there are barriers to its implementation with few professionals “very prepared to deal with the subject”.  In addition, knowledge of the guideline amongst the general public has yet to be evaluated.

As part of the 2011 public health responsibility deal a commitment to 80% of products having labels which include warnings about drinking when pregnant forms part of the alcohol pledges. A study in 2014 showed that 90% of all labels did indeed include this information. However, it has also been shown that this form of education is amongst the least effective in terms of alcohol interventions, and the pledge is no longer in effect.

Pregnancy is recognised as a good time for the initiation of behaviour change yet in the context of alcohol consumption it is arguably too late. An estimated half of all pregnancies are unplanned and there remains therefore a window of early pregnancy before a woman is likely to have had contact with a health professional and before the guidelines can be explained during which unintentional damage to her unborn baby could occur.  The same argument can be used when considering the suggestion of banning the sale of alcohol to pregnant women – visible identification of pregnancy tends only to be possible at the very latest stages.

How then to address consumption of alcohol during pregnancy? 

Consumption of alcohol is doubtless shaped by the culture and context of the society in which one is living.  Highest levels of alcohol consumption in pregnancy are, unsurprisingly, seen in countries where the population consumption of alcohol is also highest.  Current UK policy that is directed to reducing population consumption of alcohol will likely have a knock-on effect of reducing alcohol consumption in pregnancy.

Many women will however be familiar with the barrage of questions that they encounter when not drinking on a night out.  From the not-so-subtle “Not drinking, eh… Wonder why that is? <nudge, nudge, wink, wink>” to the more overt “Are you pregnant?”.  The road to conception and pregnancy is littered with enough stumbling blocks and pressures that the additional unintentional announcement of either fact of conception or intention to conceive is an unnecessary cause of potential further anxiety. Until society accepts that not drinking is an acceptable choice, without any need for clarification or explanation, then pregnant women or those hoping to conceive who are adhering to guidelines will continue to identify themselves, perhaps before they want to.

What next?

The UK’s All Party Parliamentary Group for FASD had its inaugural meeting in June 2015.  This group calls for an increased awareness of FASD particularly regarding looked

after children and individuals within the criminal justice system, sectors where the prevalence of FASD is particularly high. Concerted efforts need to be made to identify children with FASD to ensure that the appropriate support pathways are in place. Alongside this, efforts to ensure the best mechanisms for education of the dangers of alcohol consumption in pregnancy need to be increased, including training for midwives, and other health professionals who may be able to offer brief intervention and advice to women both before and after conception.

The views expressed by the authors are theirs alone and do not represent the views of Liverpool John Moores University, the UK National FASD clinic at Surrey and Borders Partnership NHS Foundation Trust. NOFAS run a national FASD helpline on on 020 8458 5951 as do the FASD Trust on 01608 811 599.

Source:  http://www.alcoholpolicy.net/2017/05/drinking-in-pregnancy-where-next-for-fasd-in-the-uk.html

Addiction Advocacy Needs A Bill Gates, David Geffen, Warren Buffett, Or Tom Steyer

Addiction doesn’t need someone to put their name on a building, or name a research institute. Addiction desperately needs bold philanthropists who want to leverage the people power of the grassroots. Addiction and drug overdoses claim one life every four minutes in America. In the time it takes to order a latte, someone dies—from an illness that is highly treatable. The addiction crisis is the result of social prejudice; criminal justice policies that incarcerate people with addiction instead of giving them treatment; health care policies that make it difficult or impossible to get medical help for substance use disorders; ignorance; and “abstinence-only” drug policies that are ineffective and backwards.

The fact is, people who struggle with substance use disorder are treated like second-class citizens. Admitting there’s a problem can mean losing your job, home, and custody of your children. That makes addiction a civil rights issue. And, thanks to the work of advocates across the nation, it’s finally being recognized as a moral issue, as well. Thought leaders like Tom Steyer are helping to drive this message home. I first met Tom during the Democratic National Convention. I had just shared my experience with addiction and recovery when Tom approached me. I was taken aback by the story he shared. He, too, lost someone very dear to him due to addiction: his best friend, who struggled with addiction for decades. His friend contracted HIV and Hepatitis C through drug use, and died of medical complications due to his illnesses. A few months later, Tom joined me at the Facing Addiction in America summit in Los Angeles, where we invited him to share his story on stage with the U.S. Surgeon General. As Tom talked, tears filled my eyes. He said, “We must embrace our shared humanity and recognize that addiction is a deadly, chronic illness, not a personal failing.” I’d lost friends, too. I was at risk, too. It was time to bridge the gap between policies and public awareness.

People like Tom Steyer and other pioneering philanthropists, who give tens of millions to progressive causes such as medical research, environmental causes, and water quality, must also step up to end the addiction crisis in America. Our fight is America’s fight. The sooner they do, the quicker we can heal this nation from our generation’s most urgent public health crisis.

Working alongside lobbyists, nonprofit groups, social organizers, and peer recovery groups, they can help fill the gaps left by policies and laws that omit or punish people with substance use disorder. As the current administration takes steps toward a health care bill that will leave people suffering from addiction without medical care, these philanthropic giants are in a unique position to help. Why? Because their involvement would not be tied to political party or personal gain. Rather, they would focus on the solution, plain and simple.

Addiction should be one of the issues on the list of social problems we urgently address, next to finding a cure for cancer and ending childhood hunger. Addiction permeates the social fabric of America. Nobody is exempt. As many people suffer from addiction as diabetes; more people use pain medications than tobacco products. For every person who’s developed full blown substance use disorder, another dozen are on the road to addiction. Substance use disorder affects every corner of society, including our collective health, family unity, the economy, workplace productivity, and our reliance on social programs. It also keeps jails full of people who may struggle to find jobs to support their families once they’re released, and will never be able to vote again.

The recovery advocacy movement has been built slowly, through the efforts of individuals and highly fragmented groups. We have an incredible grassroots movement that addresses an issue that directly impacts one in every three families in America, and indirectly touches all of us. But fundraising for recovery advocacy has been largely through family and friend donations—which, although heartfelt, aren’t sufficient to fund serious research, create desperately needed social infrastructure, or provide education about the true nature of addiction. While organizations dedicated to battling cancer, heart disease, and diabetes raise hundreds of millions of dollars annually, the “addiction field,” such as it is, raises perhaps $25 million from private sources. This is unconscionable.

Gates, Geffen, Buffett, Steyer, and other philanthropic giants have the potential to be visionaries in this space. They could quickly stem the addiction epidemic without waiting for policy makers to hammer out yet another law that places people’s recovery at risk. They could find the solution that keeps families intact. With their help, nobody will lose another friend to this disease or the health problems that come with it. Bob and Suzanne Wright demonstrated the power and possibility of this kind of giving when they funded Autism Speaks. Their philanthropy helped move autism front and center: why not do the same for addiction?

What will our society, our culture, be like when we finally take addiction out of the equation? For many people, and their families, the answer is coming much too slowly.

It’s time to apply our knowledge, build a coalition, and offer the solutions our country so desperately needs. It’s time to change the framework of this crisis and confront our deepest values. Instead of punishment, we need to help the people who are sick—dying from this illness. It’s time to work together and end America’s addiction crisis for good.

What we need now is for America’s philanthropic visionaries to step up to help us dramatically accelerate the pace of progress in this urgent effort. Addiction doesn’t need someone to put their name on a building, or name a research institute. Addiction desperately needs bold philanthropists who want to leverage the people power of the grassroots. Ryan Hampton is an outreach lead and recovery advocate at Facing Addiction, a leading nonprofit dedicated to ending the addiction crisis in the United States.

Source:  http://www.huffingtonpost.com/entry/addiction-advocacy-needs-a-bill-gates-david-geffen_us_592ddfaae4b075342b52c0f5   30th May 20127

SAN FRANCISCO – Visits by teens to a Colorado children’s hospital emergency department and its satellite urgent care centers increased rapidly after legalization of marijuana for commercialized medical and recreational use, according to new research being presented at the 2017 Paediatric Academic Societies Meeting in San Francisco.

The study abstract, “Impact of Marijuana Legalization in Colorado on Adolescent Emergency Visits” on Monday, May 8 at the Moscone West Convention Center in San Francisco.

Colorado legalized the commercialization of medical marijuana in 2010 and recreational marijuana use in 2014. For the study, researchers reviewed the hospital system’s emergency department and urgent care records for 13- to 21-year-olds seen between January 2005 and June 2015.

They found that the annual number of visits with a cannabis related diagnostic code or positive for marijuana from a urine drug screen more than quadrupled during the decade, from 146 in 2005 to 639 in 2014.

Adolescents with symptoms of mental illness accounted for a large proportion (66%) of the 3,443 marijuana-related visits during the study period, said lead author George Sam Wang, M.D., FAAP, with psychiatry consultations increasing from 65 to 442. More than half also had positive urine drug screen tests for other drugs. Ethanol, amphetamines, benzodiazepines, opiates and cocaine were the most commonly detected.

Dr. Wang, an assistant professor of paediatrics at the University of Colorado Anschutz Medical Campus, said national data on teen marijuana use suggest rates remained roughly the same (about 7%) in 2015 as they’d been for a decade prior, with many concluding no significant impact from legalization. Based on the findings of his study, however, he said he suspects these national surveys do not entirely reflect the effect legalization may be having on teen usage.

“The state-level effect of marijuana legalization on adolescent use has only begun to be evaluated,” he said. “As our results suggest, targeted marijuana education and prevention strategies are necessary to reduce the significant public health impact of the drug can have on adolescent populations, particularly on mental health.”

Dr. Wang will present the abstract, “Impact of Marijuana Legalization in Colorado on Adolescent Emergency Department (ED) Visits,” from 8 a.m. to 10 a.m. Numbers in this news release reflect updated information provided by the researchers. The abstract is available at https://registration.pas-meeting.org/2017/reports/rptPAS17_abstract.asp?abstract_final_id=3160.11.

The Paediatric Academic Societies (PAS) Meeting brings together thousands of individuals united by a common mission: to improve child health and well-being worldwide. This international gathering includes paediatric researchers, leaders in academic paediatrics, experts in child health, and practitioners. The PAS Meeting is produced through a partnership of four organizations leading the advancement of paediatric research and child advocacy: Academic Paediatric Association, American Academy of Paediatrics, American Paediatric Society, and Society for Paediatric Research. For more information, visit the PAS Meeting online at www.pas-meeting.org, follow us on Twitter @PASMeeting and #pasm17, or like us on Facebook. For additional AAP News coverage, visit http://www.aappublications.org/collection/pas-meeting-updates.

Source:   http://www.aappublications.org/news/2017/05/04/PASMarijuana050417

 A New Agenda to  Turn Back the Drug Epidemic

Robert L. DuPont, MD, President , Institute for Behavior and Health, Inc.

A. Thomas McLellan, PhD, Senior Strategy Advisor , Institute for Behavior and Health, Inc.  May 2017

Institute for Behavior and Health, Inc. , 6191 Executive Blvd , Rockville, MD 20852 , www.IBHinc.org 1

Background 

The Institute for Behavior and Health, Inc. (IBH) is a 501(c)3 non-profit substance use policy and research organization that was founded in 1978. Non-partisan and non-political, IBH develops new ideas and serves as a force for change.

Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs and Health was published in November 2016. Four months later, in March 2017, IBH held a meeting of 25 leaders in addiction treatment, health care, insurance, government and research to discuss the scope and implications of this historic document. The US Surgeon General, VADM Vivek H. Murthy, MD, was an active participant in the meeting. The significance of this new Surgeon General’s Report is analogous to the historic 1964 Surgeon General’s report, Smoking and Health, a document that inspired an extraordinarily successful public health response in the United States that has reduced the rates of cigarette smoking by over 64% and continues its impact even today, more than 50 years following its release.

The following is a summary of the discussion at the March 2017 meeting and the conclusions and recommendations that were developed.

Introduction: The 2016 Surgeon General’s Report 

The two primary objectives of the US Surgeon General’s Report of 2016 are first to provide scientific evidence that shows that in addition to nicotine, other substance misuse and addiction issues (e.g., alcohol, opioids, marijuana, etc.) also are best understood and addressed as public health problems; and second to encourage the inclusion of addiction – its prevention, early recognition and intervention, treatment and active long-term recovery management – into the mainstream of American health care. At present these elements are not integrated either as a stand-alone continuum or within the general medical system. As is true for other widespread illnesses, addiction to nicotine, alcohol, marijuana, opioids, cocaine and other substances is a serious chronic illness. This perspective is contrary to the common perception that addiction reflects a moral failing, a personal weakness or poor parenting. Such opinions have stigmatized individuals who are suffering from these often deadly substance use disorders and have led to expensive and ineffective public policies that segregate prevention and treatment outside of mainstream medical care. A better public health approach encourages afflicted individuals and their family members to seek and receive help within the current health care system for these serious health problems.

An informed public health approach to reducing the prevalence and the harms associated with substance use disorders requires more than the brief treatment of serious cases. Particularly important are substance use prevention programs in schools, healthcare and in all other parts of the community to protect adolescents (ages 12 – 21), the group most at risk for the initiation of substance-related harms and substance use disorders.  Importantly, abundant tragic experience and accumulating science show that substance use disorders are not effectively treated with only short-term care. Because substance use disorders produce 2 significant long-lasting changes in the brain circuits responsible for memory, motivation, inhibition, reward sensitivity and stress tolerance, addicted individuals remain vulnerable to relapse years following specialized treatment.1, 2, 3 Thus, as is true for all other chronic illnesses, long periods of personalized treatment and monitoring are necessary to assure compliance with care, continued sobriety, and improved health and social function. In combination, science-based prevention, early intervention, continuing care and monitoring comprise a modern continuum of public health care. The overall goals of this continuum comport well with those of other chronic illnesses:

1 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 2. The Neurobiology of Substance Use, Misuse, and Addiction. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available: https://addiction.surgeongeneral.gov/

2 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 5. Recovery: The Many Paths to Wellness. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available: https://addiction.surgeongeneral.gov/

3 Betty Ford Institute Consensus Panel. (2007). What is recovery? A working definition from the Betty Ford Institute. Journal of Substance Abuse Treatment, 33(3), 221-228.

4 White, W. L. (2012). Recovery/remission from substance use disorders: An analysis of reported outcomes in 415 scientific reports, 1868-2011. Philadelphia, PA: Philadelphia Department of Behavioral Health and Intellectual Disability Services.

· sustained reduction of the cardinal symptom of the illness, i.e., substance use;

· improved general health and function; and,

· education and training of the patient and the family to self-manage the illness and avoid relapses.

In the addiction field achieving these goals is called “recovery.” This word is used to describe abstention from the use of alcohol, marijuana and other non-prescribed drugs as well as improved personal health and social responsibility.3,4 Over 25 million formerly addicted Americans are in stable, long-term recovery of a year or longer.4 Understanding how to consistently accomplish the life-saving goal of recovery must inform health care decisions.

The 2016 Surgeon General’s Report offers a science-informed vision and path to recovery in response to the nation’s serious addiction problem, including specifically the opioid overdose epidemic. Research shows that it is possible to prevent or delay most cases of substance misuse; and to effectively treat even the most serious substance use disorders with recovery as an expectable result of comprehensive, continuous care and sustained monitoring. To do this, substance use disorders must be recognized as serious, chronic health conditions that are both preventable and treatable. The nation must integrate the short-term siloed episodes of specialty treatment that now are isolated from mainstream healthcare into a fully integrated continuum of care comparable to that currently available to those with other chronic illnesses such as diabetes, hypertension, asthma and chronic pain.

Meeting Discussion and Conclusions 

The Surgeon General’s Report and the meeting convened by the Institute for Behavior and Health, Inc. (IBH) to promote its recommendations are significant responses to the expanding epidemic of opioid 3 and other substance use disorders, an epidemic that struck nearly 21 million Americans aged 12 and older in 2015 alone.5 That year saw more than 52,000 overdose deaths.6 This drug epidemic has devastated countless families and communities throughout the US. Unlike earlier and smaller drug epidemics, the current opioid epidemic is not limited to a few regions or communities or a narrow range of ethnicities or incomes in the United States. Instead it afflicts all communities and all socioeconomic groups; its impacts include smaller communities and rural areas as well as suburban areas and inner cities. Fuelled by the suffering of countless grieving families, the nation is in the early stages of confronting the new epidemic. A growing national determination to turn back this deadly epidemic has opened the door to innovation that is sustained by strong bipartisan political support for new and improved efforts in both prevention and treatment of substance use disorders.

5 Center for Behavioral Health Statistics and Quality. (2015). Behavioral health trends in the United States: Results from the 2014 National Survey on Drug Use and Health (HHS Publication No. SMA 15-4927, NSDUH Series H-50). Available: http://www.samhsa.gov/data/

6 Rudd, R. A., Seth, P., David, F., & Scholl, L. (2016, December 30). Increases in drug and opioid-involved overdose deaths – United States. Morbidity and Mortality Weekly Report, 65(50-51), 1445-1452. Available: https://www.cdc.gov/mmwr/volumes/65/wr/mm655051e1.htm

7 Levy, S. J., Williams, J. F., & AAP Committee on Substance Use and Prevention. (2016). Substance use screening, brief intervention, and referral to treatment. Pediatrics, 138(1), e20161211. Available: http://pediatrics.aappublications.org/content/138/1/e20161211

8 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 3. Prevention Programs and Policies. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available: https://addiction.surgeongeneral.gov/

Abstinence is an Achievable Goal, both for Prevention and for Treatment 

Embracing and synthesizing the 30 years of science supporting the findings of the 2016 Surgeon General’s Report, the group discussed a single goal for the prevention of addiction: no use of alcohol, nicotine, marijuana or other non-prescribed drugs by youth for reasons of health. This goal should be the core prevention message to all children from a very young age. Health care professionals, educators and parents should understand the importance of this simple, clear health message. They should continue to reinforce this message of no-use for health as children grow to adulthood. Even when prevention fails, it is possible for parents, other family members, friends, primary care clinicians, educators and others to identify and to intervene quickly to stop youth substance use from becoming addiction.7

The science behind this ambitious but attainable prevention goal is clear. Alcohol, nicotine products, marijuana and other non-prescribed drug use is uniquely harmful to the still-developing brains of adolescents. Thus any substance “use” among youth must be considered “misuse” – use that may harm self or others. The goal of no substance use is not just for the purpose of preventing addiction, though that is one clear and important by product of successful prevention. Addiction is a biological process that can take years to develop. In contrast, even a single episode of high-dose use of alcohol or other substance could immediately produce an injury, accident or even death. While it is true that most episodes of substance misuse among adults do not produce serious problems, it is also true that substance misuse is associated with 70% or more of the injuries, disabilities and deaths of young people.8 These figures are even higher for minority youth. Many adolescent deaths are preventable 4 because most are related to substance use – including substance-related motor vehicle crashes and overdose.9

9 Subramaniam, G. A., & Volkow, N. D. (2014). Substance misuse among adolescents. To screen or not to screen? JAMA Pediatrics, 168(9), 798-799. Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827336/

10 Data analyzed by the Center for Behavioral Health Statistics and Quality. CBHS. (2015). Behavioral health trends in the United States: Results from the 2014 National Survey on Drug Use and Health (HHS Publication No. SMA 15- 4927, NSDUH Series H-50).

11 2014 data obtained by IBH from the Monitoring the Future study. For discussion of data through 2013 see DuPont, R. L. (2015, July 1). It’s time to re-think prevention; increasing percentages of adolescents understand they should not use any addicting substances. Rockville, MD: Institute for Behavior and Health, Inc. Available: https://www.ibhinc.org/s/IBH_Commentary_Adolescents_No_Use_of_Substances_7-1-15.pdf

Youth who use any one of the three most common “gateway” substances, i.e., alcohol, nicotine and marijuana, are many times more likely than those who do not use that single drug to use the other two substances as well as other illegal drugs.10 The use of any drug opens the door to an endless series of highly risky decisions about which drugs to use, how much to use, and when to use them. This perspective validates the public health goal for youth of no use of any drug.

Complete abstinence from the use of alcohol or any other drug among adolescents is not simply an idealistic goal – it is a goal that can be achieved. Data were presented at the meeting from the nationally representative Monitoring the Future study showing that 26% of American high school seniors in 2014 reported no use of alcohol, cigarettes, marijuana or other non-prescribed drugs in their lifetimes. 11 This is a remarkable increase from only 3% reported by American high school seniors in 1983. Moreover, in the same survey, 50% of high school seniors had not used any alcohol, cigarettes, marijuana or other non-prescribed substance in the past 30 days, up from 16% in 1982. These largely overlooked and important findings show that youth abstinence from any substance use is already widespread and steadily increasing.

In parallel with the goal of abstinence for prevention, the recommended goal for the treatment of those who are addicted is sustained abstinence from the use of alcohol and other drugs, with the caveat, explicitly acknowledged by the group, that individuals who are taking medications as-prescribed in the treatment of substance use disorders (e.g., buprenorphine, methadone and naltrexone) and who do not use alcohol or other non-prescribed addictive substances – are considered to be abstinent and ”in recovery.” Abstinence from all non-prescribed substance use is the scientifically-informed goal for individuals in addiction treatment. This treatment goal is widely accepted in the large national recovery community. The long-lasting effects of addiction to drugs are easily seen among cigarette smokers: smoking only a single cigarette is a serious threat to the former smoker, even decades after smoking the last cigarette. There is incontrovertible evidence from brain and genetic research showing the long-term effects of substance misuse on critical brain regions.2 It is unknown when or if these brain changes will return to being entirely normal following cessation of substance use; however, it is known that the recovering brain is particularly vulnerable to the effects of return to any substance use, often leading to overdose or rapid re-addiction. 5

Participants in the IBH meeting supported the idea that abstinence is the high-value outcome in addiction treatment; and that while any duration of abstinence is valuable, longer-term, stable abstinence of 5 years is analogous to the widely-used standard in cancer treatment of 5-year survival. The scientific basis for the value of sustained recovery is validated by the experience of the estimated 25 million Americans now in recovery. This increasingly visible recovery community is a remarkable and very positive new force in the country.

Measuring and Attaining these Goals 

The mantra from the IBH meeting was, if you don’t measure it, it won’t happen. The group of leaders recognized the paucity of current models for systematic integration of addiction treatment and general healthcare. The group encouraged the identification of promising models and the promotion of innovation to achieve the goal of sustained recovery. Even programs that include fully integrated care of other diseases, managed care and other comprehensive health programs do not reliably achieve the goal of sustained or even temporary recovery for substance use disorders. The meeting participants noted the absence of long-term outcome studies of the treatment of substance use disorders and encouraged all treatment programs not only to extend the care of discharged patients but also to systematically study the trajectories of discharged patients to improve their long-term treatment outcomes. The increasing range of recovery support services after treatment is an important and promising new trend that is now actively promoting sustained recovery.

Meeting participants noted one particularly promising model of public health goal measurement and attainment – the 90-90-90 goals for the treatment of HIV/AIDS: 90% of people with HIV will be screened to know their infection status; 90% of all people with diagnosed HIV infection will receive sustained antiretroviral therapy; and 90% of all patients receiving antiretroviral therapy will have viral suppression (i.e., zero viral load).12 These measurable goals provide an operational definition of public health success for the country, states and individual healthcare organizations.

12 UNAIDS. (2014). 90-90-90: An Ambitious Treatment Target to Help End the AIDS epidemic. Geneva, Switzerland: Joint United Nations Programme on HIV/AIDS. Available: http://www.unaids.org/sites/default/files/media_asset/90-90-90_en_0.pdf

With this model as background, the IBH group concluded that a similar public health approach and similarly specific numeric goals should be established for preventing and treating substance use disorders. Examples of parallel national prevention goals could include 90% rates of screening for substance misuse among adolescents; 90% provision of interventions and follow-up for those screening positive; and 90% total abstinence rates among youth aged 12-21. While these are admittedly ambitious prevention goals, adoption of them could incentivize families, schools and communities to increase the percentage of youth who do not use any alcohol, nicotine, marijuana or other drugs every year.

A similar approach was adopted by the IBH group to improve the impact of addiction treatment. Again, there would be significant public health value if the US adopted the following goals: 90% of individuals aged 12 or older receive annual screening for substance misuse and substance use disorders; 90% of those who receive a diagnosis of a substance use disorder are referred and meaningfully engaged (at 6 least three sessions) in some form of addiction treatment; and 90% of those engaged in treatment achieve sustained abstinence as measured by drug testing, during and for six months following treatment.

Source:  IBH-Report-A-New-Agenda-to-Turn-Back-the-Drug-Epidemic  May 2017

In Southern Ohio, the number of drug-exposed babies in child protection custody has jumped over 200%.  The problem is so dire that workers agreed to break protocol to invite a reporter to hear their stories.  Foster care placements are at record levels, and the number of drug-exposed newborns in their custody has jumped over 200% in the past decade

Inside the Clinton County child protection office, the week has been tougher than most.

Caseworkers in this thinly populated region of southern Ohio, east of Cincinnati, have grown battle-weary from an opioid epidemic that’s leaving behind a generation of traumatized children. Drugs now account for nearly 80% of their cases. Foster-care placements are at record levels, and the number of drug-exposed newborns in their custody has jumped over 200% in the past decade. Funding, meanwhile, hasn’t budged in years.

“Many of our children have experienced such high levels of trauma that they can’t go into traditional foster homes,” said Kathi Spirk, director of Clinton County job and family services. “They need more specialized care, which is very expensive.”

The problem is so dire that workers agreed to break protocol and invite a reporter to camp out in a conference room and hear their stories. For three days, they relived their worst cases and unloaded their frustrations, in scenes that played out like marathon group therapy, for which they have no time. Many agreed that talking about it only made them feel worse, yet still they continued, one after another.

Hence the bad week.

Given the small size of their community, they asked that their names be changed out of concern for their own safety and the privacy of the children.

The caseworkers, like most, are seasoned in despair. Many worked in the 1990s when crack cocaine first arrived, followed by crystal meth in the early 2000s. In 2008, after the shipping giant DHL shuttered its domestic hub here in Wilmington and shed more than 7,000 jobs, prescription pill mills flourished while the economy staggered. Back then, a typical month saw 30 open cases, only a few of them drug-related. But the flood of cheap heroin and fentanyl, now at its highest point yet, has changed everything. A typical month now brings four times as many cases, while institutional knowledge has been flipped on its head.

“At least with meth and cocaine, there was a fight,” said Laura, a supervisor with over 20 years of experience. “Parents used to challenge you to not take their kids. And now you have them say: ‘Here’s their stuff. Here’s their formula and clothes.’ They’re just done. They’re not going to fight you any more.”

Heroin has changed how they approach every step of their jobs, they said, from the first intake calls to that painstaking decision to place a child into temporary foster care or permanent custody. Intake workers now fear what used to be routine.

“Occasionally, we’d get thrown a dirty house, something easy to close and with little trauma to the child,” said Leslie, another worker. “We’re not getting those any more.

Now they’re all serious, and most of them have a drug component. So you may get a dirty house, but it’s never just a dirty house.”

‘I had a four-year old whose mom had died in front of her and she described it like it was nothing’ Children come into the system in two ways. The first is through a court order after caseworkers deem their environment unsafe, and if no friends or family can be found.

Because of the added trauma, removing a child is always the last option, caseworkers said. But in a county with only 42,000 people spread out over 400 square miles, the magnitude of the epidemic has compromised an already delicate safety net. Relatives are overwhelmed financially. Multiple generations are now addicted, along with cousins, uncles, and neighbors. In many cases, a safe house with a grandparent or other relative will eventually attract drug activity.

Law enforcement will also bring children in, usually after parents overdose. These cases often reveal the most horrendous neglect: a three-year old who needed every tooth pulled because he’d never been made to brush them, or kids found sleeping on bug-infested mattresses, going to the toilet in buckets because the water had been shut off. Children are coming in more hardened, they said, older than their years.

“I had a four-year-old whose mom had died in front of her and she described it like it was nothing,” said Bridgette, another caseworker. “She knew how to roll up a dollar bill and snort white powder off the counter. That’s what she thought dollar bills were for.” She added that many of the children could detail how to cook heroin. One foster family had a five-year-old boy who put his medicine dropper in his shoe. “Because that’s where daddy hid his needles,” she said.

“The kids are used to surviving in that mess,” added Carole, another veteran. “Now all the sudden the system is going in and saying it’s not safe. All their survival instincts are taken away and they go ballistic. They don’t know what to do.”

During the first weeks of foster care, meltdowns, tantrums, and violence are common as children navigate new landscapes and begin to process what they’ve experienced.

One afternoon, the caseworkers brought in a foster couple who’d taken in two sisters, an infant born drug-exposed, and her four-year old sister. The baby had to be weaned off opioids and now suffered chronic respiratory problems. Part of her withdrawal had included non-stop hiccups. The older girl had lived with her parents in a drug house and displayed clear signs of post-traumatic stress. Once, a family friend sitting next to her in a car had overdosed and turned purple. She’d witnessed domestic abuse, and one day a neighbor shot and killed her dog while she watched (she’d let the dog out). After a meltdown at a classmate’s pool party, over a year after entering foster care, she revealed having seen a toddler drown in a pond while adults got high. Through therapy, she’d also revealed sexual assault. The foster mother described how the girl suffered flashbacks, triggered by stress and certain anniversaries, like the day of her removal, and other seemingly random events. When this happened, she slipped into catatonic seizures.

“Her eyes are closed and you can’t wake her,” she said. “It’s like narcolepsy, a deep, unconscious sleep. We later discovered it was a coping mechanism she’d developed in order to survive.”

Despite what they’ve endured, most children wish desperately to return to their parents. Many come to see themselves as their parents’ caretakers and feel guilty for being taken away, especially if they were the ones to report an overdose, as in the case of a four-year-old girl who climbed out of a window to alert a neighbor. “She asked me: if I took her away, who was going to take care of mommy?” Bridgette remembered.

For caseworkers, reunification is the endgame. After children enter temporary foster care, the agency spends up to two years working closely with the family while the parents try to stay sober. The only contact with their children comes in the form of twice-weekly visits held in designated rooms here at the office. Each contains a tattered sofa and some second-hand toys. Currently, the agency runs about 200 visits each week. The encounters are monitored through closed-circuit cameras. For everyone involved, it can be the most trying period.

Many parents use the time to build trust and re-establish bonds. “During those first four years, a child gets such good stuff from their parents,” said Sherry, the caseworker who monitors the visits. “The kids are just trying to get that back.” Some parents bring doughnuts and pictures, while others need more guidance. Caseworkers hold parenting classes. Some moms lost newborns at the hospital after they tested positive for drugs; workers teach them how to feed and hold the child, and encourage them to bring outfits to dress their babies.

For other children, the visits trigger a storm of emotion that churns up the trauma of removal. “We had one girl who’d scream and wail at the end of every visit,” Laura, the supervisor, remembered. “Each time she thought she’d never see her mother again. We’d have to pry her out of mom’s arms and carry her down the hallway.”

“We’d sit in our offices and just sob,” added another worker. “But that girl’s cries weren’t enough to keep Mom off heroin.”

The number of available foster families is dwindling, while the cost of supporting them has never been higher

Perhaps the greatest difference with heroin and opioids, caseworkers said, is their iron grasp. Staying sober is a herculean task, especially in this rural community short on resources, where the nearest treatment facilities are over 30 miles away in Dayton, Cincinnati, or Columbus. At some point, nearly every parent falls off the wagon. They disappear and miss visits, leaving children to wait. One of the hardest parts of the job is telling a child that mom or dad isn’t coming, or that they can’t even be found.

“You see the hurt in their eyes,” Sherry said. “It’s a look of defeat, and it just breaks your heart.” She remembered a mother who’d failed to show up for months, then made it for her twin boys’ birthday. “The next day she overdosed and died.”

A tally sheet is used to track how many times prospective clients waiting to enter the program call a detox center, in Huntington, West Virginia. Photograph: Brendan Smialowski/AFP/Getty Images

When parents fail drug screenings during the 18-month period, caseworkers use discretion. Parents might be doing better in other areas like landing a job, or finding secure housing, so workers help them to get back on the wagon. “It’s all about showing progress,” Laura said. Some parents make it 16, 17 months sober and fully engaged. “And they’re the toughest cases, because we’ve been rooting for them this whole time and helping them. We’re giving kids pep talks, saying: ‘Mom’s doing great, she’s getting it together!’ They’re so happy to be going home. And then it all falls apart.”

With heroin, defeat is something the workers have learned to reckon with. Lately they’ve started snapping photos of parents and children during their first visit together, getting medical histories and other vital information – something they used to do much later. “Because we know the parents probably aren’t going to make it,” Laura admitted. “And if we never see them again, this is the info we need.” When asked how many opioid cases had ended in reunification, only two workers raised their hands.

The repeated disappointments come as resources and morale have reached their tipping point. The number of available foster families is dwindling, they said, while the cost of supporting them – over $1.5m a year – has never been higher.

Spirk, the agency’s director, said that all the agency’s budget was paid for with federal dollars and a county tax levy, although they’ve been flat-funded for nearly 10 years. The state contributes just 10%. When it comes to investing in child protection, Ohio ranks last in the country – despite having spent nearly $1bn fighting its opioid problem in 2016 alone.

The Ohio house of representatives recently passed a new state budget with an additional $15m for child protective services, but the state senate has yet to pass its own version. The only bit of hope came in March, when the Ohio attorney general’s office announced a pilot program that will give Clinton County, along with others, additional resources to help treat children for trauma, and to assist with drug treatment. It starts in October.

The epidemic’s unrelenting barrage has also taken a toll on mental health. “Our caseworkers are experiencing secondary trauma and frustration at not being able to reunify children with their parents because of relapses,” Spirk said.

Almost every caseworker said they had experienced depression or some form of PTSD, although no one had sought professional help. The privacy of their cases also means that few can speak openly with friends or family members. Some chose to drink, while others leaned on their faiths. But most said coping mechanisms they once relied on had failed.

“I used to have a routine on my drive home,” Laura said. “I’d stop in front of a church, roll down my window, and throw out all the day’s problems. The next morning I’d pick them back up. These days, I can’t do that anymore.”

“There’s no more outlet,” added Shelly, another supervisor. “You think you’re able to separate but you can’t let it go anymore. You try to eat healthy, do yoga, whatever they tell you to do. But it’s just so horrific now, and it keeps getting worse.”

At some point, the inevitable happens. When a parent can’t stay sober, or stops showing progress, the decision is made to place the child into permanent custody and put them up for adoption. For everyone, including caseworkers, it’s the most wrenching day.

The final act of every case is the “goodbye visit”, held in one of the nicer conference rooms. It’s a chance for parents to let their children know they love them and will miss them, and that it’s time to move on. Adoptive parents can choose to stay in contact, but it isn’t mandatory.

To make the time less stressful, Sherry, the worker who monitors the visits, has them draw pictures together, which she scans and gives to them as mementoes. She also tapes the meetings for them to keep. Watching from her tiny room full of TV screens, she can’t help but cry. “What people don’t realize is that when a baby comes into our custody, they’re still in a carrier seat. By the time the case is over, we’ve helped to potty train them. Two years is a very long time with a child. So in a way, it’s like my goodbye visit, too.”

Caseworkers have started making “life books” for kids once they come into the system. It’s where they put the photos they’ve taken, plus any pictures of birth parents or relatives they can find, report cards, ribbons and medals – the souvenirs of any childhood.  “It’s their history,” Sherry said, “so that one day they can make sense of their lives.”   She noted that one kid, after turning 18, tore his to pieces, taking with him only the good memories.

Source:  https://www.theguardian.com/us-news/2017/may/17/ohio-drugs-child-protection-workers

Abstract

Childhood maltreatment increases the risk of subsequent depression, anxiety and alcohol abuse, but the rate of resilient victims is unknown. Here, we investigated the rate of victims that do not suffer from clinical levels of these problems after severe maltreatment in a population-based sample of 10980 adult participants.

Compared to men, women reported more severe emotional and sexual abuse, as well as more severe emotional neglect. For both genders, severe emotional abuse (OR = 3.80 [2.22, 6.52]); severe physical abuse (OR = 3.97 [1.72, 9.16]); severe emotional neglect (OR = 3.36 [1.73, 6.54]); and severe physical neglect (OR = 11.90 [2.66, 53.22]) were associated with depression and anxiety while only severe physical abuse (OR = 3.40 [1.28, 9.03]) was associated with alcohol abuse.

Looking at men and women separately, severe emotional abuse (OR = 6.05 [1.62, 22.60] in men; OR = 3.74 [2.06, 6.81] in women) and severe physical abuse (OR = 6.05 [1.62, 22.60] in men; OR = 3.03 [0.99, 9.33] in women) were associated with clinical levels of depression and anxiety. In addition, in women, severe sexual abuse (OR = 2.40 [1.10, 5.21]), emotional neglect (OR = 4.78 [2.40, 9.56]), and severe physical neglect (OR = 9.86 [1.99, 48.93]) were associated with clinical levels of depression and anxiety.

Severe emotional abuse in men (OR = 3.86 [0.96, 15.48]) and severe physical abuse in women (OR = 5.18 [1.48, 18.12]) were associated with alcohol abuse. Concerning resilience, the majority of severely maltreated participants did not report clinically significant levels of depression or anxiety (72%), or alcohol abuse (93%) in adulthood. Although the majority of severely abused or neglected individuals did not show clinical levels of depression, anxiety or alcohol use, severe childhood maltreatment increased the risk for showing clinical levels of psychopathology in adulthood.

Introduction

Severe child maltreatment is conventionally defined within child protection practice as severe physical, emotional, sexual abuse and/or severe physical and emotional neglect by adults [1]. Severity can be defined on the basis of the type of maltreatment, its frequency, if the child was subjected to multiple forms of maltreatment, if a weapon had been used, if the maltreatment resulted in an injury, and if the abuse was considered severe by the victim. For sexual abuse, even a single experience is often considered to be severe [1].

Childhood maltreatment and its psychosocial consequences

There are annually over one million victims of childhood maltreatment in the USA alone and childhood maltreatment has a large public health impact [2]. Several studies show that childhood physical, emotional, and sexual abuse are all related to an increased risk of depression and anxiety disorders in adulthood [3–9]. Other studies have found that the severity of abuse and neglect is associated with increased depression and anxiety symptoms in adulthood [10–12]. This means that as a general rule, the more severe the abuse and neglect, the more likely the abused individuals are to show symptoms of depression and anxiety.

There is also a robust relationship between childhood maltreatment and later alcohol abuse [13–16]. For example, Young-Wolff et al. [17] found that men who had experienced childhood maltreatment were 1.7 times more likely to suffer from alcohol abuse in adulthood than men who did not report experiences of childhood maltreatment. Similar findings have been made when investigating the consequences of abuse and neglect in women (e.g., [18]). Findings from a study by Schwandt et al. [19] suggested that the severity of emotional and physical abuse plays a prominent role in the development of alcohol abuse. In line with these results suggesting a role of the severity of childhood abuse on later substance misuse, Hyman et al. [20] found that the severity of abuse was predictive of cocaine use after having been discharged from an inpatient treatment for cocaine addiction.  This was true for women but not for men. Kendler et al. [21] showed that women who had experienced child sexual abuse reported higher incidences of alcohol abuse. Twin studies have also shown that childhood sexual abuse increases the risk of alcohol abuse and addiction later in life [21–24]. To summarize, there is a strong, robust relationship between childhood maltreatment and mental disorders in adulthood. These associations include associations between childhood experiences of physical abuse, emotional abuse, and neglect, respectively, and mental disorders such as depression and anxiety disorders, and alcohol abuse [25–26]. Moreover, multi-type maltreatment in childhood is associated with greater impairment in adulthood, and this association also includes a range of psychological and behavioral problems, such as depression, anxiety, and alcohol abuse [27].

However, not all victims of childhood maltreatment develop symptoms of substance abuse or psychopathology in adulthood. Meta-analyses suggest that many (but not all) children who have experienced abuse succeed in overcoming some of the possible negative outcomes [28]. For example, Klika and Herrenkohl [28] found that some individuals who have experiences of abuse in childhood do not suffer long-term negative sequelae. Collishaw et al. [29] reported that despite serious experiences of childhood sexual or physical abuse, some individuals did not develop psychiatric problems during adulthood. Moreover, Hamilton et al. [30] reported that emotional neglect did not significantly predict increases in depressive or anxiety symptoms later in life. It has been estimated that 12–22% of maltreated individuals are functioning well despite experiencing childhood maltreatment [31].

The current study

Several studies have focused on only experiencing one type of maltreatment (e.g., sexual abuse) or one type of outcome (e.g., depression). Moreover, most previous studies have relied on either convenience samples or samples from health care services, and especially samples of the latter kind might bias the results and show less resilience than is actually the case.

In the present study, we used a large, population-based sample of Finnish men and women. The types of maltreatment included emotional, physical, and sexual abuse as well as emotional and physical neglect.   Thus, the aims of the present study were to:

1. Investigate gender differences in severe experiences of different types of childhood abuse;

2. Compare if and how individuals reporting severe experiences of different types of childhood abuse differ from individuals who did not report experiencing childhood abuse, in terms of presence of clinically significant symptoms of depression and anxiety in adulthood; and

3. Compare if and how individuals reporting severe experiences of different types of childhood abuse differ from individuals who did not report experiencing childhood abuse in terms of presence of alcohol abuse symptoms in adulthood.

Results

Descriptive results

The proportion of participants with severe experiences of emotional abuse was 0.6% (n = 64). The corresponding proportion for severe experiences of physical abuse was 0.2% (n = 26) while the proportions for severe experiences of sexual abuse was 0.4% (n = 43). For severe experiences of emotional neglect, the proportion was 0.4% (n = 44) and for severe experiences of physical neglect 0.1% (n = 7).  With regard to gender differences in the different types of severe experiences of abuse, Table 2 shows that there were statistically significant differences between men and women in the proportion of individuals with severe experiences of emotional abuse, sexual abuse and emotional neglect. All of these were more prevalent in women. There were no statistical differences between men and women in terms of having severe experiences of physical abuse and physical neglect.

We then investigated whether the proportion of individuals having clinical levels of depression and anxiety was higher in individuals with severe experiences of abuse and neglect compared to individuals with less severe (or no) experiences of abuse and neglect. Table 3 shows that, for both genders, severe experiences of emotional and physical abuse and emotional and physical neglect increased the likelihood of suffering from clinical depression or anxiety compared to less severe experiences of the said forms of childhood maltreatment.

In men, severe abuse experiences were significantly associated with increases in the prevalence of clinical depression or anxiety when it came to experiences of severe emotional and physical abuse and physical neglect. No association was observed for severe sexual abuse and severe emotional neglect. For women, severe experiences of all childhood maltreatment types increased the likelihood of suffering from clinical depression or anxiety compared to other lower experiences of maltreatment.

Next, we explored the proportions of both men and women who were resilient to severe experiences of childhood maltreatment with regards to not suffering from clinical levels of depression or anxiety in adulthood. Depending on the abuse type, 55.6% to 100% of men with experiences of severe abuse did not show clinically significant levels of depression or anxiety. For women, 50% to 80.5% did not show clinically significant levels of depression or anxiety.

Discussion

The present study investigated five types of maltreatment: emotional, physical and sexual abuse, and physical and emotional neglect; and their relationships to depression, anxiety and alcohol abuse. The study used a population-based sample of 10980 participants and used validated measures of experiences of childhood maltreatment, current depression and anxiety, and current alcohol abuse.

More particularly, our aim was to investigate gender differences in victims of severe childhood maltreatment, as well as to compare if and how individuals reporting severe experiences of different types of childhood abuse differ from individuals without such severe experiences in terms of presence of clinically significant symptoms of depression, anxiety and alcohol abuse in adulthood.

The present study found that women reported more childhood experiences of severe emotional, sexual abuse and emotional neglect than men. Our findings are inconsistent with the results of those of previous studies indicating that men reported more childhood experiences of abuse than women [3, 38]. However, our results are consistent with findings suggesting that women are more sensitive than men to the effects of experiences abuse in childhood [29].

Compared to another Finnish population based sample, the frequencies of severe abuse were relatively low in our sample. This could be due to samples being obtained at different times, as abuse in Finland has been decreasing [39], or that in the present study the complete CTQ was used: in the study by Albrecht’s et al. [33], only one item per factor was used. The decrease in measurement reliability that follows from removing 80% of the original items might have inflated the estimates in Albrecht’s study [33].

More specifically, our results revealed that, in men, severe experiences of emotional and physical abuse as well as physical neglect were significantly associated with increases in the prevalence of depression and anxiety symptoms. For women, there was an association between all types of severe childhood maltreatment (emotional, physical and sexual abuse, and physical and emotional neglect) with depression and anxiety symptoms in adulthood.

These results were consistent with previous literature indicating that physical abuse and/or emotional abuse are related to depression and anxiety disorders [4–5, 40–41]. These findings also corroborate findings from meta-analyses and extend previous reports of severe experiences of abuse or neglect being associated with greater risk of developing depressive and anxiety disorders in adulthood [26].

When we examined each type of maltreatment for associations with alcohol abuse, the results showed that severe emotional abuse was associated with alcohol abuse in men. For women, severe physical abuse emerged as a predictor for problematic alcohol use. This is consistent with research suggesting that childhood experiences of emotional and physical abuse were found to be the primary predictor of alcohol abuse [19, 42].

It is intriguing, however, that there appears to be a gender difference in response to abuse type, with men having a considerably more severe response to emotional abuse in terms of propensity to develop alcoholism later in life. For example, an explanation for why women appear to suffer greater consequences in terms of abusing alcohol later in life could be that boys are more likely to engage in rough-and-tumble play and play fights [43], and are thus desensitized to physical abuse to a higher extent than women. It is also, however, possible that measurement invariance could explain the perceived gender differences.

Our current findings suggest that, fortunately, more than half of the participants who have severe experiences of abuse and neglect in childhood seem to succeed in overcoming some of the possible consequences with regards to depression and anxiety symptoms and alcohol abuse in adulthood. While the present study did not investigate mediators of resilience, many studies have considered successful psychosocial adjustment as a mediator of psychological resilience following adverse events [44–45]. It should also be mentioned that some individuals likely have heritable factors that have been shown to protect against adverse effects of maltreatment, by means of gene–environment interaction (i.e., the concept that individuals respond differently to environmental stressors depending on their genotype) [46].

Limitations of the research

Despite the strengths of the present study, it is also characterized by some limitations worth mentioning. First, memories are usually influenced by later experiences, and since the questionnaire was about events that happened during childhood, the obtained information might be somewhat biased. Second, we did not consider the possible overlap between experiences of maltreatment types. Because experiencing one type of abuse or form of neglect is associated with experiencing also another type of abuse or form of neglect [10, 47], it is possible that also severe forms of abuse and neglect are correlated across types or maltreatment. This could, for example, mean that several of the individuals with clinical cases of depression and anxiety or alcohol abuse, not only had experienced one form of severe abuse, but several. Should this be the case, the additive effect of multiple types of abuse could influence the results.

In the present study, it is possible that the true prevalence of anxiety, depressive symptoms or alcohol abuse has been underestimated, as we have only one cross-sectional assessment of the above mentioned indicators (i.e., some individuals may have experienced clinically significant symptoms before study participation, or may experience symptoms in the future, but did not do so at the time of assessment). A longitudinal assessment of adulthood symptoms would thus arguable have been more appropriate than a single, cross-sectional measure.

Also, some of our results and group comparisons were based on very few individuals. This might both influence the estimated prevalence of depression and anxiety or problematic alcohol use and undermines the statistical power to detect differences. Finally, we only included three known consequences of experiencing childhood maltreatment: Depression and anxiety and problematic alcohol use. It is possible that individuals showing resilience on these possible consequences of maltreatment are not resilient with respect to other negative outcomes, such as social functioning or health-risk behavior.

Conclusions  

To our knowledge, this is the first study that has looked at the effects of severe experiences of abuse in childhood on depression and anxiety symptoms and alcohol abuse in adulthood in a relatively large sample.

We found that a majority of individuals with severe experiences of childhood maltreatment did not meet the criteria for clinical of levels depression and anxiety or clinical significant levels of alcohol abuse. Although this is a positive message, it is important to remember that experiences of child maltreatment increase the risk of psychosocial problems in adulthood and several of the victims of severe maltreatment included in our study may have had increased, but non-clinical significant levels of depression, anxiety, and alcohol abuse.

Source: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0177252

Addiction is treatable. So why aren’t more people receiving quality care?

The crisis is well documented and reported: More people are dying of drug overdose than any other non-natural cause—more than from guns, suicide, and car accidents. Politicians have held press conferences, formed commissions and task forces, and convened town-hall meetings. Vivek Murthy, the Surgeon General under President Obama (fired by Donald Trump), issued an historic report on America’s drug-use and addiction crises. Pharmaceutical companies have been blamed. Drug cartels. Physicians who hand out pain pills like Skittles.

In the meantime, the problem worsens. In 2015, 52,000 people died because of overdose, including 33,000 on OxyContin, heroin, and other opioids. Almost three times that number died of causes related to the most-used mood-altering addictive drug, alcohol. The 2016 and 2017 overdose numbers are predicted to be higher. Currently, fentanyl deaths are skyrocketing. If not politicians, to whom can we turn to address the crisis? Since addiction is a health problem, the logical answer would be the addiction-treatment system, but it’s in disarray.

Currently most people who enter treatment are subjected to archaic care, some of which does more harm than good. Only about 10 percent of people who need treatment for drug-use disorders get any whatsoever. Of those who do, a majority enter programs with practices that would be considered barbaric if they were common in treatment systems for other diseases.

Many programs reject science and employ one-size-fits-all-addicts treatment. Patients are often subjected to a slipshod patchwork of unproven therapies. They pass talking sticks and bat horses with Nerf noodles. In some programs, patients are subjected to confrontational therapies, which may include the badgering of those who resist engaging in 12-Step programs, participation in which is required in almost every program. These support groups help some people, but alienate others. When compulsory, they can be detrimental.

Patients are routinely kicked out of programs for exhibiting symptoms of their disease (relapse or breaking rules), which is unconscionable. They are denied life-saving medications by practitioners who don’t believe in them—as Richard Rawson, PhD, research professor, UVM Center for Behavior and Health, says, “this is tantamount to a doctor not believing in Coumadin to prevent heart attacks or insulin for diabetes.”

Patients are put in programs for arbitrary periods of time. Three or five days of detox isn’t treatment. Many residential programs last for twenty-eight days, but research has shown that a month is rarely long enough to treat this disease. Some of those who enter residential treatment do get sober, but they relapse soon after they’re discharged, with, as addiction researcher Thomas McLellan, PhD, sums, “a hearty handshake and instructions to go off to a church basement someplace.” As he says, “It just won’t work.” Finally, people afflicted with this disease are almost never assessed and treated for co-occurring psychiatric disorders, in spite of the fact they almost always accompany and underlie life-threatening drug use. If both illnesses aren’t addressed, relapse is likely.

The disastrous state of the system suggests that addiction-medicine specialists don’t know how to treat substance-use disorders (or even if they can be treated). It’s not the case. The National Institute on Drug Abuse (NIDA) and organizations of addiction-care professionals like the American Society of Addiction Medicine (ASAM) and American Association of Addiction Psychiatry (AAAP) have identified effective treatments. There’s no easy cure for many complex diseases, including addiction. However, cognitive-behavior therapy, motivational interviewing, and addiction medications, often used in concert with one another and in concert with assessment and treatment dual diagnoses, are among many proven treatments. However, most patients are never offered these treatments because of a fatal chasm between addiction science and practitioners and programs.

Fixing the system requires modeling it on the one in place for other serious illnesses. Most people enter the medical system in their primary-care doctors’ offices, health clinics, or emergency rooms. Currently, most doctors in these settings have had little or no education about addiction. A recent ASAM survey of two thirds of U.S. medical schools found that they require an average of less than an hour of training in addiction treatment.

Doctors must be taught to recognize substance-use disorders and treat them immediately—the archaic “let them hit bottom” paradigm has been discredited. They should offer or refer for brief interventions. A program called SBIRT (Screening, Brief Intervention and Referral to Treatment), which seeks to identify risky substance use and includes as few as three counselling sessions, has proven effective in many cases, and may be implemented in general healthcare settings.

Primary-care doctors should be trained and certified to prescribe buprenorphine, a medication that decreases craving and prevents overdose on opioids. Currently, there are limitations on the number of patients doctors can treat. Still, in Vermont, for example, almost 50 percent of opioid users in treatment receive care in their doctors’ offices- they don’t have to go to addiction specialists or intensive treatment programs to receive care.

When a patient requires a higher level of care, doctors must refer them to addiction specialists, which excludes many current practitioners whose only qualification to treat addiction is their own experience in recovery. Instead, patients must be seen by psychiatrists and psychologists trained to diagnose and treat the wide range of substance use disorders. There’s a shortage of these doctors; there needs to be a concerted effort to fill the void.

According to Larissa Mooney, MD, director of the UCLA Addiction Medicine Clinic, “Individuals entering treatment should be presented with an informed discussion about treatment options that include effective, research-based interventions.  In our current system, treatment recommendations vary widely and may come with bias; medication treatments are either not offered or may be presented as a less desirable option in the path to recovery. Treatment should be individualized, and if the same form of treatment has been repeated over and over with poor results (i.e. relapse), an alternative or more comprehensive approach should be suggested.”

When determining if a patient should be treated in physicians’ offices, intensive-outpatient, or residential setting, doctors should rely on ASAM guidelines, not guesses. The length of treatment must be determined by necessity, not insurance. If a patient relapses, is recalcitrant, or breaks rules, treatment should be re-evaluated. They may need a higher level of care, but sick people should never be put out on the street. In addition, all practitioners must reject the archaic proscriptions against medication-assisted treatment; Rawson says that failing to prescribe addiction medications in the case of opioid addiction “should be considered malpractice.”

Programs must also address the fact that a majority of people with substance-use disorders have interrelated psychiatric illnesses. Patients should undergo clinical evaluation, which may include psychological testing. Those with dual diagnoses must be treated for their co-occurring disorders. Finally, initial treatments must be followed by aftercare that’s monitored by an addiction psychiatrist, psychologist, or physician. In short, the field must adopt gold-standard, research-based best practices.

People blame politicians, drug dealers, and pharmaceutical companies for the overdose crisis. However, that won’t help the millions of addicted Americans who need treatment now. Even the most devoted and skilled addiction professionals must acknowledge that they’re part of a broken system that’s killing people. No one can repair it but them.

Source:https://www.psychologytoday.com/blog/overcoming-addiction/201705/sobering-truth-about-addiction-treatment-in-america  May 2017

O, let me not be mad, not mad, sweet heaven. Keep me in temper and keep the Liberal Democrats away from government. For they would make us all mad.

On Friday, new meaning was given to the Progressive Alliance. Maybe the Lib Dems have taken pity seeing Labour struggling to convince even the BBC that the nationalisation of everything can be paid for just by whacking more taxes on the rich. That was my first thought on reading of their pledge to completely legalise cannabis.

In the spirit of cooperation, I thought they have dreamt up a way to raise a billion quid of Labour’s shortfall. People won’t notice, not when they are stoned anyway.

Yes, the Lib Dems’ great money-raising wheeze depends on getting all us puffing away on the weed, just like we knock back the alcohol or used to grab a fag at the first excuse. Why not? Cigarettes and alcohol have always proved nice little earners, even if smuggling went up with every tax hike.  So why not add dope and kill two birds with one stone (no pun intended) and make yourself popular with all those ageing liberal hippies like Simon Jenkins, Mary Ann Seighart and Camilla Cavendish, former head of David Cameron’s policy unit, who are all forever bellyaching on about accepting drugs as part of the fabric of life and restoring sanity to society.

Hang on a minute – that’s the Lib Dem plan! It’s nothing to do with helping Labour out of a hole. It’s to finance their own mental health programme. Yes, you have read that. Wasn’t it last week that the well-meaning Norman Lamb earmarked, guess what, but a billion quid to fight that historic injustice, he says, is faced by people with mental ill health? An historic injustice that goes back all of 2 years.

‘Under the Conservative Government, services have been stretched to breaking point at a time when the prevalence of mental ill health appears to be rising.’

It is more than bizarre that the Lib Dems fail to join up the dots of mental illness and treatment (on which they have been campaigning vigorously) with increased use of drugs, particularly cannabis (which is what legalisation means).

Have they missed entirely the connection between cannabis use and mental ill health? Are they unaware that cannabis use triples psychosis risk? And from 17 to 38 can lose you 8 IQ points? Perhaps they are suffering that IQ loss already.

In Lib Dem happy land, everything can be squared – even Tiny Tim’s evangelical religious beliefs with gay marriage – and on drugs it is back to the future of hippy protest.

They have all been out straggling the airwaves, forgotten but former Lib Dem MPs – Dr Evan Harris (Dr Death as he was better known) and Dame Molly Meacher’s former sidekick Dr Julian Huppert – emerging into the daylight blinking to press their old cause, along with their Frankenstein master, the suitably named Professor David Nutt, of magic mushroom and alcohol antidote research fame.

One wonders whether the God-fearing Tim knows what he’s conjured up.  As a concerned parent, he should know that if legalisation means anything at all it means drug use going up as the latest stats from Colorado underline. Past-month marijuana use among 12-to-17 year-olds there has increased from 9.82 per cent to 12.56 per cent, according to the most recent year-by-year comparison looking at pre-legalisation data.

Well I for one am looking forward to seeing the contortions he’ll have to go through to join up the dots on his mental health and drugs legalisation policies. I suggest before he finds himself being asked to justify adding to our already overcrowded and underfunded secure psychiatric units – peopled with male psychotics addicted to cannabis – he reads one of the many comprehensive reviews of the link between cannabis and mental illness.

However, I am not holding my breath that Andrew Marr or any other progressive liberal BBC interviewer will press him on it.

Source:  http://www.conservativewoman.co.uk/kathy-gyngell-potty-lib-dems-want-legalise-cannabis-boost-mental-health/   14th May 2017

How do you know when you are being softened up for something? One sure sign is when what you are being asked to give your support to is sold to you as entirely unproblematic or as a panacea to a host of problems. Never believe it.

My antennae began twitching when the latest round in the campaign for legalised ‘medical cannabis’ began back last autumn. The instigator was the All Party Parliamentary Group for Drugs Policy Reform chaired by one Baroness Molly Meacher and its ammunition a misleading and derivative report: Accessing Medicinal Cannabis: Meeting Patients’ Needs.

With a general election under way it seems the good Baroness and her backers have decided to give their ‘medipot’ campaign another crack of the whip, ever hopeful of a change of government heart over legalising so-called medicinal cannabis.

What could be wrong with that, I hear you ask. Well, if I was sceptical about the stated purpose of this report when it was first published, I am even more so this time. Why? First, because the case for medicinal cannabis is based on a false premise, which the recent licensing of cannabidiol demonstrates again. Second, the scientific research on its efficacy doesn’t stack up too well. And third, there no safe way of using the unprocessed plant for recreational let alone medical purposes.

To recap, contrary to received wisdom, no one has stopped or is stopping  the scientific study of the chemicals in cannabis for medicinal purposes. Two approved cannabis-derived medications, Marinol and Sativex, exist already and a third, Epidiolex is undergoing clinical trials at the moment. In addition to this, the non psycho-active CBD or cannabidiol has been approved by Britain’s medicines regulatory authority, the MHRA, and the compound is now to be licensed and regulated as a medicine. Evidence of the efficacy of the derived compounds of cannabis for the wide range of symptoms they have been tested on is at best weak. This is what a dispassionate systematic research review conducted by the American Academy of Neurology and endorsed by the American Autonomic Society, the American Epilepsy Society, the Consortium of Multiple Sclerosis Centers, the International Organization of Multiple Sclerosis Nurses, and the International Rett Syndrome Foundation, shows.

There are indisputable  scientific and safety reasons for why the whole unprocessed cannabis plant is not and will never be approved as a medicine; that’s unless we chose to revert to medieval quackery and throw all scientific and safety advances  out of the window. It is not just that cannabis risks (addiction, psychosis, cancer, impaired cognitive functioning, to name but some) outweigh any possible benefits, but that as a natural ‘herb’ it is untested for pathogens and bacteria. Who is their right mind would chose mould over an approved antibiotic? And where is the luminary who thinks smoking is a sensible medication delivery system? – which how most cannabis users chose to ingest the weed.

But rational science hasn’t stopped the medipot activists in their tracks. Over the last few months they’ve been relentlessly pressing their victimhood status on the media and the inequity they suffer of not having a free and easy access to their preferred untested drug, i.e. dope.  They have really been doing rather well at convincing the media of their non-existent problem. The Daily Mail even fell for it this week, reiterating the campaigners’ victim meme of being sick people unjustly prosecuted by harsh and uncompromising authorities for the crime of tending to their pain when, in fact, it is the regulatory authorities who are protecting people from poisoning themselves. No wonder Baroness Meacher, chair of the aforesaid APPG, sounded so triumphant on the airwaves yesterday as she pushed the case for medipot to an all believing radio host. Even the Mail (all that has stood between us and drugs legalisation, she as much as said) had finally written a balanced article on the topic, she crowed.

She herself certainly was not balanced. I cannot make up my mind, given her ‘economy with truth’ regarding drug statistics on previous occasions that I have taken her up on, here, and here whether the Baroness is just daft and deluded, genuinely ingenuous, or, more worryingly, actively disingenuous. Running true to form, Baroness Meacher failed in her interview (go to circa one hour, 6 minutes into the programme) to either mention the medicines approval system or the recent licensing of cannabidiol as a medicine.  She also misled the public, deliberately it seemed, by giving the impression that the UK government has actively frustrated cannabis-based research when it hasn’t. In fact, the opposite is the case, as drugs policy analyst David Raynes made clear on the same programme.  The UK government broke ground when it licensed research into cannabis in 1998.

In the  absence of research, her spurious argument went, there remains a medical need for public access to the raw cannabis plant and therefore an end to its classification as a harmful recreational drug. There we had it.

The truth is that the APPG on Drugs Policy Reform she chairs is hardly an independent or dispassionate body. It is funded by The Open Society, which is in turn is a George Soros front. According to the Washington Times (Source: www.washingtontimes.com 2nd April 2014) this is the billionaire philanthropist who, with a cadre of like-minded, wealthy donors, has dominated the pro-legalisation side of the marijuana debate in the US by funding grass-roots movements in every state. No wonder so many capitulated.  Through a network of nonprofit groups,  Mr. Soros has spent at least $80 million on these drugs legalisation efforts since 1994. And more in the last three years. I fear the APPG’s effort (ably backed by Nick Clegg who also seems oblivious to the relationship between cannabis and mental illness) is but the latest in a line of such campaigns whose objective is effectively to legalise recreational cannabis. These go back to 1979 when Keith Stroup of NORML, the group “that speaks for pot users’ originally admitted that medipot was  a red herring to get pot a good name.  More recently he revealed that he was not too keen on cannabis compounds being subjected to scientific drug research trials. He said that the “pharmaceuticalisation” of cannabis was a battleground to be fought in order to protect ‘the options of patients’ – to smoke dope as it is.

I wonder if this too is why Meacher is so reluctant to give a full account of cannabis research and medical regulation? It rather pulls her medi-pot carpet from under her feet.

Source:  http://www.conservativewoman.co.uk/kathy-gyngell-the-push-for-medipot-remains-a-push-for-pot/   May 2017

“We should all be dead,” said Jonathan Goyer one bright morning in January as he looked across a room filled with dozens of his co-workers and clients. The Anchor Recovery Community Center, which Goyer helps run, occupies the shell of an office building in Pawtucket, Rhode Island. Founded seven years ago, Anchor specializes in “peer-to-peer” counselling for drug addicts. With state help and private grants, Anchor throws everything but the kitchen sink at addiction. It hosts Narcotics Anonymous meetings, cognitive behavioral therapy sessions, art workshops, and personal counselling. It runs a telephone hotline and a hospital outreach program. It has an employment center for connecting newly drug-free people to sympathetic hirers, and banks of computers for those who lack them. And all the people who work here have been in the very pit of addiction—shoplifting to pay for a morning dose, selling their bodies, or dragging out their adult lives in prison. Some have been taken to emergency rooms and “hit” with powerful anti-overdose drugs to bring them back from respiratory failure.

That is how it was with Goyer. His father died of an overdose at forty-one, in 2004. His twenty-nine-year-old brother OD’d and died in 2009. When he was shooting heroin he slept on the floor of a public garage. He would pick up used hypodermic needles if they were new enough that the volume gauges inked on the outside hadn’t been rubbed off with use. He OD’d several times before getting clean in 2013. Now he visits people after overdoses and tells them, “I was right where you’re at.”

There have always been drug addicts in need of help, but the scale of the present wave of heroin and opioid abuse is unprecedented. Fifty-two thousand Americans died of overdoses in 2015—about four times as many as died from gun homicides and half again as many as died in car accidents. Pawtucket is a small place, and yet 5,400 addicts are members at Anchor. Six hundred visit every day. Rhode Island is a small place, too. It has just over a million people. One Brown University epidemiologist estimates that 20,000 of them are opioid addicts—2 percent of the population.

Salisbury, Massachusetts (pop. 8,000), was founded in 1638, and the opium crisis is the worst thing that has ever happened to it. The town lost one young person in the decade-long Vietnam War. It has lost fifteen to heroin in the last two years. Last summer, Huntington, West Virginia (pop. 49,000), saw twenty-eight overdoses in four hours. Episodes like these played a role in the decline in U.S. life expectancy in 2015. The death toll far eclipses those of all previous drug crises.

And yet, after five decades of alarm over threats that were small by comparison, politicians and the media have offered only a muted response. A willingness at least to talk about opioid deaths (among other taboo subjects) surely helped Donald Trump win last November’s election. In his inaugural address, President Trump referred to the drug epidemic (among other problems) as “carnage.” Those who call the word an irresponsible exaggeration are wrong.

Jazz musicians knew what heroin was in the 1950s. Other Americans needed to have it explained to them. Even in the 1960s and 1970s, with bourgeois norms and drug enforcement weakening, heroin lost none of its terrifying underworld associations. People weren’t shooting it at Woodstock. Today, with much of the discourse on drug addiction controlled by medical bureaucrats, it is common to speak of addiction as an “equal-opportunity disease” that can “strike anyone.” While this may be true on the pharmacological level, it was until quite recently a sociological falsehood. In fact, most of the country had powerful moral, social, cultural, and legal immunities against heroin

and opiate addiction. For 99 percent of the population, it was an adventure that had to be sought out. That has now changed.

America had built up these immunities through hard experience. At the turn of the nineteenth century, scientists isolated morphine, the active ingredient in opium, and in the 1850s the hypodermic needle was invented. They seemed a godsend in Civil War field hospitals, but many soldiers came home addicted. Zealous doctors prescribed opiates to upper-middle-class women for everything from menstrual cramps to “hysteria.” The “acetylization” of morphine led to the development of heroin. Bayer began marketing it as a cough suppressant in 1898, which made matters worse. The tally of wrecked middle-class families and lives was already high by the time Congress passed the Harrison Narcotics Tax Act in 1914, threatening jail for doctors who prescribed opiates to addicts. Americans had had it with heroin. It took almost a century before drug companies could talk them back into using drugs like it.

If you take too much heroin, your breathing slows until you die. Unfortunately, the drug sets an addictive trap that is sinister and subtle. It provides a euphoria—a feeling of contentment, simplification, and release—which users swear has no equal. Users quickly develop a tolerance, requiring higher and higher amounts to get the same effect. The dosage required to attain the feeling the user originally experienced rises until it is higher than the dosage that will kill him. An addict can get more or less “straight,” but approaching the euphoria he longs for requires walking up to the gates of death. If a heroin addict sees on the news that a user or two has died from an overly strong batch of heroin in some housing project somewhere, his first thought is, “Where is that? That’s the stuff I want.”

Tolerance ebbs as fast as it rises. The most dangerous day for a junkie is not the day he gets arrested, although the withdrawal symptoms—should he not receive medical treatment—are painful and embarrassing, and no picnic for his cellmate, either. But withdrawals are not generally life-threatening, as they are for a hardened alcoholic. The dangerous day comes when the addict is released, for the dosage he had taken comfortably until his arrest two weeks ago may now be enough to kill him.

The best way for a society to avoid the dangers of addictive and dangerous drugs is to severely restrict access to them. That is why, in the twentieth century, powerful opiates and opioids (an opioid is a synthetic drug that mimics opium) were largely taboo—confined to patients with serious cancers, and often to end-of-life care. But two decades ago, a combination of libertarian attitudes about drugs and a massive corporate marketing effort combined to instruct millions of vulnerable people about the blessed relief opioids could bring, if only mulish oldsters in the medical profession could get over their hang-ups and be convinced to prescribe them. One of the rhetorical tactics is now familiar from debates about Islam and terrorism: Industry advocates accused doctors reluctant to prescribe addictive medicines of suffering from “opiophobia.”

In 1996, Purdue Pharmaceuticals brought to market OxyContin, an “extended release” version of the opioid oxycodone. (The “-contin” suffix comes from “continuous.”) The time-release formula meant companies could pack lots of oxycodone into one pill, with less risk of abuse, or so scientists claimed. Purdue did not reckon with the ingenuity of addicts, who by smashing or chewing or dissolving the pills could release the whole narcotic load at once. That is the charitable account of what happened. In 2007, three of Purdue’s executives pled guilty to felony misbranding at the time of the release of OxyContin, and the company paid $600 million in fines. In 2010, Purdue brought out a reformulated OxyContin that was harder to tamper with. Most of Purdue’s revenues still come from OxyContin. In 2015, the Sackler family, the company’s sole owners,

suddenly appeared at number sixteen on Forbes magazine’s list of America’s richest families.

Today’s opioid epidemic is, in part, an unintended consequence of the Reagan era. America in the 1980s and 1990s was guided by a coalition of profit-seeking corporations and concerned traditional communities, both of which had felt oppressed by a high-handed government. But whereas Reaganism gave real power to corporations, it gave only rhetorical power to communities. Eventually, when the interests of corporations and communities clashed, the former were in a position to wipe the latter out. The politics of the 1980s wound up enlisting the American middle class in the project of its own dispossession.

OxyContin was only the most commercially successful of many new opioids. At the time, the whole pharmaceutical industry was engaged in a lobbying and public relations effort to restore opioids to the average middle-class family’s pharmacopeia, where they had not been found since before World War I. The American Pain Foundation, which presented itself as an advocate for patients suffering chronic conditions, was revealed by the Washington Post in 2011 to have received 90 percent of its funding from medical companies.

“Pain centers” were endowed. “Chronic pain” became a condition, not just a symptom. The American Pain Society led an advertising campaign calling pain the “fifth vital sign” (after pulse, respiration, blood pressure, and temperature). Certain doctors, notoriously the anaesthesiologist Russell Portenoy of the Beth Israel Medical Center, called for more aggressive pain treatment. “We had to destigmatize these drugs,” he later told the Wall Street Journal. A whole generation of doctors was schooled in the new understanding of pain. Patients threatened malpractice suits against doctors who did not prescribe pain medications liberally, and gave them bad marks on the “patient satisfaction” surveys that, in some insurance programs, determine doctor compensation. Today, more than a third of Americans are prescribed painkillers every year.

Very few of them go on to a full-blown addiction. The calamity of the 1990s opioid revolution is not so much that it turned real pain patients into junkies—although that did happen. The calamity is that a broad regulatory and cultural shift released a massive quantity of addictive drugs into the public at large. Once widely available, the supply “found” people susceptible to addiction. A suburban teenager with a lot of curiosity might discover that Grandpa, who just had his knee replaced, kept a bottle of hydrocodone on the bedside table. A construction boss might hand out Vicodin at the beginning of the workday, whether as a remedy for back pain or a perquisite of the job. Pills are doseable—and they don’t require you to use needles and run the risk of getting AIDS. So a person who would never have become a heroin addict in the old days of the opioid taboo could now become the equivalent of one, in a more antiseptic way.

But a shocking number of people wound up with a classic heroin problem anyway. Relaxed taboos and ready supply created a much wider appetite for opioids. Once that happened, heroin turned out to be very competitively priced. Not only that, it is harder to crack down on heavily armed drug gangs that sell it than on the unscrupulous doctors who turned their practices into “pill mills.” Addicts in Maine complain about the rising price of black-market pharmaceutical pills: They have risen far above the dollar-a-milligram that used to constitute a kind of “par” in the drug market. An Oxy 30 will now run you forty-five bucks. But you can shoot heroin when the pills run out, and it will save you money. A lot of money. Heroin started pouring into the eastern United States a decade ago, even before the price of pills began to climb. Since then, its price

has fallen further, its purity has risen—and, lately, the number of heroin deaths is rising sharply everywhere. That is because, when we say heroin, we increasingly mean fentanyl.

Fentanyl is an opioid invented in 1959. Its primary use is in transdermal patches given to people for end-of-life care. If you steal a bunch of these, you can make good money with them on the street. Addicts like to suck on them—an extremely dangerous way to get a high. Fentanyl in its usual form is about fifty times as strong as street heroin. But there are many different kinds of fentanyl, so the wallop it packs is not just strong but unpredictable. There is butyrfentanyl, which is about a quarter the strength of ordinary fentanyl. There is acetylfentanyl, which is also somewhat weaker. There is carfentanil, which is 10,000 times as strong as morphine. It is usually used as an animal tranquilizer, although Russian soldiers used an aerosol version to knock out Chechen hostage-takers before their raid on a Moscow theater in 2002. A Chinese laboratory makes its own fentanyl-based animal tranquilizer, W-18, which finds its way into Maine through Canada.

China manufactures a good deal of the fentanyl that comes to the U.S., one of those unanticipated consequences of globalization. The dealers responsible for cutting it by a factor of fifty are unlikely to be trained pharmacists. The cutting lab may consist of one teenager flown up from the Dominican Republic alone in a room with a Cuisinart and a box of starch or paracetamol. It takes considerable skill to distribute the chemicals evenly throughout a package of drugs. Since a shot of heroin involves only the tiniest little pinch of the substance, you might tap into a part of the baggie that is all cutting agent, no drug—in which case you won’t get high. On the other hand, you could get a fentanyl-intensive pinch—in which case you will be found dead soon thereafter with the needle still sticking out of your arm. This is why fentanyl-linked deaths are, in some states, multiplying year on year. The federal CDC has lagged in reporting in recent years, but we can get a hint of the nationwide toll by looking at fentanyl deaths state by state. In Maryland, the first six months of 2015 saw 121 fentanyl deaths. In the first six months of 2016, the figure rose to 446.

Sometimes arrested or hospitalized users are surprised to find that what they thought was heroin was actually fentanyl. But there are addicts who swear they can tell what’s in the barrel of their needles. One in Rhode Island, whom we’ll call Gilberto, says heroin has a pleasant caramel brown tint, like the last sip of Coca-Cola in a glass. Fentanyl is clear. And many addicts claim they can recognize the high. “Fentanyl just hits you. Hard,” Gilberto says. “But it’s got no legs on it. It lasts about two hours. Heroin will hold you.” This makes fentanyl a distinctly inconvenient drug, but many addicts prefer it. All dealers, at least around Rhode Island, describe their heroin as “the fire,” in the same way all chefs describe their ribs as so tender they just fall off the bone.

“I knew we were screwed, as a state and as a country,” Jonathan Goyer says, “when I had a conversation with a kid who was going through withdrawals.” Although he had enough money to get safer drugs, the kid was going to wait through the sweats and the diarrhea and the nausea until his dealer came in at 5 p.m. That would allow him to risk his life on fentanyl.

Those in heroin’s grip often say: “There are only two kinds of people—the ones I get money from and the ones I give money to.” A man who is dead to his wife and his children may be desperate to make a connection with his dealer. They don’t buy much besides heroin—perhaps a plastic cup of someone else’s drug-free urine on a day when they need to take a drug test for a hospital or employer. This will set them back twenty or thirty dollars. In addiction, as in more mainstream endeavors, the lords of hedonism

are the slaves of money. Gilberto in Rhode Island claims to have put a million dollars into each of his needle-pocked arms, at the rate of three fifty-bag “bricks” of heroin a day.

Dealers are businessmen and behave like businessmen, albeit heavily armed ones. They may “throw something” to a particularly reliable customer—that is, give him enough heroin from time to time to allow him to deal a bit on his own account and stay solvent. An addict who discovers that the 10mg pills he is paying $18 each for in Maine are available for $10 in Boston, a three-hour drive away, may be tempted to sell them to support his own habit. The line between users and pushers blurs, rendering impractical the policy that most people prefer—be merciful to drug users, but come down hard on dealers.

Addicts wake up “sick,” which is the word they use for the tremulous, damp, and terrifying experience of withdrawal. They need to “make money,” which is their expression for doing something illegal. Some neighborhood bodegas—the addicts know which ones—will pay 50 cents on the dollar for anything stolen from CVS. That is why razor blades, printer cartridges, and other expensive portable items are now kept under lock and key where you shop. Addicts shoplift from Home Depot and drag things from the loading docks. They pull off scams. They will scavenge for thrown-out receipts in trash cans outside an appliance store, enter the store, find the receipted item, and try to return it for cash. On the edge of the White Mountains in Maine, word spread that the policy at Hannaford, the dominant supermarket chain, was not to dispute returns of under $25. For a while, there was a run on the big cans of extra virgin olive oil that sold for $24.99, which were brought to the cash registers every day by a succession of men and women who did not, at first sight, look like connoisseurs of Mediterranean cuisine. Women prostitute themselves on Internet sites. Others go into hospital emergency rooms, claiming a desperately painful toothache that can be fixed only with some opioid. (Because if pain is a “fifth vital sign,” it is the only one that requires a patient’s own testimony to measure.) This is generally repeated until the pain-sufferer grows familiar enough to the triage nurses to get “red-flagged.”

The population of addicts is like the population of deer. It is highest in rustic places with access to urban supplies. Missouri’s heroin problem is worst in the rural counties near St. Louis. New Hampshire’s is worst in the small cities and towns an hour or so away from the drug markets of Massachusetts: Lawrence, Lowell, and Boston. But the opioid epidemic of the past decade is unusually diverse. Anchor’s emergency room clients are 82 percent white, 9 percent Hispanic, and 6 percent black. The state of Rhode Island is 85 percent white, 9 percent Hispanic, and 5 percent black. “I try to target outreach,” Goyer says, “but the demographics are too random for that.”

Drug addiction used to be a ghetto thing. Now Oxycodone has joined shuttered factories and Donald Trump as a symbol of white working-class desperation and fecklessness. The reaction has been unsympathetic. Writes Nadja Popovich in The Guardian: “Some point to this change in racial and economic demographics as one reason many politicians have re-evaluated the tough ‘war on drugs’ rhetoric of the past 30 years.”

The implicit accusation is that only now that whites are involved have racist authorities been roused to act. This is false in two ways. First, authorities have not been roused to act. Second, when they do, they will have epidemiological, and not just tribal, grounds for doing so. A plague afflicting an entire country, across ethnic groups, is by definition more devastating than a plague afflicting only part of it. A heroin scourge in America’s housing projects coincided with a wave of heroin-addicted soldiers brought back from Vietnam, with a cost peaking between 1973 and 1975 at 1.5 overdose deaths per 100,000. The Nixon White House panicked. Curtis Mayfield wrote his soul ballad

“Freddie’s Dead.” The crack epidemic of the mid- to late 1980s was worse, with a death rate reaching almost two per 100,000. George H. W. Bush declared war on drugs. The present opioid epidemic is killing 10.3 people per 100,000, and that is without the fentanyl-impacted statistics from 2016. In some states it is far worse: over thirty per 100,000 in New Hampshire and over forty in West Virginia.

In 2015, the Princeton economists Angus Deaton and Anne Case released a paper showing that the life expectancy of middle-aged white people was falling. Prominent among the causes cited were “the increased availability of opioid prescriptions for pain” and the falling price and rising potency of heroin. Census figures show that Case and Deaton had put the case mildly: Life expectancy was falling for all whites. Although they are the only racial group to have experienced a decline in longevity—other races enjoyed steep increases—there are still enough whites in the United States that this meant longevity fell for the country as a whole.

Bill Clinton alluded to the Case-Deaton study often during his wife’s presidential campaign. He would say that poor white people are “dying of a broken heart.” Heroin has become a symbol of both working-class depravity and ruling-class neglect—an explosive combination in today’s political climate.

Maine’s politicians have taken the opioid epidemic as seriously as any in the country. Various new laws have capped the maximum daily strength of prescribed opioids and limited prescriptions to seven days. The levels are so low that they have led some doctors to warn that patients will go onto the street to get their dosages topped off. “We were sad,” State Representative Phyllis Ginzler said in January, “to have to come between doctor and patient.” She felt the deadly stakes of Maine’s problem gave her little alternative.

Paul LePage, the state’s garrulous governor, has been even more direct. Speaking of drug dealers at a town hall in rural Bridgton in early 2016, he said: “These are guys with the name D-Money, Smoothie, Shifty, these types of guys. They come from Connecticut and New York, they come up here, they sell their heroin, they go back home. Incidentally, half the time they impregnate a young white girl before they leave.” This is what the politics of heroin threatens to become nationwide: To break the bureaucratic inertia, one side will go to any rhetorical length, even invoking race. To protect governing norms, the other side will invoke decency, even as the damage mounts. It is what the politics of everything is becoming nationwide. From town to town across the country, the correlation of drug overdoses and the Trump vote is high.

The drug problem is already political. It is being reframed by establishment voices as a problem of minority rights and stigmatization. A documentary called The Anonymous People casts the country’s 20 million addicts as a subculture or “community” who have been denied resources and self-respect. In it, Patrick Kennedy, who was Rhode Island’s congressman until 2011 and who was treated for OxyContin addiction in 2006, says: “If we can ever tap those 20 million people in long-term recovery, you’ve changed this overnight.” What’s needed is empowerment. Another interviewee says, “I refuse to be ashamed of what I am.”

This marks a big change in attitudes. Difficult though recovery from addiction has always been, it has always had this on its side: It is a rigorously truth-focused and euphemism-free endeavor, something increasingly rare in our era of weasel words. The face of addiction a generation ago was that of the working-class or upper-middle-class man, probably long and intimately known to his neighbors, who stood up at an AA meeting in a church basement and bluntly said, “Hi, I’m X, and I’m an alcoholic.”

The culture of addiction treatment that prevails today is losing touch with such candour. It is marked by an extraordinary level of political correctness. Several of the addiction professionals interviewed for this article sent lists of the proper terminology to use when writing about opioid addiction, and instructions on how to write about it in a caring way. These people are mostly generous, hard-working, and devoted. But their codes are neither scientific nor explanatory; they are political.

The director of a Midwestern state’s mental health programs emailed a chart called “‘Watch What You Call Me’: The Changing Language of Addiction and Mental Illness,” compiled by the Boston University doctor Richard Saltz. It is a document so Orwellian that one’s first reaction is to suspect it is a parody, or some kind of “fake news” dreamed up on a cynical website. We are not supposed to say “drug abuse”; use “substance use disorder” instead. To say that an addict’s urine sample is “clean” is to use “words that wound”; better to say he had a “negative drug test.” “Binge drinking” is out—“heavy alcohol use” is what you should say. Bizarrely, “attempted suicide” is deemed unacceptable; we need to call it an “unsuccessful suicide.” These terms are periphrastic and antiscientific. Imprecision is their goal. Some of them (like the concept of a “successful suicide”) are downright insane. This habit of euphemism and propaganda is not merely widespread. It is official. In January 2017, less than two weeks before the end of the last presidential administration, drug office head Michael Botticelli issued a memo called “Changing the Language of Addiction,” a similarly fussy list of officially approved euphemisms.

Residents of the upper-middle-class town of Marblehead, Massachusetts, were shocked in January when a beautiful twenty-four-year-old woman who had excelled at the local high school gave an interview to the New York Times in which she described her heroin addiction. They were perhaps more shocked by her description of the things she had done to get drugs. A week later, the police chief announced that the town had had twenty-six overdoses and four deaths in the past year. One of these, the son of a fireman, died over Labor Day. At the burial, a friend of the dead man overdosed and was rushed to the hospital. One fireman there said to a mourner that this was not uncommon: Sometimes, at the scene of an overdose, they will find a healthy- and alert-looking companion and bring him along to the hospital too, assuming he might be standing up only because the drug hasn’t hit him yet. In communities like this, concerns about “hurtful” words and stigma can seem beside the point.

Former Bush administration drug czar John Walters and two other scholars wrote last fall, “There is another type of ‘stigma’ afflicting drug users—that their crisis is somehow undeserving of the full resources necessary for their rescue.” Walters is talking largely about law enforcement. As he said more recently: “If someone were getting food poisoning from cans of tuna, the whole way we’re doing this would be more aggressive.”

Which is not the direction we’re going. In state after state, voters have chosen to liberalize drug laws regarding marijuana. If you want an example of mass media–induced groupthink, Google the phrase “We cannot arrest our way out of the drug problem” and count the number of politicians who parrot it. It is true that we cannot arrest our way out of a drug problem. But we cannot medicate and counsel our way out of it, either, and that is what we have been trying to do for almost a decade.

Calling addiction a disease usefully describes certain measurable aspects of the problem—particularly tolerance and withdrawal. It fails to capture what is special and dangerous about the way drugs bind with people’s minds. Almost every known disease is something people wish to be rid of. Addiction is different. Addicts resist known cures—even to the point of death. If you do not reckon with why addicts go to such

lengths to continue suffering, you are unlikely to figure out how to treat them. This turns out to be an intensely personal matter.

Medical treatment plays an obvious role in addressing the heroin epidemic, especially in the efforts to save those who have overdosed or helping addicts manage their addictions. But as an overall approach, it partakes of some of the same fallacies as its supposed opposite, “heartless” incarceration. Both leave out the addict and his drama. Medicalizing the heroin crisis may not stigmatize him, but it belittles him. Moral condemnation is an incomplete response to the addict. But it has its place, because it does the addict the compliment of assuming he has a conscience, a set of thought processes. Those thought processes are what led him into his artificial hell. They are his best shot at finding a way out.

In 1993, Francis F. Seeburger, a professor of philosophy at the University of Denver, wrote a profound book on the thought processes of addicts called Addiction and Responsibility. We tend to focus on the damage addiction does. A cliché among empathetic therapists, eager to describe addiction as a standard-issue disease, is that “no one ever decides to become an addict.” But that is not exactly true, Seeburger shows. “Something like an addiction to addiction plays a role in all addiction,” he writes. “Addiction itself . . . is tempting; it has many attractive features.” In an empty world, people have a need to need. Addiction supplies it. “Addiction involves the addict. It does not present itself as some externally imposed condition. Instead, it comes toward the addict as the addict’s very self.” Addiction plays on our strengths, not just our failings. It simplifies things. It relieves us of certain responsibilities. It gives life a meaning. It is a “perversely clever copy of that transcendent peace of God.”

The founders of Alcoholics Anonymous thought there was something satanic about addiction. The mightiest sentence in the book of Alcoholics Anonymous is this: “Remember that we deal with alcohol—cunning, baffling, powerful!” The addict is, in his own, life-damaged way, rational. He’s too rational. He is a dedicated person—an oblate of sorts, as Seeburger puts it. He has commitments in another, nether world.

That makes addiction a special problem. The addict is unlikely ever to take seriously the counsel of someone who has not heard the call of that netherworld. Why should he? The counsel of such a person will be, measured against what the addict knows about pleasure and pain, uninformed. That is why Twelve Step programs and peer-to-peer counselling, of the sort offered by Goyer and his colleagues, have been an indispensable element in dragging people out of addiction. They have authority. They are, to use the street expression, legit.

The deeper problem, however, is at once metaphysical and practical, and we’re going to have a very hard time confronting it. We in the sober world have, for about half a century, been renouncing our allegiance to anything that forbids or commands. Perhaps this is why, as this drug epidemic has spread, our efforts have been so unavailing and we have struggled even to describe it. Addicts, in their own short-circuited, reductive, and destructive way, are armed with a sense of purpose. We aren’t. It is not a coincidence that the claims of political correctness have found their way into the culture of addiction treatment just now. This sometimes appears to be the only grounds for compulsion that the non-addicted part of our culture has left.

Christopher Caldwell is a senior editor at the Weekly Standard.

Source:  https://www.firstthings.com/article/2017/04/american-carnage

Meet Ryan Hampton, 36, recovery advocate, political activist and recovering heroin addict igniting America’s social media feeds with stories of hope, recovery and activism. From his advocacy that led Sephora to take their eyeshadow branded “druggie” off the shelves to the activism that urged an Arizona politician to apologize for a statement stigmatizing addiction, he’s certainly become a social media powerhouse for all things addiction, recovery and policy. And with an estimated 7 out of 10 people on social media platforms, it’s no coincidence he’s found success taking the addiction advocacy fight digital.

Today, more than 22 million people are struggling with addiction, and it’s estimated that as a result, more than 45 million people are affected. But what many people don’t realize is that there are more than 23 million people living in active, long-term recovery today. Yet, because of shame and stigma, many stay silent. To fight this often-lethal silence, Hampton has urged the public to speak up and share personal stories of recovery through his recently launched Voices Project. The project, a collaborative effort to encourage people across the nation to share their story, exists to put real faces and names behind the addiction epidemic.

A Personal Struggle

Before becoming a national recovery advocate and social media powerhouse, Hampton himself faced a personal struggle with addiction. A former staffer in the Clinton White House, Hampton did not appear to be a likely candidate for heroin addiction, or so stigma would say. But after an injury and subsequent prescription for pain medication, Hampton found himself addicted to opiates, eventually leading to a heroin addiction that would span more than a decade.  After a long struggle, Hampton decided to get help.

It was the phone call that started his recovery journey that changed everything – his life and his view on the power of his phone. After getting sober, he began connecting with others in recovery, amazed at the magnitude of the digital community. But still, while uncovering these online stories of recovery, Hampton lost four friends to opioid addiction.

It was a breaking point for Hampton – one that led to the beginning of a movement that would someday reach and impact millions.

A Notable Partner

Hampton began reaching out to others in recovery and started realizing the power of digital tools to connect and build an online recovery community. And as he was slowly networking and meeting others in recovery, on October 4, 2015, Hampton’s advocacy met its catalyst: Facing Addiction.   The non-profit organization hosted a concert at the National Mall in Washington, D.C., an event that drew thousands to the capitol with celebrities, musicians and other well-known names willing to publicly celebrate the reality of recovery and call for reform in the addiction industry. Hampton, a Los Angeles resident, tuned into the event from across the country through Facebook Live and was again inspired by the content delivered through his mobile phone.

After meeting co-founders of Facing Addiction, Jim Hood and Greg Williams, Hampton plugged in, partnered and even joined the Facing Addiction team as a recovery advocate.

The importance of online advocacy aligns with Facing Addictions’ national priorities, shares CEO Jim Hood, “When enough people tell enough stories and the people who are impacted by addiction look like all of us and our kids and neighbors and relatives, the stigma has to start going away. And then we can get to work.”

After partnering with Facing Addiction, Hampton understood the priorities, the strategy and the mechanism. Said by Hampton, “I stand on the shoulders of giants”.

Leveraging the power of the algorithms at his fingertips every day, Hampton has grown his online presence to be one of the most influential in the recovery movement. Digital communication helped him get to treatment, connected him with Facing Addiction, and now is the platform in which he is sharing recovery stories from across the nation.

In just one week, more than 200 stories were submitted to the Voices Project and over 500 people sent in personal messages to express their support. Among those speaking up are notable voices such as pro skateboarder and former Jackass member Brandon Novak;   Grammy Award-winning musician Sirah;  rapper Royce da 5’9’’;   American politician and mental health advocate Patrick Kennedy;  former child actress and now-addiction counselor Mackenzie Phillips, and more.

According to Royce da 5’9’’, “Addiction is a problem that we all have to deal with. It affects us all in one way or another, and having someone giving it a voice, a name and a face not only helps get rid of the stigma regarding addiction, but he’s [Ryan] on the forefront letting people know there are solutions out there and recovery is real.”

Patrick Kennedy shares the importance of building a digital recovery movement to influence and support political reform in the addiction recovery space. “With the push of a button we’ll be able to have others show up to support communities across the nation,” says Kennedy, “because their fight is our fight.”

“The face of addiction is everyone,” Sirah shares. “The Voices Project gives people a voice and a connection to hope.”

The hope offered through open dialogue about addiction and recovery has now grown into a digital movement.

The pages that Hampton started with $20 and an old computer have gained more than 200,000 followers across platforms, reaching nearly 1 million people each week. “We’re the fastest-growing social movement in history – and the funny thing is, we’re a community that nobody ever wanted to be a part of,” Novak says.

“This is the one space where we cannot be ignored. The time has come for us to speak out, and we’re a community that speaks loudly. With addiction, we’re dealing with imminent death every day,” Hampton says. “Through social media, we’ve found an innovative way to communicate with each other and connect with people we haven’t met, and now, we’re having this conversation with the rest of the world.”

Perhaps the most intriguing impact of Hampton’s work is the paradoxical ability to bring the work of addiction recovery advocacy online – only to take it back offline through real-world change in communities across the country. According to Hampton, the work he’s doing shouldn’t stay digital – it should impact community laws, help new non-profits emerge and influence real people to seek treatment and find it.

“No matter if you have social media or not – your way of doing this is talking about addiction at the dinner table, to a parent or a friend or an employer. You should not be afraid to tell your story of recovery or loss and, most importantly, your story of struggle and how you need help. It may not just change your life, it may change someone else’s life,” Hampton says.

At the crux of digital advocacy in the addiction recovery realm are real lives being saved – people finding treatment, families finding hope and those in recovery being freed of stigma that can keep them in shame and silence.  This is the mission that has fuelled Hampton’s work since the beginning. And Hampton’s reason is hard to refute: “My story is powerful, but our stories are powerful beyond measure.”

Source: https://www.forbes.com/sites/toriutley/2017/04/18/the-recovering-heroin-addict-shaking-social-media/2/#273606f0689c

Kuei Y. Tseng was awarded $1.95 million by NIH for a five-year study of “Adolescent Maturation of the Prefrontal Cortex: Modulation by Cannabinoids.” Regular marijuana use by teens can stop the brain from maturing, according to a new study by scientists at Rosalind Franklin University of Medicine and Science, North Chicago, IL. Published March 4 in the journal Molecular Psychiatry, the study is the first to establish a causal link between repeated cannabinoid exposure during adolescence and an interruption of the normal maturation processes in the prefrontal cortex, a region in the brain’s frontal lobe, which regulates decision making and working memory and undergoes critical development during adolescence.

The findings apply to natural cannabinoids, including those in marijuana, and a new generation of more potent, synthetic cannabinoid products. THC, the compound in marijuana that produces feelings of euphoria, is of particular concern. The chemical can be manipulated, resulting in varying concentrations between marijuana strains – from 2 to 28 percent. A higher concentration of THC and increasing use by younger teens poses a greater risk for long term negative effects, the study finds. Kuei Y. Tseng, MD, PhD, associate professor of cellular and molecular pharmacology at the Chicago Medical School at RFUMS and principal investigator of the study, blames the CB1 cannabinoid receptor, which governs neuronal communication, for the drug’s long -lasting effect.

Tseng and his team of researchers used rat models in testing the effect of cannabinoid exposure during narrow age windows and analyzed the way information is later processed by the adult prefrontal cortex. They discovered that when CB1 receptors are repeatedly activated by cannabinoids during early adolescence, development of the prefrontal cortex stalls in that phase. The window of vulnerability represents two thirds of the span of adolescence. Test animals showed no such effect when exposure occurred in late adolescence or adulthood.

“We have conclusively demonstrated that an over activation of the CB1 receptor during the window equivalent to age 11 to 17 in humans, when the prefrontal cortex is still developing, will inhibit its maturation and have a long lasting effect on its functions,” Tseng said.

The study shows how chronic cannabis use by teens can cause persistent behavioral deficits in adulthood, including problems with attention span and impulse control. The findings also add to prior research that draws a correlation between adolescent marijuana abuse and the development of schizophrenia.

The discovery, which comes as a growing number of states are considering legalization of marijuana for both medicinal and recreational use, calls for the attention of physicians who prescribe medical marijuana and policy makers who, according to Tseng, “will have to establish regulations to take advantage of the beneficial effects of marijuana while minimizing its detrimental potential.”

Researchers are focusing on developing outcome measures to reveal the degree of frontal lobe maturation and history of drug exposure. The challenge now, Tseng said, is to find ways to return the frontal lobe back to a normal state either through pharmacological or cognitive interventions.

“Future research will tell us what other mechanisms can be triggered to avoid this type of impairment of the frontal lobe,” Tseng said. “Ultimately, we want to restore the prefrontal cortex.”

Supported by RFUMS, the research was funded primarily through NIH Grant R01-MH086507 to Tseng and also by a 2012 seed grant from the Brain Research Foundation.

Source:  https://www.rosalindfranklin.edu/news/profiles/study-shows-marijuana-use-interrupts-adolescent-brain-development/   4th March 2017

Chairman Murphy, Ranking Member DeGette, and Members of the Committee: thank you for inviting the National Institute on Drug Abuse (NIDA), a component of the National Institutes of Health (NIH), to participate in this important hearing to provide an overview of what we know about the role of fentanyl in the ongoing opioid overdose epidemic and how scientific research can help us address this crisis.

The misuse of and addiction to opioids – including prescription pain medicines, heroin, and synthetic opioids such as fentanyl – is a serious national problem that affects public health as well as social and economic welfare.  The Centers for Disease Control and Prevention (CDC) recently estimated that the total “economic burden” of prescription opioid misuse alone in the United States is $78.5 billion a year, including the costs of health care, lost productivity, addiction treatment, and criminal justice involvement.1  In 2015, over 33,000 Americans died as a result of an opioid overdose.2  That year, an estimated 2 million people in the United States suffered from substance use disorders related to prescription opioid pain medicines (including fentanyl), and 591,000 suffered from a heroin use disorder (not mutually exclusive).3

This issue has become a public health epidemic with devastating consequences including not just increases in opioid abuse and related fatalities from overdoses, but also the rising incidence of neonatal abstinence syndrome due to opioid use during pregnancy, and the increased spread of infectious diseases, including HIV and hepatitis C.4-6  Recent research has also found a significant increase in mid-life mortality in the United States particularly among white Americans with less education.  Increasing death rates from drug and alcohol poisonings are believed to have played a significant role in this change.7

The Pharmacology of Fentanyl and Other Synthetic Opioids

Prescription opioids, heroin, and synthetic opioid drugs all work through the same mechanism of action.  Opioids reduce the perception of pain by binding to opioid receptors, which are found on cells in the brain and in other organs in the body.  The binding of these drugs to opioid receptors in reward regions in the brain produces a sense of well-being, while stimulation of opioid receptors in deeper brain regions results in drowsiness and respiratory depression, which can lead to overdose deaths.  The presence of opioid receptors in other tissues can lead to side effects such as constipation and cardiac arrhythmias through the same mechanisms that support the use of opioid medications to treat diarrhea and to reduce blood pressure after a heart attack.  The effects of opioids typically are mediated by specific subtypes of opioid receptors (mu, delta, and kappa) that are activated by the body’s own (endogenous) opioid chemicals (endorphins, enkephalins).  With repeated administration of opioid drugs (prescription or illicit), the production of endogenous opioids decreases, which accounts in part for the discomfort that ensues when the drugs are discontinued (i.e., withdrawal).8

The rewarding effects of opioids – whether they are medications, heroin, or illicitly produced synthetic opioids – are increased when they are delivered rapidly into the brain, which is why non-medical users often inject them directly into the bloodstream.9 Fentanyl, in particular, is highly fat-soluble, which allows it to rapidly enter the brain, leading to a fast onset of effects. This high potency and rapid onset are likely to increase the risk for both addiction and overdose, as well as withdrawal symptoms.10  In addition, injection use increases the risk for infections and infectious diseases.  Another important property of opioid drugs is their tendency, when used repeatedly over time, to induce tolerance.  Tolerance occurs when the person no longer responds to the drug as strongly as he or she initially did, thus necessitating a higher dose to achieve the same effect.  The establishment of tolerance results from the desensitization of the brain’s natural opioid system, making it less responsive over time.11  Furthermore, the lack of sufficient tolerance contributes to the high risk of overdose during a relapse to opioid use after a period of abstinence whether it is intentional – for example, when a person tries to quit using – or situational – for example, if a person cannot obtain opioid drugs while incarcerated or hospitalized.  Users no longer know what dose of the drug they can safely tolerate, resulting in overdoses.

While all of these opioids belong to a single class of drugs, each is associated with distinct risks. The risk of overdose and negative consequences is generally greater with illicit opioids due to the lack of control over the purity of the drug and its potential adulteration with other drugs.  All of these factors increase the risk for overdose, since users have no way of assessing the potency of the drug before taking it.  In the case of adulteration with highly potent opioids such as fentanyl or carfentanil, this can be particularly deadly.12-14  Another contributing factor to the risk of opioid-related mortality is the combined use with benzodiazepines or other respiratory depressants, like some sleeping pills or alcohol.15

The Role of Fentanyl in the Opioid Crisis

The emergence of illicitly manufactured synthetic opioids including fentanyl, carfentanil, and their analogues represents an escalation of the ongoing opioid overdose epidemic.  Fentanyl is a µ-opioid receptor agonist that is 80 times more potent than morphine in vivo. While fentanyl is available as a prescription – primarily used for anesthesia, treating post-surgical pain, and for the management of pain in opioid-tolerant patients – it is the illicitly manufactured versions that have been largely responsible for the tripling of overdose deaths related to synthetic opioids in just two years – from 3,105 in 2013 to 9,580 in 2015.2  A variety of fentanyl analogues and synthetic opioids are also included in these numbers, such as carfentanil (approximately 10,000 times more potent than morphine), acetyl-fentanyl (about 15 times more potent than morphine), butyrfentanyl (more than 30 times more potent than morphine), U-47700 (about 12 times more potent than morphine), and MT-45 (roughly equivalent potency to morphine), among others.17

The opioid crisis began in the mid-to late 1990’s, following a confluence of events that led to a dramatic increase in opioid prescribing, including: a regulatory, policy and practice focus on opioid medications as the primary treatment for all types of pain;18 an unfounded concept that opioids prescribed for pain would not lead to addiction;19 the release of guidelines from the American Pain Society in 1996 encouraging providers to assess pain as “the 5th vital sign” at each clinical encounter; and the initiation of aggressive marketing campaigns by pharmaceutical companies promoting the notion that opioids do not pose significant risk for misuse or addiction and promoting their use as “first-line” treatments for chronic pain.19-21

The sale of prescription opioids more than tripled between 1999 and 2011, and this was paralleled by a more than four-fold increase in treatment admissions for opioid abuse and a nearly four-fold increase in overdose deaths related to prescription opioids.22  Federal and state efforts to curb opioid prescribing resulted in a leveling off of prescriptions starting in 2012;23 however, heroin-related overdose deaths had already begun to rise in 2007 and sharply increased from just over 3,000 in 2010 to nearly 13,000 in 2015.2  We now know prescription opioid misuse is a significant risk factor for heroin use; 80 percent of heroin users first misuse prescription opioids.24  While only about four percent of people who misuse prescription opioids initiate heroin use within 5 years,24,25 for this subset of people the use of the cheaper, often easier to obtain street opioid is part of the progression of an opioid addiction.26

The opioid overdose epidemic has now further escalated, with the rise in deaths related to illicitly manufactured synthetic opioids.  Often, the population of people using and overdosing on fentanyl looks very similar to the population using heroin. However, the drivers of fentanyl use can be complicated as the drug is often sold in counterfeit pills – designed to look like common prescription opioids or benzodiazepines (e.g. Xanax) – or is added as an adulterant to heroin or other drugs, unbeknownst to the user.14  And there are also market forces supporting the proliferation of higher-potency opioids, as people with opioid addictions develop increasing tolerance to these drugs.27

History of Fentanyl Misuse

The first fentanyl formulation (Sublimaze) received approval by the Food and Drug Administration (FDA) as an intravenous anesthetic in the 1960s.  Other formulations, including a transdermal patch, a quick acting lozenge or “lollipop” for breakthrough pain, and dissolving tablet and film, have since received FDA approval.28  Misuse of prescription fentanyl was first described in the mid-1970s among clinicians,29 and continues to be reported among the people misusing prescription opioids.3  More recently, between April 2005 and March 2007 there was an uptick in deaths related to illicitly manufactured fentanyl that was traced to a single laboratory in Mexico. Once the laboratory shut down the rate of overdose declined.30  However, over the last few years there has been a growing production of illicitly manufactured fentanyl, much of which is imported from China, Mexico, and Canada.14  The increase in illicitly manufactured fentanyl availability in the U.S. is reflected by the substantial increase in seizures of fentanyl by law enforcement which jumped from under 1,000 seizures in 2013 to over 13,000 in 2015.31 Research shows that the increasing availability of illicitly manufactured fentanyl closely parallels the increase in synthetic opioid overdose deaths in the U.S.32

HHS Response and NIDA-Supported Research Related to Fentanyl

Within HHS, the Office of the Assistant Secretary for Planning and Evaluation (ASPE) has been leading a targeted and coordinated policy and programmatic effort to reduce opioid abuse and overdose, including fentanyl use and overdose. The effort focuses on strengthening surveillance, improving opioid prescribing practices and the treatment of pain, increasing access to treatment for opioid addiction, expanding use of naloxone to reverse opioid overdose, and funding and conducting research to better understand the epidemic and identify effective interventions. Under this effort, NIDA is engaged in number critical activities.

NIDA supports the National Drug Early Warning System (NDEWS), which monitors emerging drug use trends to enable health experts, researchers and others to respond quickly to potential outbreaks of illicit drugs.  In partnership with the NDEWS, the Northeast Node of the NIDA’s Clinical Trials Network (CTN) has been funded to complete a Fentanyl Hot Spot Study in New Hampshire.  In 2015, New Hampshire had the highest rate of fentanyl-related deaths in the country and this study is investigating the causes of increased fentanyl use and related deaths in this region.

In the first phase of the study, multiple stakeholders throughout the state, including treatment providers, medical responders, law enforcement, state authorities and policymakers were interviewed about their perspectives on the fentanyl crisis.33  Many expressed that better user-level data was imperative to answer pointed questions to more accurately inform policy, such as the trajectory of fentanyl use, supply chain, fentanyl-seeking behavior versus accidental ingestion, value of testing kits, treatment preferences, etc. The researchers reported that, “Some may seek out a certain dealer or product when they hear about overdoses because they think that it must be good stuff.”  According to the group leader, only approximately a third of users knowingly use fentanyl, but the number of users is slowly increasing.

The second phase of the study is conducting a rapid epidemiological investigation of fentanyl users’ and first responders’ perspectives, so that real-time data can inform policy in tackling the fentanyl overdose crisis.

Another ongoing NIDA funded study is characterizing the fentanyl crisis in Montgomery County, Ohio – an area experiencing one of the largest surges of illicitly manufactured fentanyl in the country. This study will explore the scope of the fentanyl crisis in this area, collecting data from postmortem toxicology and crime laboratories, and will explore active user knowledge and experiences with fentanyl.  Other NIDA funded research is working to develop faster methods for screening for fentanyl and other synthetic opioids to track overdoses through emergency department screening and improve surveillance of the fentanyl threat across the country.

NIDA-supported research is also working to develop new treatments for opioid addiction, including treatments targeting fentanyl specifically. One ongoing NIDA-funded study is in the early stages of developing a vaccine for fentanyl that could prevent this drug from reaching the brain.34

Evidence-Based Approaches

With the emergence of very high potency opioids addressing supply becomes increasingly difficult because the quantities transported may be much lower.  Thus, it is critical to address demand reduction through the deployment of evidence-based prevention and treatment strategies to reduce the number of people developing an opioid addiction and treating the population of Americans who already suffer from this addiction.

Evidence-Based Treatments for Opioid Addiction

Three classes of medications have been approved for the treatment of opioid addiction : (1) agonists, e.g. methadone , which activate opioid receptors; (2) partial agonists, e.g. buprenorphine, which also activate opioid receptors but produce a diminished response; and (3) antagonists, e.g. naltrexone, which block the opioid receptor and interfere with the rewarding effects of opioids.35  These medications represent the first-line treatments for opioid addiction.

The evidence strongly demonstrates that methadone, buprenorphine, and injectable naltrexone (e.g., Vivitrol) all effectively help maintain abstinence from other opioids and reduce opioid abuse-related symptoms.  These medications have also been shown to reduce injection drug use and HIV transmission and to be protective against overdose.36-40  These medications should be administered in the context of behavioral counseling and psychosocial supports to improve outcomes and reduce relapse.  Two comprehensive Cochrane reviews, one analyzing data from 11 randomized clinical trials that compared the effectiveness of methadone to placebo, and another analyzing data from 31 trials comparing buprenorphine or methadone treatment to placebo, found that38,39:

* Patients on methadone were over four times more likely to stay in treatment and had 33 percent fewer opioid-positive drug tests compared to patients treated with placebo;

* Methadone treatment significantly improves treatment outcomes alone and when added to counseling; long-term (beyond six months) outcomes are better for patients receiving methadone, regardless of counseling received;

* Buprenorphine treatment significantly decreased the number of opioid-positive drug tests; multiple studies found a 75-80 percent reduction in the number of patients testing positive for opioid use;

* Methadone and buprenorphine are equally effective at reducing symptoms of opioid addiction; no differences were found in opioid-positive drug tests or self-reported heroin use when treating with these medications.

To be clear, the evidence supports long-term maintenance with these medicines in the context of behavioral treatment and recovery support, not short-term detoxification programs aimed at abstinence.41  Abstinence from all medicines may be a particular patient’s goal, and that goal should be discussed between patients and providers.  However, the scientific evidence suggests the relapse rates are extremely high when tapering off of these medications, and treatment programs with an abstinence focus generally do not facilitate patients’ long-term, stable recovery.42,43

Treatment Challenges

Unfortunately, medications approved for the treatment of opioid abuse are underutilized and often not delivered in an evidence based manner.44,45  Fewer than half of private-sector treatment programs offer these medications; and of patients in those programs who might benefit, only a third actually receive it.45  Further, many people suffering with opioid addiction do not seek treatment. Identifying the need for and engaging them in treatment is an essential element of addressing the opioid crisis. For example, recent research suggests that initiating patients on buprenorphine following an opioid overdose can increase treatment retention and improve outcomes.46  Overcoming the misunderstandings and other barriers that prevent wider adoption of these treatments is crucial for tackling the opioid crisis.

In addition, to achieve positive outcomes, treatments must be delivered with fidelity. To be effective, methadone and buprenorphine must be given at a sufficiently high dose.38,39  Some treatment providers wary of using methadone or buprenorphine have prescribed lower doses for short treatment durations, leading to treatment failure and the mistaken conclusion that the medication is ineffective.38,47

As of 2011, more than 22 percent of patients in a methadone treatment programs were receiving less than the minimum recommended dose of methadone.48  Interestingly, a recent study identified a genetic variant near the mu opioid receptor gene associated with a higher required dose of methadone (corresponding to a need for about an additional 20 mg per day) in African American patients but not European Americans with this gene variant.49  This highlights the need for dosing flexibility to achieve the effective dose for an individual patient.  The NIH Precision Medicine Initiative and other ongoing research projects are working to define the genetic, biological, and clinical factors that influence the efficacy of treatment to help clinicians deliver care precisely tailored for a specific patient to improve outcomes.

Research has also shown that tapering off of buprenorphine can present significant risks for relapse.43,50  A recent analysis of five studies that examined outcomes following buprenorphine taper found that on average only 18 percent (a range of 10 to 50 percent) of patients remained abstinent one to two months after tapering off of buprenorphine.50  In addition, some state programs and insurance providers limit the duration of treatment a patient may receive.  There is no evidence base to support this practice, and the available evidence suggests that it poses a significant risk for patient relapse.  This is also an important consideration in the context of the two years of funding for the opioid crisis authorized through the 21st Century Cures Act. This funding will be critical for helping states address the ongoing opioid epidemic, however, opioid addiction is a chronic condition and many patients will need ongoing treatment for many years.  It will be important to develop sustainability strategies to ensure that patients do not lose access to these life-saving medications when a particular funding program is discontinued.

While users seeking treatment are on a wait list they generally continue to engage in opioid use and this may contribute to failure to enter treatment when a slot becomes available.  Research has shown that providing interim treatment with medications while patients are awaiting admission to a treatment program increases the likelihood that they will engage in treatment.  In one study, over 64 percent of study participants receiving interim methadone entered comprehensive care within six months, compared with only 27 percent in the control group, and the group receiving methadone had lower rates of heroin use and criminal behavior.51 One model for interim treatment with buprenorphine would use urine testing call backs and a special medicine dispensing device to prevent diversion.52  Implementation would require a regulatory change because take home buprenorphine is not allowed under interim regulations currently. When this model was tested, patients showed strong adherence to the interim treatment plan and reported strong satisfaction with the treatment. State regulations and payment system issues (bundled payment that does not accommodate billing for interim treatment) are often barriers to this type of program and they are not frequently used.

Fentanyl specific challenges

While specific data on treatment outcomes for patients addicted to fentanyl or other high potency synthetic opioids are not available, the same principles of treatment still apply.  In addition, patients regularly using these substances and surviving would be expected to have a strong opioid dependency. At this time we are not sure how many people fit this clinical picture. In this scenario the withdrawal symptoms are likely to be severe, and could lead to life threatening cardiac arrhythmias and seizures if untreated or if extreme opioid withdrawal is potentiated during overdose reversal.53 There is an urgent need for more research to determine if people using fentanyl or other high potency opioids respond differently to medications for overdose reversal as well as treatment and to determine the most effective approaches for utilizing medications and psychosocial supports in this population.

In general outcomes are better predicted by the strength of the psychosocial supports around patients to support their recovery – educational or job opportunities, supportive friends and family, stable housing, access to child care – than the severity of their addiction.  Providing behavioral counseling and wrap around services to address these needs is important for achieving the best outcomes.

Prevention of Opioid Misuse and Addiction

Since the majority of people who develop an opioid addiction begin by misusing prescription opioids, the Department of Health and Human Services (HHS) continues to focus efforts on improving opioid prescribing and preventing the misuse of prescription drugs as the long-run strategy to stop the opioid epidemic.  NIDA supports research to understand the impact of federal and state policy changes on rates of opioid abuse and related public health outcomes.  This and other federally supported research has demonstrated the efficacy of multiple types of interventions, including:

* Educational initiatives delivered in school and community settings (primary prevention)54

* Supporting consistent use of prescription drug monitoring programs (PDMPs)

* Aggressive law enforcement efforts to address doctor shopping and pill mills56,57

* Providing healthcare practitioners with tools for managing pain, including prescribing guidelines and enhanced warnings on drug labels with expanded information for prescribers58-61

In states with the most comprehensive initiatives to reduce opioid overprescribing, the results have been encouraging.  Washington State’s implementation of evidence-based dosing and best-practice guidelines, as well as enhanced funding for the state’s PDMP, helped reduce opioid deaths by 27 percent between 2008 and 2012.58  In Florida, new restrictions were imposed on pain clinics, new policies were implemented requiring more consistent use of the state PDMP, and the Drug Enforcement Administration (DEA) worked with state law enforcement to conduct widespread raids on pill mills, which resulted in a dramatic decrease in overdose deaths between 2010 and 2012.62  These examples show that state and Federal policies can reduce the availability of prescription opioids and related overdose deaths.  However, the increasing supply of heroin and illicit fentanyl in the United States is undermining the effects of these improvements. While we have seen a leveling off of overdose deaths related to commonly prescribed opioids over the last few years, overdose deaths related to illicit opioids have risen dramatically during this time.

In early 2016 CDC released guidelines for prescribing opioids for chronic pain.60  We believe they represent an important step for improving prescriber education and pain prescribing practices in our nation.  NIDA is advancing addiction awareness, prevention, and treatment in primary care practices through seven Centers of Excellence for Pain Education.63  Intended to serve as national models, these centers target physicians-in-training, including medical students and resident physicians in primary care specialties (e.g. internal medicine, family practice, and pediatrics).

Addressing the Public Health Consequences of Opioid Misuse

Other evidence-based strategies can be used to reduce the health harms associated with opioid use, including increasing access to the opioid-overdose-reversal drug naloxone.

Preventing Overdoses with Naloxone

The opioid overdose-reversal drug naloxone can rapidly restore normal respiration to a person who has stopped breathing as a result of an overdose from heroin or prescription opioids.  Naloxone is widely used by emergency medical personnel and some other first responders.  Beyond first responders, a growing number of communities have established overdose education and naloxone distribution programs that make naloxone more accessible to opioid users and their friends or loved ones, or other potential bystanders, along with brief training in how to use these emergency kits.  Such programs have been shown to be effective, as well as cost-effective, ways of saving lives.64,65  CDC reported that, as of 2014, more than 152,000 naloxone kits had been distributed to laypersons and more than 26,000 overdoses had been reversed since 1996.66  In addition, the majority of states now allow individuals to obtain naloxone from retail pharmacies without a patient-specific prescription.67

Two naloxone formulations specifically designed to be administered by family members or caregivers have recently been developed.  In 2014 the FDA approved a handheld auto-injector of naloxone, and in late 2015 the FDA approved a user-friendly intranasal formulation that was developed through a NIDA partnership with Lightlake Therapeutics, Inc. (a partner of Adapt Pharma Limited).68

The availability of naloxone is critical to reduce opioid-related fatalities.69  However, research examining past fentanyl outbreaks shows that higher than typical naloxone doses were required to reverse fentanyl overdose.70  As the use of fentanyl and other highly potent opioids is increasing, it would be prudent to promote the use of naloxone while recognizing that multiple doses may be needed to revive someone experiencing a fentanyl overdose.71  It is also important for first responders to know that, while fentanyl has a short duration of action (30-90 minutes), it can stay in fat deposits for hours, and patients should be monitored for up to 12 hours after resuscitation.72  More research may be needed to develop new naloxone formulations tailored to higher-potency opioids.

Ongoing Opioid-Related Research: Implementation Science

Despite the availability of evidence based treatments for opioid abuse, we have a significant and ongoing treatment gap in our Nation.  Among those who need treatment for an addiction, few receive it.  In 2014, less than 12 percent of the 21.5 million Americans suffering with addiction received specialty treatment.3   Further, many specialty treatment programs do not provide current evidence based treatments – fewer than half provide access to MAT for opioid use disorders.45  In addition, it is clear that preventing drug use before it begins—particularly among young people—is the most cost-effective way to reduce drug use and its consequences.73  Evidence based prevention interventions also remain highly underutilized.

Ongoing NIDA research is working to better understand the barriers to successful and sustainable implementation of evidence based practices and to develop implementation strategies that effectively overcome these barriers.  This work also seeks to understand the role environment—be it social, familial, structural, or geographic—plays in preventing opioid use and in the success of prevention and treatment interventions, as well as how to tailor prevention and treatment interventions to individuals with unique needs, including those in the criminal justice system or with HIV.

Other NIDA supported research is looking at how to improve access to treatment among other high risk populations.  For example, patients with opioid addiction are at increased risk of adverse health consequences and often seek medical care in emergency departments (EDs). NIDA is also collaborating with the Baltimore County Health Department on a pilot study to explore the possibility of providing methadone through pharmacies to increase access to treatment in underserved parts of the city. In the pilot, pharmacies would be considered satellite locations of licensed methadone treatment facilities; this model has been used in Pennsylvania and New York. Discussions are underway to explore whether regulatory exceptions can be granted to make this possible. Similarly, ongoing research is examining on the impact of providing opioid addiction treatment within infectious disease clinics.  This type of research is essential for translating evidence based strategies into real-world interventions that will reach the greatest number of people and get the most out of limited prevention and treatment resources.

Implementation Research to Address the Opioid Crisis in Rural Communities

Our efforts are also focused on addressing the opioid crisis in the epicenter of the epidemic – Appalachia.  NIDA is partnering with the Appalachian Regional Commission (ARC) to fund one-year services planning and needs assessment research grants to provide the foundation for future intervention programs and larger scale research efforts to test interventions to address opioid misuse in rural Appalachia.  Four grants were awarded in FY 2016 that will address issues related to injection drug use and associated transmission of infectious disease as well as the coordination of care for prisoners with opioid addiction as they re-enter the community.

A second funding opportunity announcement in partnership with the Substance Abuse and Mental Health Services Administration (SAMHSA), CDC, and ARC was released in October 2016 to support comprehensive, integrated approaches to prevent opioid injection and its consequences, including addiction, overdose, HIV and hepatitis C, as well as sexually transmitted diseases.  High rates of injection drug use in Appalachia has led to a rapid increase in the transmission of hepatitis C, raising concern about an outbreak of HIV.6 These projects will work with state and local communities to develop best practices that can be implemented by public health systems in the Nation’s rural communities including opioid abuse treatment  and other strategies to increase the testing and treatment for HIV.

HIV Testing and Treatment

NIDA supported research has helped to develop the seek, test, treat, and retain model of care (STTR) that involves reaching out to high-risk, hard-to-reach drug users who have not been recently tested for HIV; engaging them in HIV testing; engaging those testing positive in antiretroviral therapy; and retaining patients in care. Research has shown that implementation of STTR has the potential to decrease the rate of HIV transmission by half.75

Ongoing Opioid-Related Research: Development of Pain Treatments with Reduced Potential for Misuse

NIDA is one of multiple institutes of the NIH supporting research into novel pain treatments with reduced potential for misuse and diversion, including abuse resistant opioid analgesics, non-opioid medication targets, and non-pharmacological treatments. Some of the most promising potential therapies include:

* Abuse Resistant Opioid Analgesics: Efforts are underway to identify new opioid pain medicines with reduced misuse, tolerance, and dependence risk, as well as alternative delivery systems and formulations for existing drugs that minimize diversion and misuse (e.g., by preventing tampering) and reduce the risk of overdose deaths.  Multiple recent NIH-funded studies have reported progress in the discovery of opioid compounds with selective analgesic effects with reduced respiratory depressive effects and reduced abuse liability.76-78

* Non-Opioid Medications: Some non-opioid targets with promising preliminary data include fatty acid binding proteins, the G-protein receptor 55, cannabinoids, and transient receptor potential cation channel A1.

* Nervous Stimulation Therapies: Several non-invasive nervous stimulation therapies – including transcranial magnetic stimulation and transcranial direct current stimulation, as well as electrical deep brain stimulation, spinal cord stimulation, and peripheral nerves/tissues stimulation – have shown promise for the treatment of intractable chronic pain.  These devises have been approved by the FDA for treatment of other conditions but more research is needed on their effectiveness for pain.

* Neurofeedback: Neurofeedback is a novel treatment modality in which patients learn to regulate the activity of specific brain regions by getting feedback from real-time brain imaging.  This technique shows promise for altering the perception of pain in healthy adults and chronic pain patients and may also be effective for the treatment of addiction.

*

Ongoing Opioid-Related Research: Accelerating Development of New Treatments for Addiction

While the three available medications have represented significant advances in the ability to treat opioid use disorders the efficacy of these medications is far from ideal.  NIDA is funding research to accelerate development of new treatments.  This includes development of non-pharmacological interventions including biologics – such as vaccines, monoclonal antibodies, and bioengineered enzymes designed to prevent a drug from entering the brain – and novel brain stimulation techniques – such as TMS and transcranial direct current stimulation (tDCS), that target brain circuits impaired in addiction with improved specificity and temporal and spatial resolutions, and thus, with less adverse effects.  One ongoing NIDA-funded study is in the early stages of developing a vaccine for fentanyl that could prevent this drug from reaching the brain.34

Since the pharmaceutical industry has traditionally made limited investment in the development of medications to treat SUDs, NIDA has focused on forming alliances between strategic partners (pharmaceutical and biotechnology companies as well as academic institutions) with the common goal of advancing medications through the

development pipeline toward FDA approval.  NIDA conducts research to decrease the risks associated with medications development to make it more appealing for pharmaceutical companies to complete costly phase IIb and III clinical studies.  An example of such a project is a partnership with US World Meds, is in late stage development of lofexidine, a medication for the treatment of opioid withdrawal symptoms that might also hold promise for the treatment of other addictions.

Conclusion

NIDA will continue to closely collaborate with other federal agencies and community partners with a strong interest in preserving public health to address the interrelated challenges posed by misuse of prescription opioids, heroin, and synthetic opioids such as fentanyl.  We commend the committee for recognizing the serious and growing challenge associated with this exceedingly complex issue.  Under the leadership of the Department of Health and Human Services and the Office of National Drug Control Policy, NIDA will continue to support the implementation of the multi-pronged, evidence-based strategies to improve opioid prescribing and pain management, reduce overdose deaths, and increase access to high quality opioid abuse treatment.

Source:https://www.drugabuse.gov/about-nida/legislative-activities/testimony-to-congress/2016/americas-addiction-to-opioids-heroin-prescription-drug-abuse 

March 2017

‘What can we do?’ This was the question that dominated the weekend’s news and current affairs in the aftermath of the Westminster ‘terror’ attack. We still do not know if it was organised by so-called Islamic State or, as seems increasingly likely, was the savage work of a ‘lone wolf’.

The discussion I heard on Any Questions centred on rooting out radicalisation, smartening up security, or accepting ‘the new normal’ that the likes of Sadiq Khan and Dominic Grieve (the security services have done well and something was bound to happen at some point) seem resigned to – a world where increasingly frequent human sacrifices are subliminally accepted as a price worth paying to protect our democracy and ‘our way of life’.

Two factors were not considered. One, the role of family dysfunction and two, the role of drugs, in catalysing the sort of violence perpetrated in Westminster last Wednesday.

From the moment he was born to a 17-year-old lone mother, Adrian Ajao was statistically at risk. Newspapers referred to his ‘well to do’ Home Counties upbringing but of far more significance for this baby’s future life path was a birth certificate that listed only his mother. I am not asking you to weep but to accept, statistically, that Adrian didn’t get off to a very good start. The hard statistical fact is that children who live continuously with lone mothers have poorer cognitive and socio-emotional outcomes compared to children who have biological fathers as a stable part of the household and family life.

Any idea that the presence of a stepfather helps can be forgotten. It doesn’t stack up statistically either – children are no less at risk of poor outcomes in step households. Adrian adopted his stepfather’s name only symbolically to abandon it later.

While some children in Africa are named after the unfortunate circumstances they are born to, in the modern West the unfortunate circumstance is not to have a biological father to name you.

Here is where the trajectory from pain to violence begins. As the young Adrian hit his late teens, his chances of his hitting drugs too were high. From the graphic descriptions volunteered by former friends it was to prove disastrous. Cannabis, it seems likely, triggered the psychosis that was a key factor in his increasingly psychotic and violent behaviour.

Before his final horrific killing spree in Westminster last week, Khalid Masood (as he became) had gone from troubled teen to terror of his neighbourhood; once he tried to run a neighbour down and the wife he married in 2004 fled for her life. He would be jailed twice for slashing people with knives.

For anyone in a culture of denial about cannabis, schizophrenia and violence let me refer them to the epidemiological evidence in the public domain. It not only identifies cannabis use as a risk factor for schizophrenia, but in individuals with a predisposition for schizophrenia, it results in an exacerbation of symptoms and worsening of the schizophrenic prognosis (Simona A. Stilo,MD; Robin M. Murray RM. Translational Research 2010: The epidemiology of schizophrenia: replacing dogma with knowledge. Dialogues Clin Neurosci. 2010 Sep;12(3):305–315). A recently published Cambridge Study in Delinquent Development – a 50-year cohort study – has categorically found that cannabis caused a seven-fold increase in a violent behaviour and that continued use of cannabis over the lifetime of the study was strongest predictor of violent convictions, even when all other factors that contributed to violent behaviour were accounted for. A study of Norwegian youths similarly found an association between cannabis use and violence and that frequency of cannabis use relates to frequency of incidents of violent behaviour. The preliminary findings of another study have found the changes in brain function that suggest the mechanism for cannabis-induced violence.

Ajao is not the only young British drug user to become prone to sudden bursts of violence, to dream about killing someone or to harbour a blood lust. Our NHS psychiatric wards are full of them on anti-psychotic medication to stop them hearing voices while they yet still abuse cannabis.

An analysis of hospital episode statistics I investigated a few years ago revealed the extent of the cannabis mental health crisis in the UK, despite an overall fall in use. Between 1998 and 2011, mental and behavioural disorders due to cannabis use increased overall by 54 per cent. This included an 108 per cent increase in harmful use episodes, a 51 per cent increase in dependence, a 61.8 per cent increase in psychotic disorders, and a 450 per cent increase in ‘other mental and behavioural disorders. Drug-related hospital admissions have reached record highs too in recent years. Most, 70 per cent are men and most of these are young men. The science is there for the behavioural unit in the Home Office to investigate, as Amber Rudd promised would be the case last year when she was asked.

Since Wednesday police have been searching for explanations for Khalid Masood’s violence. They are checking all possible contacts with ISIL cells and the influence of Islamist radicals, quite rightly. Masood, I have no doubt, was ripe for radicalisation in his own unhappy quest for personal ‘justice’.

Like Lee Rigby’s killers before him, I suspect the drugs came first and the conversion followed, giving a purpose to the violent impulses lurking within. Newspaper columnist Peter Hitchens has been right to ask what violent killers have in common and to ask whether it is dope that may be the real mind-blowing terror threat in our midst and where dysfunctional families abound. For the fact is that mental illness, triggered by cannabis, increases the risk of aggressive behaviour, crime and violence.

British longitudinal data on cannabis use and schizophrenia shows that the incidence of schizophrenia in South London doubled between 1965 and 1999. The study uniquely allowed for the examination of trends in cannabis use prior to first presentation with schizophrenia. The greatest increase was found in people under 35. Its author Professor Sir Robin Murray has suggested that up to 20 per cent of schizophrenia cases could be cannabis attributable.

Despite all this, the Government in the UK has kept its head in the sand over this public health and safety time bomb. It has never fulfilled its pledge to run a major public health education campaign.

The evidence should tell Amber Rudd’s Home Office ‘behaviour unit’ that it is overdue, as is committed policing to protect young men at risk.  This has to be part of any prevention strategy in response to the carnage in Westminster last week. The link between cannabis and violence, as I argued before, can no longer be ignored.

Source:  http://www.conservativewoman.co.uk/kathy-gyngell-did-cannabis-trigger-westminster-killers-madness/   28th March 2017 

The Director of the NDPA, Peter Stoker, visited Vancouver East Side in 1999.  It was tragic to see drug dependent men and women living rough on the streets – in the alleys behind the main road – injecting in public.  A team of police officers called The Odd Squad worked the area and did everything they could to help these people – producing a great video called ‘Through the Blue Lens’ – we took this video into schools and it was the most powerful drug prevention message we had ever used.  We would urgently ask you to see this video on You Tube – https://www.youtube.com/watch?v=gwFRsfATaag

The article below is covering the same story – 19 years later.  Isn’t it about time that Canada began to promote good drug prevention instead of relaxing their drug laws? 

As overdose deaths spike, provincial health officials say more overdose prevention sites will soon open across the province.

The number of overdose deaths related to illicit drugs in British Columbia leapt to 755 by the end of November, a more than 70-per-cent jump over the number of fatalities recorded during the same time period last year.

In August, 50 people died of drug overdoses in British Columbia.  In September, 57 died. In October, the number jumped to 67 — an increase that worried health officials, who had thought that increasing the supply and training for administering the overdose reversal drug naloxone was making a difference.

In November, drug overdoses caused 128 deaths — 61 more than the previous month, and nearly double the October total. That spike has brought the total number of deaths between January and November to 755, the highest number ever recorded by the BC Coroner and a 70 per cent increase over this time last year

“We’re quite fearful that the drug supply is increasingly toxic, it’s increasingly unpredictable, and it’s very, very difficult to manage,” said Lisa Lapointe, B.C.’s chief coroner, referring to the increasing prevalence of the synthetic opioid fentanyl being added to many illicit drugs.  “Those who…attempt to use drugs safely, it’s almost impossible.”

With advance notice from the coroner that November numbers would be much higher, provincial health officials announced three weeks ago that several overdose prevention sites would open in Vancouver, Surrey and Victoria. People can go inside the sites to inject drugs, and are given first aid if they overdose.

An unofficial safe consumption site located in the alley behind the Downtown Eastside Market off East Hastings Street.

Health officials have insisted the sites are temporary and are not supervised injection sites, which are currently difficult to open because of a strict Conservative-era law that current federal health minister Jane Philpott has promised to change.

If there is any good news to be found within the grim statistics, it is that no deaths have occurred at any of those overdose prevention sites. And no one has died at a volunteer-run tent that has been operating since September, without official permission or government funding, out of an alley in the heart of the Downtown Eastside. People can smoke or snort drugs at that site, not just inject.

“We’re pretty steady, we get about 100 people a day,” said Sarah Blyth, the Downtown Eastside market coordinator and one of the organizers of the tent. “We’re coming up to welfare (day)…it’s happening this Wednesday, so I imagine up until Christmas it’s going to be pretty busy.”

A sign on the front door of VANDU’s storefront at 380 E. Hastings advertises that the location is an overdose prevention site, with volunteers trained in first aid

“A lot of people use during Christmas,” Blyth added. “Not everybody’s Christmas is as happy as others.”  At the Vancouver Area Network of Drug Users storefront further down East Hastings Street, Linda Bird confirmed the overdose prevention site located there has been busy, with around 60 people a day passing through. Volunteers, who are paid a small stipend by Vancouver Coastal Health, work two to four hour shifts. Overdoses are common, small stipend by Vancouver Coastal Health, work two to four hour shifts. Overdoses are a small stipend by Vancouver Coastal Health, work two to four hour shifts. Overdoses are common, Bird said.

“A lot of them are taking this very, very seriously,” Bird said of the volunteers. “It’s a crisis and a lot of them have seen their friends dropping.”

Vancouver Coastal Health has announced a fourth overdose prevention site in Vancouver, while Fraser Health has added more sites in Langley, Abbotsford and Maple Ridge.

Overdose deaths in November were nearly double the number seen in October

Health authorities in the Interior, Vancouver Island and the north are also planning to open sites in the future, said Perry Kendall, B.C.’s health officer.  “We’re still struggling in many communities with the idea of having these (overdose prevention) sites open,” Kendall said. “That doesn’t help.”

He urged the federal government to introduce the new legislation as soon as possible.

“You must use (drugs) in the presence of somebody who can help you,” Lapointe emphasized. “We are seeing people die with a naloxone kit open beside them, but they haven’t even had time to use it. We are seeing people die with a needle in their arm or a tablet nearby…You must go somewhere where someone is able to give you immediate medical assistance.”

Source:  http://www.metronews.ca/news/vancouver/2016/12/19/bc-drug-deaths

As part of the ongoing efforts of the International Narcotics Control Board (INCB) to raise awareness of key issues relevant to international drug control, I have the pleasure to share with you three short texts:

* Application of principle of proportionality for drug-related offences

* Ensuring availability of narcotic drugs for medical purposes

* Carrying by international travellers of small quantities of preparations containing controlled substances

Application of principle of proportionality for drug-related offences

  1. The application of the principle of proportionality in the context of drug offences is a key aspect of a sound and effective drug policy. Some States have made extensive use of incarceration of low-level drug offenders, despite the fact that this approach is not mandated by the international drug control treaties, and some have even applied extrajudicial responses to drug-related offences, notwithstanding the fact that such actions are contrary to the treaties. It is essential to distinguish between the criminal justice provisions contained within the Conventions1,2,3, and the criminal justice policy measures which have been taken by some Governments.
  2. Implementation of the international treaties is subject to the internationally recognized principle of proportionality, which requires that a State’s treatment of illegal behaviour to be proportionate and that a punishment in response to criminal offences should be proportionate to the seriousness of the crime.
  3. The INCB has repeatedly called upon States to give due regard to the principle of proportionality in the elaboration and implementation of criminal justice policy in their efforts to address drug-related crime.
  4. While the choice of legislative or policy measures to address drug-related crime, including the determination of sanctions is the prerogative of States, the international drug control treaties require that these sanctions should be adequate and proportionate, taking into account the gravity of the offence and the degree of responsibility of the alleged offender.
  5. The international drug control treaties do not automatically require the imposition of conviction and punishment for drug-related offences, including those involving the possession, purchase or cultivation of illicit drugs, in appropriate cases of minor nature or when committed by drug users. While “serious offences shall be liable to adequate punishment, particularly by imprisonment or other penalties of deprivation of liberty”, offences of a minor or lesser gravity need not necessarily be subject to harsh criminal sanctions, such as incarceration. The Conventions afford discretion for Parties to provide, either as an alternative to conviction and punishment or in addition to conviction and punishment, that drug users undergo measures of treatment, education, after-care, rehabilitation and social reintegration.

*

Ensuring availability of narcotic drugs for medical purposes

  1. Some decades ago the international community made a solemn commitment with the SingleConvention on Narcotic Drugs of 1961 and the Convention on Psychotropic Substances of 1971: to ensure the availability, to make adequate provision and not to unduly restrict the availability of drugs that were considered indispensable for medical and scientific purposes. Over the past decades that promise has not been fully met. . Too many people suffer or die in pain or do not have access to the medications they need. Unnecessary suffering because of the lack of appropriate medication due to the inaction, lack of know-how or unnecessary administrative requirements is a scandal that shames us all.
  2. Around 5.5 billion people still have limited or no access to medicines containing narcotic drugs such as codeine or morphine, leaving 75 per cent of the world population without access to proper pain relief treatment. Around 92 per cent of morphine used worldwide is consumed by only 17 per cent of the world population, primarily living in the United States, Canada, Western Europe, Australia and New Zealand. Inadequate access violates the notion of article 25 of the Universal Declaration of Human Rights, including the Right to medical care, which also encompasses palliative care.
    1. This situation is caused by a variety of factors, including health care professionals, that meansThe imbalance in the availability of opioid analgesics is particularly worrying as the latest data show that many of the conditions requiring pain management, particularly cancer, are prevalent and increasing in low- and middle-income countries.doctors and nurses, not receiving adequate education and training as part of their professional education, lack of know-how and capacity of government authorities, concerns about overprescribing and addiction and overly onerous regulatory and administrative requirements. Many patients in most of the countries in Africa, Central America and the Caribbean, and South Asia are affected, but patients in other parts of the world are also affected.
    2. Concrete steps and rapid action by Member States, the international community and the pharmaceutical industry can go a long way to remedy the situation. The most important and urgent actions would involve providing specialised training for health care professionals enabling them to prescribe and administer pain medication as well as training for the competent national authorities.
    3. Governments must bring about partnerships with the pharmaceutical industry, which has a duty to act in a socially responsible manner, to ensure access to and availability of affordable medications, placing emphasis on generics.
    4. Governments need also ensure that the training curricula of doctors and nurses contain, ab initio, content on the prescribing and rational use of medicines containing controlled substances.
    5. At the same time, where necessary, legislation and regulations should be revised, prescribing practices brought up to day and the capacity of national agencies involved strengthened.
    6. If Governments, together with the relevant international agencies, were to put together a sufficiently well-resourced plan of action, Member States would be on their way to significantly contributing towards achieving a major element of Sustainable Development Goal 3 on Ensuring healthy lives and promote wellbeing for all at all ages.

 

Carrying by international travellers of small quantities of preparations containing narcotic drugs and psychotropic substances for personal medical use

  1. The Board’s continuing endeavour to assist travellers carrying small quantities of controlled substances for personal medical use across international borders gained, both, high visibility and prominent usefulness.
  2. An ever increasing inflow of queries from individual travellers and organizations on the aforementioned subject has been observed. The secretariat regularly receives requests for assistance and/or clarification of the applicable national rules and regulations. The requests come from organizations and individual travellers residing in various countries. In 2016, requests came from Australia, France, Italy, United Kingdom, and the United States; their countries of interest included Cambodia, Canada, Colombia, France, Germany, Guinea Bissau, Malaysia, Saudi Arabia, Thailand, Turkey and the USA.
  3. Several requests relate to common rules and regulations of the European Union and the Schengen area. The substances referenced in the queries included psychotropic substances listed in Schedules II, III and IV such as amfetamine, alprazolam, buprenorphine, dextroamphetamine, diazepam, methylphenidate, nitrazepam, tramadol, zolpidem and others that are not under international control.
  4. Since 2013, the information furnished by Governments on national requirements for travellers under medical treatment carrying preparations containing narcotic drugs or psychotropic substances under international control has been summarized in a standardized table format and made available in six official UN languages on INCB website.
  5. To date, such information is available for 109 Governments (up from 79 in May 2014)and is uploaded to the Board’s webpage, more than half are already available in the form of standardized tables translated into six official UN languages:http://www.incb.org/incb/en/psychotropic-substances/travellers_country_regulations.html
  6. In September 2016, given the increasing interest in this pertinent information, inparticular the international guidelines for national regulations concerning travellers under treatment with internationally controlled drugs, and the compilation of standardized summary tables of regulations by country, the secretariat sent out a reminder letter to all countries and territories, requesting all Governments to visit the above website and to inform the Board if the information pertaining to their countries accurately reflects current provisions of their national laws and regulations.
    1. The Governments that have not yet furnished any information were requested to

    provide the requisite description of all relevant legal/regulatory or administrative measures

    adopted to allow travellers entering/leaving the country to carry medical preparations

    containing controlled substances for personal medical use. In addition to full texts of relevant

    pieces of information, these Governments were also requested to fill in and to submit to the

    Board the standardized summary tables that were attached to the circular letter.

    1. The secretariat will continue to augment the list of national rules and regulations

    pertaining to travellers carrying internationally controlled substances for personal medical use,

    provide requisite assistance and attend to all inquiries in this regard.

    Source:  http://www.incb.org/incb/en/news/alerts.html

    INCB is the independent, quasi-judicial body charged with promoting and monitoring Government compliance with the three international drug control conventions: the 1961 Single Convention on Narcotic Drugs, the 1971 Convention on Psychotropic Substances, and the 1988 Convention against Illicit Traffic in Narcotic Drugs and Psychotropic Substances.

 

 

 

 

 

I was just a year old when I had my first experience with opioids. I was born with a hiatal hernia, which constricted my esophagus and caused me to reflux like crazy. I couldn’t keep breast milk down and I became malnourished, tiny and weak. One night, my parents, Gayle and Morty Gebien, rushed me to the hospital. I was dehydrated and spitting up everything they tried to get me to eat or drink. The doctors told my parents to prepare themselves for the possibility that I wouldn’t live through the night. They brought me into surgery and gave me morphine for the pain. Maybe that’s where it all began.

I’ve always had a difficult time coping with stress. I sucked my thumb until I was eight years old. I started smoking at age 14 and never stopped. In high school, I was a pothead, and so were most of my friends. I dropped acid and did ecstasy a handful of times. Academically, I was apathetic, skipping class often and bringing home terrible report cards. One day, when I was 17, I went golfing with friends. When I got home, my back began to ache, a dull pain like a hand wrapping around my spine and squeezing it tight. I didn’t know it then, but I had a herniated disc. I lay down on the floor of my bedroom, and it felt like my vertebrae were shifting beneath me. Eventually, the sensation passed, and I got up.

The next year, I started volunteering at a hospital in Richmond Hill, folding blankets, mopping floors and stocking shelves. That’s when I first considered becoming a doctor. I studied science at the University of Toronto Scarborough, but my grades weren’t strong enough to get me into medical school, so I moved to Montreal and did a master’s in molecular biology at McGill. After that, I went to med school at the University of Queensland in Australia and did my residency in emergency medicine in Michigan.

In 2007, I visited my parents on vacation in Florida. I slept on the couch and, during the night, I displaced the disc in my back. The pain was much stronger than what I’d experienced in high school. My mother, who had prescriptions for her own back issues—she’d slipped on wet stairs a few years before I was born—gave me a powerful opioid called Dilaudid to soothe it. I knew I liked it too much. The back pain melted away, but so did everything else. It was like taking a happy pill. I immediately felt calm, relaxed, brighter and more wakeful than usual. Later that month, I sprained my thumb playing hockey. I went to the hospital, where the doctor asked me if I wanted codeine-based Tylenol 3s or oxycodone-based Percocet. I chose the latter. I knew Percs were the stronger of the two and I wanted to know just how strong. The feeling was great—similar to how I’d felt on Dilaudid that morning in Florida. My first bottle of Percocets—30 tiny white pills—lasted about a year.

In 2008, following stints as a cruise-ship doctor and an air-ambulance physician, I landed an ER job in Saint John, New Brunswick. At the bar one night, I met a blond girl named Katie, a personal support worker at a pain clinic. I was taken by her eyes, a light bluish-grey I’d never seen before. It took me a couple of tries, but, eventually, she agreed to go out with me. In February 2009, I moved back to Toronto to take a job as an ER doctor at the York Central Hospital, and Katie and her two-year-old daughter soon followed. They rented an apartment at Bathurst and Steeles, and began settling into a routine.

I found a new doctor in Toronto who prescribed me another 30 Percocets for my back, and I started taking them more often. After a few weeks, the pain subsided, and I stopped using them, but I stashed the extras, maybe half the bottle, in my medicine cabinet. One Friday night, some buddies came over for a few beers and some PlayStation golf, and I popped a few Percocets. It wasn’t some big decision, but, in hindsight, I realize that was the moment I crossed the line. It was the first time I took them purely recreationally. They gave me a fuzzy, happy feeling I couldn’t access any other way. Soon, I was dipping into my bottle once every few weeks—if Katie and I were going camping with friends or if I needed a boost of energy to play with Katie’s daughter after a long shift. She couldn’t tell when I was high and, at first, neither could Katie. The following year, in early 2011, we learned that Katie was pregnant with a boy and we bought a five-bedroom stone house at Bathurst and Sheppard.

My parents lived a short drive away and were proud grandparents. They were over at least once a week, but my mom and Katie didn’t get along. Katie felt they were too involved in her daughter’s life—they weren’t biologically related, after all. My mom would get upset if Katie’s daughter didn’t call her on her birthday. A series of slights, real and imagined, between my mother and Katie culminated in an exchange of profanity-laden emails. I became the rope in a vicious tug-of-war. My mother would tell me to assert myself and “be a man.” Katie would say I wasn’t standing up for her. Eventually, Katie asked me to choose between her and my parents. I was dedicated to making my life with Katie work, so I told my parents that they weren’t welcome at the house anymore. Shortly after that, Katie and I flew to Las Vegas to get married. A little more than a year later, she gave birth to our second child together, a girl. My parents weren’t there for the birth, which broke my heart.

Over time, I began to rely on the pills not just to help my back pain but also to cope emotionally. Initially, I went to my doctor every couple of months, then once a month and then every couple of weeks. He recommended that I exercise, lose weight and see a physiotherapist, but he always filled my prescription. He never told me it was too much.

In August 2012, I got a job as an emergency room doctor at the Royal Victoria Regional Health Centre in Barrie. Katie and I bought a spectacular five-bedroom house on the waterfront, at the end of a cul-de-sac. We had a dock and a boat. I was making roughly $300,000 a year. I bought Katie a Lexus SUV, which we eventually traded in for an Audi Q7. But our marriage was deteriorating. We were arguing all the time—about my family, about my parenting. I’d reprimand her daughter for misbehaving, and Katie would undermine me, saying, “Daddy’s just had a bad day.” Katie had also noticed my drug use, which had gone from two pills a day to as many as eight. We fought about it at least once a week.

She wanted me to get help, but I always refused. Seeking help would have meant two things: one, admitting that I had a problem; and two, admitting that I was no longer in control. The pills helped me get through my days, and I wasn’t ready to let that go. Sometimes I slept in my car to avoid another fight.

The first time it occurred to me that I might have a drug problem, I was standing next to a lumber pile in Rona, waiting for my contractor to pick out aluminum framing for our basement renovation. I felt irritation wash over me, totally unprovoked. I couldn’t figure out what was wrong, but I popped a Percocet and immediately felt relieved. I wondered if I had been experiencing withdrawal symptoms, but I felt ashamed even considering it. I dealt with patients every day and didn’t see myself as one. Throughout my career as a doctor, I was trained to believe I was infallible. As far back as medical school, we were told that, no matter what, you don’t call in sick; you show up. So, even though I knew I was in trouble, I didn’t ask for help.

As the months went on, I continued using. That May, I was visiting my folks when I started having withdrawal symptoms. I asked my mom for a few fentanyl patches and she obliged, thinking that I just needed relief for my back pain. She had a prescription for the opioid, which is up to a hundred times more powerful than morphine. The intensely potent drug is usually doled out in surgery or given to patients with chronic pain who have built up a tolerance to other opioids. The transparent squares, which at the time looked a little like clear Band-Aids, contained two layers: one with the slow-release drug and one that’s skin adhesive. I slapped one on my back and stashed the others for later.

About a week later, I got home after a long shift and typed, “How to smoke fentanyl” into Google. My kids were with their nanny at the park near our house. I went to the garage and cut a patch into one-centimetre squares. I lined each piece up on a larger square of tin foil, then I held the lighter under the first piece, watched the puff of smoke come up and inhaled. The sweet smell of burnt plastic filled my nose and travelled deep into my lungs. It was as if I were being pushed by a powerful but gentle wave. Calm washed over me. My anxiety and fear were gone. I slowly lowered myself backward into a chair. I was higher than I’d ever been. Imagine a surge of confidence kicking in, a worldly reassurance that all of your problems will just dissolve. A soft happiness sets in, then a creativity spike. You feel totally alert, more awake and sharper than ever. Everything around you feels warmer. Now, imagine those sensations happening within a few milliseconds of each other. And that’s what it’s like to smoke fentanyl. I sat there, eyes glazed, staring out at the street for 20 minutes. I was in heaven.

Gayle Gebien, above, gave her son a few fentanyl patches for his back pain. He took them home and Googled “How to smoke fentanyl”

A drug like fentanyl doesn’t inject your body with new feelings; it borrows from the ones you already have. When the high starts to wear off, the positive sensations retreat and the negative ones become amplified. And addicts have no shortage of negative emotions. A dark cloud descends upon your brain. You become scared, anxious, agitated. The warmth rolls away and leaves you in cold sweats, shivering. Self-loathing kicks in, followed by guilt, fear, sadness, paranoia. Coming down off that first rush, my body began to ache. All I could focus on was escaping those feelings as quickly as possible, and the only solution was to smoke again. And again—each iteration sinking me deeper into dependency. From that day on, I smoked fentanyl at least six times a day and sometimes as many as 15 times.

The scariest part was that, as a doctor, I knew exactly what I was getting into, and I didn’t care. Fentanyl is one of the most dangerous opioids on the market. It can be smoked, injected or dissolved under your tongue. The federal health minister, Jane Philpott, has called Canada’s opioid problem a national public health crisis. In Ontario, 162 people died of fentanyl overdoses in 2015. In B.C., 332 people died in the first nine months of 2016.

Doctors are part of the problem. One of the most common complaints we get from patients is that we under-treat chronic pain. And, because pain is subjective and difficult to diagnose, we tend to take patients’ word for it when they say they’re in pain. Late last year, the College of Physicians and Surgeons announced it was investigating 86 doctors for prescribing daily opioid dosages that wildly exceeded national guidelines. One patient was prescribed the equivalent of 150 Tylenol 3s per day. Some of those cases occur because patients undergoing cancer treatment or living with multiple sclerosis may need very high dosages. But, in other cases, like mine, there’s rampant abuse of the system.

When I think about it now, I’m disgusted that I kept drugs in the same house as my children. At first, I locked up my patches in my toolbox in the garage. Later, I would smoke in the shower stall in our basement and hide my fentanyl under the sink behind the pipes. I convinced myself that, by taking those precautions, I was being a responsible father. I was high-functioning, but, still, my kids were getting a stoned daddy, even if they were too young to realize it. I wanted to believe that I was like any other doting dad—I took my kids to the beach in the summer, dunking the little ones in the water and wading hand in hand with the eldest. I took them apple-picking in the fall and tobogganing in the winter. The only difference was that, 15 times a day, I’d head to the basement to smoke up. That I was high around my kids is one of the hardest things for me to forgive of myself.

That summer, my cravings were ruthless, and I had no legitimate access to patches. I knew I couldn’t write prescriptions in my own name, so I came up with a plan: I began to write prescriptions for Katie, then I’d go to the pharmacy to pick them up. But I didn’t want pharmacists getting suspicious of Katie, so I began to recruit other pretend patients. I had become friendly with one of the contractors renovating our basement. At one point, I asked him: “Can you do me a favour?” I explained that I needed someone to pick up my fentanyl and that I could supply him with Percocet if he agreed, which he did. I’d write two prescriptions in his name: one for fentanyl and one for Percocet. He’d get them both filled and keep the Percs. One night, my supply was dry and I was going through withdrawal. Katie and I were arguing, and I left the house. I got in a taxi and went into town. I was so desperate that I began going from taxi to taxi, knocking on windows and asking strangers, “Are you interested in doing a swap? I can get you Percocet, but I need you to pick up some fentanyl for me.” The first three weren’t interested. The fourth was.

From August to October, I also cajoled two assistants and a nurse into giving me painkillers from the hospital. I never offered to pay them; I just told them I was in a lot of pain and couldn’t write prescriptions in my own name. I put them in a terrible position and I minimized the stakes. “Oh, it’s not a big deal,” I said. They saw I was hurting and agreed. (They were later fired for it.) Over 16 months, I acquired 445 patches of fentanyl with fraudulent prescriptions, smoking about a patch a day.

At home, my relationship with Katie was in tatters. Instead of offering support, Katie would yell at me, and I would yell back or retreat in silence. “You’re smoking again,” she would shout when she caught me going downstairs. She threatened to leave. She called me a junkie.

I never smoked before work. But I did wear a patch to stave off withdrawal symptoms. Twice I had to leave work because my cravings were too intense to keep going. I lost more than 30 pounds, my cheeks were sunken and I became irritable and jittery. Once, a colleague asked me if I was okay. I told her there were problems at home and left it at that. She didn’t ask again.

My mom had noticed my ragged state and, unbeknownst to me, called and told the hospital I might have a drug problem. My supervisor and the hospital’s chief of staff called me into a meeting and asked me if I had any problems they should be aware of. I lied. I said that things were rocky with Katie but, otherwise, no. They gave me pamphlets on addiction and mental health, and I went back to work.

I decided to change tactics. For the next four months, I forged prescriptions from other doctors in my own name. I’d go to the pharmacy and sweet-talk the staff—it was usually the same guy—into not faxing my prescription over to the hospital. Pharmacists hate to bother busy doctors, and I played on that. Every time I went to get one filled, I threatened everything: my job, my family, my freedom. I didn’t care.

One Sunday in November 2014, the pharmacist was too busy administering flu shots to speak to me and faxed the prescription. I could have tried harder to intervene, but, for some reason, I didn’t. My endless scheming had worn me down. The doctor who happened to pick it up in the ER was the same doctor whose signature I’d forged on the script, which requested a dozen patches. I didn’t know it then, but the doctor reported me to my supervisor. After 20 minutes of nervously waiting, I was waved over by the pharmacist. “We’ve run out of supplies, actually,” she said. She gave me what she claimed were her last few patches, and I went home none the wiser. Two days later, the chief of emergency and the chief of staff greeted me in the doctors’ change room. They told me that they knew about the false prescriptions, that the pharmacy had called the police and that I couldn’t work—I’d be going on unofficial leave without pay, and my medical licence would be suspended. I was scared shitless. The shame of being caught in a tangle of lies was overwhelming. I was afraid for my family, afraid I’d lose my job, afraid of what other people would say. I should have felt lucky to be alive—at that point I was a bag of skin and bones—but I just felt dizzying fear for the future. And yet, on top of all that was an unexpected wave of relief. My life had just come crashing down; at least I couldn’t deny it anymore.

I was arrested at home. Police charged me with three counts of forgery and gave me a notice to appear in court. Three days later, I went to Homewood Health Centre in Guelph, a facility recommended to me by a psychiatrist at my hospital, for five weeks. My parents covered the $10,000 bill. There, the doctors decided I should go into a rapid wean, a process intended to produce intense withdrawal and, with it, a deterrent to using drugs again. First, doctors gave me Suboxone, a pill used to get addicts off opiates. The drug satisfies some of the body’s narcotic cravings but doesn’t get you high. Coming off the Suboxone was vicious, as my endorphin levels plummeted and my brain began to rewire itself. I thought I was going to die. When I tried to walk, my body curled inward, neck down, arms tight to my chest, in a position known in rehab as the Suboxone shuffle. My ears were ringing. My body temperature began to swing like crazy: one moment I’d soothe my chills in a hot shower and the next I’d be running aimlessly outside, rubbing snow on my face. I remember telling the doctor that I couldn’t handle the pain. He agreed to give me another two milligrams of Suboxone to stave off my withdrawal. I knew that would only delay the inevitable, but, at that point, I didn’t care—I was so desperate I considered throwing myself in front of a bus. My body felt like it was disintegrating. Lifting a spoon to my mouth was tiring; walking up a ramp left me winded. The next day, I thought I was progressing, but, 32 hours later, I was still in the throes of withdrawal. I lay down on the hospital bed in my room to take a nap. When I woke up four hours later, the weakness was gone, my limbs had uncurled and my gait returned to normal. The week from hell was over.

On my 14th day in rehab, Katie brought the kids to visit. She told them that I was sick, and they assumed Homewood was a regular hospital. I’ll never forget my son asking why I wasn’t coming home with them that day.

My return from rehab was strange. Katie was exhausted from caring for the kids by herself for five weeks, and we were soon back to our bickering. I was sleeping on the couch and I was still on leave from my job, so my days were empty.

There’s a grieving process that comes with addiction, and I was grieving the loss of my drug of choice. The cycles of shame, self-loathing, rationalization and apathy returned. So I did what I always did to cope: I wrote a prescription for fentanyl using one of my old prescription pads. I didn’t realize the police were monitoring me.

Within a week, I was back to getting high 15 times a day. On the morning of January 4, I lost track of how much I’d smoked. I overdosed and collapsed in my basement shower stall. My face was a putrid shade of green, drool was dribbling down my chin and my dry tongue was hanging from my open mouth. I was barely breathing when Katie walked in. She had seen me high many times before, and she could spot the telltale bursts of energy, hoarse voice and constricted pupils, but that day was different. I’d been downstairs for longer than usual, and she hadn’t seen my face like that before. I remember her screams tearing through the fog in my head. “I’m calling an ambulance,” she cried. I jolted awake, flailing my arms as my paraphernalia went flying. I gasped for breath a few times, head lolling, then lunged for the toilet and vomited. “I thought you were dead,” she said. I told her I didn’t need an ambulance and, eventually, she stopped insisting, worn down from so many arguments. A few hours later, I was back in the stall lighting up another patch.

At 7 a.m. on January 19, 2015, 10 officers from the Barrie drug crimes unit showed up at my front door. If I have a rock bottom, I hit it that day. I woke to my three dogs barking and peered out the window to see the cops on the front steps. I opened the door in my underwear. “Sorry to do this, but your life is never going to be the same,” one of them said to me. I asked for a minute to put the dogs out in the backyard, and the officer

agreed. Another went upstairs to tell Katie she would be arrested, too, wrongly thinking she was involved. They let me put my clothes on and have a cigarette in the garage. They handcuffed me as we were walking outside, so that my kids wouldn’t see if they came downstairs. I was taken to the police station and charged with 72 counts of trafficking—for compelling the pharmacist to supply drugs under false pretences—plus six counts of forging prescriptions.

From January 19 to February 5, I was in jail at the North Correctional Centre in Penetanguishene awaiting my bail hearing. I was despondent. There was a stairwell on the second storey that overlooked the unit’s concrete floor, and I figured that if I jumped headfirst I would die. I told one guy I’d made friends with about my plan, and he pulled me aside. “Wait a second, motherfucker,” he said. “You’ve got your wife, your kids. That’s the most selfish thing you could do.” I went back to my cell. I hadn’t been using long enough after my first stint in rehab to go through acute withdrawal again, but I had the munchies like crazy, a sign of early recovery. I had an appetite so ferocious I’d chug the syrup that came with our French toast in the morning. My cellmate let me eat some of his snacks, too—Rice Krispies Treats, ketchup chips, Twix bars.

With the help of my parents, I made the $80,000 bail, but one of the conditions was that I live with my mom and dad at their Yonge and Sheppard condo. I went home briefly to collect my things. Katie wanted a stable environment for the kids, so she moved them back to New Brunswick 10 days later. I was devastated but didn’t have a choice. In April, I enrolled in Renascent, a clinic at Spadina and Bloor, for my second stint in rehab. I stayed for four weeks. During my daily walks in the neighbourhood, every time I saw a homeless person, I’d think to myself that I was closer to becoming one of them than I was prepared to admit. I was nearly out of money, my marriage was probably over and my network of friends had dwindled. I was initially represented by Marie Henein and Danielle Robitaille, the lawyers who represented former attorney general Michael Bryant and CBC host Jian Ghomeshi. I put the first payment of $35,000 on a line of credit but changed lawyers shortly after. I was still paying the mortgage on our home in Barrie and couldn’t keep up with their retainer.

In August, I walked into the Vitanova Foundation recovery centre in Woodbridge, another government-funded facility, not knowing how long I would be there. The centre offered a free rehab program and dorm-style residence, and, as the weeks passed, I felt my strength and clarity returning.

Three months later, on November 2, 2015, my 45th birthday, I got a call from my dad telling me that my mom had died. He’d found her in bed, non-responsive, wearing three 50-milligram fentanyl patches that we think she applied by accident. Her usual dose was a 25-milligram patch. It was the worst day of my life. I redoubled my efforts to stay clean. I checked out of Vitanova and moved back into my father’s condo. I slept on the couch and have continued to for the past two years. I FaceTime with my kids every couple of days, but it feels like no way to be a father. I’m on social assistance and help my dad with rent when I can—his pension isn’t enough to support both of us. Our Barrie home sold shortly after my mom’s death, and I gave most of the money to Katie, knowing that I might not be working much in the next few years. I run a flooring company with an old friend to make extra cash. And I’m still drug-free.

But my body hasn’t fully recovered: my short-term memory is spotty, I have hearing loss in my right ear and, for the first time in my life, I suffer from panic attacks. I apologized to the City of Barrie for betraying the trust of its residents. And I’ve done some outreach work, speaking to officials at the Ontario Ministry of Health and Toronto Public Health about how to tackle the opioid epidemic.

In April 2016, I filed for bankruptcy. Katie sent divorce papers a few months later. I had been hoping we’d find a way to make it as a couple, but I understood. In February, my biological kids came to stay with me for a week. I got to see my son—now five years old—skate for the first time; my little girl, who’s four, was so excited with the Hatchimal we picked out at Toys’R’Us that she carried the box around with her everywhere and showered me with hugs. I didn’t explain what was going on—I just said I’d talk to them soon. They’re too young to understand what happened. I worry about what they’ll think of me when they do find out. I hope they can be proud of my recovery, but that day is a long way away.

In December 2016, I pleaded guilty, and, as part of the deal, Katie’s charges were finally dropped. I’m awaiting my sentence. The Crown wants me locked up for eight years; my lawyer is arguing for house arrest. Most likely, the judge will settle on a multi-year prison term. My dad has early-stage Alzheimer’s, and I’m concerned about how he’ll cope while I’m gone. I worry constantly about Katie and our kids, too. I’m embarrassed that my life has become a cautionary tale, but I’m thankful that I got caught. Had I not been arrested, I’m certain I’d be dead right now.

When I get out, I will have to face the College of Physicians and Surgeons’ discipline committee, as is standard in cases like mine. My medical licence is currently suspended, and they’ll probably revoke it entirely. If they don’t, I plan to practise again, ideally in the area of addiction. I became a doctor so that I could help people. I messed up my life, but I can still help others avoid the same fate.

Correction  March 30, 2017

An earlier version of this story indicated that Darryl Gebien’s stay at Renascent was covered by OHIP, when in fact the fees there are covered by the Ministry of Health, as well as the centre’s foundation.

Source:  http://torontolife.com/city/crime/doctor-perfect-life-got-hooked-fentanyl/

Ontario opted not to follow B.C.’s lead on harm reduction, rejecting the idea of creating safe injection sites similar to the one in Vancouver. Postmedia News files

In December, the Liberal government introduced Bill C-37 in response to an epidemic of illicit drug use. The bill facilitates the creation of additional supervised injection sites by reducing previously established restrictions.

The decision to promote supervised injection sites is in line with the latest philosophy guiding addiction management — that of harm reduction. Proponents claim harm-reduction institutions will save lives while averting hundreds of thousands in medical and criminal-legal expenses.

Much in the harm-reduction philosophy is laudable — the desire to destigmatize and protect those with severe illnesses for one — but the field is slipping into dangerous, almost Brave-New-World territory.

In Toronto and Ottawa, supposedly inveterate alcoholics receive calculated amounts of alcohol hourly throughout the day at designated wet shelters and managed alcohol programs. Residents line up on the hour to receive just enough house-made wine to keep withdrawal symptoms at bay. Some drink almost three bottles of wine daily with little to do in between scheduled drinks.

Vancouver, which was Canada’s first city to establish a safe injection site in 2003, has now progressed to experimenting with “heroin-assisted treatment” as a means of further protecting addicts from the harms of tainted street drugs. Participants receive pharmaceutical-grade heroin injections two to three times daily. Recently, in place of heroin, the more innocuous-sounding but no less potent opiate, hydromorphone, is being administered instead.

Is their drug use no longer a problem because they’re off the street? And where exactly do the patients go from here?

Most lay supporters of harm-reduction policy assume a gradual attempt is made to wean the addict off the substance of abuse. Proponents claim that harm reduction isn’t about “giving up” on the addict but is actually a temporary stepping stone towards the ultimate goal of recovery.

But the reality is different.

Dr. Jeffrey Turnbull, who established Ottawa’s managed alcohol program, offers a more sober portrayal of the goals of harm reduction. In a Fifth Estate documentary, he compares his program for those with chronic and severe addictions to palliative care. He agrees his facility is a place for alcoholics to “die with dignity” as opposed to dying on the streets. One resident featured in the episode had been using the program’s services for four years; he was only 24 when he first entered the managed alcohol program.

No doubt, the medical community is frustrated by the high failure rates associated with abstinence-based treatment programs but the criteria for determining when an addict now warrants a harm-reduction approach is unclear. Addiction does not follow a linear natural history akin to metastatic cancer; rather, there exists a variable trajectory and the possibility for recovery is always there.

However, Turnbull’s admission points to an uncomfortable belief underlying the harm-reduction philosophy — the view that some addicts are without hope of ever leading a full, productive life free of drug use.

It may be true that, for some, the best we can do is safe, controlled sedation. But the medical community and society should not be so quick to condemn many others to the compromised mental prison that is the life of the addict.

Proponents argue that harm reduction and abstinence are not mutually exclusive, and some even suggest that harm-reduction institutions actually improve recovery rates. But this is a fiction and is without evidence.

Harm-reduction researchers have conveniently neglected to investigate any potentially negative findings of their policies. Their studies focus exclusively on the obvious benefits such as decreased overdose deaths, cost savings, and so-called “treatment retention.” That addicts will remain “in treatment” longer when freely administered their drug of choice is not surprising, but that this is in their best interests is highly questionable.

Politicians insist supervised injection sites and managed substance programs are effective “evidence-based” interventions, but these assertions are problematic when the evidence only tells half the story.

Canada is quickly moving towards an addiction defeatist infrastructure. Toronto, Montreal, Ottawa and Victoria are all following Vancouver’s lead in constructing further supervised injection sites. Widespread creation of managed substance programs is the next logical step of the harm-reduction approach. Unless vigilance is exercised, we risk relegating addicts to a half-conscious state whereby life is maintained but not really lived.

It is both tragic and ironic that the activist responsible for implementing widespread harm reduction policies in Toronto, Raffi Balian, recently died from an accidental overdose while attending a harm-reduction conference in Vancouver. His death highlights the inadequacy of half measures when dealing with the insidious and powerful disease that is addiction.

Jeremy Devine is a medical student at the University of Toronto’s Faculty of Medicine and a CREMS research scholar in the medical humanities and social sciences

Source: http://www.nationalpost.com/m/search/blog.     2nd March 2017

Summary:

Long-term heavy use of alcohol in adolescence alters cortical excitability and functional connectivity in the brain, according to a new study. These alterations were observed in physically and mentally healthy but heavy-drinking adolescents, who nevertheless did not fulfil the diagnostic criteria for a substance abuse disorder.

Long-term heavy use of alcohol in adolescence alters cortical excitability and functional connectivity in the brain, according to a new study from the University of Eastern Finland and Kuopio University Hospital. These alterations were observed in physically and mentally healthy but heavy-drinking adolescents, who nevertheless did not fulfil the diagnostic criteria for a substance abuse disorder. The findings were published in Addiction Biology.

Constituting part of the Adolescents and Alcohol Study, the study analysed the effects of heavy adolescent drinking on the electrical activity and excitability of the cortex. The study did a follow-up on 27 adolescents who had been heavy drinkers throughout their adolescence, as well as on 25 age-matched, gender-matched and education-matched controls with little or no alcohol use. The participants were 13 to 18 years old at the onset of the study.

At the age of 23-28, the participants’ brain activity was analysed using transcranial magnetic stimulation (TMS) combined with simultaneous electroencephalogram (EEG) recording. In TMS, magnetic pulses are directed at the head to activate cortical neuronal cells. These magnetic pulses pass the skull and other tissues, and they are safe and pain-free for the person undergoing TMS. The method allows for an analysis of how different regions of the cortex respond to electrical stimulation and what the functional connectivities between the different regions are. Indirectly, the method also makes it possible to analyse chemical transmission, i.e. mediator function. The effects of long-term alcohol use haven’t been studied among adolescents this way before.

The cortical response to the TMS pulse was stronger among alcohol users. They demonstrated greater overall electrical activity in the cortex as well as greater activity associated with the gamma-aminobutyric acid, GABA, neurotransmission system. There were also differences between the groups in how this activity spread into the different regions of the brain. Earlier research has shown that long-term, alcoholism-level use of alcohol alters the function of the GABA neurotransmission system. GABA is the most important neurotransmitter inhibiting brain and central nervous system function, and GABA is known to play a role in anxiety, depression and the pathogenesis of several neurological disorders.

The study found that alcohol use caused significant alterations in both electrical and chemical neurotransmission among the study participants, although none of them fulfilled the diagnostic criteria of a substance abuse disorder. Moreover, in an earlier study completed at the University of Eastern Finland, also within the Adolescents and Alcohol Study, cortical thinning was observable in young people who had been heavy drinkers throughout their adolescence. For young people whose brain is still developing, heavy alcohol use is especially detrimental. The findings of the study warrant the question of whether the diagnostic criteria for substance abuse disorders should be tighter for adolescents, and whether they should be more easily referred to treatment. The use of alcohol may be more detrimental to a developing brain than previously

thought, although it takes time for alcohol-related adverse effects to manifest in a person’s life

Source:  https://www.sciencedaily.com/releases/2016/12/161208085850.htm? February_2017)

I totally agree that we all need to let Attorney General Jeff Sessions know that the majority of Americans suffer because of marijuana …. whether they choose to use it or not.  It is a factor in crime, physical and mental health, academic failure, lost productivity, et al.  American cannot be great again if we continue to allow poison to be grown and distributed to the masses.

The President has taken a position that “medical marijuana” should be a State’s right, because he is not yet enlightened on the reality of what that means.  If asked to define “medical marijuana” that has helped his friends, I doubt that he would say gummy bears, Heavenly brownies and other edibles with 60 to 80% potency, sold in quantities that are potentially lethal; smoked pot at 25% THC content; or waxes and oils used for dabbing and vaping that are as high as 98% potency that cause psychotic breaks, mental illness, suicides, traffic deaths and more.

Further, if states are to have a right to offer “medical marijuana”, it has to be done under tightly controlled conditions and the profit motive eliminated.  Privately owned cultivation and dispensaries must be banned … including one’s ability to grow 6 plants at home.  6 plants grown hydroponically with 4 harvests a year could generate 24 lbs of pot, the equivalent of about 24,000 joints. That obviously would not be for personal use.  We would just have thousands of new drug dealers, with more crime, more child endangerment, more BHO labs blowing up, more traffic deaths, et al.

Source:   Letter from Roger Morgan to DrugWatch International  Feb. 2017

Abstract

Background Amphetamine abuse is becoming more widespread internationally. The possibility that its many cardiovascular complications are associated with a prematurely aged cardiovascular system, and indeed biological organism systemically, has not been addressed.

Methods

Radial arterial pulse tonometry was performed using the SphygmoCor system (Sydney). 55 amphetamine exposed patients were compared with 107 tobacco smokers, 483 non-smokers and 68 methadone patients (total=713 patients) from 2006 to 2011. A cardiovascular-biological age (VA) was determined.

Results

The age of the patient groups was 30.03±0.51–40.45±1.15 years. This was controlled for with linear regression. The sex ratio was the same in all groups. 94% of amphetamine exposed patients had used amphetamine in the previous week. When the (log) VA was regressed against the chronological age (CA) and a substance-type group in both cross-sectional and longitudinal models, models quadratic in CA were superior to linear models (both p<0.02). When log VA/CA was regressed in a mixed effects model against time, body mass index, CA and drug type, the cubic model was superior to the linear model (p=0.001). Interactions between CA, (CA)2 and (CA)3 on the one hand and exposure type were significant from p=0.0120. The effects of amphetamine exposure persisted after adjustment for all known cardiovascular risk factors (p<0.0001).

Conclusions

These results show that subacute exposure to amphetamines is associated with an advancement of cardiovascular-organismal age both over age and over time, and is robust to adjustment. That this is associated with power functions of age implies a feed-forward positively reinforcing exacerbation of the underlying ageing process.

To read the whole research study log on to:

Source:    http://dx.doi.org/10.1136/heartasia-2016-010832

Outdoor cannabis cultivation in northern California has damaged forestlands and their inhabitants. Will legalization of recreational marijuana make things worse or better?

A visit to a marijuana farm in Willow Creek, the heart of northern California’s so-called Emerald Triangle feels like strolling through an orchard. At 16 feet high and eight feet around, its 99 plants are too overloaded with cannabis buds to stand on their own. Instead each plant has an aluminium cage for support.

Welcome to America’s “pot basket.” The U.S. Drug Enforcement Administration estimates 60 percent of cannabis consumed nationwide is grown in California. According to the Department of Justice, the bulk of that comes from the three upstate counties of the Emerald Triangle: Mendocino, Humboldt and Trinity. Conditions here are said to be perfect for outdoor marijuana cultivation. But that has proved to be a very mixed blessing for the region, bringing with it a litany of environmental disturbances to local waterways and wildlife. Creek diversions threaten fish habitat and spur toxic algal blooms. Road building and clear-cuts erode soil and cloud streams. Deep within, illegal “guerilla grows” pepper forestlands with banned rodent poisons that are intended to eradicate crop pests but are also fatal to other mammals.

On November 8 voters in four states—Massachusetts, Maine, California and Nevada—legalized recreational marijuana. These states join Colorado, Washington, Oregon and Alaska, along with the District of Columbia, where one can already legally buy the drug for recreational use. Will this expanded market mean more environmental damage? Or will legalization pave the way for sounder regulation?

In 1996 California legalized marijuana for medical use, providing the first legal space for pot cultivation since the federal government’s blanket ban on the crop some 60 years before. As grow operations in the state flourished, California Department of Fish and Wildlife biologist Scott Bauer analyzed satellite imagery to examine the impact of cultivation on water levels in four Emerald Triangle watersheds. His study, published in PLoS ONE in 2015, found that in three of the four watersheds, “water demand for marijuana cultivation exceeds stream flow during the low-flow [summer] periods.”

The real problem is not marijuana’s overall water consumption, which still falls far short of California staples like walnuts or almonds, explains environmental scientist Van Butsic of the University of California, Berkeley. Rather it is an issue of where and when pot is

grown. Analyzing aerial imagery of 4,428 grow sites in 60 Humboldt county watersheds, Butsic found that one in 20 grow sites sat within 100 meters of fish habitat and one in five were located on steep land with a slope of 17 degrees or more. “The problem is that cannabis is being grown in the headwaters, and much of the watering is happening in the summer,” Butsic says.

If that arrangement goes on unchecked, U.C. Berkeley ecologist Mary Powers warns, summer plantations could transform local rivers from cool and “salmon-sustaining” to systems full of toxic cyanobacteria. Over eons of evolution native salmon species have adapted to “deluge or drought” conditions, she says. But the double whammy of climate change and water extraction could prove to be a game-changer.

Powers spelled out the unprecedented stresses in a 2015 conference paper focused on the Eel River that flows through Mendocino and southern Humboldt. She and her team found riverbed-scouring floods in winter, followed by dry, low-flow conditions in summer, led to warm, stagnant, barely connected pools of water. That is bad news for salmon, but ideal for early summer algal blooms. The algae then rot, creating an oxygen-deficient paradise for toxic cyanobacteria, which have been implicated in the poisoning deaths of 11 dogs along the Eel River since 2002.

Dogs are not the only terrestrial creatures endangered by the grow operations. Between 2008 and 2013 Mourad Gabriel, then a doctoral candidate at the University of California, Davis, Veterinary Genetics Lab, carried out a study of the American fisher, a small carnivorous mammal that is a candidate for the endangered species list. He wanted to suss out the threats to fisher populations in northern California. So he radio-tagged fishers from Trinity County’s Hoopa Valley Reservation and public lands near Yosemite National Park to track their movements. Between 2006 and 2011, 58 of the fishers Gabriel and his team tracked turned up dead. Gabriel studied the necropsies and found that 46 of the animals had been exposed to anticoagulant rodenticides—rat poisons that block liver enzymes, which enable blood clotting. Without the enzyme the exposed mammals bled to death from flesh wounds.

The finding puzzled Gabriel at first, because rat poison is more common in agricultural and urban settings than in remote forests. But then he started visiting the remnants of guerilla grows that had been busted under the guidance of lawmen such as Omar Brown, head of the Narcotics Division at the Trinity County Sheriff’s Office. “We have found [anticoagulant rodenticides] carbofuron on grows in the national forest,” Brown reports. “These are neurotoxin-laced pesticides that have been banned in the U.S. since 2011. And even for allowed pesticides, we’ve found instances where trespass grows are using them in illegally large quantities.” The poisons hit female fishers particularly hard, because the early, pest-prone phase of marijuana cultivation coincides with the fishers’ nesting season, when pregnant females are actively foraging.

Gabriel, now director of the Integral Ecology Research Center based in Humboldt County, says other states may be dealing with rodenticides, water diversions and other problems from guerilla grows, too. “The climate in Colorado, Oregon and Washington is conducive for marijuana cultivation,” he observes. But “there just isn’t the scientific data to prove whether other states have these problems because there has not been research funding put towards answering these questions.”

In California headwater ecosystems could get a reprieve if a greatly expanded legalized pot industry moves to the Central Valley, where production could take place indoors and costs would be less. In pot-growing pioneer states like Colorado or Washington much of the production has moved indoors, where temperatures can be more closely managed. But other factors may hinder that move. “Bud and pest problems are always worse indoors, which biases farmers toward a chemically intensive regime,” says Marie

Peterson of Downriver Consulting, a Weaverville, Calif.–based firm that helps growers fill out the paperwork for state and county permits as well as assesses water management plans for their plantations. And besides, the Central Valley already suffers from prolonged drought.

Of the eight states that legalized the cultivation of recreational marijuana, only Oregon and California allow outdoor grows. But regulating open-air pot plantations in these states remains challenging, even though legal operations for medical marijuana have been around since 1998 and 1996, respectively. In 2015 California passed the Medical Marijuana Regulation and Safety Act, which calls on the state’s departments of Food and Agriculture, Pesticide Regulation, and Fish and Wildlife, along with the state’s Water Board—to oversee environmental impacts of the industry. The board came up with a list of requirements for a marijuana plantation water permit, which in turn became a necessary condition for a license to grow medical pot in any of the three Emerald Triangle counties. Counties have until January 2018 to decide whether to create similar stipulations for recreational marijuana growing permits.

Butsic is optimistic about a more regulated future for the marijuana industry in California. “I think five years from now things will be more sustainable. Permitting shows growers that the state is interested in water use and their crop.”

Source:  https://www.scientificamerican.com/article/burgeoning-marijuana-market-prompts-concerns-about-crop-rsquo-s-environmental-impact/  2nd Feb. 2017

GW intends to advance oncology research and development efforts

GW Pharmaceuticals plc (Nasdaq:GWPH) (“GW,” “the Company” or “the Group”), a biopharmaceutical company focused on discovering, developing and commercializing novel therapeutics from its proprietary cannabinoid product platform, today announced positive top-line results from an exploratory Phase 2 placebo-controlled clinical study of a proprietary combination of tetrahydrocannabinol (THC) and cannabidiol (CBD) in 21 patients with recurrent glioblastoma multiforme, or GBM. GBM is a particularly aggressive brain tumour, with a poor prognosis. GW has received Orphan Drug Designation from the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) for THC:CBD in the treatment of glioma.

The study showed that patients with documented recurrent GBM treated with THC:CBD had an 83 percent one year survival rate compared with 53 percent for patients in the placebo cohort (p=0.042). Median survival for the THC:CBD group was greater than 550 days compared with 369 days in the placebo group. THC:CBD was generally well tolerated with treatment emergent adverse events leading to discontinuation in two patients in each group. The most common adverse events (three patients or more and greater than placebo) were vomiting (75%), dizziness (67%), nausea (58%), headache (33%), and constipation (33%). The results of some biomarker analyses are still awaited.

“The findings from this well-designed controlled study suggest that the addition of a combination of THC and CBD to patients on dose-intensive temozolomide produced relevant improvements in survival compared with placebo and this is a good signal of potential efficacy,” said Professor Susan Short, PhD, Professor of Clinical Oncology and Neuro-Oncology at Leeds Institute of Cancer and Pathology at St James’s University Hospital and principal investigator of the study. “Moreover, the cannabinoid medicine was generally well tolerated. These promising results are of particular interest as the pharmacology of the THC:CBD product appears to be distinct from existing oncology medications and may offer a unique and possibly synergistic option for future glioma treatment.”

We believe that the signals of efficacy demonstrated in this study further reinforce the potential role of cannabinoids in the field of oncology and provide GW with the prospect of a new and distinct cannabinoid product candidate in the treatment of glioma.

These data are a catalyst for the acceleration of GW’s oncology research interests and over the coming months, we expect to consult with external experts and regulatory agencies on a pivotal clinical development program for THC:CBD in GBM and to expand our research interests in other forms of cancer.

The study, designed to evaluate a number of safety and efficacy endpoints, comprised an initial phase where the safety of THC:CBD in combination with dose-intense temozolomide (an oral alkylating agent that is a standard first-line treatment for GBM) was assessed in 2 cohorts of 3 patients each.  Following a satisfactory independent safety evaluation, the study then entered a randomized placebo-controlled phase where 12 patients were randomized to THC:CBD as add-on therapy compared with 9 patients randomized to placebo (plus standard of care).

Beginning in 2007 and prior to initiating this study, GW conducted substantial pre-clinical oncologic research on several cannabinoids in various forms of cancer including brain,

lung, breast, pancreatic, melanoma, ovarian, gastric, renal, prostate and bladder. These studies have resulted in approximately 15 publications and show the multi-modal effects of cannabinoids on a number of the key pathways associated with tumour growth and progression. Cannabinoids have been shown to promote autophagy (the process of regulated self-degradation by cells) via several distinct mechanisms, including acting on the AKT/mTOR pathway, an important intracellular signalling pathway that is overactive in many cancers.

In glioma, THC and CBD appear to act via distinct signalling pathways. The combination of THC and CBD showed good efficacy in various animal models of glioma, particularly when used in combination with temozolomide. Initial in vitro studies showed that the combined administration of THC and CBD led to a synergistic reduction in the viability of U87MG glioma cells when compared to the administration of each cannabinoid individually. The co-administration of temozolomide with THC and CBD had further synergistic effects, causing a significant reduction in cell viability. These pre-clinical studies justified the initiation of the Phase 2 clinical study.

GW’s portfolio of intellectual property related to the use of cannabinoids in oncology includes a number of issued patents and pending applications in both the U.S. and Europe. This portfolio is designed to protect the use of various cannabinoids individually or in combination, in the treatment of a variety of oncology-specific disorders and product formulations.

About GBM

Gliomas are tumours that arise from glial cells mainly in the brain but can also be found within the spinal cord. Within the category of Glioma there are multiple different tumor types. GBM is the most common Glioma and is one of the most common primary brain tumors, accounting for 15.6% of all primary brain tumors (Ostrom et al. 2013). They are also the most aggressive with only 28.4% of patients surviving one year and only 3.4% surviving to year five (Brodbelt et al. 2015). Studies of patients with high-grade gliomas showed that headache was the most common initial presenting symptom. These headaches can be persistent lasting more than six months and are often associated with other symptoms, including seizures, visual disturbances, cognitive impairment and nausea and vomiting depending on the location and growth rate of the tumor.

About GW Pharmaceuticals plc

Founded in 1998, GW is a biopharmaceutical company focused on discovering, developing and commercializing novel therapeutics from its proprietary cannabinoid product platform in a broad range of disease areas. GW is advancing an orphan drug program in the field of childhood epilepsy with a focus on Epidiolex® (cannabidiol), which is in Phase 3 clinical development for the treatment of Dravet syndrome, Lennox-Gastaut syndrome, Tuberous Sclerosis Complex and Infantile Spasms. GW commercialized the world’s first plant-derived cannabinoid prescription drug, Sativex® (nabiximols), which is approved for the treatment of spasticity due to multiple sclerosis in 31 countries outside the United States. The Company has a deep pipeline of additional cannabinoid product candidates which includes compounds in Phase 1 and 2 trials for glioma, schizophrenia and epilepsy. For further information, please visit www.gwpharm.com.

Original press release: http://ir.gwpharm.com/releasedetail.cfm?ReleaseID=1010672

Source:  https://www.newcannabisventures.com/gw-pharma  17th Feb. 2017

Once you drop, you can’t stop – sometimes for up to 15 hours. Images revealing how LSD interacts with receptors in the brain could explain why a trip lasts so long, while another study involving a similar receptor unpicks how the drug makes these experiences feel meaningful.

LSD acts on with a number of different receptors in the brain, including ones for the chemicals serotonin and dopamine, but it’s not known exactly which receptors are responsible for its various effects. Daniel Wacker and his colleagues at the University of North Carolina, Chapel Hill, used crystallography to look at the structure of LSD when it binds to a receptor in the brain that normally detects serotonin. They discovered that part of this serotonin 2B receptor acts as a lid, closing around the LSD molecule and trapping it.

This could explain the extended trips the drug produces. “It takes LSD very long to get into the receptor, and once it’s stuck it doesn’t go away,” says Wacker.

However, there is conflicting evidence. Other studies have shown that LSD hangs around in the blood for a long time. “No prolonged action at the receptor is needed to explain the duration of action,” says Matthias Liechti at the University of Basel, Switzerland.

But if Wacker is right, the fact that LSD seems to get stuck inside the receptor might mean it can have effects at very low doses. In recent years, there have been reports of some people taking LSD in amounts too small to cause hallucinations, in an attempt to boost creativity or general well-being.

There’s little hard evidence about whether this microdosing works, but Wacker says psychoactive effects at low doses are plausible. “Our study suggests even very low amounts of LSD may be enough to cause psychoactive effects.” Scientific interest in LSD’s clinical use has revived in recent years – notably to relieve severe psychiatric conditions such as PTSD and anxiety. There are also signs that LSD has helpful non-psychoactive effects on other ailments, such as cluster headaches.

Suppressing bliss

A second study finds evidence that LSD affect the brain by binding to serotonin receptors, and hints at possible ways to harness some of its effects therapeutically. Katrin Preller and her colleagues at the University of Zurich, Switzerland, gave 22 volunteers 100 micrograms of LSD each to determine the role of the serotonin 2A receptor, which is similar to the one studied by Wacker’s team.

In some of the tests, subjects were also given ketanserin, a drug that blocks the serotonin 2A receptor. In those tests, the trippy effects of LSD – including hallucinations, feeling separate from the body, and feelings of bliss – were completely blocked, showing that this receptor must be responsible for them.

The researchers also played songs to the participants. Some of the songs were ones the volunteers had chosen as meaningful beforehand, while others were not. While on LSD, they rated what had been non-meaningful songs as highly meaningful – an effect that, once again, ketanserin blocked.

Preller thinks these findings suggest that the serotonin 2A receptor is important for how we decide which things are relevant to us. “This is something that’s incredibly important for our everyday life,” she says. “We do it constantly, for example if you see a familiar face.”

Some psychiatric conditions, such as schizophrenia and phobias, are associated with paying too much attention to unimportant stimuli. Preller speculates that LSD might help people refocus their attention in a different direction.

“If you have a depressed patient ruminating about negative thoughts, LSD might facilitate a process where you attribute meaning to other things,” says Preller.

Alternatively, people with these conditions might benefit from drugs that reduce the action of the serotonin 2A receptor, like ketanserin.

Source: Journal reference: Current Biology, DOI: 10.1016/j.cub.2016.12.030 Journal reference: Cell, DOI: 10.1016/j.cell.2016.12.033

This Report reviews what we know about substance use and health and how we can use that knowledge to address substance misuse and related health consequences.

First, a general Introduction and Overview of the Report (PDF | 1.5 MB) describes the extent of the substance use problem in the United States. Then it lays a foundation for readers by explaining what happens in the brain of a person with an addiction to these substances.

Chapter 2 – The Neurobiology of Substance Use, Misuse, and Addiction (PDF | 6.0 MB) describes the three main circuits in the brain involved in addiction, and how substance use can “hijack” the normal function of these circuits. Understanding this transformation in the brain is critical to understanding why addiction is a health condition, not a moral failing or character flaw.  Few would disagree with the notion that preventing substance use disorders from developing in the first place is ideal. Prevention programs and policies are available that have been proven to do just that.

Chapter 3 – Prevention Programs and Policies (PDF | 1.5 MB) describes a range of programs focused on preventing substance misuse including universal prevention programs that target the whole community as well as programs that are tailored to high-risk populations. It also describes population-level policies that are effective for reducing underage drinking, drinking and driving, spread of infectious disease, and other consequences of alcohol and drug misuse.

If a person does develop a substance use disorder, treatment is critical. Substance use disorders share some important characteristics with other chronic illnesses, like diabetes. Both are chronic conditions that can be effectively managed with medications and other treatments that focus on behavior and lifestyle.

Chapter 4 – Early Intervention, Treatment, and Management of Substance Use Disorders (PDF | 629 KB) describes the clinical activities that are used to identify people who have a substance use disorder and engage them in treatment. It also describes the range of medications and behavioral treatments that can help people successfully address their substance use disorder.

As with other chronic conditions, people with substance use disorders need support through the long and often difficult process of returning to a healthy and productive life.

Chapter 5 – Recovery: The Many Paths to Wellness (PDF | 335 KB) describes the growing array of services and systems that provide this essential function and the many pathways that make recovery possible.  Responsive and coordinated systems are needed to provide prevention, treatment, and recovery services. Traditionally, general health care and substance use disorder treatment have been provided through distinct and separate systems, but that is now changing.

Chapter 6 – Health Care Systems and Substance Use Disorders (PDF | 1.3 MB) explains why integrating general health care and substance use services can result in better outcomes and describes policies and activities underway to achieve that goal.

The final chapter, Chapter 7 – Vision for the Future: A Public Health Approach (PDF | 255 KB), provides concrete recommendations on how to reduce substance misuse and related harms in communities across the United States.

Source:  https://addiction.surgeongeneral.gov/executive-summary/report

Currently, 29 states and Washington, DC, have passed laws to legalize medical marijuana. Although evidence for the effectiveness of marijuana or its extracts for most medical indications is limited and in many cases completely lacking, there are a handful of exceptions. For example, there is increasing evidence for the efficacy of marijuana in treating some forms of pain and spasticity, and 2 cannabinoid medications (dronabinol and nabilone) are approved by the US Food and Drug Administration for alleviating nausea induced by cancer chemotherapy.

A systematic review and meta-analysis by Whiting et al1 found evidence, although of low quality, for the effectiveness of cannabinoid drugs in the latter indication. The anti -nausea effects of tetrahydrocannabinol (THC), the main psychoactive ingredient in marijuana, are mediated by the interactions of THC with type cannabinoid (CB1) receptors in the dorsal vagal complex. Cannabidiol, another cannabinoid in marijuana, exerts antiemetic properties through other mechanisms. Nausea is a medically approved indication for marijuana in all states where medical use of this drug has been legalized. However, some sources on the internet are touting marijuana as a solution for the nausea that commonly accompanies pregnancy, including the severe condition hyperemesis gravidarum.

Although research on the prevalence of marijuana use by pregnant women is limited, some data suggest that this population is turning to marijuana for its antiemetic properties, particularly during the first trimester of pregnancy, which is the period of greatest risk for the deleterious effects of drug exposure to the foetus. Marijuana is the most widely used illicit drug during pregnancy, and its use is increasing. Using data from the National Survey of Drug Use and Health, Brown et al report in this issue of JAMA that 3.85%of pregnant women between the ages of 18 and 44 years reported past-month marijuana use in 2014, compared with 2.37%in 2002. In addition, an analysis of pregnancy data from Hawaii reported that women with severe nausea during pregnancy, compared with other pregnant women, were significantly more likely to use marijuana (3.7%vs 2.3%, respectively).

Although the evidence for the effects of marijuana on human prenatal development is limited at this point, research does suggest that there is cause for concern. A recent review and a meta-analysis found that infants of women who used marijuana during pregnancy were more likely to be anaemic, have lower birth weight, and require placement in neonatal intensive care than infants of mothers who did not use marijuana. Studies have also shown links between prenatal marijuana exposure and impaired higher-order executive functions such as impulse control, visual memory, and attention during the school years.

The potential for marijuana to interfere with neurodevelopment has substantial theoretical justification. The endocannabinoid system is present from the beginning of central nervous system development, around day 16 of human gestation, and is increasingly thought to play a significant role in the proper formation of neural circuitry early in brain development, including the genesis and migration of neurons, the outgrowth of their axons and dendrites, and axonal pathfinding. Substances that interfere with this system could affect foetal brain growth and structural and functional neurodevelopment.

An ongoing prospective study, for example, found an association between prenatal cannabis exposure and foetal growth restriction during pregnancy and increased frontal cortical thickness among school-aged children. Some synthetic cannabinoids, such as those found in “K2/Spice” products, interact with cannabinoid receptors even more strongly than THC and have been shown to be teratogenic in animals.

A recent study in mice found brain abnormalities, eye deformations, and facial disfigurement (cleft palate) in mouse foetuses exposed at day 8 of gestation to a potent full cannabinoid agonist, CP-55,940. The percentage of mouse foetuses with birth defects increased in a linear fashion with dose. (The eighth day of mouse gestation is roughly equivalent to the third or fourth week of embryonic development in humans, which is before many mothers know they are pregnant.) It is unknown whether these kinds of effects translate to humans; thus far, use of synthetic cannabinoids has not been linked to human birth defects, although use of these substances is still relatively new.

THC is only a partial agonist at the CB1 receptor, but the marijuana being used both medicinally and recreationally today has much higher THC content than in previous generations (12% in 2014 vs 4% in 1995), when many of the existing studies of the teratogenicity of marijuana were performed. Marijuana is also being used in new ways that have the potential to expose the user to much higher THC concentrations—such as the practice of using concentrated extracts (eg, hash oil). More research is needed to clarify the neurodevelopmental effects of prenatal exposure to marijuana, especially high-potency formulations, and synthetic cannabinoids.

One challenge is separating these effects from those of alcohol, tobacco, and other drugs, because many users of marijuana or K2/Spice also use other substances. In women who use drugs during pregnancy, there are often other confounding variables related to nutrition, prenatal care, and failure to disclose substance use because of concerns about adverse legal consequences.    Even with the current level of uncertainty about the influence of marijuana on human neurodevelopment, physicians and other health care providers in a position to recommend medical marijuana must be mindful of the possible risks and err on the side of caution by not recommending this drug for patients who are pregnant. Although no states specifically list pregnancy-related conditions among the allowed recommendations for medical marijuana, neither do any states currently prohibit or include warnings about the possible harms of marijuana to the foetus when the drug is used during pregnancy. (Only 1 state, Connecticut, currently includes an exception to the medical marijuana exemption in cases in which medical marijuana use could harm another individual, although potential harm to a foetus is not specifically listed.)

In 2015, the American College of Obstetricians and Gynecologists issued a committee opinion discouraging physicians from suggesting use of marijuana during preconception, pregnancy, and lactation. Pregnant women and those considering becoming pregnant should be advised to avoid using marijuana or other cannabinoids either recreationally or to treat their nausea.

Source:  http://jamanetwork.com/ on 12/21/2016

NIH Monitoring the Future survey shows use of most illicit substances down, but past year marijuana use relatively stable

December 13, 2016

The 2016 Monitoring the Future (MTF) annual survey results released today from the National Institutes of Health (NIH) reflect changing teen behaviors and choices in a social media-infused world. The results show a continued long-term decline in the use of many illicit substances, including marijuana, as well as alcohol, tobacco, and misuse of some prescription medications, among the nation’s teens. The MTF survey measures drug use and attitudes among eighth, 10th, and 12th graders, and is funded by the National Institute on Drug Abuse (NIDA), part of the NIH.

Findings from the survey indicate that past year use of any illicit drug was the lowest in the survey’s history for eighth graders, while past year use of illicit drugs other than marijuana is down from recent peaks in all three grades.

Marijuana use in the past month among eighth graders dropped significantly in 2016 to 5.4 percent, from 6.5 percent in 2015. Daily use among eighth graders dropped in 2016 to 0.7 percent from 1.1 percent in 2015. However, among high school seniors, 22.5 percent report past month marijuana use and 6 percent report daily use; both measures remained relatively stable from last year. Similarly, rates of marijuana use in the past year among 10th graders also remained stable compared to 2015, but are at their lowest levels in over two decades.

The survey also shows that there continues to be a higher rate of marijuana use among 12th graders in states with medical marijuana laws, compared to states without them. For example, in 2016, 38.3 percent of high school seniors in states with medical marijuana laws reported past year marijuana use, compared to 33.3 percent in non-medical marijuana states, reflecting previous research that has suggested that these differences precede enactment of medical marijuana laws.

Further, some 40.2 percent of seniors in so-called medical marijuana (MMJ) states are using edibles—foods infused with marijuana concentrates—compared to 28.1 percent of seniors in states that have not medicalized pot. High school seniors are in the healthiest part of the life span. One wonders why so many young people need so much “medicine.”

The survey indicates that marijuana and e-cigarettes are more popular than regular tobacco cigarettes. The past month rates among 12th graders are 12.4 percent for e-cigarettes and 10.5 percent for cigarettes. A large drop in the use of tobacco cigarettes was seen in all three grades, with a long-term decline from their peak use more than two decades ago. For example, in 1991, when MTF first measured cigarette smoking, 10.7 percent of high school seniors smoked a half pack or more a day. Twenty-five years later, that rate has dropped to only 1.8 percent, reflecting the success of widespread public health anti-smoking campaigns and policy changes.

There has been a similar decline in the use of alcohol, with the rate of teens reporting they have “been drunk” in the past year at the survey’s lowest rates ever. For example, 37.3 percent of 12th graders reported they have been drunk at least once, down from a peak of 53.2 percent in 2001.

Although non-medical use of prescription opioids remains a serious issue in the adult population, teen use of prescription opioid pain relievers is trending downwards among 12th graders with a 45 percent drop in past year use compared to five years ago. For example, only 2.9 percent of high school seniors reported past year misuse of the pain reliever Vicodin in 2016, compared to nearly 10 percent a decade ago.

“Clearly our public health prevention efforts, as well as policy changes to reduce availability, are working to reduce teen drug use, especially among eighth graders,” said Nora D. Volkow, M.D., director of NIDA. “However, when 6 percent of high school seniors are using marijuana daily, and new synthetics are continually flooding the illegal marketplace, we cannot be complacent. We also need to learn more about how teens interact with each other in this social media era, and how those behaviors affect substance use rates.”

“It is encouraging to see more young people making healthy choices not to use illicit substances,” said National Drug Control Policy Director Michael Botticelli. “We must continue to do all we can to support young people through evidence-based prevention efforts as well as treatment for those who may develop substance use disorders. And now that Congress has acted on the President’s request to provide $1 billion in new funding for prevention and treatment, we will have significant new resources to do this.”

The MTF survey, the only large-scale federal youth survey on substance use that releases findings the same year the data is collected, has been conducted by researchers at the University of Michigan at Ann Arbor since 1975.

Other highlights from the 2016 survey:

Illegal and Illicit Drugs

* Illicit Drugs other than Marijuana: Past year rates are the lowest in the history of the survey in all three grades. For example, 14.3 percent of 12th graders say they used an illicit drug (other than marijuana) compared to its recent peak of 17.8 percent in 2013.

* Marijuana-Past year use: Past year marijuana use among eighth graders dropped significantly to 9.4 percent in 2016, from 11.8 percent last year. Past year rates were somewhat stable for sophomores at 23.9 percent, and for seniors at 35.6 percent when compared to last year. However, past year marijuana use has dropped in the last five years among eighth and 10th graders.

* Marijuana-Daily use: Daily rates among 10th and 12th graders remained relatively stable at 2.5 percent and 6 percent for the past few years.

* Marijuana Edibles: Teens who live in states where medical marijuana is legal report a higher use of marijuana edibles. For example, among 12th graders reporting marijuana use in the past year, 40.2 percent consumed marijuana in food in states with medical marijuana laws compared to 28.1 percent in states without such laws.

* Synthetic Cannabinoids: Past year “synthetic marijuana” (K2/Spice) use among 10th and 12th graders dropped significantly from last year. For example, the rate for seniors fell to 3.5 percent compared to 5.2 percent in 2015, with a dramatic drop from its peak of 11.4 percent the first year it was measured in 2011.

* Cocaine: Past year cocaine use was down among 10th graders to 1.3 percent from 1.8 percent last year. Cocaine use hit its peak in this measure at 4.9 percent in 1999.

* Inhalants: Inhalant use, usually the only category of drugs used more by younger teens than their older counterparts, was down significantly among eighth graders compared to last year, with past year use at 3.8 percent, compared to 4.6 percent in 2015. Past year inhalant use peaked among eighth graders in 1995 at 12.8 percent.

* MDMA (Ecstasy or “Molly”): Past year use is down among eighth graders to 1 percent, from last year’s 1.4 percent. MDMA use is at its lowest point for all three grades in the history of the MTF survey.

* Heroin: Heroin rates remain low with teens still in school. High school seniors report past year use of heroin (with a needle) at 0.3 percent, which remains unchanged from last year. In the history of the survey, heroin (with a needle) rates have never been higher than 0.7 percent among 12th graders, as seen in 2010.

* Cold and Cough Medicine: Eighth graders alone reported an increase in misuse of over-the-counter cough medicine at 2.6 percent, up from 1.6 percent in 2015, but still lower than the peak of 4.2 percent when first measured in 2006.

* Attitudes and Availability: Attitudes towards marijuana use have softened, but perception of harm is not necessarily linked to rates of use. For example, 44 percent of 10th graders perceive regular marijuana smoking as harmful (“great risk”), but only 2.5 percent of them used marijuana daily in 2016. This compares to a decade ago (2006) when 64.9 percent of 10th graders perceived marijuana as harmful and 2.8 percent of them used it daily. The number of eighth graders who say marijuana is easy to get is at its lowest in the history of the survey, at 34.6 percent.

Prescription Drugs

* Opioid Pain relievers (described as “Narcotics other than Heroin” in the survey):  The  past year rate for non-medical use of all opioid pain relievers among 12th graders is at 4.8 percent, down significantly from its peak of 9.5 percent in 2004.

* Vicodin/OxyContin: The past year non-medical use of Vicodin among high school seniors is now lower than misuse of OxyContin (2.9 percent compared to 3.4 percent). The past year data for 12th graders 10 years ago was 9.7 percent for Vicodin and 4.3 percent for OxyContin.

* ADHD Medicines: Past year non-medical use of Adderall is relatively stable at 6.2 percent for 12th graders; however, non-medical use of Ritalin dropped to 1.2 percent, compared to 2 percent last year, and a peak of 5.1 percent in 2004.

* Tranquilizers: Non-medical use of this drug category, which includes benzodiazepines, has seen a general decline. For example, among 12th graders the 2016 past year rate is 4.9 percent, compared to its peak in 2002 at 7.7 percent.

* Attitudes and Availability: The majority of teens continue to say they get most of their opioid pain relievers (for non-medical use) from friends or relatives,

either taken, bought or given. The only prescription drugs seen as easier to get in 2016 than last year are tranquilizers, with 11.4 percent of eighth graders reporting they would be “fairly easy” or “very easy” to get, up from 9.8 percent in 2015. Also, when eighth graders were asked if occasional non-medical use of Adderall is harmful (“great risk”), 35.8 percent said yes, compared to 32 percent last year.

Tobacco

* Daily Smoking: The 2016 daily smoking rates for high school seniors was 4.8 percent compared to 22.2 percent two decades ago (1996). For 10th graders, the 2016 daily smoking rate is 1.9 percent, compared to 18.3 percent in 1996.

* Hookah Use: For past year tobacco use with a hookah, the 2016 rate dropped to 13 percent among high school seniors, from 22.9 percent two years ago, its peak year since the survey began measuring hookah use in 2010.

* E-Cigarettes (Vaporizers): The rate for e-cigarettes among high school seniors dropped to 12.4 percent from last year’s 16.2 percent. Of note: only 24.9 percent of 12th graders report that their e-cigarettes contained nicotine (the addictive ingredient in tobacco) the last time they used, with 62.8 percent claiming they contain “just flavoring.”

* Little Cigars: The 2016 past year rate dropped to 15.6 percent among 12th graders, from a peak of 23.1 percent in 2010, when first included in the survey.

* Attitudes and Availability: This year, more 10th graders disapprove of regular use of e-cigarettes than last year. For example, 65 percent of 10th graders say they disapprove, up from last year’s 59.9 percent. In addition, more 10th graders think it is harder to get regular cigarettes than last year; 62.9 percent said they are easy to get, compared to 66.6 percent last year. This represents a dramatic shift from survey findings two decades ago, when 91.3 percent of 10th graders thought it was easy to get cigarettes.

Alcohol

* Past year use: More than half (55.6 percent) of 12th graders report having used alcohol in the past year, compared to the peak rate of about 75 percent in 1997. Thirty-eight percent of 10th graders and 17.6 percent of eighth graders report past year use, compared to the peaks of 65.3 percent in 2000 among 10th graders and 46.8 percent in 1994 among eighth graders.

* Binge drinking: Among eighth graders, binge drinking (described as five or more drinks in a row in the last two weeks) continues to significantly decline, now

at only 3.4 percent, the lowest rate since the survey began asking about it in 1991, down from a peak of 13.3 percent in 1996. Binge drinking among high school seniors is down to 15.5 percent, half its peak of 31.5 percent in 1998.

* Been drunk: Representing a long-term downward trend, 37.3 percent of 12th graders say they have been drunk in the past year; 20.5 percent of 10th graders say they have been drunk, down from a peak of 41.6 percent in 2000. Eighth graders reported a rate of 5.7 percent, down from a peak of 19.8 percent in 1996.

* Attitudes: Just over 71 percent of 10th graders think it is easy to get alcohol, compared to last year’s rate of 74.9 percent, and down from 90.4 percent two decades ago.

Overall, 45,473 students from 372 public and private schools participated in this year’s MTF survey. Since 1975, the survey has measured drug, alcohol, and cigarette use and related attitudes in 12th graders nationwide. Eighth and 10th graders were added to the survey in 1991. Lloyd D. Johnston, Ph.D., who has been the principal investigator at the University of Michigan’s Institute for Social Research for all 42 years, is retiring from that position this year, but the survey of teens will continue under the leadership of Richard A. Miech, Ph.D., who is currently a member of the MTF scientific team.

“The declining use of many drugs by youth is certainly encouraging and important,” said Dr. Johnston. “But we need to remember that future cohorts of young people entering adolescence also will need to know why using drugs is not a smart choice. Otherwise we risk having another resurgence of use as was seen in the 90s.”

“We want to thank Dr. Johnston for his lifetime of work building this survey into the important public health tool it is today,” added Dr. Volkow.

Source:  National Families in Action’s The Marijuana Report srusche=nationalfamilies.org@mail230.atl101.mcdlv.net  12th Dec.2016

Robert J. Tait, et al

Abstract

Context: Synthetic cannabinoids (SCs) such as “Spice”, “K2”, etc. are widely available via the internet despite increasing legal restrictions. Currently, the prevalence of use is typically low in the general community (<1%) although it is higher among students and some niche groups subject to drug testing. Early evidence suggests that adverse outcomes associated with the use of SCs may be more prevalent and severe than those arising from cannabis consumption.

Objectives: To identify systematically the scientific reports of adverse events associated with the consumption of SCs in the medical literature and poison centre data.

Method: We searched online databases  and manually searched reference lists up to December 2014. To be eligible for inclusion, data had to be from hospital, emergency department, drug rehabilitation services or poison centre records of adverse events involving SCs and included both self-reported and/or analytically confirmed consumption.

Results: From 256 reports, we identified 106 eligible studies including 37 conference abstracts on about 4000 cases involving at least 26 deaths. Major complications include cardiovascular events (myocardial infarction, ischemic stroke and emboli), acute kidney injury (AKI), generalized tonic-clonic seizures, psychiatric presentations (including first episode psychosis, paranoia, self-harm/suicide ideation) and hyperemesis. However, most presentations were not serious, typically involved young males with tachycardia (≈37–77%), agitation (≈16–41%) and nausea (≈13–94%) requiring only symptomatic care with a length of stay of less than 8 hours.

Conclusions: SCs most frequently result in tachycardia, agitation and nausea. These symptoms typically resolve with symptomatic care, including intravenous fluids, benzodiazepines and anti-emetics, and may not require inpatient care. Severe adverse events (stroke, seizure, myocardial infarction, rhabdomyolysis, AKI, psychosis and hyperemesis) and associated deaths manifest less commonly. Precise estimates of their

incidence are difficult to calculate due to the lack of widely available, rapid laboratory confirmation, the variety of SC compounds and the unknown number of exposed individuals. Long-term consequences of SCs use are currently unknown. Keywords: Emergency medical services, street drugs, drug overdose, mental disorders, drug-related side effects and adverse reactions

Discussion

The prevalence of SC consumption is low in the general population.   However, the risk of requiring medical attention following use of SC seems to be greater than that for cannabis consumption.  Our systematic review of adverse events found that typically events were not severe, only required symptomatic or supportive care and were of short duration.

Nevertheless, a number of deaths have been attributed either directly or indirectly to SC consumption, together with other major adverse sequelae, including a significant number with persistent effects including new on-set psychosis with no family history of psychosis

We did not include popular media reports or the grey literature in the search, which would probably reveal further cases but would be less likely to contain reliable medical information. We were unable to determine the exact number of cases in the scientific literature due to the potential overlap between poison centre data and hospital reports. We could not even definitively establish the number of deaths attributed to SC consumption. Of the 28 531 ED visits in 2011 recorded in the DAWN database, 119 (0.4%) led to death potentially related to SC use

Our review of published cases identified only 22 fatal cases in the USA through to the end of 2014. As not all presentations especially for psychiatric problems or palpitations will include assessment of SC use, SC presentations may currently be seriously underreported. This suggests that the magnitude of the health burden due to SC use is considerably greater than that currently documented. Most of the data were based on self-reported consumption of SC, with no simple screening test available yet for clinicians.

Some of the information on adverse effects of SCs arises from poison centre data. Wood et al. outlined the strengths and weakness of poison centre data for novel psychoactive substances.  In brief, poison centres may detect new and unfamiliar exposures, but the rates of detection may decline with familiarity with the substances involved. In addition, the data depend upon voluntary reporting, often lack analytical confirmation, and may not discern which symptoms to attribute to a given substance, in cases of poly-drug exposure. Similarly, novel adverse events and events involving new SCs are more likely to be reported or published in the medical literature.

The consumption of cannabis affects the cardiovascular system and increases the risk of myocardial infarction.  Similarly, cannabis has been implicated in ischemic stroke, especially multifocal intracranial stenosis among young adults.   Cannabis use, ischemic stroke, and multifocal intracranial vasoconstriction, a prospective study in 48 consecutive young patients. The potential mechanisms include cardiac ischemia due to increased heart rate, postural hypotension, impaired oxygen supply arising from raised carboxyhemoglobin levels, especially in conjunction with tobacco smoking, and catecholamine-mediated pro-arrhythmic effects.  Marijuana as a trigger of cardiovascular events: speculation or scientific certainty? It is thus perhaps unsurprising that similar adverse outcomes have occurred following the use of SCs given their increased potency at CB1 receptors. Whether these compounds have significant direct effects on other receptors is still unknown.

The comparatively short period for which SC have been available and used in the general community means that long-term outcomes are currently unknown. However, the occurrence of AKI has implications for future health with a meta-analysis estimating a nearly nine-fold increase in the risk of developing chronic kidney disease, and a three-fold increase in the risk of end stage renal disease, compared to those who have not had AKI.   Thus, even low prevalence events with apparently limited duration, like AKI, have the potential to result in significant health costs following the resolution of acute symptoms. The other effects with long-term potential health consequences are initiation or exacerbation of psychiatric disorders, particularly psychosis. These are extremely debilitating and disabling conditions with large societal and health impacts for patients, families and the health system.

Clinical implications

SC intoxication appears to be a distinct and novel clinical entity. Use of SCs can cause more significant clinical effects than marijuana. There also appear to be qualitative differences in the nature of the symptoms with which patients present. The sheer number of SCs available and the rate at which they continue to change confound examinations of the scale and extent of the problem.   More recent formulations (in the UK termed “Third Generation”) are typically more potent that earlier SCs and seem to be associated with greater harms.  Trecki and colleagues report that the incidence of clusters and severity of adverse events involving SCs appears to be increasing.   This increase could be due to greater familiarity with presentations, better coordination between public health authorities and laboratories or the characteristics of newer SCs.   The overall effects of SC can resemble those of cannabis, but other than anxiety and paranoia these are not usually the symptoms associated with acute hospital presentation. Instead, patients seem to present in EDs because of behavioural abnormalities (agitated behaviour, psychosis, anxiety) or symptoms associated with acute critical illness. The latter includes seizures (which if prolonged can lead to rhabdomyolysis and hyperthermia), AKI, myocardial ischaemia and infarction in demographic groups where this would be most unusual. The majority of mild intoxications only require symptomatic treatment and generally do not require hospital admission. Severe intoxications, involving seizures, severe agitation or mental health disturbances, arrhythmias and significant chest pain, should be admitted to hospital for further investigation.

The lack of an antidote to SCs, analogous to that for opioid overdose, complicates management, as does the unpredictable effects and lack of a clear toxidrome to distinguish SCs from other recreational drugs.   The differential diagnosis requires the elimination of diverse conditions including hypoglycaemia, CNS infection, thyroid hyperactivity, head trauma and mental illness.  Benzodiazepines are usually sufficient to control agitation: while the use of haloperidol has also been described.  Caution is advised in undifferentiated agitation. Benzodiazepine failure should prompt consideration of definitive airway control. In addition to intravenous fluids for dehydration, the primary goals are protecting the airway, preventing rhabdomyolysis and to monitor for either cardiac or cerebral ischemia.

Traditionally, most recreational drug overdoses have been easily explicable based on clinical presentation alone. From an epidemiological perspective, this position should be revisited. Both the Welsh Emerging Drugs and Identification of Novel Substances (WEDINOS) and the Australian Capital Territory Novel Substances (ACTINOS) projects, routinely analyse raw product samples in the possession of patients, associated with severe or unusual presentations. This protocol has been able to characterize novel products well before their identification by law enforcement, arguably generating important information, not just for the patient concerned but also for population health services.

Conclusions

Data from poison centres and drug monitoring systems in Europe, the UK, the USA, and Australia illustrate trends of increased use of SCs. The number of unique SCs appears to continue growing, but the SCs seem to share common characteristics within the class. The most common effects include tachycardia, agitation and nausea; these generally respond to supportive care. However, physicians should be aware of the severe cardiovascular, cerebrovascular, neurological, psychiatric and renal effects, which occur in a minority of cases.

Differences among compounds in the class are difficult to assess. Methods to detect, identify and confirm new SCs lag behind the appearance of these drugs. Further, many of the cases depend upon self-report of the patients, whose information may be unreliable or inaccurate. Improving the availability of advanced laboratory resources will improve our ability to recognize SCs with higher risk of severe toxicity.

Source:  Extracts from Clinical Toxicology  Volume 54, 2016 – Issue 1  Nov.2015

A recognized deficiency: Inadequate protective protocols

An evaluation of risk applied to marijuana products for medical purposes concludes that advanced mitigation strategies and new protective delivery protocols are necessary to adequately protect the public from harm. The Risk Evaluation and Mitigation Strategies (REMS) program is already an approved protocol in the United States (US) by the US Food and Drug Administration and in Canada a similar controlled distribution program is in place including RevAid®.1,2    These programs are intended to assure patients are monitored to prevent or minimize major side effects and or reactions.   There are a number of medications that fall into existing REMS restrictions include thalidomide, clozapine, isotretinoin, and lenilidomide.  In both of these programs only prescribers and pharmacists who are registered or patients who are enrolled and who have agreed to meet all the conditions of the program are given access to these drugs.1,2

Current Government-approved Cannabinoid Products

Dronabinol (Marinol®, generic), nabilone (Cesamet®, generic) are synthetic cannabinoids to mimic delta-9-THC and nabiximols (Sativex®) is a combination of delta-9-THC and cannabidiol. They all lack the pesticides, herbicides and fungicides placed on marijuana plants during growth.

The longest approved agents, dronabinol and nabilone are indicated for short term use in nausea and vomiting due to chemotherapy and appetite stimulation.3,4  Nabiximols is used as a buccal spray for multiple sclerosis and as an adjunct for cancer pain.5  The maximum delta-9-THC strengths available are 10 mg for dronabinol and 2.7 mg/spray of nabiximols.3,5  Cannabidiol (CBD), a non-psychoactive compound, is one of many cannabinoids found in marijuana.   CBD is currently available for free from the U.S. National Institute of Health in government-sponsored clinical trials as potential treatment of resistant seizures (Dravet’s Syndrome and Lennox-Gastaut Syndrome).6

‘Medical’ Marijuana products

All marijuana products, including marijuana for medical purposes, fit the prerequisites for a REMS program. The average potency of marijuana more than doubled between 1998 and 2009.7 In 2015 common leaf marijuana averaged 17.1% THC in Colorado.8  Examples of oral marijuana products contain 80 mg of THC in chocolates, cookies and drinks and even 420 mg of THC in a “Dank Grasshopper” bar.9  Butane hash oil (BHO) is a concentrated THC product used in water bongs and/or e- cigarettes and contains upwards of 50 – 90% THC with a Colorado average of 71.7 % THC.8   One “dab” (280 mg) of 62.1% BHO is equal to 1 gram of 17% THC in marijuana leaf form.8  These extremely elevated levels of THC make true scientific research with these products incapable of passing Patient Safety Committee standards.10

The Thalidomide Parallel

The risks are so severe for thalidomide, in terms of use in pregnancy that a special protocol that educates, evaluates, mitigates and monitors has been made obligatory.11

Thalidomide (Contergan®) was developed by a German company, Chemie Gruenenthal, in 1954 and approved for the consumer market in 1957.12 It was available as an over-the-counter drug for the relief of “anxiety, insomnia, gastritis, and tension” and later it was used to alleviate nausea and to help with morning sickness by pregnant women. Thalidomide was present in at least 46 countries under a variety of brand names and was available in “sample tablet form” in Canada by 1959 and licensed for prescription on December 2, 1961. Although thalidomide was withdrawn from the market in West Germany and the UK by December 2, 1961, it remained legally available in Canada until March of 1962. It was still available in some Canadian pharmacies until mid-May of 1962.12

Canada had permitted the drug onto the Canadian market when many warnings were already available

An association was being made in 1958 of phocomelia (limb malformation) in babies of mother’s using thalidomide.  A trial conducted in Germany against Gruenenthal, for causing intentional and negligent bodily injury and death, began in 1968 ending in 1970 with a claim of insufficient evidence.  Later, the victims and Gruenenthal settled the case for 100 million dollars.11

In 1962 the American pharmaceutical laws were increased by the Kefauver-Harris Drug Amendment of 1962 and proof for the therapeutic efficiency through suitable and controlled studies would be required for any government approved medication.13 According to paragraph 25 of the Contergan foundation law, every 2 years a new report is required to determine if further development of these regulations are necessary.13

In 1987 the War Amputations of Canada established The Thalidomide Task Force, to seek compensation for Canadian-born thalidomide victims from the government of Canada.12

In 1991, the Ministry of National Health and Welfare (the current Health Canada) awarded Canadian-born thalidomide survivors a small lump-sum payment.12

In 2015 the Canadian government agreed on a settlement of $180 million dollars to 100 survivors of thalidomide drug exposure and damage.14 Through Rona Ambrose, in her capacity as the Health Minister for the government of Canada at the time of the negotiations, an attempt was made to involve the drug companies related to the thalidomide issue in the survivor’s settlement agreement. Negotiations with the drug companies failed.  The Canadian taxpayer alone paid to amend the survivors by way of monetary award.

Thalidomide continues to be sold under the brand name of Immunoprin®, among others in a REMS program. It is an immunomodulatory drug and today, it is used mainly as a treatment of certain cancers (multiple myeloma) and leprosy.11

Question: If the drug thalidomide included psychotropic properties and offered the “high” of marijuana would it be prudent or responsible to allow it to be legally sold and marketed for non-medical purposes – acknowledging thalidomide’s record for toxicity in pregnancy?

Marijuana Risk Assessment and Government Acknowledgement

Risks demonstrated in the scientific literature include genetic and chromosomal damage.15, 16

When exposure occurs in utero, there is an association with many congenital abnormalities including cardiac septal defects, anotia, anophthalmos, and gastroschisis. Marijuana use can disrupt foetal growth and the development of organs and limbs and may result in mutagenic alterations in DNA. Cannabis has also been associated with foetal abnormalities in many studies including low birth weight, foetal growth restriction, preterm birth spontaneous miscarriage, spina bifida and others.15

Phocomelia has been shown in testing in a similar preclinical model (hamster) to that which revealed the teratogenicity of thalidomide.15

THC has the ability to interfere with the first stages in the formation of the brain of the fetus; this event occurs two weeks after conception.  Exposure to today’s high potency marijuana in early pregnancy is associated with anencephaly, a devastating birth defect in which infants are born with large parts of the brain or skull missing.15

The existence of specific health risks associated with marijuana products are acknowledged by national and various local governments and a plethora of elected officials in both Canada and the United States.16, 17, 18

Warnings and the contraindications for use by specific populations and in association with identified conditions, have been publicized by the Federal Government of Canada and the Federal Government of the United States of America through their respective health agencies.16, 17, 18

A government of Canada leaflet produced by Health Canada and updated in December 2015: Consumer Information – Cannabis (Marihuana, marijuana) reads19:

“The use of this product involves risks to health, some of which may not be known or fully understood. Studies supporting the safety and efficacy of cannabis for therapeutic purposes are limited and do not meet the standard required by the Food and Drug Regulations for marketed drugs in Canada.”19

“Using cannabis or any cannabis product can impair your concentration, your ability to think and make decisions, and your reaction time and coordination. This can affect your motor skills, including your ability to drive. It can also increase anxiety and cause panic attacks, and in some cases cause paranoia and hallucinations.”19

“When the product should not be used: under the age of 25, are allergic to any cannabinoid or to smoke, have serious liver, kidney, heart or lung disease, have a personal or family history of serious mental disorders such as schizophrenia, psychosis, depression, or bipolar disorder, are pregnant, are planning to get pregnant, or are breast-feeding, are a man who wishes to start a family, have a history of alcohol or drug abuse or substance dependence.”19

“A list of health outcomes related to long term use includes the following:

Increased risk of triggering or aggravating psychiatric and/or mood disorders (schizophrenia, psychosis, anxiety, depression, bipolar disorder), decrease sperm count, concentration and motility, and increase abnormal sperm morphology. Negatively impact the behavioural and cognitive development of children born to mothers who used cannabis during pregnancy.”19

In Canada, the College of Family Physicians has issued guidelines for issuing marijuana prescriptions.20

“Dried cannabis is not appropriate for patients who: a) Are under the age of 25 (Level II) b) Have a personal history or strong family history of psychosis (Level II) c) Have a current or past cannabis use disorder (Level III) d) Have an active substance use disorder (Level III) e) Have cardiovascular disease (angina, peripheral vascular disease, cerebrovascular disease, arrhythmias) (Level III) f) Have respiratory disease (Level III) or g) Are pregnant, planning to become pregnant, or breastfeeding (Level II)”20

“Dried cannabis should be authorized with caution in those patients who: a) Have a concurrent active mood or anxiety disorder (Level II) b) Smoke tobacco (Level II) c) Have risk factors for cardiovascular disease (Level III) or d) Are heavy users of alcohol or taking high doses of opioids or benzodiazepines or other sedating medications prescribed or available over the counter (Level III)”20

In February 2013 The College of Family Physicians of Canada issued a statement advancing the position that physicians should sign a declaration rather than write a prescription as the potential liability, as well as the ethical obligations, for health professionals prescribing marijuana for medical purposes appears not to have been adequately addressed by Health Canada. 21

“In our view, Health Canada places physicians in an unfair, untenable and to a certain extent unethical position by requiring them to prescribe cannabis in order for patients to obtain it legally. If the patient suffers a cannabis-related harm, physicians can be held liable, just as they are with other prescribed medications. Physicians cannot be expected to prescribe a drug without the safeguards in place as for other medications – solid evidence supporting the effectiveness and safety of the medication, and a clear set of indications, dosing guidelines and precautions.”21

Representatives of the government of the United States held a press conference at the Office of National Drug Policy (ONDCP) in 2005. Mental health experts and scientists joined high-ranking government officials to discuss an emerging body of research that identified clear links between marijuana use and mental health disorders, including depression, suicidal thoughts and schizophrenia.22

The US Substance Abuse and Mental Health Service Administration (SAMHSA) report about the correlation between age of first marijuana use and serious mental illness; and an open letter to parents on “Marijuana and Your Teen’s Mental Health,” signed by twelve of the Nation’s leading mental health organizations, ran in major newspapers and newsweeklies across the country.23

Included were the following announcements:

“Regular use of the drug has appeared to double the risk of developing a psychotic episode or long-term schizophrenia.”23

“Research has strongly suggested that there is a clear link between early cannabis use and later mental health problems in those with a genetic vulnerability – and that there is a particular issue with the use of cannabis by adolescents.” 23

“Adolescents who used cannabis daily were five times more likely to develop depression and anxiety in later life.” 23

In 2016 the Obama Administration steadfastly opposes legalization of marijuana and other drugs because legalization would increase the availability and use of illicit drugs, and pose significant health and safety risks to all Americans, particularly young people.24 The US government still maintains marijuana is classified as a Schedule I drug, meaning it has a high potential for abuse and no currently accepted medical use in treatment in the United States.17, 18

Risk Evaluation and Mitigation Strategy for Marijuana Products

The dispensing of marijuana for medical purposes must follow a strict dispensing and monitoring protocol; no less arduous than that used for the delivery of drugs such as thalidomide.

Recommendation – The implementation of a REMS for marijuana products (REMSMP).

1. The first order for a government is to protect the public. As such, it befits a government approving marijuana for medical purposes to implement a REMS program.

2. Medical cannabis/marijuana dispensaries/stores/delivery systems will be       required to comply with all necessary components of a rigorous REMS program prior to selling and dispensing marijuana products.

3. Governmental regulatory organizations must be responsible for the cannabis/marijuana for medical purposes programs and obtain the required evaluations [(i.e. laboratory tests (pregnancy, HCG, etc.), physical and mental health examination documentation], signed patient consent, provider contract and education forms – performed in the required time frames both before initiation, during and after continued usage of marijuana products for medical purposes.

4. Quarterly audits will be performed, by the government regulatory organization, on each medical marijuana/cannabis dispensary for compliance.  Failure to comply with the REMSMP program will result in fines and other appropriate penalties to the marijuana dispensaries.

A REMS for Marijuana Product Potential Framework:

EMBRYO-FETAL TOXICITY & BREASTFEEDING

* Marijuana causes DNA damage in male and female patients.15  If marijuana is used during conception or during pregnancy, it may cause birth defects, cancer formation in the offspring, Downs Syndrome or embryo-fetal death.15, 16, 18

* Pregnancy must be ruled out before the start of marijuana treatment.  Pregnancy must be prevented by both the male and female patients during marijuana treatment by the use of two reliable methods of contraception.

* When there is no satisfactory alternative treatment, females of reproductive potential may be treated with marijuana provided adequate precautions are taken to avoid pregnancy.

* Females of Reproductive Potential: Must avoid pregnancy for at least 4 weeks before beginning marijuana therapy, during therapy, during dose interruptions and for at least 4 weeks after completing therapy.  Females must commit to either abstain continuously from heterosexual intercourse or use two methods or reliable birth control as mentioned.  They must have two negative pregnancy tests prior to initiating marijuana therapy and monthly pregnancy test with normal menses or two months with abnormal menses and for at least 1 month after stopping marijuana therapy.

* Males (all ages): DNA damage from marijuana is present in the semen of patients receiving marijuana.15 Therefore, males must always use a latex or synthetic condom during any sexual contacts with females of reproductive potential while using marijuana and for up to at least 28 days after discontinuing marijuana therapy, even if they have undergone a successful vasectomy.  Male patients using marijuana may not donate sperm.

* Blood Donation: Patients must not donate blood during treatment with marijuana and for at least 1 month following discontinuation of marijuana because the blood might be given to a pregnant female patient whose fetus should not be exposed to marijuana.

* Marijuana taken by any route of administration may result in drug-associated DNA damage resulting in embryo-fetal toxicity. Females of reproductive potential should avoid contact with marijuana through cutaneous absorption, smoke inhalation or orally.

* If there is contact with marijuana products topically, the exposed area should be washed with soap and water.

* If healthcare providers or other care givers are exposed to body fluids of a person on marijuana, the exposed area should be washed with soap and water.  Appropriate universal precautions should be utilized, such as wearing gloves to prevent the potential cutaneous exposure to marijuana.

* Several psychoactive cannabinoids in marijuana are fat soluble and are found to concentrate in breast milk.  Nursing mothers must not be receiving marijuana.16 Consult the primary care provider about how long to be off of marijuana before considering breast feeding.

NON-SEMINOMA TESTICULAR GERM CELL CARCINOMA

* Marijuana use is a known risk factor in the development of non-seminoma testicular germ cell carcinoma in males.25 – 28

* The presence of non-seminoma testicular germ cell carcinoma must be excluded before the start of marijuana treatment.  The patient’s primary care provider must perform a testicular examination and review the patient’s human chorionic gonadotropin (HCG) blood test before starting marijuana.  Male patients must perform weekly testicular self-evaluations while receiving marijuana.  They are also required to have their primary care provider perform a testicular evaluation and a HCG blood test performed every 4 months while receiving marijuana.29, 30

MENTAL HEALTH:

* Short term high dose and chronic marijuana usage is a known risk factor for the development of multiple mental health disorders.16, 18, 20, 31 – 34  Depression, paranoia, mental confusion, anxiety, addiction and suicide potential are all associated with acute and chronic exposure to marijuana.16, 18   Decline in intelligence is a potential risk of adolescent-onset marijuana exposure. 16, 18, 35

The presence of these mental health disorders must be evaluated by a licensed psychiatrist or psychologist by use of the Mini International Neuropsychiatric Interview or equivalent validated diagnostic instrument before marijuana is started.  The diagnostic mental health evaluation tool will be completed every 1month by an independent licensed psychiatrist or psychologist for a minimum of 6 months until unchanging and then every 4 months thereafter while receiving marijuana ending 4 months after the last exposure to marijuana.36

PSYCHIATRIC EVALUATIONS:

History of Substance Abuse Disorder: As the prevalence of substance use disorders amongst those patients requesting medical authorization of marijuana products is known to be extremely high the patient population must be screened prior to dispensing marijuana products for risk of a substance use disorder.  Substance use must be monitored prior to onset of marijuana with the World Health Organization, Smoking and Substance Involvement Screening Test (WHO-ASSIST, V3.0), and repeated at monthly intervals until unchanging and every 3 months thereafter while receiving marijuana, ending 6 months after the last exposure to marijuana.37

Conclusion

The evidence that thalidomide and tobacco products were harmful was known to the manufacturers/distributors before government and the populous acknowledged these dangers.

To date, there continue to be legal repercussions to said manufacturers/distributors/government for knowingly placing the public at risk.  We believe that the same will happen for marijuana products and that it is our responsibility to assist the Canadian government to protect the public from a similar outcome.

Since the government is fully aware of the marijuana harms, the  government must not be complicit in risking Canadian health/lives, but rather must mitigate any and all such risk to current and future generations.38, 39

The REMSMP program described assists in providing patient education, provider education and required patient monitoring before any marijuana products are allowed to be dispensed.  The program also requires on-going data collection and analysis, to determine the actual hazards from marijuana use and whether the program should even continue.  As the stewards of the country’s human and financial resources, it is critical that government protect the public from potential irreversible harm and itself from litigation risk by harmed individuals knowing that, in the context of marijuana use, harm is not only possible but probable.

Source:  Pamela McColl,  National Director,  Smart Approaches to Marijuana Canada and The Marijuana Victims’ Association,    Vancouver BC Canada    August  2016

Endorsements

Philip Seeman, M.D. Ph.D., O.C. Departments of Pharmacology and Psychiatry University of Toronto,   Nobel Prize nominee (Science)

Elizabeth Osuch, M.D. Associate Professor Rea Chair of Affective Disorders, University of Western Ontario Schulich School of Medicine and Denistry,  London, Ontario

Ray Baker, M.D., FCFP, FASAM, Associate Clinical Professor, University of British Columbia Faculty of Medicine,  Vancouver, British Columbia

Pamela McColl, Smart Approaches to Marijuana – Canada.  Board Member Campaign for Justice Against Tobacco Fraud

Robert L. DuPont, MD,  President, Institute for Behavior and Health, Inc. Clinical Professor of Psychiatry, Georgetown University School of Medicine,  First Director, National Institute on Drug Abuse,  Second US White House Drug Chief

Bertha K Madras, PhD Professor of Psychobiology, Department of Psychiatry,Harvard Medical School

Phillip A. Drum Pharm. D., FCSHP.    Smart Approaches to Marijuana – USA

Professor Gary Hulse, School of Psychiatry and Clinical Neurosciences, University of Western Australia, Crawley, Australia

Grainne Kenny, Dublin, Ireland Co-founder and Hon. President of EURAD ,Brussels, Belgium

Peter Stoker Director, National Drug Prevention Alliance, United Kingdom

Mary Brett, BSc (Hons), Chair of Charity Cannabis Skunk Sense (CanSS) www.cannabisskunksense.co.uk ,United Kingdom

Deidre Boyd, CEO: DB Recovery Resources, Editor: Recovery Plus UK

References  1. Accessed on 7/28/16:http://www.fda.gov/Drugs/DrugSafety/Postmarket DrugSafetyInformationforPatients andProviders/ucm2008016.htm#rems  2. Accessed on 7/28/16: https://www.revaid.ca  3. Accessed on 7/31/16: http://www.fda.gov/ohrms/dockets/dockets/05n0479/05N-0479-emc0004-04.pdf

4. Accessed on 7/31/16: https://www.cesamet.com/pdf/Cesamet_PI_50_count.pdf

5. Accessed on 7/31/16: http://www.ukcia.org/research/SativexMonograph.pdf

6. Accessed on 7/28/16:https://clinicaltrials.gov/ct2/results?term=CBD+and+ epilepsy&Search=Search

7. National Center for Natural Products Research (NCNPR), Research Institute of Pharmaceutical Sciences. Quarterly Report, Potency Monitoring Project, Report 107, September 16, 2009 thru December 15, 2009. University, MS: NCNPR, Research Institute of Pharmaceutical Sciences, School of Pharmacy, University of Mississippi (January 12, 2010).

8. Orens A, et al. Marijuana Equivalency in Portion and Dosage. An assessment of physical and pharmacokinetic relationships in marijuana production and consumption in Colorado. Prepared for the Colorado Department of Revenue. August 10, 2015.

9. Accessed on7/30/16: https://weedmaps.com/dispensaries/tree-house-collective-dispensary-san-marcos

10.  Personal conversation with Marilyn Huestis, NIH researcher, June 2015.

11. Accessed on 8/4/16:http://www.contergan.grunenthal.info/grt-ctg/GRT-CTG/Die_Fakten/Chronologie/152700079.jsp

12. Accessed on 7/28/16: http://www.thalidomide.ca/the-canadian-tragedy/ 13. Accessed on 7/28/16:  http://www.fda.gov/Drugs/NewsEvents/ucm320924.htm 14. Accessed on 7/29/16: http://news.gc.ca/web/article-en.do?nid=945369&tp=1

15. Reece AS, Hulse GK. Chromothripsis and epigenomics complete causality criteria for cannabis- and addiction-connected carcinogenicity, congenital toxicity and heritable genotoxicity. Mutat Res. 2016;789:15-25. 16. Accessed on 7/28/16: http://www.hc-sc.gc.ca/dhp-mps/marihuana/med/ infoprof-eng.php 17. Accessed on 1/8/16:  https://www.whitehouse.gov/ondcp/frequently-asked-questions-and-facts-about-marijuana#harmless 18. Accessed on 1/8/16:  https://www.whitehouse.gov/ondcp/marijuana  19. Accessed on 7/20/16: http://www.hc-sc.gc.ca/dhp-mps/marihuana/info/cons-eng.php

20. College of Family Physicians of Canada. Authorizing Dried Cannabis for Chronic Pain or Anxiety: Preliminary Guidance from the College of Family Physicians of Canada. Mississauga, ON: College of Family Physicians of Canada; 2014.

21. Accessed on 3/8/16:http://www.cfpc.ca/uploadedFiles/Health_Policy/CFPC _Policy_Papers_and_Endorsements/CFPC_Policy_Papers/Medical%20Marijuana%20Position%20Statement%20CFPC.pdf 22. Accessed on 6/31/16 http://www.ovguide.com/john-p-walters-9202a8c040 00641f8000000 0003d9c0b

23. Accessed 8/1/2016: http://www.prnewswire.com/news-releases/white-house-drug-czar-research-and-mental-health-communities-warn-parents-that-marijuana-use-can-lead-to-depression-suicidal-thoughts-and-schizophrenia-54240132.html

24. Accessed on 2/8/2016. https://www.whitehouse.gov/ondcp/marijuana

25. Accessed on 8/1/2016: https://www.drugabuse.gov/news-events/nida-notes/2010/12/marijuana-linked-testicular-cancer

26. Lacson JCA, et al. Population-based case-control study of recreational drug use and testis cancer risk confirms an association between marijuana use and nonseminoma risk. Cancer. 2012;118(21):5374-5383.

27. Daling JR, et al. Association of marijuana use and the incidence of testicular germ cell tumors. Cancer. 2009;115(6):1215-1223.

28. Gurney J, et al. Cannabis exposure and risk of testicular cancer: a systematic review and meta-analysis. BMC Cancer 2015;15:1-10.  29. Accessed on 7/30/16:http://www.cancer.org/cancer/testicularcancer/ detailedguide/testicular-cancer-diagnosis

30. Takizawa A, et al. Clinical Significance of Low Level Human Chorionic Gonadotropin in the Management of Testicular Germ Cell Tumor. J Urology. 2008;179(3):930-935.

31. Moore TH, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319-328.

32. Large M, et al., Cannabis use and earlier onset of psychosis: a systematic meta-analysis. Arch Gen Psychiatry. 2011;68(6):555-61.

33. Ashton CH and Moore PB. Endocannabinoid system dysfunction in mood and related disorders. Acta Psychiatr Scand, 2011;124: 250-261.

34. Ranganathan M and D’Souza DC. The acute effects of cannabinoids on memory in humans: a review. Psychopharmacology. 2006;188: 425-444, 2006.

35. Accessed on 8/1/2016:https://www.drugabuse.gov/publications/drug facts/marijuana

36. Sheehan D, et al. Mini International Neuropsychiatric Interview, DSM-IV English Version 5.0.0 2006.

37.  Accessed on 8/1/2016: http://www.who.int/substance_abuse/activities/assist/ en/

38. Accessed on 8/1/16: http://news.gc.ca/web/article-en.do?nid=844329 39. Accessed on 8/3/16: http://www.healthlinkbc.ca/healthtopics/content.asp? hwid=abl2153

Thanks to advances in science, we have never known so much about the effects marijuana use has on the human body, particularly, the fragile brain. Yet, in a political era when scientific research is regularly marshalled to end public policy debates, the powerful, growing scholarship on marijuana has largely been ignored or dismissed. Indeed, marijuana use seems to be one of the glaring areas in modern life where wishful thinking reigns over rationality.

Yet, as the lesson of tobacco demonstrates, when Americans are given the scientific facts about serious threats to their health, they adjust their behavior and insist on measures to safeguard their communities. In the instance of marijuana, the public can be forgiven for not knowing the true threat. With the assistance of a sympathetic media, marijuana legalization advocates, many seeking to profit off the drug, continue to sell romantic falsehoods and outright lies. They casually dismiss the growing list of serious concerns about marijuana emerging from scientific scholarship and survey research, or just cry “reefer madness” without examining the evidence.

Amidst the current marijuana public policy discussion, more than ever, concerned citizens, community leaders, lawmakers, educators, and parents need to better understand the growing body of research about this drug. What follows is a compilation and discussion of the latest research, including reports that are beginning to come in on the effects legalization has had in Colorado and neighbouring states—including increased criminal activity even with legalization. While all research has limitations, what we do know is becoming clearer by the day, and it will make many question what they thought they knew about this drug of abuse.

Key Recent Findings:

Journal of the American Medical Association: “There is little doubt about the existence of an association between substance use and psychotic illness…studies suggest that the association between cannabis use and later psychosis might be causal, a conclusion supported by studies showing that cannabis use is associated with an earlier age at onset of psychotic disorders, particularly schizophrenia.”

Society for the Study of Addiction: “Regular cannabis use in adolescence approximately doubles the risks of early school-leaving and of cognitive impairment and psychoses in adulthood. Regular cannabis use in adolescence is also associated strongly with the use of other illicit drugs

World Psychiatric Association: “Evidence that is a component cause of psychosis is now sufficient for public health messages outlining the risk, especially of regular use of high-potency cannabis and synthetic cannabinoids.”

American Academy of Paediatrics: “The adverse effects of marijuana have been well documented” and include “impaired short-term memory, decreased concentration, attention span, and problem solving” which “interfere[s] with learning.”

American Psychological Association: “Heavy marijuana use in adolescence or early adulthood has been associated with a dismal set of life outcomes including poor school performance, higher dropout rates, increased welfare dependence, greater unemployment and lower life satisfaction.”

Proceedings of the National Academy of Sciences: “Persistent adolescent-onset cannabis users” showed “an average 8-point IQ decline from childhood to adulthood.”

Clinical Psychological Science Journal: Duke University and UC Davis researchers “found that those dependent on cannabis experienced more financial difficulties, such as paying for basic living expenses and food, than those who were alcohol dependent.”

Journal of Drug and Alcohol Dependence: States that have legalized “medical” marijuana find an association with higher 12th grade drop-out rates, lessened college attainment, and increases in daily smoking. Further, there is a dose/response relationship between adverse impact and years of increased exposure under legalization.

U.S. Department of Health and Human Services, SAMHSA: Since legalizing marijuana, Colorado climbed to number one among states for both youth (12-17) and college age adults (18-25) marijuana use.

Discussion:

The further acceptance of marijuana legalization and commercialization in some states will lead to a greater availability of the drug. Greater availability and acceptance will lead to greater use of marijuana, both in the sense of more users, and likely further in the sense of more frequent and greater consumption.

In states that have legalized already there is strong evidence that adult use has surged upward. There is further evidence that use by youth will also increase.

Youth use of marijuana in states that have now commercialized sales was already more extensive than national norms, however, reports since the first commercialization began in January, 2014, indicate growing use amongst all age groups.

As marijuana use intensifies, the consequences of such use and abuse accelerates. These consequences are considerable, and will impose significant costs, both personal and economic, on health and social well-being.

Finally, and perversely, evidence is strong that the consequences will include not only continued, but intensified and entrenched criminal activity associated with drug use. Indications are clear that the criminal and violent black market capitalizes on increased marijuana availability and use. Marijuana commercialization/legalization is advancing both a public health and a public safety disaster.

We shall review recent evidence of the health-related consequences in this document. In a later accompanying document we will assess the impact on use of drugs beyond marijuana, as well as the impact on further criminal drug markets.

Though comparisons between marijuana and other substances of abuse are frequently made to the effect that marijuana is not proportionally lethal, there are nevertheless other measures of the drug’s dangers. Former National Institute on Drug Abuse Director Dr. Bob DuPont has termed marijuana “the most dangerous drug,” in part because of the sheer prevalence of what is the most widely used illegal substance in the world, and in part because the effects are not always felt or experienced by those affected. They can nevertheless be measured and are real. In some instances, research shows that they appear irreversible, even after abstinence.

Among the more troubling findings are those showing a relationship between marijuana use and psychotic episodes, diminished memory, verbal skill, and other cognitive performance, lowered life achievements, criminal and anti-social behavior, school leaving and academic failure, and even lowered life satisfaction.

Most concerning, perhaps, are the findings that heavy, early marijuana use is associated with a loss of intelligence over the life course. Specific supporting citations for other statements will be found below.

Further, Dr. Wayne Hall’s twenty-year review of the literature in the journal Addiction, as we will present in greater detail in the review, showed a clear relationship between youth marijuana use and subsequent use of other drugs. As Hall has argued:

The relationships between regular cannabis use and other illicit drug use have persisted after statistical adjustment for the effects of confounding variables in both longitudinal studies and discordant twin studies… The order of involvement with cannabis and other illicit drugs, and the increased likelihood of using other illicit drugs, are the most consistent findings in epidemiological studies of drug use in young adults.

In general, the health risks of marijuana use are reasonably well known, and based on long-standing research that now consists in multiple studies across many nations, exploring many dimensions of what is a very complex drug.

The last decade has witnessed an intensification of concern and stimulated even more studies of marijuana’s manifold impact, involving several areas of the body and the mind. The comprehensive nature of the physiological impact mirrors, to some extent, the widespread dispersal of the body’s naturally-occurring endocannabinoid receptor system.

There are additional physiological concerns, many based on smoking as the manner of consumption, focused on its effects on the cardiac and respiratory systems. These threats are real and mounting.

But the most compelling investigations regarding risk are emerging from studies of the brain, however the drug is consumed. These include both the structure and the functioning of the neurophysiology of the brain, and they further extend into discoveries regarding the consequences of brain activity, as we have mentioned, such as cognition, memory, learning, executive performance, and general behavior. Moreover, they also include examinations of drug dependency and what is termed “marijuana use disorder.”

That is, both the brain as an organ as well as “the mind,” the very personhood, of the individual are affected by the chemistry of the drug. Most concern is focused on the principle intoxicating element, THC , which shows signs of being actively toxic to the nervous system, the potency of which in modern forms is escalating dramatically under marijuana commercialization.

We must acknowledge that many studies demonstrate a risk that is emergent, and not fully known; multiple factors and confounders do coincide and must be accounted for before we argue “causation” for the effects that have been shown. Nevertheless, a substantial and repeated body of research that, taken piece by piece, showing “associations” or “correlations” or “predispositions,” must now be seen as sufficient, when taken together, to establish a clear and present danger.

In some measure, the worst effects are contingent, in the sense that not all forms of use by all individuals will produce the direst impact. But by now the evidence is compelling that certain forms of use, under certain circumstances, is deeply damaging.

Simply put, any honest observers must accept that the preponderance of evidence, as suggested by our review of recent literature which follows, demonstrates a high risk from marijuana use that is now overwhelming.

What we find is research from several related lines of inquiry, all pointing in the same direction. The risks are only worsening with time, in each line of inquiry, serving to confirm a congruence with the findings from other arena.

Studies of various marijuana disorders of behavior are being underpinned and given a basis by studies of the brain and its performance; showing consistent patterns from several interrelated domains of impact. Moreover, as over time the tools brought to bear have become more sophisticated and able to measure subtle and consequential effects, the sense of concern over what we are doing to youth is only mounting.

Though all users, even adult non-frequent users, have been shown to suffer some deficits through marijuana intoxication, and though there are further indications that even young adult casual users undergo structural brain changes, the evidence is far more robust and more worrying in other circumstances.

Danger increases, that is, when any of the following conditions are co-present with marijuana use: the existence of co-morbidities (or even predispositions), especially collateral substance dependencies or psychological deficits; certain genetic profiles that confer greater susceptibility; heavy, frequent use (daily use being the most threatening), especially of high-potency varieties; and especially exposure at a developmentally young age, during periods of highly consequential brain formation and calibration, generally ranging from prenatal or paediatric exposure up to young adulthood.

Where more than one of these factors is present, the risks escalate; where the developmentally young smoke high-potency cannabis frequently for an extended period – most markedly those with predisposing psychological deficits – the effects can be catastrophic in their lives, including dramatic “psychotic breaks.” These effects appear to be, in some cases, largely irreversible.

And it is this “worst-case scenario” that, perversely, is being fostered by state legalization and commercialization measures, thereby ensuring the greatest magnitude of damage.

A further implication of these facts concerns our emerging knowledge of the risks, given that most longitudinal studies showing long-term adult impacts were carried out without an appreciation of how the various factors above conferred greater vulnerability.

Often, studies that failed to find major impact were based on samples of adults, not adolescents, who were not exposed to heavy, frequent, newly-potent doses. Yet the commercialization of marijuana has resulted in marijuana potency that eclipses anything we have ever previously seen, in some cases by orders of magnitude. Highly potent “edibles” and concentrated cannabis extractions, like “shatter” are taking potency levels once common in the two- to three-percent range up to 80 percent. The consequence is that most everything we thought we knew about marijuana’s risks needs to be re-assessed under contemporary conditions, and most every danger, as we progressively uncover them, turns out to be heightened.

These finding are warnings of grave danger, with the promise of yet more to be discovered. Not all is “proven,” and not all establishes independent causation, but the evidence is strong enough, and growing daily, to activate in public policy a “precautionary principle.” That is, the evidence is strong enough to warrant a clear directive not to proceed further. Simply put, the pathway of legalization must not be pursued.

Recent Research and Findings: An Annotated Review

What has research over the past two decades revealed about the adverse health effects of recreational cannabis use? (full article), Addiction, (2014).

“Regular cannabis use in adolescence approximately doubles the risks of early school-leaving and of cognitive impairment and psychoses in adulthood. Regular cannabis use in adolescence is also associated strongly with the use of other illicit drugs.”

Unintentional Pediatric Exposures to Marijuana in Colorado: 2009-2015, Pediatrics, (2016).

“Annual pediatric marijuana cases increased more than 5-fold from 2009 (9) to 2015 (47). Colorado had an average increase in cases of 34% (P < .001) per year while the remainder of the United States had an increase of 19% (P < .001).”

Wants Marijuana Products to Have Warnings Against Use in Pregnancy, National Council on Alcoholism and Drug Dependence, (2015).

The American Medical Association seeks warnings against marijuana use in pregnancy.

Cannabis Use and Earlier Onset of Psychosis, Psychiatry, (2011).

“There is little doubt about the existence of an association between substance use and psychotic illness. National mental health surveys have repeatedly found more substance use, especially cannabis use, among people with a diagnosis of a psychotic disorder. There is a high prevalence of substance use among individuals treated in mental health settings,6 and patients with schizophrenia are more likely to use substances than members of the wider community. Prospective birth cohort and population studies suggest that the association between cannabis use and later psychosis might be causal, a conclusion supported by studies showing that cannabis use is associated with an earlier age at onset of psychotic disorders, particularly schizophrenia.”

The Impact of Marijuana Policies on Youth: Clinical, Research, and Legal Update, American Academy of Pediatrics, (2015).

“The adverse effects of marijuana have been well documented, and studies have demonstrated the potential negative consequences of short- and long-term recreational use of marijuana in adolescents. These consequences include impaired short- term memory and decreased concentration, attention span, and problem solving, which clearly interfere with learning. Alterations in motor control, coordination, judgment, reaction time, and tracking ability have also been documented; these may contribute to unintentional deaths and injuries among adolescents (especially those associated with motor vehicles if adolescents drive while intoxicated by marijuana).

Negative health effects on lung function associated with smoking marijuana have also been documented, and studies linking marijuana use with higher rates of psychosis in patients with a predisposition to schizophrenia have recently been published, raising concerns about longer-term psychiatric effects. New research has also demonstrated that the adolescent brain, particularly the prefrontal cortex areas controlling judgment and decision-making, is not fully developed until the mid-20s, raising questions about how any substance use may affect the developing brain. Research has shown that the younger an adolescent begins using drugs, including marijuana, the more likely it is that drug dependence or addiction will develop in adulthood. A recent analysis of 4 large epidemiologic trials found that marijuana use during adolescence is associated with reductions in the odds of high school completion and degree attainment and increases in the use of other illicit drugs and suicide attempts in a dose-dependent fashion that suggests that marijuana use is causative.”

American Academy of Pediatrics Reaffirms Opposition to Legalizing Marijuana for Recreational or Medical Use, American Academy of Pediatrics, (2015).

The American Academy of Pediatrics () reaffirms its opposition to legalizing marijuana, citing the potential harms to children and adolescents.

Half-Baked — The Retail Promotion of Marijuana Edibles, New England Journal of Medicine, (2015).

“Edibles that resemble sugary snacks pose several clear risks. One is over-intoxication….At high doses, can produce serious anxiety attacks and psychotic-like symptoms. This problem is augmented by differences in the pharmacokinetic and metabolic effects of marijuana when it is ingested rather than smoked. In addition, case reports document respiratory insufficiency in young children who have ingested marijuana.”

Adverse Health Effects of Marijuana Use, New England Journal of Medicine, (2014).

A review of the current state of the science related to the adverse health effects of the recreational use of marijuana, focusing on those areas for which the evidence is strongest.

A New England Journal of Medicine Article about Marijuana, Psychology Today, (2014) summarizes the adverse health effects as published in the New England Journal of Medicine.

UN: cannabis law changes pose ‘very grave danger to public health’, The Guardian, (2014).

United Nations International Narcotics Control Board warns of “very grave danger” from legalizing marijuana.

Damaging Effects of Cannabis Use on the Lungs, Advances in Experimental Medicine and Biology, (2016).

“Cannabis smoke affects the lungs similarly to tobacco smoke, causing symptoms such as increased cough, sputum, and hyperinflation. It can also cause serious lung diseases with increasing years of use. Cannabis can weaken the immune system, leading to pneumonia. Smoking cannabis has been further linked with symptoms of chronic bronchitis. Heavy use of cannabis on its own can cause airway obstruction. Based on immuno-histopathological and epidemiological evidence, smoking cannabis poses a potential risk for developing lung cancer.”

Marijuana use in adolescence may increase risk for psychotic symptoms, American Journal of Psychiatry, (2016).

Regular marijuana use significantly increased risk for subclinical psychotic symptoms, particularly paranoia and hallucinations, among adolescent males.

Heavy, persistent pot use linked to economic, social problems at midlife: Study finds marijuana not ‘safer’ than alcohol, Clinical Psychological Science, (2016).

Science Daily’s review of a research study that followed children from birth up to age 38 has found that people who smoked cannabis four or more days of the week over many years ended up in a lower social class than their parents, with lower-paying, less skilled and less prestigious jobs than those who were not regular cannabis smokers. These regular and persistent users also experienced more financial, work-related and relationship difficulties, which worsened as the number of years of regular cannabis use progressed.

The impact of adolescent exposure to medical marijuana laws on high school completion, college enrolment and college degree completion, Drug & Alcohol Dependence, (2016).

States that have legalized marijuana find an association with higher 12th grade drop out rates, lessened college attainment, and increases in daily smoking. Further, there is a dose/response relationship between adverse impact and years of increased exposure under legalization.

Early marijuana use associated with abnormal brain function, lower IQ, Lawson Health Research Institute, (2016).

“Previous studies have suggested that frequent marijuana users, especially those who begin at a young age, are at a higher risk for cognitive dysfunction and psychiatric illness, including depression, bipolar disorder and schizophrenia.”

Marijuana Users Have Abnormal Brain Structure and Poor Memory, Northwestern Medicine, (2013).

“Teens who were heavy marijuana users — smoking it daily for about three years — had abnormal changes in their brain structures related to working memory and performed poorly on memory tasks, reports a new Northwestern Medicine® study. A poor working memory predicts poor academic performance and everyday functioning. The brain abnormalities and memory problems were observed during the individuals’ early twenties, two years after they stopped smoking marijuana, which could indicate the long-term effects of chronic use. Memory-related structures in their brains appeared to shrink and collapse inward, possibly reflecting a decrease in neurons.”

Young adult sequelae of adolescent cannabis use: an integrative analysis, Lancet Psychiatry, (2014).

Adolescent cannabis use has adverse consequences in young adulthood:

“We recorded clear and consistent associations and dose-response relations between the frequency of adolescent cannabis use and all adverse young adult outcomes. After covariate adjustment, compared with individuals who had never used cannabis, those who were daily users before age 17 years had clear reductions in the odds of high-school completion…and degree attainment…, and substantially increased odds of later cannabis dependence…, use of other illicit drugs…, and suicide attempt.”

Traditional marijuana, high-potency cannabis and synthetic cannabinoids: increasing risk for psychosis, World Psychiatry, (2016).

“Evidence that [THC] is a component cause of psychosis is now sufficient for public health messages outlining the risk, especially of regular use of high-potency cannabis and synthetic cannabinoids.”

Monitoring Marijuana Use in the United States; Challenges in an Evolving Environment, (2016).

“Use of marijuana or any of its components, especially in younger populations, is associated with an increased risk of certain adverse health effects, such as problems with memory, attention, and learning, that can lead to poor school performance and reduced educational and career attainment, early-onset psychotic symptoms in those at elevated risk, addiction in some users, and altered brain development.”

Marijuana use and use disorders in adults in the , 2002–14: analysis of annual cross-sectional surveys, Lancet Psychiatry, (2016).

Commenting on this study to the Associated Press, Dr. Wilson Compton, Deputy Director of said, “if anything, science has shown an increasing risk that we weren’t as aware of years ago.” He added that other research has increasingly linked marijuana use to mental impairment, and early, heavy use by people with certain genes to increased risk of developing

psychosis.

Prenatal marijuana exposure, age of marijuana initiation, and the development of psychotic symptoms in young adults, Psychological Medicine, (2015).

Prenatal marijuana exposure linked to bad childhood outcomes; if effect is further “mediated” through early onset marijuana use, strong association with negative adult outcomes, such as arrest, low educational performance, unemployment.

One in six children hospitalized for lung inflammation positive for marijuana exposure, American Academy of Pediatrics, (2016).

Colorado: 16% of exposed children admitted to hospital for lung inflammation tested positive for MJ metabolite.

Cannabis use increases risk of premature death, American Journal of Psychiatry, (2016).

Cannabis use in youth increases the risk of early death.

Scientists Call for Action Amidst Mental Health Concerns, The Guardian, (2016).

“Most research on cannabis, particularly the major studies that have informed policy, are based on older low-potency cannabis resin.” According to Sir Robin Murray, professor of psychiatric research at King’s College London: “It’s not sensible to wait for absolute proof that cannabis is a component cause of psychosis. There’s already ample evidence to warrant public education around the risks of heavy use of cannabis, particularly the high-potency varieties. For many reasons, we should have public warnings.””

Marijuana use in adolescence may increase risk for psychotic symptoms, American Journal of Psychiatry, (2016).

Chronic marijuana use in adolescent boys increases risk of developing persistent subclinical psychotic symptoms (hallucinations, paranoia). “For each year adolescent boys engaged in regular marijuana use … subsequent symptoms increased by 21% and… paranoia or hallucinations increased by 133% and 92%, respectively. This effect persisted even when [study] participants stopped using marijuana for 1 year.”

Heavy, persistent pot use linked to economic, social problems at midlife, Clinical Psychological Science, (2016).

“Regular long-term [marijuana] users also had more antisocial behaviors at work, such as stealing money or lying to get a job, and experienced more relationship problems, such as intimate partner violence and controlling abuse.”

Effects of Cannabis Use on Human Behavior, Including Cognition, Motivation, and Psychosis: A Review, Psychiatry, (2016).

This longitudinal study documented adolescent-onset (but not adult-onset) persistent cannabis users showed neuropsychological decline ages 13 to 38 years. “Longitudinal investigations show a consistent association between adolescent cannabis use and psychosis. Cannabis use is considered a preventable risk factor for psychosis… strong

physiological and epidemiological evidence supporting a mechanistic link between cannabis use and schizophrenia… raise[s] the possibility that our current, limited knowledge may only apply to the ways in which the drug was used in the past.”

Marijuana use disorder is common and often untreated, National Institute of Health/NESARC, (2016).

“People with marijuana use disorder are vulnerable to other mental health disorders … onset of the disorder was found to peak during late adolescence. …People with marijuana use disorder…experience considerable mental disability. …Previous studies have found that such disabilities persist even after remission of marijuana use disorder.”

The health and social effects of nonmedical cannabis use, World Health Organization, (2016).

“There is a worrying increasing demand for treatment for cannabis use disorders and associated health conditions in high- and middle-income countries, and there has been increased attention to the public health impacts of cannabis use and related disorders in international policy dialogues.”

AKT1 genotype moderates the acute psychotomimetic effects of naturalistically smoked cannabis in young cannabis smokers, Translational Psychiatry, (2016).

“Smoking cannabis daily doubles an individual’s risk of developing a psychotic disorder, yet indicators of specific vulnerability have proved largely elusive. Genetic variation is one potential risk modifier.”

What’s That Word? Marijuana May Affect Verbal Memory, Internal Medicine, (2016).

Researchers found a “dose-dependent independent association between cumulative lifetime exposure to marijuana and worsening verbal memory in middle age.”

Adolescent Cannabinoid Exposure Induces a Persistent Sub-Cortical Hyper-Dopaminergic State and Associated Molecular Adaptations in the Prefrontal Cortex., Cerebral Cortex, (2016).

“We report that adolescent, but not adult, exposure induces long-term neuropsychiatric-like phenotypes similar to those observed in clinical populations…. findings demonstrate a profound dissociation in relative risk profiles for adolescent versus adulthood exposure to in terms of neuronal, behavioral, and molecular markers resembling neuropsychiatric pathology.”

Cannabis increases the noise in your brain, Biological Psychiatry, (2015).

“At doses roughly equivalent to half or a single joint, ∆9- produced psychosis-like effects and increased neural noise in humans. The dose-dependent and strong positive relationship between these two findings suggest that the psychosis-like effects of cannabis may be related to neural noise which disrupts the brain’s normal information processing activity.”

Marijuana Use: Detrimental to Youth, American College of Pediatricians, (2016).

“Marijuana is the leading illicit substance mentioned in adolescent emergency department admissions and autopsy reports, and is considered one of the major contributing factors leading to violent deaths and accidents among adolescents.”

Chronic Adolescent Marijuana Use as a Risk Factor for Physical and Mental Health Problems in Young Adult Men, Psychology of Addictive Behaviors, (2015).

Evidence suggests that youth who use marijuana heavily during adolescence may be particularly prone to health problems in later adulthood (e.g., respiratory illnesses, psychotic symptoms).

Developmental Trajectories of Marijuana Use among Men, Journal of Research in Crime and Delinquency, (2015).

“Young men who engage in chronic marijuana use from adolescence into their 20s are at increased risk for exhibiting psychopathic features, dealing drugs, and enduring drug-related legal problems in their mid-30s.”

Appraising the Risks of Reefer Madness, Cerebrum, (2015).

“Cannabis is generally accepted as a cause of schizophrenia (though less so in North America, where this topic has received little attention),” notes Dr. R. Murray, an Oxford University Professor of Psychiatry.

Prenatal exposure to cannabinoids evokes long-lasting functional alterations by targeting CB1 receptors on developing cortical neurons, Adán de Salas-Quiroga, (2015).

“Prenatal exposure to cannabinoids evokes long-lasting functional alterations by targeting CB1 receptors on developing cortical neurons.” “This study demonstrates that remarkable detrimental consequences of embryonic exposure on adult-brain function, which are evident long after withdrawal, are solely due to the impact of on CB1 receptors located on developing cortical neurons.” Embryonic exposure increased seizures in adulthood and the consequences of prenatal were lifelong; even though the cannabinoid receptors after withdrawal appear normal, there is an apparent impact on connectivity.

Association Between Use of Marijuana and Male Reproductive Hormones and Semen Quality: A Study Among 1,215 Healthy Young Men, American Journal of Epidemiology, (2015).

“Regular marijuana smoking more than once per week was associated with a 28% … lower sperm concentration and a 29% … lower total sperm count after adjustment for confounders.”

Is Marijuana Use Associated With Health Promotion Behaviors Among College Students? Health-Promoting and Health-Risk Behaviors Among Students Identified Through Screening in a University Student Health Services Center, Journal of Drug Issues, (2015).

“Results showed marijuana users were more likely to use a variety of substances and engage in hazardous drinking than non-users.”

Psychosocial sequelae of cannabis use and implications for policy: findings from the Christchurch Health and Development Study, Social Psychiatry and Psychiatric Epidemiology, (2015).

“Findings…suggest that individuals who use cannabis regularly, or who begin using cannabis at earlier ages, are at increased risk of a range of adverse outcomes, including: lower levels of educational attainment; welfare dependence and unemployment; using other, more dangerous illicit drugs; and psychotic symptomatology.”

Young brains on cannabis: It’s time to clear the smoke, Clinical Pharmacology and Therapeutics, (2015).

“There is certainly cause for concern about the amount and frequency of cannabis use among youth….Recent evidence shows that early and frequent use of cannabis has been linked with deficits in short-term cognitive functioning, reduced IQ, impaired school performance, and increased risk of leaving school early – all of which can have significant consequences on a young person’s life trajectory….Heavy cannabis use in adolescence is also a risk factor for psychosis….Youth aged 15-24 spent the largest number of days in a hospital for a primary diagnosis of mental and behavioral disorders due to the use of cannabinoids.”

Association Between Lifetime Marijuana Use and Cognitive Function in Middle Age and Long-term Marijuana Use and Cognitive Impairment in Middle Age, Internal Medicine, (2016).

“These studies have generally shown reduced activity in those with long-term marijuana use in brain regions involved in memory and attention, as well as structural changes in the hippocampus, prefrontal cortex, and cerebellum.”

Denial of Petition To Initiate Proceedings To Reschedule Marijuana, Federal Register/DEA Review of “Scientific Evidence of [Marijuana’s] Pharmacological Effects, If Known”, (2016).

“Individuals with a diagnosis of marijuana misuse or dependence who…initiated marijuana use before the age of 15 years, showed deficits in performance on tasks assessing sustained attention, impulse control, and general executive functioning compared to non-using controls. These deficits were not seen in individuals who initiated marijuana use after the age of 15 years…. Additionally, in a prospective longitudinal birth cohort study of 1,037 individuals, marijuana dependence or chronic marijuana use was associated with a decrease in IQ and general neuropsychological performance compared to pre-marijuana exposure levels in adolescent onset users.

The decline in adolescent-onset users’ IQ persisted even after reduction or abstinence of marijuana use for at least 1 year…. The deficits in IQ seen in adolescent-onset users increased with the amount of marijuana used. Moreover, when comparing scores for measures of IQ, immediate memory, delayed memory, and information-processing speeds to pre-drug-use levels, the current, heavy, chronic marijuana users showed deficits in all three measures.”

The health and social effects of nonmedical cannabis use, World Health Organization, (2016).

“Cannabis is globally the most commonly used psychoactive substance under international control. In 2013, an estimated 181.8 million people aged 15−64 years used cannabis for nonmedical purposes globally (uncertainty estimates 128.5–232.1 million) (UNODC, 2015). There is a worrying increasing demand for treatment for cannabis use disorders and associated health conditions in high- and middle-income countries, and there has been increased attention to the public health impacts of cannabis use and related disorders in international policy dialogues.[…] This publication builds on contributions from a broad range of experts and researchers from different parts of the world. It aims to present the current knowledge on the impact of nonmedical cannabis use on health.”

Source:  https://hudson.org/research/12975-marijuana-threat-assessment-part-one-recent-evidence-for-health-risks-of-marijuana-use

October 19, 2016 2.02am BST

Currently 25 states and the District of Columbia have medical cannabis programs. On Nov. 8, Arkansas, Florida and North Dakota will vote on medical cannabis ballot initiatives, while Montana will vote on repealing limitations in its existing law.

We have no political position on cannabis legalization. We study the cannabis plant, also known as marijuana, and its related chemical compounds. Despite claims that cannabis or its extracts relieve all sorts of maladies, the research has been sparse and the results mixed. At the moment, we just don’t know enough about cannabis or its elements to judge how effective it is as a medicine.

What does the available research suggest about medical cannabis, and why do we know so little about it?

What are researchers studying?

While some researchers are investigating smoked or vaporized cannabis most are looking at specific cannabis compounds, called cannabinoids.

From a research standpoint, cannabis is considered a “dirty” drug because it contains hundreds of compounds with poorly understood effects. That’s why researchers tend to focus on just one cannabinoid at a time. Only two plant-based cannabinoids, THC and cannabidiol, have been studied extensively, but there could be others with medical benefits that we don’t know about yet. THC is the main active component of cannabis. It activates cannabinoid receptors in the brain, causing the “high” associated with cannabis, as well as in the liver, and other parts of the body. The only FDA-approved cannabinoids that doctors can legally prescribe are both lab produced drugs similar to THC. They are prescribed to increase appetite and prevent wasting caused by cancer or AIDS.

Cannabidiol (also called CBD), on the other hand, doesn’t interact with cannabinoid receptors. It doesn’t cause a high. Seventeen states have passed laws allowing access to CBD for people with certain medical conditions.

Our bodies also produce cannabinoids, called endocannabinoids. Researchers are creating new drugs that alter their function, to better understand how cannabinoid receptors work. The goal of these studies is to discover treatments that can use the body’s own cannabinoids to treat conditions such as chronic pain and epilepsy, instead of using cannabis itself.

Cannabis is promoted as a treatment for many medical conditions. We’ll take a look at two, chronic pain and epilepsy, to illustrate what we actually know about its medical benefits.

Is it a chronic pain treatment? Research suggests that some people with chronic pain self-medicate with cannabis. However, there is limited human research on whether cannabis or cannabinoids effectively reduce chronic pain. Research in people suggest that certain conditions, such as chronic pain caused by nerve injury, may respond to smoked or vaporized cannabis, as well as an FDA-approved THC drug. But, most of these studies rely on subjective self-reported pain ratings, a significant limitation. Only a few controlled clinical trials have been run, so we can’t yet conclude whether cannabis is an effective pain treatment.

An alternative research approach focuses on drug combination therapies, where an experimental cannabinoid drug is combined with an existing drug. For instance, a recent study in mice combined a low dose of a THC-like drug with an aspirin-like drug. The combination blocked nerve-related pain better than either drug alone.

In theory, the advantage to combination drug therapies is that less of each drug is needed, and side effects are reduced. In addition, some people may respond better to one drug ingredient than the other, so the drug combination may work for more people. Similar studies have not yet been run in people.

Well-designed epilepsy studies are badly needed Despite some sensational news stories and widespread speculation on the internet, the use of cannabis to reduce epileptic seizures is supported more by research in rodents than in people. In people the evidence is much less clear. There are many anecdotes and surveys about the positive effects of cannabis flowers or extracts for treating epilepsy. But these aren’t the same thing as well-controlled clinical trials, which can tell us which types of seizure, if any, respond positively to cannabinoids and give us stronger predictions about how most people respond.

While CBD has gained interest as a potential treatment for seizures in people, the physiological link between the two is unknown. As with chronic pain, the few clinical studies have been done included very few patients. Studies of larger groups of people can tell us whether only some patients respond positively to CBD.

We also need to know more about the cannabinoid receptors in the brain and body, what systems they regulate, and how they could be influenced by CBD. For instance, CBD may interact with anti-epileptic drugs in ways we are still learning about. It may also have different effects in a developing brain than

in an adult brain. Caution is particularly urged when seeking to medicate children with CBD or cannabis products.

Cannabis research is hard

Well-designed studies are the most effective way for us to understand what medical benefits cannabis may have. But research on cannabis or cannabinoids is particularly difficult. Cannabis and its related compounds, THC and CBD, are on Schedule I of the Controlled Substances Act, which is for drugs with “no currently accepted medical use and a high potential for abuse” and includes Ecstasy and heroin.

In order to study cannabis, a researcher must first request permission at the state and federal level. This is followed by a lengthy federal review process involving inspections to ensure high security and detailed record-keeping.

In our labs, even the very small amounts of cannabinoids we need to conduct research in mice are highly scrutinized. This regulatory burden discourages many researchers.

Designing studies can also be a challenge. Many are based on users’ memories of their symptoms and how much cannabis they use. Bias is a limitation of any study that includes self-reports. Furthermore, laboratory-based studies usually include only moderate to heavy users, who are likely to have formed some tolerance to marijuana’s effects and may not reflect the general population. These studies are also limited by using whole cannabis, which contains many cannabinoids, most of which are poorly understood.

Placebo trials can be a challenge because the euphoria associated with cannabis makes it easy to identify, especially at high THC doses. People know when they are high. Another type of bias, called expectancy bias, is a particular issue with cannabis research. This is the idea that we tend to experience what we expect, based on our previous knowledge. For example, people report feeling more alert after drinking what they are told is regular coffee, even if it is actually decaffeinated. Similarly, research participants may report pain relief after ingesting cannabis, because they believe that cannabis relieves pain. The best way to overcome expectancy effects is with a balanced placebo design, in which participants are told that they are taking a placebo or varying cannabis dose, regardless of what they actually receive.

Studies should also include objective, biological measures, such as blood levels of THC or CBD, or physiological and sensory measures routinely used in other areas of biomedical research. At the moment, few do this, prioritizing self-reported measures instead.

Cannabis isn’t without risks

Abuse potential is a concern with any drug that affects the brain, and cannabinoids are no exception. Cannabis is somewhat similar to tobacco, in that some people have great difficulty quitting. And like tobacco, cannabis is a natural product that has been selectively bred to have strong effects on the brain and is not without risk. Although many cannabis users are able to stop using the drug without problem, 2-6 percent of users have difficulty quitting. Repeated use, despite the desire to decrease or stop using, is known as cannabis use disorder.

As more states more states pass medical cannabis or recreational cannabis laws, the number of people with some degree of cannabis use disorder is also likely to increase.

It is too soon to say for certain that the potential benefits of cannabis outweigh the risks. But with restrictions to cannabis (and cannabidiol) loosening at the state level, research is badly needed to get the facts in order.

Source: https://theconversation.com/what-do-we-know-about-marijuanas-medical-benefits-two-experts-explain-the-evidence-64200   Oct.2016

Dramatic acceleration of reproductive aging, contraction of biochemical fecundity and healthspan-lifespan implications of opioid-induced endocrinopathy—FSH/LH ratio and other interrelationships

Highlights

· The classically described opioid related female reproductive endocrinopathy including central dysregulation and peripheral ovarian resistance is confirmed.

· Advance of the age of the inversion of the ratio of FSH/LH by 18.06 years from 46.26+4.76 to 28.06+9.36 is demonstrated by statistical modelling

· This important finding is likely related to the sexual differential in opioid pathophysiology in which females are significantly disadvantaged.

· Statistical modelling showed that many elements of the reproductive endocrinopathy had a non-linear relationship to chronological age, including squared, cubed and quartic functions of age suggesting a feed-forward bidirectional relationship with age and the ageing process.

· These findings have major implications for the incidence of morbidity and mortality events, and for frequently recommended treatments such as indefinite opioid agonist replacement therapies for opioid dependence.

Abstract

Whilst disturbances of female reproductive hormones and function are commonplace in opioid dependence, their pathophysiological interrelationships are not well understood. Hormonal levels in females were compared in 77 opioid dependent patients (ODP) and 148 medical controls (MC) including 205 and 364 repeat studies. Significant changes in FSH, LH, oestradiol, testosterone and SBG were noted including power functions with age.

The FSH/LH was lower in ODP (P=0.0150) and the ratio inversion point occurred at 28.06+9.36 v. 46.26+4.76 years, implying a 58% reduction in fertility duration. FSH has been shown to induce ovarian failure and GnRH (controlling LH and FSH) has been shown to regulate longevity systemically. This implies that, far from being benign, these findings explicate the adverse experience of female compared to male ODP, exacerbate opioid-dependent aging amongst females, and informs the care of opioid dependent women, particularly relating to the choice, dose and duration of agonist or antagonist therapy.

Introduction

Rates of morbidity and mortality from medical and illicit opioid dependence are rising in manyparts of the world, with the proportion of female consumers increasing [1-3].

Accordingly, increasing attention is not only being paid to the effects of chronic opiate exposure on traditional areas of women’s health such as pregnancy, lactation and contraception, but also domestic violence, child abuse, manner of initiation into opiate use, time to from first use to dependence and physical and mental health morbidity [4-9].

Reports from this centre [10] and elsewhere [11, 12] indicate that the health of opioid dependent women is significantly worse than that of non-opiate using women or their male counterparts.

It has been shown that the hypothalamopituitary-gonadal (HPG) axis is coordinated and integrated particularly by the triple positive Kisspeptin-Neurokinin B-Dynorphin (KNDy) cells of the lateral hypothalamus [13, 14]; that cytokines have a powerful impact on brain structure and function [15, 16]; and HPG and hypothalamic function [17]; that the hypothalamus integrates and controls mammalian lifespan via gonadotrophin releasing hormone (GnRH) [18]; and that sexual reproductive and fecundity factors are powerful predictors of longevity [19, 20].

This suggests that disruption of these integrated systems through opiate use would have a profound pathophysiological impact that extends beyond gynaecological, endocrine or addiction medicine. While different gender associated health outcomes are, in part, attributed to different sex hormones or ratios, more recent data of profound genetic [21], immunological [21-25] and epigenetic [26] gender differences imply that the total aetiological “palette” of factors with which the hormonal milieu bi-directionally interacts may be significantly richer and more complex than has previously been appreciated.

Reduced fertility, impaired lactation, and aberrant, late and scanty menses are all well described in the literature relating to female opioid dependent patients [27-29]. Premature ovarian failure may also be part of the picture. Osteoporosis and osteopaenia are also known to be common in male and female opioid dependent patients (30,31), and impaired bone homeostasis is known to be related to both hypogonadal and hypothalamic failure and immune stimulation (24,29).

Of particular interest hypothalamic GnRH [18] and FSH [30] have recently been causally implicated in reduced mammalian lifespan, and oocyte depletion and ovarian failure respectively. The hypothalamic GnRH pulse generator in the arcuate nucleus is known to be the master regulator of both commencement of menstrual cycles at menarche and the cyclicity of the cycles once established [31, 32]. Age at menarche is linked with lifespan, cardiovascular disorders, type 2 diabetes and breast cancer [31]. Its activity is governed by nuclear hormone (estrogen, progesterone, thyroid hormone and vitamin D) signalling, by many genes of the δ- aminobutyric acid B receptor (GABABR) 2 system, by nutritional signals including the leptin receptor, histone and polycomb silencing complex demethylation patterns and steroidal biogenesis pathways amongst others [31]. Opioids have been shown to be directly suppressive of GnRH release both directly [33] and via their effects in elevating prolactin [27, 28].

Indeed the proopiomelanocortin cells of the arcuate nucleus are physiological negative regulators of the GnRH pacemaker cells [33]. Moreover a direct effect of oestradiol on telomerase expression in human stem cells has been demonstrated [34]. Hence multiple interacting mechanistic pathways exist by which opioids can interact with nutritional and metabolicfunction and reproductive hormonal status.

Thus while it has long been recognized that systemic health factors impact upon a woman’s reproductive fitness, these considerations imply that HPG physiology may itself be a sensitive – if complex – readout of the female hypothalamic function. Female HPG factors may integrate and provide an output of systemic health, and thereby formulate a prospective predictor of longevity and thus health-based morbidity and mortality [18, 35, 36].

For these reasons this study reviewed and compared female reproductive hormones of opioid dependent and general medical controls with particular attention to FSH, LH and their relationship. Other key ratios of physiological significance are also described.

Methods

Patient Selection As hepatitis C serology is only performed in this clinic on drug dependent patients this test is a surrogate marker for the drug dependent state. Patients were therefore assigned to either the medical control group or the drug dependent group based upon whether or not they had had hepatitis C serology performed.

The analysis included results from all patients for whom pathology was requested. Two patients who were pregnant were excluded from the analysis. The age range was restricted to 15-50 years in view of the dramatic changes in the hormonal milieu in females in the reproductive age group compared to other periods ofa woman’s life. This is also the period in which the majority of addiction occurs.  Blood tests were taken in the period 1995-2015 as clinically indicated for patient care in the course of their routine medical care.

Pathology Analysis.

All pathology was performed by Queensland Medical Laboratory (QML) according to National Association of Testing Authorities Australia (NATA) accredited methods to the Australian Laboratory standard AS-15189. QML is accredited both with NATA and to the international clinical laboratory standard ISO 9001. The Free Androgen Index (FAI) was obtained from the laboratory and is defined as 100x Total Testosterone / Sex Hormone Binding Globulin (SBG). The Free Estradiol Index (FEI) was defined similarly as 100x Total Estradiol / Sex Hormone Binding Globulin [37]. Other ratios which were specifically defined and studied include the FSH/LH, LH/Testosterone, LH/Estradiol and FSH/ Progesterone indices.

Statistics.

Pathology data was downloaded as an Excel comma separated file (csv file) from QML and re-formatted as a Microsoft Excel worksheet. Categorical data were compared in EpiInfo 7.1.4.0 from Centres for Disease control in Atlanta Georgia, USA. Bivariate statistics were compared by categories in Statistica 7.1 from Statsoft, Oklahoma, USA. All t-tests were two tailed. “R” version 3.0.1 was downloaded from the University of Melbourne Central “R” Archive Network (CRAN) mirror. Continuous data was compared in “R”. Continuous data was log transformed to satisfy normality assumptions, as indicated by the Shapiro test. Linear regression was performed in “R”. Graphs were drawn using ggplot2 in “R”. Loess curves of best fit were drawn as localized polynomials. Linear regression was performed by the classicalmethod with deletion of the least significant term until only significant terms remained.

In view of the fluctuating levels of sex hormones across the lifespan, polynomial models in age were fitted as suggested by the form of the graphical loess curves. Final models for analysis were chosen based on an Analysis of Variance (Anova) comparison of final polynomial models for each dependent variable, as indicated in the text. Special interest centred on the log (FSH/LH) ratio. As explained in the text the points at which it crossed zero in each group were of particular interest. These points were estimated based on Fieller’s theorem, as were the associated confidence intervals. P<0.05 was considered significant.

Ethics. Ethical approval for this study was given by the Human Research Ethics Committee (HREC) of the Southcity Medical Centre (SMC). The SMC HREC has been accredited by the National Health and Medical Research Centre (NHMRC). The conduct of this study complied with the Declaration of Helsinki.

Results

753 opioid dependent patients (ODP’s) and 1867 medical control (MC) patients were  compared. All patients were in the age range 15-50 years. The mean ages in the two groups were 31.42+0.27 (mean+SEM) and 30.34+0.22 years respectively (Student’s t = 2.96,df =1727, P = 0.0020). Their clinical pathology was sampled on 1360 and 4310 occasions. All patients were female. In seven cases their group assignment changed based on their drug use dependency status which changed over the course of the study.

Since this data is derived from our clinical pathology no other demographic or drug use data is available. Drug use and demographic data for this cohort has previously been presented [38- 41]. Similarly no menstrual or contraceptive data is available. Table 1 shows a bivariate comparison of the two groups. The data presented relates only to the first occasion on which each patient was studied. The data are presented by category.

Significant differences are noted between the two groups on metabolic, hepatic, immune and infectious parameters, and on the two hormonal parameters oestradiol and the sex hormone binding globulin SBG. SBG is produced from the liver and is not usually classified as a hormone, but many aspects of its function resemble hormonal activity since its level and binding characteristics and subtypes determine the hormonal availability particularly of oestradiol and testosterone to the tissues. It’s level is known to rise in hepatic dysfunction [42,43]. It is therefore considered as a hormone for the purposes of this analysis. This table also

presents the sample sizes of the different groups on the first occasion they were analyzed and

in the cross-sectional dataset. As opioids are known to impact metabolic, immune and hepatic

function [44, 45] these various parameters are reported and show many significant differences.

The sample size in the longitudinal dataset is shown in Supplementary Table 1.

Figure 1 presents the hormonal levels by age. The rise of the gonadotrophins LH and FSH, the decline of the sex hormones oestradiol, progesterone and testosterone with age, is well known. SBG is also noted to fall with age. It is noted that all the figures show the changes up to age 60 years, whilst the statistical analysis is limited to changes occurring less than age 50 years.

This allows the changes in the data trend lines to be shown graphically, but allows the analysis to be conducted without the confounding effect of the dramatic hormonal changes which occur in females as they enter their sixth decade of life. Supplementary Figure 1 shows the same hormones over time. Figure 2 shows various selected hormone ratios as a function of chronologic age. Interestingly the FAI and FEI both appear lower throughout life, apparently due to the higher SBG noted in Figure 1.

The relationship of LH/estradiol, FSH/Progesterone and LH/testosterone, which are all

physiologically meaningful, is shown. Supplementary Figure 2 shows these ratio relationships over time.

Figure 3 displays the mean log ratios between the hormones and ratios in the opioid dependent group to that in the opioid naive group. The figure shows that SBG is elevated the most, and LH is depressed the most severely in ODP. Similarly the FSH/LH ratio is most elevated whilst the LH/Estradiol ratio is most depressed. The presentation in this manner allows the direct and rapid comparison of the various changes across the spectrum of parameters examined.

Table 2 summarizes the results from mixed effects repeated measures linear regressions in which terms for the addictive status were significant. The first column lists the biological parameter of interest. The second column gives the form of the model. The third column gives the statistical parameter measured. The remainder of the table lists the parameter and model values respectively. One notes that progesterone, LH/estradiol and LH/Testosterone are missing from the table, as the optimal model for these contained no significant term in addictive status. One will note that the higher order design of the optimal model chosen in this table closely parallels the form of the curves in Figures 1and 2. This Table emphasizes the polynomial relationship of these hormonal parameters with age.

Table 3 is a statistical technical table which formally presents a concise extract from Anova analyses of model comparisons which lead to the choice of model design in Table 2. Naturally it would have been too cumbersome to present all the model comparisons, so typically the linear model is compared with the best or next best model determined by Anova. This Table emphasizes that models polynomial in age account for the variance in the data very significantly better than simple linear models.

The serum prolactin levels were not different between the two groups considered either by chronological age or by time (data not shown). Interestingly the FSH and LH appear to have a very different relationship, even when plotted as logarithms in Figure 1. This is of particular interest, as the FSH is normally lower than the LH in the reproductive years, but the relationship reverses premenopausally and in the postmenopause. This crossover point is therefore of particular biochemical and endocrinologic interest. We then returned to the fascinating subject of the point at which the log(FSH/LH) ratio became equal to zero in Figure 1. Clearly a log(FSH/LH) = 0 has a similar physiological meaning to FSH/LH = 1. It was possible to estimate this point using Fieller’s theorem.

The estimates given for the ODP was 28.06+9.36 years, and for the medical controls 46.26+4.76 years. Clearly this is a truncation of this measure of the perimenopause by 18.20 years. If one assumes a menarche occurring at 15 years [46], this represents a compression of this measure of hormonal fertility from 31.26 years in MC patients to 13.06 years in ODP, a 58.2% reduction.

Since liver disease is known to elevate both estrogen and SBG it may be considered that the high rates of liver disease in this population were significant confounding effects for the primary comparison described in this study. Importantly hepatitic inflammation is known to elevate both estradiol and SBG [27, 32] so that these hepatofugal effects on their relative relationship, and thus their effect on the free circulating estrogen is uncertain. These confounding factors were therefore evaluated formally. By comparing controls with opioid dependent patients who were both infected and uninfected with hepatotrophic viridae the effect of drug dependency alone can be isolated from a concomitant effect of hepatic inflammation.

Supplementary Figures 3-5 show the effect of seropositivity for HbsAg (Hepatitis B surface antigen) , HBcAb (Hepatitis B core antibody) and HCV (Hepatitis C virus) on the estradiol, SBG, Free Estrogen Index (FEI) FSH, LH and FSH/LH ratio respectively. Patients were considered to be hepatitis C positive if the HCV PCR (Polymerase chain reaction) was positive or the HCV antibody was positive in the absence of a negative HCV PCR result. These results are shown in the Supplementary Figures. Three groups were considered – non hepatitic control patients, patients tested and found to be negative, and patients tested and found to be positive.

Formal statistical analysis of these data by selected hormonal parameters in mixed effects repeated measures models are shown in Supplementary Tables 2-4. In each case the medical control patients were used as statistical comparator controls for linear regression modeling which was undertaken in R. Only statistically significant results are listed in the Tables.

Figure 4 illustrates the effect of Hepatitis B or C seropositivity considered together on these hormones and their ratios, and Table 4 provides the applicable statistical analysis for log (FSH/LH) compared to the medical control group. These studies show that in uninfected opioid dependent patients estradiol is mildly elevated at trend level significance (P=0.08-0.09) except in the case of HBcAb where this elevation reaches significance (P=0.0135, Supplementary Table 2). Estradiol is further elevated by chronic viral hepatitis (all P<0.02). Our analysis shows that opioid dependency alone without chronic viral hepatitis (CVH) significantly elevates SBG (most P≤0.01), an elevation which is furthered by CVH (P≤0.001, Supplementary Table 3). However when these two indices are considered together as the (log) Free Estrogen Index these effects are mostly abrogated

(Supplementary Table 4).

Opioid dependency elevates the FSH and reduces LH so that the net effect of opioid dependency on the (log) FSH/LH ratio is to raise it in both CVH -infected and -uninfected opioid dependent patients. As shown graphically in the Figures and quantitated in Table 4, theeffect is actually more marked in uninfected ODP (most P≤0.002) in the case of Hepatitis B,and is highly statistically significant in both HCV -infected and -uninfected ODP patients.

Another way in which to compare the relationship between hepavirus infection and drug dependency status directly from our data is to include both factors as independent variables in models of our main parameter of interest. In such models the classical regression process of model reduction from initial to final model should either completely remove extraneous variables, or indicate their relative weights. Unsurprisingly this was not possible when addictive status and Hepatitis C status was considered concurrently, or when all hepaviridae were considered together with addictive status, as all such models both linear and quadratic for age failed to converge due to collinearity. However it was possible to compare HBsAg and addictive status together with age directly in mixed effects models of Estradiol, SBG, FEI and log (FSH/LH). Whilst models linear in age were functional in this analysis higher order models as suggested by Table 3 in general failed to converge (other than as shown in Supplementary Table 5). Detailed results for linear mixed effects models are presented in Supplementary Table 5 which shows that opioid dependency features in five terms in this table and HBsAg status is included in four terms with effect sizes broadly comparable. This result indicates that both addictive status and Hepatitis B virus infection together are statistically significant determinants of these parameters.

When models accounting for the variance of the log (FSH/LH) ratio were formally directly compared by Anova comparisons of mixed effects maximum likelihood models the addictive status was more highly predictive than the HbsAg serostatus. The addition of addictive status to age as dependent variables was more significant than the addition of HBsAg to age (AIC’s 1257.84 v 1274.49. Log Ratio = 14.65, P = 0.0001) and the addition of a term for HbsAg status did not significantly improve an additive model between age and addictive status (AIC’s 1259.22 v 1257.84, Log Ratio = 2.61, P=0.2703).

Overall these data show that whilst both HBV and HCV CVH elevate both estradiol and SBG,their rise is proportional so that when considered as the Free Estrogen Index there is little change seen in opioid dependence. This result implies that the biologically available level of oestradiol is unchanged by hepaviridae infection. However when one considers the gonadotrophins both CVH -infected and -uninfected opioid dependent patients display elevated FSH, depressed LH and therefore a markedly and highly significantly elevated FSH/LH ratio which is therefore independent of the CVH status. These data indicate therefore that particularly in the case of the gonadotrophins, the observed changes relate more to the opioid dependency than the chronic viral hepatitis infection as confirmed in the analysis of log(FSH/LH) when both addictive and infective independent variables are included as factors concurrently.

Discussion

These data confirm and extend previous data showing perturbation of reproductive hormonal axes in opioid dependence amongst females. Data indicate that opioid dependence is characterized by marked fluctuation from normal in the mean levels of several sex hormones and their key physiological ratios from 50% elevated to 50% reduced. A key factor in this is the increased SBG level which rises presumably due to hepatic stimulation which is known to occur in ODP related to cytokine stimulation and often infection with hepatotrophic viridae including Hepatitis B and C [42, 43]. Significant alterations in FSH, LH, estradiol, testosterone and SBG, and in the FAI, FEI, FSH/LH, LH/estradiol, and FSH/Progesterone ratio were demonstrated in sensitive models, mostly polynomial in chronological age.

Particularly interesting findings relate to the altered FSH/LH ratio.

Early in a young woman’s life the FSH is low and the LH generally higher. After the menopause the reverse situation applies, so that the crossover or equality point becomes a sensitive biochemical and endocrinologic marker of the premenopause. Because FSH has been shown to have an aetiological role in ovarian failure and therefore the decline in systemic health [30], this is a very important biochemical harbinger of systemic health and likely foreshadows healthspan.

Study data indicate the FSH/LH equality point for opioid dependent women is reached at 28.06+9.36 years as opposed to 46.26+4.76 in controls. This likely represents a severe reduction in this measure of the reproductive lifespan and optimal reproductive fitness from 31.26 years to 13.06 years (58.2% ). This in turn implies an increased incidence of premature ovarian failure in opioid dependence. None of these findings were simply explainable on the basis of co-existing hepatitic liver disease alone.

Earlier studies showing that altered gonadotrophin levels have a systemic effects contributing to longevity [18] and in particular the role of FSH in contributing causally to ovarian compromise [30], together with the well described impact of fertility and fecundity on lifespan and longevity [19, 20] implies in turn that the clearly demonstrated failure of physical health across all body systems [11] may in fact be related to systemically impaired health and indeed reduced healthspan. Healthspan is a term which refers to the period of life for which individuals maintain optimal health [47, 48].

Hence this dramatic alteration of reproductive fitness is likely to impact both the healthspan of women, and their lifespan or longevity as the rate of aging is known to accelerate dramatically after both the menopause and in the fifth decade (after the age of forty) when the FSH/LH ratio normally inverts. This is turn carries major implications for the type and duration of treatment for the illicit opiate user. For example whilst internationally most opioid dependent patients are maintained on methadone, an opioid agonist or buprenorphine, a partial agonist, however it may be that maintenance on an opioid antagonists such as naltrexone or nalmefene may re-awaken and reignite the HPG axis following extended chronic illicit opiate use [27, 28, 32, 49] and thereby repair and renovate the healthspan. Similarly most opiate agonist or partial agonist treatment regimes are usually recommended to be of indefinite duration. The principal aim of such treatment appears to be to minimize reduce crime and illicit opiate use, overdose related death, and spread of blood borne viral infection (i.e. HCV; HIV). However it would appear from exhaustive analyses [11] that such treatment comes at an inexorable cost of pan-systemic disease, potentially relating to allostasis in multiple systems [50, 51] and generalized derangement of health including dysmetabolism [52] and immune stimulation [35, 53] and ultimately immune exhaustion [54, 55].

It is of some interest that the OPD in this study have been shown elsewhere to be maintained upon a relatively low dose of buprenorphine with a mean of 6.98mg [10]. It is likely therefore that in cohorts managed more traditionally with high dose full agonists, these effects may be more profound. This heightens the concerns expressed at other points herein. The hormonal ratios chosen in this study were of physiological import, as LH controls estradiol and testosterone secretion, and FSH is a prime determinant of progesterone secretion. The importance of the FAI and the FEI relate to the free availability of physiologically active levels of androgen and estrogen respectively. The importance of the FSH/LH ratio as a sensitive endocrinological measure of the premenopause has been mentioned above.

Of particular concern is the repeated demonstration that the effects of opioid dependence may be more severe in female patients [10-12]. The present clear demonstration of the altered female hormonal milieu of opioid dependence implies that endocrine factors may be an important, if likely not the only factor in this heightened disease severity. Whilst this finding is clearly suggestive it cannot be regarded as demonstrating a necessarily causal relationship between hormonal dysregulation and heightened female sensitivity to opioid induced pathophysiology. Although this study did not show any differences in either the time- or age- dependent changes in serum prolactin levels by group, it is well established that long term opioid administration is associated with hyperprolactinaemia [27, 28, 32, 49]. Greying of the temporal hair is well known to be the sine qua non of human aging [56] and this key metric has previously been shown to be greatly advanced in opioid dependency [39].

It is fascinating therefore that both the cellular stress system mediated in all addictions by Activator Protein-1 (AP-1) and c-Jun terminal kinase (JNK) activity [57], together with the prolactin receptor (prlr) were recently demonstrated to be the most salient signalling transduction pathways of extrinsic pro-ageing signals to the stem cells of the hair bulge where they were integrated with cell-intrinsic epigenetic processes particularly Foxc1 status to regulate hair follicle stem cell aging and thus hair physiological status [58], which are clearly therefore important and powerful metrics of ageing in accelerated aging syndromes such as opioid dependency. Of particular interest is the clear demonstration in Tables 2 and 3 that many of these hormones and ratios are best modelled by non-linear functions polynomial in chronological age. This is a very important finding as it suggests not only that opioids effect hormonal function in a deleterious manner, but that a feed forward relationship is in operation. That is that opioids effect the hormonal status negatively, but this advance in biological-hormonal age then further exacerbates the reproductive ageing effects themselves. This is consistent with the effects of sexuality and fecundity on the ageing process itself as has been previously documented [19, 56].

The present study has a number of strengths and limitations. It is of significant size, and has both cross-sectional and longitudinal components. It uses advanced statistical polynomial repeated measures mixed effects modelling in conjunction with graphical and Anova model comparison analyses. Whilst the study is descriptive only and not mechanistically oriented, this observational framework is placed within a relatively sophisticated pathophysiological conceptual framework as a stimulus and springboard to future work. The shortcomings of this study include that it does not have drug use data included in it, and that hormonal and contraceptive details are not available. All of these features may be improved in future iterations or replications of this work. It is also noted that the mean ages of the two groups is significantly different.  Extensive use of linear regression techniques has been made in the analysis of this dataset to account for this.

In conclusion this observational study replicates and confirms previously noted reproductive endocrinopathies. However while earlier authors frequently discount the clinical significance of these findings it is likely that they contribute meaningfully both to the experience of females in opioid dependence, and also the heightened morbidity and organ specific mortality frequently experienced by OPD women. The dramatic reduction of the modelled FSH – LH age of equality from 46.26 to 28.06 years is of particular concern in signalling system-wide metabolic and reproductive dysfunction. The far reaching impact of these findings on immune [21], genetic [21] and epigenetic [26] and longevity factors implies that treatment type and agonist administration and duration are key concerns deserving of further close attention. The present findings emphasize concerns derived from other studies of the particular and remarkable sensitivity of females to long term opioid agonist therapies [10-12] and introduce further endocrinologic concerns in relation to the common practice of indefinite opioid agonist treatment [59, 60] as have been previously expressed [10, 35, 38, 61-64]. Overall these findings powerfully and meaningfully inform our appreciation of, and insights into, the experience of females entrapped by the perils of opioid dependence.

Source:  Reece Albert Stuart, Thomas Mervyn Rees, Norman Amanda, Hulse GaryKenneth.Dramatic acceleration of reproductive aging, contraction of biochemical fecundity and healthspan-lifespan implications of opioid-induced endocrinopathy—FSH/LH ratio and other interrelationships

Reproductive Toxicology    http://dx.doi.org/10.1016/j.reprotox.2016.09.006

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Filed under: Medical Studies :

There are many reports of drug use leading to mental health problems, and we all know of someone having a few too many drinks to cope with a bad day. Many people who are diagnosed with a mental health disorder indulge in drugs, and vice versa. As severity of both increase, problems arise and they become more difficult to treat. But why substance involvement and psychiatric disorders often co-occur is not well understood.

In addition to environmental factors, such as stress and social relationships, a person’s genetic make-up can also contribute to their vulnerability to drug use and misuse as well as mental health problems. So could genetic risk for mental illness be linked to a person’s liability to use drugs?

This question has been addressed in a new study, published in the open-access journal Frontiers in Genetics.

“Our research shows that if someone is genetically predisposed towards having mental illness, they are also prone to use licit and illicit substances and develop problematic usage patterns,” says Caitlin E. Carey, a PhD student in the BRAINLab at Washington University in St. Louis and lead author of this new study. “This is important because if a mental illness, like depression, runs in your family, you are presumed at risk of that disorder. But we find that having a genetic predisposition to mental illness also places that person at risk for substance use and addiction.”

This is the first study to compare genetic risk for mental illness with levels of substance involvement across a large sample of unrelated individuals. Rather than analysing family history, Carey and her co-authors used information across each person’s genetic code to calculate their genetic risk for psychiatric disorders.

“Previous research on the genetic overlap of mental illness and drug use has been limited to family studies. This has made it difficult to examine some of the less common disorders,” says Carey. “For example, it’s hard to find families where some members have schizophrenia and others abuse cocaine. With this method we were able to compare people with various levels of substance involvement to determine whether they were also at relatively higher genetic risk for psychiatric disorders.” As well as finding an overall genetic relationship between mental health and substance involvement, the study revealed links between specific mental illnesses and drugs. Dr. Ryan Bogdan, senior author of the study and Director of the BRAINLab, notes, “We were fortunate to work with data from individuals recruited for various forms of substance dependence. In addition to evaluating the full spectrum of substance use and misuse, from never-using and non-problem use to severe dependence, this also allowed us to evaluate specific psychiatric disorder-substance relationships”. He continues, “For example, we found that genetic risk for both schizophrenia and depression are associated with cannabis and cocaine involvement.”

The study opens up new avenues for research evaluating the predictive power of genetic risk. For example, could genetic risk of schizophrenia predict its onset, severity and prognosis in youth that experiment with cannabis and other drugs?

Dr. Bogdan concludes, “It will now be important to incorporate the influence of environmental factors, such as peer groups, neighborhood, and stress, into this research. This will help us better understand how interplay between the environment and genetic risk may increase or reduce the risk of co-occurring psychiatric disorders and substance involvement. Further, it will be important to isolate specific genetic pathways shared with both substance involvement and psychiatric illness. Ultimately, such knowledge may help guide the development of more effective prevention and treatment efforts decades in the future.”

Source:  Caitlin E. Carey et al, Associations between Polygenic Risk for Psychiatric Disorders and Substance Involvement, Frontiers in Genetics (2016). DOI: 10.3389/fgene.2016.00149 

Please share this post with every concerned parent you know! Spread the Word about Pop Pot!

Pew Research released a new poll from late August and early September that shows 57% of American voters favor marijuana legalization.  Based on the question and the article, the poll probably means that 57% of the voters favor marijuana decriminalization.   Next time the poll should be more specific in its meaning.  The same day this poll was released, a headline from the Cape Cod News in supposedly “liberal” Massachusetts read Support Scarce for Legal Pot.   There could not be a bigger difference in meaning  between these headlines.  Why the difference?

Despite this poll, all 5 states with ballots for marijuana legalization this November poll at less than 57% in favor of legalization.  There is a disparity between the survey question and legalization in practice. Legalization creates a new industry expected to make a lot of money for investors.   It is the reason that Weed Maps, ArcView group  and Soros-funded groups contribute to the ballots.  There’s a big difference between legalization and decriminalization.  Did those conducting the survey explain what legalization means?

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Since the Sacramento Bee made this chart, at least $10 million more has been raised by  California’s Yes on 64 campaign. With the business Weed Maps, MJ Freeway and George Soros funding so much, it’s obviously a good business venture.  George Soros gave at least $4 million.

Legalization creates commercial marijuana stores regulated by the state .   Administering and implementing it is very difficult to do.   Pot sales are taxed at various levels and earn some money.  But as Colorado marijuana director, Andrew Freedman said, it’s not worth legalizing for the benefit of tax revenues.

When presented with facts, voters are  sceptical of commercialization and don’t want more impaired drivers.  The cost of regulation is  high.   On October 1 in Colorado, new rules began,  and the packaging must make it more difficult for children to access. Gummy candies in the shape of animals are now forbidden. The number of hospitalizations and overdose deaths from marijuana edibles which make up nearly 50% of the market necessitated these changes.

Opting out of commercial pot is very tough, too.  Dealing with inconsiderate neighbors who grow a lot of pot plants is difficult.  In Colorado, city governments are often greedy for tax money while residents say no to pot.  When voters want to ban dispensaries, other forces such as the marijuana industry fight them.   It’s one of the reasons Colorado now has buyer’s remorse

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Why Marijuana Decriminalization ?

Decriminalization means that marijuana is not treated as a crime but as a mistake; offenders are charged with a small fine, like a speeding ticket.   In legal terms, it’s the difference between a misdemeanor and a felony.  The marijuana lobbyists have successfully convinced Americans that large numbers of people go to jail for marijuana possession only.

The only people who go to jail for marijuana possession charges have committed other crimes and have plea bargained to get convicted of lesser charges.   Other crimes include drug dealing, transportation of drugs or possession of a large amount of drugs that indicates intent to sell.  Selling drugs is not a victimless crime.

Marijuana lobbyists omit information about drug courts which allows users an alternative and provides addiction treatment.

The reason that marijuana possession is a felony crime in some states is so that it can be used as evidence to convict when there are more serious crimes.  Drugs and drug paraphernalia become supporting evidence when other crimes may be harder to prove.

How are Minorities Really Affected by Drug Laws?

Minorities have the most to lose by using marijuana.  Daily or near daily use of marijuana by teens nearly doubles the risk of dropping out of high school.   Dropping out of high school makes future education and job prospects dim.  Furthermore, a study of long-term marijuana users in New Zealand over a 25-year period found an average 7-point drop in IQ by age 38.   People who complain that this study did not adjust for IQ differences as reflected by socio-economic class should realize that IQ differences resulting from socio-economic factors are in play seen before age 13, when participants first entered the study.

A recent study from UC Davis showed how chronic marijuana users faced more downward mobility than chronic alcohol users.  In the US, the disproportionate arrest of minorities may reflect concern about dropping out of school and what that means for the future. The higher conviction rate for minorities is probably a reflection of income disparity and poverty.  A disproportionate number of black and Hispanic drug dealers go to jail.   Minorities are less likely to be able to afford the legal fees that allow wealthy white drug dealers to get less time in jail or wiggle their way out of going to jail.  Justice reform should not be centered on legalizing drugs, but on giving minorities better legal representation. Retired Judge Arthur Burnett, National Executive Director of the  National African-American Drug Policy Coalition, says that  African-American communities already suffer from a liquor store on every corner. Black voters know commercial marijuana would prey on their communities at a much higher rate.  “Do we really want to substitute mass incapacitation for mass incarceration?” he asked.

There’s a strong misconception that people go to jail just for having a joint.   (The threat of jail is not the reason to tell kids not to use pot, but defense of your brain is!)   There’s also a misconception that inequities in the justice system would be solved by legalization.

Maybe next time Pew Research present the polls with a bunch of different options between decriminalization, allowing home grows only or commercialization.   Or Pew Research should a better job at explaining what they mean by legalization.

Source:  http://www.poppot.org/2016/10/13/pew-research-poll-actually-reflects-pot-decriminalization   OCTOBER 13, 2016 EDITOR

Drug education is the only part of the middle school curriculum I remember — perhaps because it backfired so spectacularly. Before reaching today’s legal drinking age, I was shooting cocaine and heroin.

I’ve since recovered from my addiction, and researchers now are trying to develop innovative prevention programs to help children at risk take a different road than I did.

Developing a public antidrug program that really works has not been easy. Many of us grew up with antidrug programs like D.A.R.E. or the Nancy Reagan-inspired antidrug campaign “Just Say No.” But research shows those programs and others like them that depend on education and scare tactics were largely ineffective and did little to curb drug use by children at highest risk.

But now a new antidrug program tested in Europe, Australia and Canada is showing promise. Called Preventure, the program, developed by Patricia Conrod, a professor of psychiatry at the University of Montreal, recognizes how a child’s temperament drives his or her risk for drug use — and that different traits create different pathways to addiction. Early trials show that personality testing can identify 90 percent of the highest risk children, targeting risky traits before they cause problems.

Recognizing that most teenagers who try alcohol, cocaine, opioids or methamphetamine do not become addicted, they focus on what’s different about the minority who do.

The traits that put kids at the highest risk for addiction aren’t all what you might expect. In my case, I seemed an unlikely candidate for addiction. I excelled academically, behaved well in class and participated in numerous extracurricular activities.

Inside, though, I was suffering from loneliness, anxiety and sensory overload. The same traits that made me “gifted” in academics left me clueless with people.

That’s why, when my health teacher said that peer pressure could push you to take drugs, what I heard instead was: “Drugs will make you cool.” As someone who felt like an outcast, this made psychoactive substances catnip.

Preventure’s personality testing programs go deeper.

They focus on four risky traits: sensation-seeking, impulsiveness, anxiety sensitivity and hopelessness.

Importantly, most at-risk kids can be spotted early. For example, in preschool I was given a diagnosis of attention deficit/hyperactivity disorder (A.D.H.D.), which increases illegal drug addiction risk by a factor of three. My difficulty regulating emotions and oversensitivity attracted bullies. Then, isolation led to despair.

A child who begins using drugs out of a sense of hopelessness — like me, for instance — has a quite different goal than one who seeks thrills.

Three of the four personality traits identified by Preventure are linked to mental health issues, a critical risk factor for addiction. Impulsiveness, for instance, is common among people with A.D.H.D., while hopelessness is often a precursor to depression. Anxiety sensitivity, which means being overly aware and frightened of physical signs of anxiety, is linked to panic disorder.

While sensation-seeking is not connected to other diagnoses, it raises addiction risk for the obvious reason that people drawn to intense experience will probably like drugs.

Preventure starts with an intensive two- to three-day training for teachers, who are given a crash course in therapy techniques proven to fight psychological problems. The idea is to prevent people with outlying personalities from becoming entrenched in disordered thinking that can lead to a diagnosis, or, in the case of sensation-seeking, to dangerous behavior.

When the school year starts, middle schoolers take a personality test to identify the outliers. Months later, two 90-minute workshops — framed as a way to channel your personality toward success — are offered to the whole school, with only a limited number of slots. Overwhelmingly, most students sign up, Dr. Conrod says.

Although selection appears random, only those with extreme scores on the test — which has been shown to pick up 90 percent of those at risk — actually get to attend. They are given the workshop targeted to their most troublesome trait.

But the reason for selection is not initially disclosed. If students ask, they are given honest information; however, most do not and they typically report finding the workshops relevant and useful.

“There’s no labeling,” Dr. Conrod explains. This reduces the chances that kids will make a label like “high risk” into a self-fulfilling prophecy.

The workshops teach students cognitive behavioral techniques to address specific emotional and behavioral problems and encourage them to use these tools.

Preventure has been tested in eight randomized trials in Britain, Australia, the Netherlands and Canada, which found reductions in binge drinking, frequent drug use and alcohol-related problems. A 2013 study published in JAMA Psychiatry included over 2,600 13- and 14-year-olds in 21 British schools, half of whom were randomized to the program. Overall, Preventure cut drinking in selected schools by 29 percent — even among those who didn’t attend workshops. Among the high-risk kids who did attend, binge drinking fell by 43 percent.

Dr. Conrod says that Preventure probably affected non-participants by reducing peer pressure from high-risk students. She also suspects that the teacher training made instructors more empathetic to high-risk students, which can increase school connection, a known factor in cutting drug use. Studies in 2009 and in 2013 also showed that Preventure reduced symptoms of depression, panic attacks and impulsive behavior.

For kids with personality traits that put them at risk, learning how to manage traits that make us different and often difficult could change a trajectory that can lead to tragedy.

Source:  http://www.nytimes.com/2016/10/04/well/family/the-4-traits-that-put-kids-at-risk-for-addiction  

September 27, 2016 |   By Renato D. Alarcón, MD, MPH

That the world is currently going through a complex and critical phase in its history is an understatement. The background is multifaceted: violence of all types with a different kind of war (but war anyway) at its peak, large migrations in all regions, religion transformed in terrorist codes and strategies with tragically massive sequelae, and politics in many countries (starting with the US) reaching levels of cheap TV shows or grotesque deformity by the words and actions of some of its protagonists. And the main victim, in addition to all the innocent lives of those who died or were injured (physically and emotionally) is humanity itself, the essence of its raison d’etre—culture—as both the repository of history and the expression of our human identity.

Culture is being demolished by grenades, guns, and incendiary speeches. And the world’s mental health is being threatened as never before by viruses of hatred, fanaticism, frivolousness, and a technology-based infectious chain. The challenges to psychiatry as the clinical armour of mental health, and to cultural psychiatry as its vanguard platoon, are indeed enormous in these dramatic and confusing times.

The preceding may sound exaggerated but an objective and close examination of worldwide events these days, conveyed by the media, social networks, or word-of-mouth, confirm the seriousness of the situation. Almost daily attacks by unknown assailants in malls, train stations, bars, churches, or in the streets reflect the contagious nature of violence—be that the result of dysmorphic preaching or the action of “lonely wolves.” Religious and even ethical principles used as reasons to kill, dressed up by coward anonymity, have used European and American cities as worldwide stages. A re-invigorated racism and its mixed-up dialectics play with fear, apprehension, or sheer ignorance to make public places or dark neighborhoods scenarios of death, invoking at times the name of the law. Homicide and suicide-related deaths have increased as a consequence.

The cultural and mental implications of all these behaviors cannot be neglected. Migration within countries or regions has been a phenomenon present for centuries around the world. To mostly socio-economic and occupational needs as main causes of migration, others have been added in the last several decades: prolonged internal political conflicts, religious wars, cruel political persecutions, bloody massive expulsions, or voluntary exile.

Psychiatry can help to alleviate, contain, and eventually prevent demolition of culture and health. That’s how powerful it is.

The other big differences are the size and frequency of the migratory waves, particularly between the Middle East and European countries, in the African continent, and the ever-present flow of Hispanics into the US.

International bureaucratic and professional organizations (World Health Organization, World Psychiatric Association, World Association of Cultural Psychiatry) have made strong pronouncements, urging governments and other agencies to study, plan, and intervene in the alleviation and prevention of the health and mental health consequences of migrations, clinical pictures of which fragilities, rejection, resentment, and uncertainties are substantial ingredients.

Moreover, we cannot deny that the political picture of the most powerful country in the world presents evidences of circus and polarization, showmanship and distrust, that make it “different.” The problem is that the “difference” now is not ideological or doctrinal; particularly on one side of the current campaign, it is the accentuation of hate,

the use of stereotypes and insults as arguments, the not-too-disguised lies or the not-too-subtle incitements to overt violence. And this fact, violence, is precisely where all the occurrences in today’s world (war, terrorism, migrations, politics) converge and show their shared umbrella.

Violence, without distinctions of age, gender, ethnicity, civil status, socio-economic level, nationality, religious or cultural features, permeates these processes. Violence—be it domestic, collective, verbal, physical, sexual, emotional, or political—is one of the most demonstrative manifestations of social as well as psychological/mental instability.

It corrodes the spaces of tolerance and reason, the roots of dialogue and communication, the capacity to judge and opine. It takes away the visions of future and progress converting them into weak presentism and facile demagoguery. Violence kills people, demolishes buildings, cities, monuments . . . and the whole of culture.

In clinical terms, the mental health consequences of this global socio-political climate affect individuals, groups, communities and the society at large. To the well-known posttraumatic stress manifestations per se, those of depression, anxiety, psychosis, substance use, as well as dissociative, somatic, conversion, and personality disorders, can be triggered or exacerbated by violence, making it the final common pathway of a variety of conditions, the overcrowded catalogue of disorganization, fright, and confusion.

It is also fed by denial, the oldest of what are known as “defense mechanisms;” by duplicities, sophisticated versions of multiplied lying, rationalism, or sloganized justifications. In the cultural realm, again, individual and group/community/ethnic identities are deformed; beliefs and traditions are betrayed or simply set aside; faith is lost. Contagiousness is, many times, an atypical collateral of violence.

In short, violence engenders more violence.

What to do under these circumstances? What can psychiatry and its allied disciplines do to alleviate, contain, and eventually prevent or avoid the demolition of culture and health? A systematic, consistent, tireless call to reason that must include an honest assessment of history and its changes, should constitute the core of a public education campaign.

An analysis of the roots of each problem, the public health/mental health response to the realities of the situation, direct invitations to and active participation in civilized dialogues with government authorities, public citizens, and political groups and academic institutions; an unequivocal protection of civil liberties and human rights, and fostering of preparedness and preventive vigilance from and for all population segments. Concomitant tasks of teaching, learning and training at all levels—students, professionals and public—strengthened by available mental health care infrastructure.

Most importantly, the restoration of cultural consciousness, of the texture of identity and genuine faith (respecting differences and welcoming coincidences), of the force of ideas and practices carrying out genuine understanding, solidarity, and teamwork. The ultimate objective is, of course, the elimination of violence as a resource, the reconstruction of culture as a unifying force, a chalice of diversity.

Globalization is far from being a comprehensive concept, in spite of its etymology. Global health and global mental health are still at the beginning of their conceptual articulation, their presence felt as undeniably strong but their entities still uncertain. Culture is being threatened worldwide, but its perpetual, basic configuration throughout millennia becomes the basis of the most important factor against its destruction: hope, the same quality that Jerome Frank intuited as the most powerful ingredient of all psychotherapies. Hope as a source of action and positive responses, as a pillar of protection and resilience for individuals and nations. Hope as a tool for the survival of human culture.

MORE ABOUT THE AUTHOR

I was born in Arequipa, the second largest city in Perú, and graduated from medical school in Lima. My parents were both high school teachers and always voiced their wish to have “a doctor” among their 3 children. I confess I liked letters and humanities but, in the end, I “compromised” by choosing psychiatry as my specialty: I am very happy because I know psychiatry is the last bastion of Humanism in medicine, and because I enjoyed the work and wisdom of great teachers. Let me just mention two: Honorio Delgado (1892-1969), a Peruvian philosopher and researcher who met and worked with giants like Freud; Jaspers; the Schneiders; Gregorio Marañón or Pedro Lain-Entralgo, who is considered the greatest Latin American psychiatrist of the 20th century; and Jerome Frank (1909-2005), an accomplished, compassionate and inspiring Hopkins academician, the first and most solid psychotherapy researcher in the world.

Trained in the US, I worked back in Lima for 8 years before returning in 1980 to work at the University of Alabama in Birmingham, Emory and, finally, the Mayo Clinic. I have always kept in close touch with Latin American psychiatry and have its visibility around the world as, perhaps, the fundamental objective of my career. In a globalized world, it is only fair to recognize the contributions of developing countries and continents. I am gratified for having helped a number of Latin American young colleagues, medical students, and residents to come to the US and enjoy learning experiences in American academic centers. I have also assisted in the organization of international events where experience-sharing, teaching, and learning from each other are substantial didactic resources. And, certainly, I plan to continue doing so for as many years as possible.

I love classical music, Latin boleros, and Peruvian waltzes. I used to play soccer and was an adolescent sports anchorman and journalist in my hometown. I lost my brother Javier, an idealist of the left, one of the 80,000 desaparecidos or victims of the “dirty war” of the 1980s in Perú; in his memory, social and political reconciliation are frequent themes of my reflections from the cultural and social psychiatry perspectives. I feel moved by Cesar Vallejo’s poetry; Hemingway’s life and novels; Bertrand Russell’s thinking; Elie Wiesel’s, M.L. King’s, or Octavio Paz’s social militancy. And count The Room, Schindler’s List, and To Kill a Mockingbird among my favorite movies.

DISCLOSURES

Dr. Alarcón is Emeritus Professor and Consultant in the department of psychiatry and psychology at Mayo Clinic College of Medicine in Rochester, MN,

* COMMENTS

Peter @ Sun, 2016-10-02 19:11

Is psychiatry really so powerful in order “to help alleviate, contain, and eventually prevent demolition of culture and health”? If that is so, how can we really measure, evaluate or discern this kind of helpfulness without incurring in another romantic case of

irremediable wishful thinking? Call me pessimist or disenchanted, but after four decades working as a clinical psychiatrist in my beloved and violent Mexico, my guess is as Paul Auster declared during the Príncipe of Asturias Award Ceremony “A book has never put food in the stomach of a hungry child. A book has never stopped a bullet from entering a murder victim’s body. A book has never prevented a bomb from falling on innocent civilians in the midst of war” (not even a psychiatry textbook or article). Nevertheless, I still do think that Dr. Alarcón words are beautiful, thoughtful and even inspiring.

Dr. Moisés Rozanes

The concept of culture is very important especially because culture and race have been misused as concepts. Most of what people call ‘race’ is culture. We live in a time of huge cultural change including the globalization of music, art, sports, and fashion. Language which communicates culture is globalizing. The internet has brought about these changes and the internet is being fought over as to which global player will control this agent of change. The danger for psychiatry is that psychiatry has too often been on the wrong side of cultural change and has supported the insider powerful over the people in past issues such as psychiatry’s shameful support of Eugenics and psychiatry’s calling being gay illness. The Populist Movement as shown by the Brexit and the Trump campaign must not be demonized by organized psychiatry and instead , need to be seen as the People culturally taking power and rejecting the mostly self-appointed ruling elite. Psychiatry needs to accept it does not have a mandate to call culture illness. Psychiatry must carefully separate culture and illness and clearly demonstrate that psychiatry can be trusted to be a medical specialty and that psychiatry will never again abuse people in the name of the powerful political elites.

Alan @ Fri, 2016-09-30 17:15

Excellent article but I wonder what is the role of culture triggering the contemporary situation? We are conditioned by our culture and use it as a reference against other social groups. I am not free from my conditioning although I can be aware of it, then a transformation takes place and I become compassionate and less violent. The other social group see my attitude and now (they seems to) listen opening the door for communication. The role of psychiatry is tainted by the damage done by it; our pseudo-diagnostic manual, Pharma and the psychotropic drugs. We are part of the problem and only after we see it there will be hope…and compassion and healing.

Manuel @ Fri, 2016-09-30 10:34

This portrayal of current cultural situation in the world is excellent, but please don’t tell me the answer is “hope”.

Psychiatry’s role should be EDUCATION, secular/Scientific education and in a good many number of years this “cultural demolition” would start to respond to treatment, I believe.

Dr. Pistone, MD Psychiatrist

Daniel @ Fri, 2016-09-30 00:04

It takes quite a bit of hubris, or delusion, to think that the times in which we live are unique or somehow special or especially threatening to culture or civilization. The world and civilization have endured fascism, the Holocaust, “Mongol hordes”, the Fall of the Roman Empire, extermination of native peoples, colonization, the Black Death, the Opium Wars, slavery, the Inquisition, ad nauseam throughout recorded history, and most certainly before. ISIS, Hillary Clinton, and Donald Trump are hardly the worst things that might “demolish” world culture.

Quentin @ Thu, 2016-09-29 10:32

My thoughts exactly. There is nothing new under the sun. The Middle Ages were far worse, especially for women and children. The Crusaders put us to shame when it comes to violent murder in the name of God. There is less violence in the streets today than in the past. Civil rights are stronger today than in the past. This is not to say, of course, that we should not be horrified about the tenor of the political climate, or the divide between those fearful who lean toward xenophobia and those who envision an open, multicultural society where every person who wants one is given a fair shot to live a safe, authentic life. “Give me your tired, your poor, your huddled masses…the wretched refuse of your teeming shore” should not be just words on a statue.

Dana @ Thu, 2016-09-29 11:23

Is not the comparison with the tranquil (civilized?) peace of America’s (e.g.) 50’s against current events in the USA? I may get eaten alive for being simple but the “world” (America) seems much more violent than even the 70’s and 80’s. I don’t believe the author was comparing today’s society against the holocaust, etc. I found the article to be interesting and a provider of Hope.

Dana @ Thu, 2016-09-29 11:12

I think the 50’s were really great for straight white folks. Otherwise, not so much.

Dana @ Thu, 2016-09-29 12:57

I think the key word is “seems” In fact, there is less violence today than in those decades. It is simply that we have access 24/7 to the sensationalized news reports about the violence that is being perpetrated today, so we are left with the impression that there is more violence when in fact there is less. It is safer to walk on city streets today than in the 70’s and 80’s. There are studies that show this.

Denise @ Thu, 2016-09-29 11:31

I think of that intermittently but not consistently enough. That’s an excellent point. Thank you for your response. I would be interesting in finding a study to reinforce my thinking. * reply

Dana @ Thu, 2016-09-29 12:59

I’m not sure I understand the context of your post. I interpreted the essay to be a commentary on current affairs and identified social trends not a look backward comparing today’s events with all recorded events since the mass extinction of mammoth and giant sloth.

If the argument is that reporting by news media is so pellucid and unreliable that current events are virtually unknowable being disinformation but that written histories are a reliable and superior source of knowledge about the world today, then I would lean toward assurance that finished and complete knowledge is enough.

Societies are being transformed. No one can argue that the world is not changing in ways unique to our times. How the people of the world interpret the transformation may not be determinative in the end, but it is important for the curious-furious to develop perspective on forces and powers influencing the future of all cultures. It’s an unusual opportunity for scholars; those with a focus on psychiatry or no.

Richard Anthony @ Thu, 2016-09-29 21:19

Reading this article reminded me the vision outlined by Jerome D. Frank in his book “Sanity and Survival”. Truly wonderful essay. John M. de Figueiredo

John @ Thu, 2016-09-29 10:23

I do not recall who said that “civilization was started by the first man who used word instead of a club to work out a disagreement.” it was well said.

Melvin @ Thu, 2016-09-29 10:21

Your words speak volumes. Working at the public school level I see first hand the “trickle down” effect the issues of this world are having on children. We must be vigilant, in continuing to address the issues you discussed, for the future of society as a whole. Thank you.

Cheryl @ Thu, 2016-09-29 10:17

Well said! Eloquent and on target.

Jennifer @ Thu, 2016-09-29 10:03

I couldn’t agree more. Listening to the political and event news feels like a daily assault to my mental health, which is generally good. I try to stay informed, but I am not allowing myself to be involved in the 24 hour / day news cycle. Quiet walks alone seems to be a good respite for me from the daily stressors of life (job, family…), but more importantly the political and global stressors (politics of hate / division, terrorism, economics, wars, climate change with devasting weather events…). It is no wonder that there is an increase in mental health issues and a growing need for medications to assist people with coping with life.

Filed under: Social Affairs (Papers) :

People with light-colored eyes may have a higher risk of alcoholism than people with dark-brown eyes, new research suggests.

In the study, researchers looked at 1,263 Americans of European ancestry, including 992 people who were diagnosed with alcohol dependence and 271 people who were not diagnosed with alcohol dependence. They found that the rate of alcohol dependence was 54 percent higher among people with light-colored eyes — including blue, green, gray and light-brown eyes — than among those with dark-brown eyes.

“This suggests an intriguing possibility — that eye color can be useful in the clinic for alcohol dependence diagnosis,” study co-author Arvis Sulovari, a graduate student in cellular, molecular and biological science at the University of Vermont, said in a statement. The prevalence of alcoholism was the highest in people with blue eyes — their rate was about 80 percent higher than that of people with other eye colors, according to the study.

Moreover, the connection between eye color and an increased risk of alcoholism was confirmed by the results of a genetic analysis, which showed a significant link between the genetic components responsible for eye color and those that studies have linked with a person’s risk of alcohol dependence, the researchers said. [7 Ways Alcohol Affects Your Health]

However, the researchers still don’t know the exact reasons that could underlie the link, and more research is needed to examine it, study co-author Dawei Li, an assistant professor of microbiology and molecular genetics at the University of Vermont, said in a statement. Previous research on people of European ancestry has shown that those with light-colored eyes may consume more alcohol on average than dark-eyed individuals, the researchers said. Other studies also have demonstrated a link between eye color and people’s risk of psychiatric illness, addiction and behavioral problems, according to the study. For example, studies have established a link between light eye color and an increased risk of seasonal affective disorder (SAD), which often co-occurs with alcohol dependence, the researchers said. A possible explanation for the link between light eye color and SAD is that light-eyed people may be more sensitive to variations in light levels, which has been associated with abnormal changes in the production of the sleep-regulating hormone melatonin and, consequently, with SAD, the researchers said.

However, the new study has shortcomings, said Gil Atzmon, an associate professor of medicine and genetics at Albert Einstein College of Medicine in New York, who was not involved in the study.

For example, although the researchers took into account participants’ gender and age, to see whether those factors may have played a role in people’s risk of alcohol dependence, they did not examine other factors that also may have affected the participants’ risk of alcoholism, such as their income level or their mental health status, Atzmon said.  The researchers did not look at whether any of the people in the study had depression, a condition that may be associated with excessive drinking, he said.

The new study was published in the July issue of the American Journal of Medical Genetics: Neuropsychiatric Genetics Part B.

Source: http://www.livescience.com/51495-eye-color-alcoholism.html  15th July 2015

Filed under: Alcohol,Medical Studies :

Abstract

The growing use and legalization of cannabis are leading to increased exposures across all age groups, including in adolescence. The touting of its medicinal values stems from anecdotal reports related to treatment of a broad range of illnesses including epilepsy, multiple sclerosis, muscle spasms, arthritis, obesity, cancer, Alzheimer’s disease, Parkinson’s disease, post-traumatic stress, inflammatory bowel disease, and anxiety. However, it is critical that societal passions not obscure objective assessments of any potential and realized short- and long-term adverse effects of cannabis, particularly with respect to age of onset and chronicity of exposure.

This critical review focuses on evidence-based research designed to assess both therapeutic benefits and harmful effects of cannabis exposure, and is combined with an illustration of the neuropathological findings in a fatal case of cannabis-induced psychosis.

The literature and reported case provide strong evidence that chronic cannabis abuse causes cognitive impairment and damages the brain, particularly white matter, where cannabinoid 1 receptors abound. Contrary to popular perception, there is little objective data supporting preferential use of cannabis over conventional therapy for restoration of central nervous system structure and function in disease states such as multiple sclerosis, epilepsy, or schizophrenia. Additional research is needed to determine if sub-sets of individuals with various neurological and psychiatric diseases derive therapeutic benefits from cannabis. David E. Mandelbaum, MD, PhD Suzanne M. de la Monte, MD MPH

Departments of Neurology, Pediatrics, Neuropathology and Neurosurgery, Hasbro Children’s Hospital and Rhode Island Hospital, and the Alpert Medical School of Brown University, Providence, RI 02903

Source:    http://dx.doi.org/10.1016/j.pediatrneurol.2016.09.004

Prior research has shown Network Support, a treatment designed to increase individuals’ support for recovery and decrease their support for drinking, provides recovery benefit. How did it fare against a well-known, evidence-based cognitive-behavioral treatment?

What problem does this study address?

An individual’s social circle, also called a social network, can serve as a major foundation to help reduce relapse risk for those that are in, or are seeking, recovery from alcohol and other drug use disorder. For example, if these social network members are in recovery themselves, they may be able to serve as recovery role models helping individuals cope with increased stress, instilling confidence that challenging situations can be handled effectively (i.e., self-efficacy), and increasing one’s recovery motivation by responding positively to recovery-related actions. In line with this, Litt and colleagues showed that an intervention called Network Support, which is designed to increase recovery supportive people in one’s network and decrease drinking-supportive individuals, led to 20% more percent days abstinent across 2 years compared to a case management intervention which helped participants set goals and provided information regarding professional and community resources to meet those goals. In the current study, the authors compared recovery benefits of this Network Support intervention to a cognitive behavioral therapy (CBT) intervention, a more active intervention than case management that has a strong scientific evidence base and is commonly delivered in treatment settings.

How was this study conducted?

Before describing the study design, it is important to first outline the content of both treatments. For Network Support, therapists leveraged the existing recovery-supportive communities within Alcoholics Anonymous (AA) to help participants increase the recovery support in their network. In this study, the treatment emphasized the social aspects of AA and recognized, but downplayed its spiritual content. In addition, Network Support also highlighted other ways by which participants could increase recovery support and decrease drinking support in their network because their prior work showed that many individuals were very resistant or unwilling to attend AA. These additional strategies included social and recreational activities that would expose them to individuals that were either recovery supportive, or at a minimum not drinking-supportive. One major difference between this version of Network Support compared to the one from the original study was the inclusion of a social skills training module to help individuals engage in these new social activities. CBT in this study was based on other CBT approaches that had been vetted in prior studies. These CBT approaches are intended to help individuals identify and avoid high-risk situations, as well as to increase their coping skills to manage cravings that might result from exposure to these high risk situations if they cannot or will not avoid them. Both Network Support and CBT consisted of 12 weekly outpatient sessions that lasted 60 minutes each.

Regarding study design, authors randomly assigned 96 adults with alcohol use disorder to Network Support and 97 to CBT, assessing participants after the treatments were delivered (post-treatment), and every 3 months thereafter up through 24-month follow-up (i.e., 27 months after they entered the study). Those with other drug use disorders apart from marijuana and those with more extensive AA experience (attending 4 or more meetings in the month before entering the study) were excluded from participatiping. The treatments were compared on percent days abstinent from alcohol, as well as percent days with heavy drinking (four or more drinks for a woman and five or more for a man in one day), number of drinks per drinking day, complete abstinence, and drinking-related consequences (i.e., effects on one’s social life, employment, and health). Authors also investigated what processes during treatment explained any differences between Network Support and CBT over time. Participants were 46 years old, on average, and 66% were Male while 93% were White. The average participant had one prior episode of alcohol use disorder treatment in their lifetime, had been to one AA meeting in the past 90 days, and drank on 69 of the past 90 days with about 9 drinks each day. Controlled or moderate drinking was the goal for 30%, while abstinence the goal for 70%. Participants in Network Support and CBT were essentially equivalent on all measured demographic and drinking-related characteristics when entering the study.

What did this study find?

The two treatments had similar rates of attendance with each group attending about 7 sessions on average. As the authors predicted, Network Support participants had more percent days abstinent over time than CBT. As illustrated in the figure on the left, participants increased their percent days abstinent in the past 90 days from about 20% in both groups upon entering the study, to about 70% in Network Support vs. 65% in CBT across 2 years after receiving the treatment. The Network Support participants also had fewer drinking consequences, on average, while percent days heavy drinking and number drinks per drinking day were similar. Complete abstinence overall was statistically similar for the groups (i.e., there was not a statistically reliable difference over time). As illustrated by the figure on the right, though, the proportion of Network Support participants that were completely abstinent during an assessment period lasting 90 days was consistently higher in Network Support than CBT with the lone exception of immediately following treatment. For example, 35% of participants in Network Support were completely abstinent for 90 days compared to only 20% for CBT at the 12-month follow-up. Also as the authors predicted, the small but statistically reliable advantage for Network Support was explained, in part, by an increase in the number of abstinent individuals in one’s close social circle, AA meeting attendance, and abstinence self-efficacy. It is important to note that adopting abstinent individuals into their network through AA, specifically, did not provide additional recovery benefit in comparison to adopting abstinent individuals into their network by other strategies. Also, about half of the Network Support group, and 60% of the CBT group never attended AA during the entire 27-month study period (3-month treatment and 2-year follow-up). Put another way, this also demonstrates that despite not being explicitly encouraged to attend AA in the CBT condition, almost as many patients in the CBT condition (40%) as the Network Support condition (50%) chose to attend AA during the follow-up period.

Why is this study important?

This study shows that specific treatments like Network Support can help individuals make changes to their social network, in particular increasing the number of abstinent individuals, if they are specifically designed to do so. In addition, these changes are important to initiating and sustaining abstinence. In other studies, like this one by Kelly and colleagues, it has been shown that decreasing the number of individuals that are heavy drinkers or who support someone’s drinking also provides benefit. Network Support and CBT provided similar benefit in this area. Another important finding was the lower drinking consequences for those in Network Support despite similar rates of heavy drinking and number of drinks on each drinking day. It could be that on days where individuals drink, networks that strongly support abstinence and recovery can help buffer against consequences, serving as a base to use coping skills and providing individuals with the support and confidence needed to get back on track after a heavy drinking episode. One critical finding was that half of the Network Support group did not attend AA at all during the study period, despite specific encouragement and support to do so. This may have been because of the lower severity of the group’s alcohol problems compared to those who attend residential treatment. Only 70% were interested in an abstinence goal, which may have turned them off to AA, which explicitly encourages abstinence as a solution to alcohol use disorder. Dozens of studies following individuals in treatment over time have shown that those who are more severe, and have more psychosocial difficulties, are more likely to attend AA and other 12-step mutual-help organizations. It is encouraging that increasing abstinent individuals in one’s network by any means, including but not limited to AA, provided recovery benefit, and that such changes can be facilitated in treatment.

Limitations of this study

The focus on the study was individuals whose primary problem was alcohol. People with drug use disorders apart from alcohol and marijuana were excluded. So it is unclear if these findings also apply to individuals that have opioid, cocaine, and amphetamine use disorders, for example.

Next steps

One possible next step is to implement this treatment with a broader patient population in real-world treatment settings. For example, it will be important to see whether Network Support is effective for individuals with primary alcohol problems that also have opioid, cocaine, and/or amphetamine use disorders, as these individuals were excluded from the current study. In addition, it will also be important to see if an adapted version of Network Support is effective for those whose primary substance is an illicit drug, such as opioids. This version of Network Support could aim to leverage the recovery-supportive social networks present in the related 12-step mutual-help group Narcotics Anonymous rather than AA, given its broader focus on all drugs.

Bottom line

For Individuals & families seeking recovery:

Making changes to one’s social circle – especially adding individuals who are abstinent or in recovery themselves – is likely to increase one’s chances of initiating and sustaining abstinence over time. Therefore, treatments that help individuals do this, like Network Support, are likely to offer greater recovery benefit.

For Scientists:

This study used a rigorous design to show that Network  Support provides similar or greater recovery benefit than CBT across a range of outcomes. Their mediation analyses offer a nice example for other clinical research, as authors also showed that Network Support worked, in part, through processes they predicted a priori (e.g., increasing number of abstinent individuals in one’s network, AA meetings, and abstinence self-efficacy).

For Policy makers:

This is the second controlled study showing that Network Support provides benefit for abstinence and other recovery outcomes. Strongly consider funding for research to test its recovery benefit in real world settings.

For Treatment professionals and treatment systems:

Interventions that target social network changes are likely to help your patients. Although research in real world treatment settings is needed before a recommendation to roll Network Support out on a large scale can be made, results to this point are positive, and suggest it is likely to provide an advantage relative to case management and CBT.

Source:Drug AlcoholDepend.doi:10.1016/j.drugalcdep.2016.06.010

Filed under: Treatment :

Seven out of 100 adolescents attend addiction treatment each year. This study used an in-depth qualitative research approach to examine the processes underlying “successful” adolescent recovery.

What problem does this study address?

Of all individuals who seek treatment for alcohol and other drug use disorders (i.e., substance use disorder), 7% are adolescents between 12 and 17 years old. For these youngest treatment seekers, relapse rates are high, with estimates from different studies suggesting 55-90% drink or use other drugs within the first year after completing treatment. From a developmental perspective, adolescents have unique clinical qualities making them different from young adults and older adults in terms of the nature of their substance use problems, and the different factors that influence these problems positive and negatively. For example, research shows that environmental influences on substance use predominate among adolescents, while family history (e.g., genetic influences) becomes more prominent during young adulthood. Yet, we often conceptualize substance use disorder recovery in adolescents like we do adults: a lifestyle marked by abstinence with an emphasis on personal growth and citizenship. This study used an intensive, qualitative approach to describe and further our understanding of the critical elements of adolescent recovery among members of Teen and Family Services, an Alternative Peer Group in the Southwestern United States nested within a recovery oriented system of care, including a hospital based treatment facility and a recovery high school. Alternative Peer Groups, also referred to as APGs, are recovery support services for adolescents with substance use disorder that engage them in a community of other recovering adolescents, to capitalize on the same desire for peer acceptance that is known to drive, in part, adolescent motivations for substance use. Alternative Peer Groups are grounded in the theory that, if centered on fun activities with peers, recovery will be perceived as more rewarding than substance use.

How was this study conducted?

A qualitative approach called clinical ethnography was used in this study, which is characterized by immersion in the environment being examined, the Alternative Peer Group at Teen and Family Services in this study. The program was designed to last 9 to 12 months, and like other Alternative Peer Groups, its explicit goal is “full engagement in the 12-step program of recovery from substance use disorder”. Study methods include field notes, observation, records examination, as well as group and individual interviews. Participants were 14 alumni of the Alternative Peer Group (11 males and 3 females; 15-30 years old) with 1 or more years abstinent (1-11 years) who were actively involved in a 12-step program. In addition to program alumni, study authors also interviewed parents of Alternative Peer Group participants, and program staff/leadership.

What did this study find?

Study findings yielded two overarching themes of adolescent recovery: 1) “Journey” and 2) Relationships. The “journey” was marked by stages of preparation, engagement, “working a program”, and recovery maintenance. Relationships were key aspects of each of these four stages, with an emphasis on recovery role models, both with similarly-aged individuals as well as those who were older and had more experience in recovery. Participants identified the preparation stage (months 1-2) as most critical given that many adolescents entered the Alternative Peer Group with a great deal of resistance and ambivalence regarding changing their substance use. Young adult staff, who were in recovery themselves, helped adolescents through this ambivalence and provided support to help them get back on track if they drank or used drugs. To work through the preparation stage, participants outlined the importance of “fun friends” and an increased “sense of belonging” in order to help increase their recovery motivation. They also cited the importance of bonding with recovery role models who demonstrated “enthusiastic sobriety”. Engagement (months 3-6 months) was the result of preparation and was typically facilitated through the benefits of a relationship, with a 12-step mutual-help sponsor for example. “Working a program” was characterized by working the 12 steps and spending time with other individuals who had active recovery lifestyles (i.e., “sticking with the winners”). These processes helped individuals cultivate and build on skills and coping strategies they learned in treatment. Recovery maintenance was characterized differently by alumni and program staff. While the alumni all described recovery as maintaining abstinence, program staff felt abstinence was key through adolescence and until their brain development was complete (i.e., through mid to late 20s). They were more open-minded about adolescents being able to engage in low-risk drinking as they entered into adulthood.

Why is this study important?

Elements specific to adolescent recovery identified by this study included participants’ desire for recovery activities and programming to be fun. Other important elements included the structure, monitoring, and reinforcement of recovery activity attendance, and bonding with positive recovery role models. Participation in fun recovery activities and forming relationships with other, particularly more experienced, recovering individuals are characteristics that map onto other qualitative research findings with adolescents and young adults. Regarding their participation and perceived benefit from 12-step mutual-help organizations, like Alcoholics Anonymous (AA) and Narcotics Anonymous (NA), for example, research has shown that finding a sense of belonging and feeling a sense of universality — having a shared experience or problem — are important subjective experiences of youth recovery. In a related study, Labbe and colleagues showed that, for young adults, the degree to which other young people are present at AA and NA meetings is related to recovery benefit early on (i.e., 3-6 months after initiating recovery), while meetings with older, more experienced individuals is more strongly related to benefit later on (e.g., 6-12 months after initiating recovery). So while connection with both peers and more experienced recovering individuals may be important, these relationships could serve different purposes depending on a person’s stage of recovery.

The mention specifically of “fun activities” is consistent with adolescent treatments for substance use disorder, such as the Adolescent Community Reinforcement Approach. This evidence-based treatment, like alternative peer groups, emphasizes the benefit of engaging adolescents in rewarding activities while abstinent, to compete with the rewarding effects of alcohol and other drug use.

In addition, the “journey” of recovery described by authors parallels the well-known “stages of change” from the transtheoretical model of changing addictive behaviors delineated by Prochaska and DiClemente, and studied extensively among individuals with SUD. The stages of pre-contemplation and contemplation from the model pre-date the beginning of the “journey” as described in this study. That said, preparation, action, and maintenance from the transtheoretical model map well onto preparation, engagement/working a program, and recovery maintenance from this study.

Limitations of this study

This study was conducted in a single program with only 14 individuals all of whom were immersed in a 12-step focused program and had achieved 1 or more years of recovery. Also, the findings reflected perceptions of parents and staff members. Consequently, the findings may not represent the population of adolescents in, or seeking, substance use disorder recovery, or the multitude of settings where adolescents may seek treatment more generally (school, outpatient, residential, etc.). That said, the similarities between members of this Alternative Peer Group and other adolescent treatment and recovery theories described above raise confidence in the applicability of these general key recovery processes across a range of settings and adolescent clinical samples. Also of note, for some of the older young adults (e.g., in their late 20s), they were reflecting on experiences that occurred several years prior. These retrospective reports may have been influenced by more recent events in the participant’s life (i.e., shaping how they remember the past), and should be interpreted with some caution.

Next steps

Recovery definitions may be variable, but all allude to outcomes beyond abstinence, such as better emotional well-being. The recovery processes described here seemed to focus more on substance use. Future studies might help illuminate adolescent recovery processes in terms of other areas of their functioning. In addition, future work might investigate change more generally among adolescents with substance use disorder. For those not interested in a “program of recovery” closely linked with 12-step mutual-help organizations, for example, how do they initiate and sustain recovery? Are the processes similar or different from those described in this study of alumni in an Alternative Peer Group who were heavily involved in 12-step organizations?

Bottom line

For Individuals & families seeking recovery:

For adolescents, engaging in fun activities with other individuals in recovery, and establishing relationships with recovery role models may be key aspects of the recovery process.

For Scientists:

Clinical ethnography was used in this study to investigate the process of adolescent recovery from substance use disorder. This intensive qualitative approach is somewhat similar to community-participatory research where researchers become well integrated into the community over time. This

model may represent a valuable methodology to understand better the complex process of recovery in subgroups like adolescents that presumably have less traditional experiences compared to adults.

For Policy makers:

Adolescent recovery remains an important field of investigation. It is recommended that policy makers continue to allot funds to investigate optimal strategies to engage and retain adolescents in treatment and recovery support services, and help them successfully re-integrate into their communities.

For Treatment professionals and treatment systems:

Adolescent and adult recovery is likely to have areas where they are similar, like the importance of having a shared experience with other individuals in the program. There might also be processes that adult and adolescents have in common, but are particularly salient in adolescent recovery. These might include, for example, engagement in fun activities with other recovering individuals and cultivating relationships with older individuals who support the adolescent’s recovery. It may be helpful to brainstorm extensively with adolescents a menu of fun activities from which they can choose.

Source: Nash, A., Marcus, M., Engebretson, J., & Bukstein, O. (2015). Recovery From Adolescent Substance Use Disorder: Young People in Recovery Describe the Process and Keys to Success in an Alternative Peer Group. Journal of Groups in Addiction & Recovery, 10(4), 290-312. doi:10.1080/1556035X.2015.1089805

Filed under: Treatment :
 September 12, 2016
Gaining scientific proof of adverse effects of cannabis, a world first
Suppression of thalamocortical projection by chronic administration of Δ9-THC (cannabinoid, active ingredient of marijuana). Photomicrograph of cerebral cortex from transgenic mice expressing GFP in thalamocortical axons at postnatal day 7 (P7). (left) : Normal thalamocortical projections. In the middle layer (layer 4), blobs of GFP showing dense termination of thalamocortical axons can be seen (under number 1~5). (right): Thalamocortical projection at P7 from a mouse received chronic administration of Δ9-THC (P2~7). Massive retraction of thalamocortical projections including middle layer (layer 4) can be observed. Credit: Osaka University

Researchers have clarified important mechanisms involved in the formation of neural circuits in the brain. This group also discovered that delta-9-tetrahydrocannabinol (THC), a psychoactive substance also found in cannabis, causes disruption of neural circuits within the cortex. These results explain why cannabis may be harmful and have potential to find application in the functional recovery of brain injury and in cases of dementia.

Neural activity is known to play an important role in the formation of neural circuits. However, we still do not know much about what kind of neural activities are involved in this formation process. This process is especially complex in projections from the thalamus to the cortex, of which so far we only knew that as these projections develop, unnecessary projections are eliminated, thereby leaving only correct projections.

A group of researchers led by Fumitaka Kimura, associate professor at the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, has now clarified the involvement of several mechanisms in the formation of this neural circuit. The researchers also put forth scientific evidence that cannabis intake causes the unnecessary trimming of neural connections, leading to a breakdown of neural circuits (Figure 1).

In their study, this group of researchers discovered that in a different section of the cortex, the rule (Spike Timing-Dependent Plasticity: STDP) by which synaptic strength (a functional measure of connections) between neurons was determined suddenly changed at a certain point in development. Building on this finding, the group examined whether a similar STDP change occurred in the projection from the thalamus and the cortex as well. They found that initially, the synapses were strengthened due to the synchronized activities of the pre- (thalamic) and post- (cortical) synaptic neurons. But after the projections had spread widely, the synchronized activities weakened all but some synapses, thereby eliminating unnecessary projections to enable more systematic ones. As the synapses are weakened, endogenous cannabinoid is released from neural cells via these synchronized activities, leading to a regression of unnecessary neuron projections (Figure 2). The researchers also confirmed such regression when cannabinoid was taken in externally.

The researchers also confirmed such regression when cannabinoid was taken in externally.

Gaining scientific proof of adverse effects of cannabis, a world first
Endogenous cannabinoid regulates the termination area of thalamocortical axons.(left): Normal thalamocortical projection terminates within a square area in layer 4 (barrel, indicated in red), revealed by visualization of individual thalamocortical axons at P12.(left): Disorganized projections of thalamocortical axons at P12 in animals in which gene of cannabinoid receptor was knocked out. Thalamocortical axons overshoot layer 4 and invade upper layers (layer 2/3); the axons seem to ignore barrels boundaries. Credit: Osaka University

These findings may have an impact on further research focused on advancing our understanding of the mechanisms involved in the formation of neural circuits and have the potential to lead to the development of new therapies to improve recovery from brain damage and dementia. In addition, the findings provide for the adverse effects of cannabis consumption on brain development and therefore may help to decrease abuse of marijuana.

This research was featured in the electronic version of Journal of Neuroscience on June 29, 2016.

More information: C. Itami et al, Developmental Switch in Spike Timing-Dependent Plasticity and Cannabinoid-Dependent Reorganization of the Thalamocortical Projection in the Barrel Cortex,Journal of Neuroscience (2016). DOI: 10.1523/JNEUROS

Source:  http://medicalxpress.com/news/2016-09-adverse-effects-cannabis-scientifically.html 12 Sept 2016

At Californian methadone clinics, group education sessions led by a nurse and focused on the risks of aggravating hepatitis infection led to the same substantial reductions in drinking as one-to-one or group motivational interviewing conducted by highly trained counsellors, offering a cost-effective means to reduce alcohol-related risks.

Summary Many methadone-maintained patients drink excessively, a particular concern among those infected with hepatitis C for whom drinking may accelerate disease progression. Motivational interviewing is the most popular counselling approach found to reduce drinking, but so far no studies have tested it among patients treated for opioid dependence in methadone maintenance programmes.

The featured study aimed to start to fill this gap in the research and at the same time (given the dominance of group counselling in US treatment services) compare one-to-one motivational interviewing with the less familiar group version, and with a nurse-led group education programme focused on the relation between drinking and disease related to hepatitis C infection.

Each of the three approaches occupied three fortnightly one-hour sessions over the first six weeks after patients started methadone treatment. Interventions were guided by set protocols and delivered by staff trained in these approaches and supervised to help ensure they delivered them as intended. Patients were paid $5 for each session they attended.

Group and individual motivational sessions were generally conducted by different counsellors. Sessions explored the impact of drinking on health and risky behaviours and while focusing on life goals, worked through ambivalence about cutting drinking. Sessions were open, meaning that patients who had not completed three sessions in their original group could join a later one. Instead of a motivational approach, the nurse-led (assisted by a hepatitis-trained research assistant) hepatitis health promotion programme adopted an educational format. Sessions focused on the progression of hepatitis infection and culturally-sensitive strategies to prevent liver damage. Content included the dangers of drinking while infected with hepatitis, strategies for avoiding drinking and drug use, diet, the dangers of reinfection with hepatitis C if patients inject, other infection routes, consistently looking after one’s health, and seeking social support and building self-esteem.

After these sessions patients suitable for this started a course of hepatitis A and B vaccinations, concluding at the same time as a six-month follow-up interview.

Participants in the study were 256 adult drinkers starting methadone treatment at five Californian clinics who scored as moderate or heavy drinkers on a baseline questionnaire. They were randomly allocated to the three approaches to reducing drinking. Typically they were black or Latino men. On entering treatment about half had drunk at least 90 US standard drinks in the past month. On average 87% of the patients completed all three of the study’s counselling/education sessions and 91% completed the six-month follow-up.

Main findings

The main outcome tested by the study was the proportion of patients who cut their drinking by half from the month before they started treatment to the month before the six-month follow-up. On this yardstick, and on the yardstick of total abstinence, there were not only no statistically significant differences between patients allocated to the three interventions, but also no substantial differences. In each group about half the patients halved their drinking, ranging from 54% after group motivational sessions to 49% after hepatitis education and 47% after one-to-one motivational sessions, and from 20–23% had not drunk at all in the past month.

Once other variables had been taken in to account, across the three sets of patients the strongest predictor of which patients would halve their drinking was how much they drank before treatment; the more they drank, the more likely they were to halve it. Women were more likely to halve their drinking than men as were better educated patients and those who took at least one dose of vaccine, while less likely were those whose partners were also drug users or who had recently used cannabis.

The authors’ conclusions

The major finding of this study was that all three interventions were followed by roughly equally substantial reductions in drinking at the six-month follow-up. Delivered by trained therapists, group and one-to-one motivational interviewing sessions neither differed in effectiveness from each other nor from a nurse-led group hepatitis education programme focused on reducing drinking.

For services the implications are that the cost-saving group format can be used without detriment to effectiveness and that costs may also be saved by implementing programmes led by nurses rather than therapists, with the potential added benefit that such programmes can be integrated within more comprehensive health promotion. Research nurses also administered the vaccines, receipt of which was associated with drinking reductions, perhaps partly because of the extra time and attention required to explain the vaccine.

It should be acknowledged that any differences between the interventions may have been obscured by differences between the staff implementing them, and that patients had volunteered for a research study rather than being counselled during routine practice.

Source:  Drug and Alcohol Dependence: 2010, 107(1), p. 23–30.Reported in Findings.org.uk

Filed under: Alcohol,Treatment,USA :

In Illinois in the USA, randomly allocating towns to enforce laws against youth smoking in public led not just to fewer youth smoking but also fewer drinking or using and being offered illegal drugs – did anti-tobacco policing spill-over to create an environment unfriendly to drinking and illegal drug use?

Summary The featured report drew its data from a study which randomly assigned 24 towns in the US state of in Illinois to either more vigorously enforce laws prohibiting under-age possession and use of tobacco, or to continue with existing low-level enforcement practices, a study which showed the intended effects on youth smoking. The issue addressed by the featured report was whether this spilled over to affect other forms of substance use and availability.

The towns selected for and which (via their officials) agreed to participate in the study were also all engaged in a state-sponsored programme intensifying enforcement of the ban on commercial tobacco sales to youngsters under the age of 18. The difference in the 12 towns allocated to enhanced enforcement was that this was supplemented by intensified enforcement of laws against young people having or using tobacco, in particular by levying civic fines against minors caught using or possessing tobacco in public. By design, at the start of the study all the towns only infrequently enforced these laws, a situation continued in the 12 control towns not allocated to enhanced enforcement.

Assignment had the intended effect; over the four years of the study, the average yearly number of anti-tobacco citations issued to minors was significantly higher (17 v. 6) in towns assigned to enhanced enforcement than in control towns.

Earlier reports on the study also showed the intended impact on youth smoking, which increased at a significantly slower rate for adolescents in towns where enforcement was extended. The researcher-administered, confidential surveys of school pupils which established this also asked about current (past 30 days) and ever use of substances other than tobacco. The key statistics for the study were the total number of different types of drugs the student had recently or ever used, averaged over pupils in the same town to assess the impacts on youth in the town as a whole. Pupils were also asked how many times over the past year someone had tried to give or sell them illegal drugs. These surveys were administered in four succeeding years to students from grade seven (age 12–13) up to grade ten in 2002, 11 in 2003, and 12 in 2004 and 2005, meaning that in each year some of the same pupils but also many new ones were sampled.

Across the four waves of data collection 52,550 pupils were eligible to be surveyed of whom 29,851 (57%) completed at least one survey. From these were selected only the 25,404 pupils (who completed 50,725 surveys) living in the 24 towns in the study.

Main findings

At the start of the study towns in the two sets of 12 did not differ in the number of substances currently or ever used by their pupils. As the different tobacco enforcement policies were implemented, over the succeeding three years the number of different drugs that a pupil currently or had ever used increased significantly less steeply in towns assigned to enhanced tobacco enforcement. There was a similar and also statistically significant result for offers of illicit drugs.

Use of substances other than tobacco was dominated by alcohol, so a further analysis focused on this substance alone. Again, increases in the average proportions of pupils who had recently or ever drank alcohol were significantly less steep in towns assigned to enhanced tobacco enforcement.

Though differences between the two sets of towns were statistically significant they were modest, and in both sets most substances had or were being used by few pupils.

The authors’ conclusions

In this study, towns allocated to heightened enforcement of laws prohibiting youth possession and use of tobacco experienced relatively lower increases in the probability that their young people had or were using a number of different substances or had been exposed to an offer of illicit drugs, providing preliminary evidence that police efforts to reduce specific substance use behaviours might have a positive spill-over effect on other high-risk activities. Given the co-occurrence of different forms of substance use, strategies that strengthen community norms against youth tobacco use might work synergistically to help reduce youth drug use and illicit drug offers.

How did an enforcement effort focused exclusively on tobacco affect use and availability of other substances? There are several possible explanations. Being punished for tobacco-related crimes might deter individual children from possessing and using other drugs, and the knowledge that police in enforcement towns approach youngsters to enforce anti-tobacco laws may deter young people and even adults from selling drugs in these communities. Possibly relevant too is the ‘broken window’ approach to enforcement, supported by studies which have shown that enforcement of laws against lower-level crimes can deter more serious offences. According to this theory, creating an environment where youth cigarette use is not tolerated might create an unfavourable environment for drug use. More directly, greater contact between young people and police enforcing underage tobacco laws might give police more chances to search for and confiscate illegal drugs.

Police believe that publicly smoking cigarettes acts as a signal to drug dealers that a young person might also be in the market for drugs. If so, making youth smoking less visible in a town may also make that town less attractive to dealers. Reduced visibility may also minimise the perception that illegal behaviour is normal and acceptable in that community. The effect could be to reduce sales attempts by make potential young customers less obvious and by making the entire town seem an undesirable dealing location. Alternatively, the findings might reflect reduced offers of alcohol or other drugs from friends rather than drug dealers, because reductions in use of tobacco spread to other substances, especially alcohol.

However, alcohol not illegal drugs might account for the bulk of the findings. Use of tobacco and alcohol tend to go together, so if police crack down on tobacco, they might also discourage drinking.

Source: Journal of Community Psychology: 2010, 38(1), p. 1–15.

 

Given that the health of American youth is in question and that so many states base their policies on reports issued by the State of Colorado, it is important to understand what the 2015 Healthy Kids Colorado Survey (HKCS) actually tells us.

The survey’s results are gleaned from voluntarily self-reported information collected every other year from Colorado middle-school and high-school students. It is produced by a partnership of the Colorado Department of Education, Colorado Department of Human Services, the Colorado Department of Public Health and the Environment and the University of Colorado.



News organizations tracking the impact of marijuana on Colorado since voters sanctioned the drug for medical and recreational use are understandably quick to report the survey’s findings — but they’re unfortunately just as quick to deliver inaccurate and misleading information. Coverage of the 2015 survey results was especially poor. Dozens of news organizations — including The Denver PostFox News, the Washington PostTimeScientific American and Reuters — should correct and clarify their work.

Why? Because for many reasons, the 2015 survey’s data do not support claims that marijuana use among Colorado teenagers has remained flat or has declined. Examination of the survey’s aggregate data, segmented by grade and geographic region, tells a different story than the Marijuana Infographic and some passages of the executive summary distributed by state officials.

New reporting should inform the public about youth marijuana use rates in several Colorado regions — particularly where marijuana is most heavily commercialized.

Here are some important things to know about the 2015 survey:

Because of its methodology and sample size, this survey is a snapshot in time that represents no one other than the Colorado youth who took it. It is inaccurate to present or describe the 2015 survey as a “state survey” or to present its findings as average use rates among Colorado youth. The 2015 survey does not include data from El Paso County (home to the state’s second largest city, Colorado Springs), Jefferson and Douglas counties (home to two of the state’s largest school districts) and Weld County. It is also important to note that Colorado’s private and parochial schools do not participate in this survey and that only students attending school are surveyed. Students with drug problems are less likely to be in school — and, therefore, less likely to be surveyed.

Differences in methodology make it difficult to compare the 2015 survey to previous HKC surveys. The randomly selected sample size dropped from 40,206 in 2013 to 15,970 in 2015. Similarly, the high school response rate dropped from 58 percent in 2013 to 46.5 percent in 2015. Counties participating in the survey also changed from 2013 to 2015. Clearly, something in the survey methods changed from 2013 to 2015, making direct comparisons risky. But if state officials and journalists insist on making these direct comparisons, there are significant increases in youth marijuana use to report from 2013 to 2015 — as detailed below. They should report this information to the public.

Because of differences in methodology, Colorado survey results should not be directly compared to other national studies of adolescent marijuana-use rates, such as the Centers for Disease Control’s Youth Risk Behavior Survey (YRBS). These surveys are different. For example, the YRBS requires a response rate of at least 60 percent. If student responses fall below that mark, the YRBS states the results “represent only the students participating in the survey.” Of note, the HKCS did not reach this threshold for high school students in either 2013 or 2015. Therefore, direct comparisons of the two studies is risky. Such differences in methodology also make it risky to compare the Colorado data and other national studies, such as the Substance Abuse and Mental Health Service Administration’s National Survey on Drug Use and Health and the Monitoring the Future (MTF), a survey from the National Institute on Drug Abuse run by contract through the University of Michigan. Further, the 2015 state report’s comparisons to a “national average” of youth marijuana use are also problematic. Please review explanations here and here from David Murray, a former chief scientist of the White House Office of National Drug Control Policy, who now serves as a senior fellow analyzing drug policy at the Hudson Institute. Among his observations:

“What is the possible source for deriving that ‘national average’? There is one genuinely national sample of youth drug use, that from the National Survey on Drug Use and Health (NSDUH) that covers all states. But this cannot be the basis for the (State of Colorado’s) claim. In their latest 2014 estimates, NSDUH reported that 7.2 percent of adolescents aged 12 to 17 across the nation used marijuana in the past month – that figure, not 21.7 percent, would be the youth ‘national average.’ Moreover, the NSDUH specifically declared that Colorado had the nation’s highest rates. Adolescent marijuana use ranged from 4.98 percent in Alabama to 12.56 percent in Colorado. Worse, the NSDUH showed for youth that from 2009, when medical marijuana took off in Colorado, there has been a stunning rise of 27 percent through 2014 (from 9.91 percent to 12.56 percent). So Colorado youth use rates in the NSDUH are not only higher than the national average, but, after freer access to marijuana, have been steeply climbing.”

To examine drug-use trends from year to year and make comparisons between states, the NSDUH is more reliable (not perfect, but more reliable). The NSDUH interviews youth who are in and out of school. It is conducted in every state — and, unlike the current version of the Colorado Healthy Kids survey, it has data from before 2013. Unfortunately, as Murray notes above, this survey shows the prevalence of past-month marijuana use among Colorado youth has increased, with Colorado ranked first among 12-17 year olds in 2014.

One strength of the HKCS is that it offers some county-level data. It is helpful to have a fine-grain look at what is happening at a local level. So, if we must compare 2013 and 2015 survey results, it is best to limit comparisons to the responses of specific regions as defined by the survey. You can find a map of those regions here. Because there are many differences between high school freshmen and seniors, combining their class data — especially given that 18-year-olds in Colorado can purchase medical marijuana legally — can give false impressions about “teen use” rates. So, it is important to segment students by grade for a more accurate look at marijuana use rates.

Remember: Because of significant differences in methodology and sample size, the 2015 HKCS shouldn’t be compared to its 2013 predecessor or any national survey — but if state officials and journalists insist on doing so, let’s all consider this closer look at student respondents by grade and region. It suggests adolescent marijuana use rates has reached levels worth considering a serious health problem in some parts of the state.

For a full breakdown of the regional data, please see this chart (produced with the significant help of Christine Miller, a Ph.D. pharmacologist and Colorado native). Among the findings:


Region 16 (Boulder, Broomfield): High school seniors in this region reported the highest rate of past-month use among 12th graders in the state. In 2015, 42.2 percent of high school seniors reported past-month use, versus 28.5 in 2013. That’s a 48.1 percent increase. The use rate among high school juniors in this region jumped from 22.3 percent to 33.4 percent, a 49.8 percent increase.

Region 20 (Denver): Use among high school seniors increased from 30 percent in 2013 to 33 percent in 2015, a jump of 10 percent. Among juniors, the use rate increased from 29 percent to 37.7 percent, an increase of 30 percent.

Region 12: Western Corridor (Summit, Eagle-Vail): Use among high school seniors increased 90 percent from 20.1 percent in 2013 to 38.2 percent in 2015. As a curious side note, this region also reported a 2.3 percent decrease in past-month marijuana use among high school juniors and a 54.7 percent increase among its high school sophomores.

Region 11: Northwest (Steamboat Springs, Craig): Marijuana use among this region’s high school students rose in grades 9-12. Among seniors the rate increased 57.3 percent from 22.5 percent in 2013 to 35.4 percent in 2015. Among juniors, use rose 18.8 percent from 18.1 percent to 21.5 percent. Among sophomores, use rose 72 percent from 8.2 percent in 2013 to 14.1 percent in 2015. Among freshmen, use rose 22.2 percent from 8.1 to 9.9 percent.

Region 19: (Mesa County/Grand Junction): Use among freshmen jumped to 13.7 percent, an increase of 57.5 percent from 2013. Use among sophomores increased 50.6 percent from 26.2 percent from 17.4 percent in 2013. The use rate among high school seniors rose to 24.4 percent, an increase of 20.8 percent.

Region 7: Pueblo: Although there was little change in use rates, the rates remain stubbornly high. They are higher than the state average for all grades; ranges from double the state average for high school freshmen to 31 percent greater than the state average for high school seniors.

A common theme among these regions is a high level of marijuana commercialization in the forms of retail and medical stores. Other commonalities should be investigated to determine the most appropriate interventions.

Analysis of the 2015 survey also found some good news — particularly in regions 8 (San Luis Valley), 10 (West Central, including Gunnison, Hinsdale and Montrose ) and 17 (Central, including Gilpin and Teller).The reasons for these reported declines in past-month use should be explored. For example, are the declines because of an effective intervention, or are they related to a change in the survey methodology from 2013 to 2015? Based on the findings, protocols for prevention and intervention should be implemented to encourage similarly favorable results in other school districts throughout the state.

This entry for DrThurstone.com was co-written by Dr. Christian Thurstone and Christine Tatum. He is an associate professor of addiction psychiatry and the director of medical training of the addiction psychiatry fellowship program at the University of Colorado. She is a longtime journalist, former national president of the Society of Professional Journalists and Dr. Thurstone’s wife. Together, they also wrote Clearing the Haze: Helping Families Face Teen Addiction(Rowman & Littlefield, 2015).

 

Source:  http://drthurstone.com/healthy-kids-colorado-survey-2015/    5th July 2016

Imagine for a minute a world in which marijuana is available in a vending machine or corner grocery store near you — like any other snack machine — pot-infused lollipops, gummy candies, baked goods and beverages available at the push of a button.

As futuristic as this farfetched tale sounds, this is Colorado’s reality, a state with the dubious distinction of becoming the first to legalize marijuana, which has helped spawn legalization efforts across the U.S., including in New Jersey.   And while Colorado’s experiment has sparked heated debate over drug legalization, a critical and unbiased look at the data clearly shows that marijuana legalization has serious and far-reaching consequences that far outweigh any of its alleged benefits.

Strong emotions on both sides of this issue should not obscure the facts. Marijuana is an addictive substance that is harmful to users, especially to its younger users. As a teen’s brain development is disturbed by chronic marijuana use, the risk for physical and psychological dependency grows exponentially.

In addition to permanently affecting brain functioning, marijuana use can lead to a wide array of negative consequences, ranging from lower grades and isolation from family to an increased risk of psychotic symptoms, depression and suicide.

According to the Office of National Drug Control Policy, legalization will cause a substantial increase in economic and social costs.  The expansion of drug use will increase crime committed under the influence of drugs, as well as family violence, vehicular crashes, work-related injuries and a variety of health-related problems. These new costs will far outweigh any income from taxes on drugs.

Few would argue that a drug that can cause such destruction is something that we should counsel people to avoid. However, legalization efforts do just the opposite. In fact, experience has shown that when drugs are legalized, drug use increases because the perception of harm is reduced.

Moreover, the Drug Enforcement Agency has estimated that legalization could double or even triple the amount of marijuana users.

While it is hard to fathom the societal impact of an additional 17 million to 34 million marijuana users, it is safe to assume that those who profit from legalization have calculated the impact on their bottom line.

Those in favor of legalization often fail to tell you that levels of drug use have gone down substantially since the 1970s when the “war” on drugs began. This is not to say that our drug laws, including those governing marijuana, are not in need of reform.

For instance, the effort to place more drug users into treatment instead of prison is a positive development, both for those struggling with addiction and for taxpayers.

However, reforming and improving our drug laws does not mean we should abandon our fight against the use of illegal drugs like marijuana.

On the contrary, the more we learn about effective methods of combating drug use, the more we learn that legalization is not the answer, and is, in fact, very much part of the problem.

Source:  Source:  www.njassemblyrepublicans.com  Daily Record 13 Apr 2014

 

At one point a few days ago I feared to turn on the radio or TV because of the ceaseless accounts of blood, death and screams, one outrage after another, which would pour out of screen or loudspeaker if I did so.

And I thought that one of the most important questions we face is this: How can we prevent or at least reduce the horrifying number of rampage murders across the world?

Let me suggest that we might best do so by thinking, and studying. A strange new sort of violence is abroad in the world. From Japan to Florida to Texas to France to Germany, Norway and Finland, we learn almost weekly of wild massacres, in which the weapon is sometimes a gun, sometimes a knife, or even a lorry. In one case the pilot of an airliner deliberately flew his craft into a hillside and slaughtered everyone on board. But the victims are always wholly innocent – and could have been us.

The culprits of the Charlie Hebdo murders, all had drugs records or connections. The same was true of the Bataclan gang, of the Tunis beach killer and of the Thalys train terrorist

I absolutely do not claim to know the answer to this. But I have, with the limited resources at my disposal, been following up as many of these cases as I can, way beyond the original headlines.

* Those easiest to follow are the major tragedies, such as the Oklahoma City bombing, the Nice, Orlando, Munich and Paris killings, the Anders Breivik affair and the awful care-home massacre in Japan last week. These are covered in depth. Facts emerge that do not emerge in more routine crimes, even if they are present.

Let me tell you what I have found. Timothy McVeigh, the 1995 Oklahoma bomber, used cannabis and methamphetamine. Anders Breivik took the steroid Stanozolol and the quasi-amphetamine ephedrine. Omar Mateen, culprit of the more recent Orlando massacre, also took steroids, as did Raoul Moat, who a few years ago terrorised the North East of England. So did the remorseless David Bieber, who killed a policeman and nearly murdered two others on a rampage in Leeds in 2003.

Eric Harris, one of the culprits of the Columbine school shooting, took the SSRI antidepressant Luvox. His accomplice Dylan Klebold’s medical records remain sealed, as do those of several other school killers. But we know for sure that Patrick Purdy, culprit of the 1989 Cleveland school shooting, and Jeff Weise, culprit of the 2005 Red Lake Senior High School shootings, had been taking ‘antidepressants’.

So had Michael McDermott, culprit of the 2000 Wakefield massacre in Massachusetts. So had Kip Kinkel, responsible for a 1998 murder spree in Oregon. So had John Hinckley, who tried to murder US President Ronald Reagan in 1981 and is now being prepared for release. So had Andreas Lubitz, the German wings pilot who murdered all his passengers last year. The San Bernardino killers had been taking the benzodiazepine Xanax and the amphetamine Adderall.

The killers of Lee Rigby were (like McVeigh) cannabis users. So was the killer of Canadian soldier Nathan Cirillo in 2014 in Ottawa (and the separate killer of another Canadian soldier elsewhere in the same year). So was Jared Loughner, culprit of a 2011 mass shooting in Tucson, Arizona. So was the Leytonstone Tube station knife attacker last year. So is Satoshi Uematsu, filmed grinning at Japanese TV cameras after being accused of a horrible knife rampage in a home for the disabled in Sagamihara.

I know that many wish to accept the simple explanation that recent violence is solely explained by Islamic fanaticism. No doubt it’s involved. Please understand that I am not trying to excuse or exonerate terrorism when I say what follows.

But when I checked the culprits of the Charlie Hebdo murders, all had drugs records or connections. The same was true of the Bataclan gang, of the Tunis beach killer and of the Thalys train terrorist.

It is also true of the two young men who murdered a defenceless and aged priest near Rouen last week. One of them had also been hospitalised as a teenager for mental disorders and so almost certainly prescribed powerful psychiatric drugs.

The Nice killer had been smoking marijuana and taking mind-altering prescription drugs, almost certainly ‘antidepressants’.

As an experienced Paris journalist said to me on Friday: ‘After covering all of the recent terrorist attacks here, I’d conclude that the hit-and-die killers involved all spent the vast majority of their miserable lives smoking cannabis while playing hugely violent video games.’

The Munich shopping mall killer had spent months in a mental hospital being treated (almost certainly with drugs) for depression and anxiety

Now look at the German events, eclipsed by Rouen. The Ansbach suicide bomber had a string of drug offences. So did the machete killer who murdered a woman on a train in Stuttgart. The Munich shopping mall killer had spent months in a mental hospital being treated (almost certainly with drugs) for depression and anxiety.

Here is my point. We know far more about these highly publicised cases than we do about most crimes. Given that mind-altering drugs, legal or illegal, are present in so many of them, shouldn’t we be enquiring into the possibility that the link might be significant in a much wider number of violent killings? And, if it turns out that it is, we might be able to save many lives in future.

Isn’t that worth a little thought and effort?

Source:  PETER HITCHENS FOR THE MAIL ON SUNDAY

PUBLISHED: 00:55, 31 July 2016 | UPDATED: 18:36, 31 July 2016

 

Pot for the poor! That could be the new slogan of marijuana legalization advocates.

In 1996, California became the first state to legalize the use of medical marijuana. There are now 25 states that permit the use of marijuana, including four as well as the District of Columbia that permit it for purely recreational use.

Colorado and Washington were the first to pass those laws in 2012. At least five states have measures on the ballot this fall that would legalize recreational use. And that number is only likely to rise with an all-time high (no pun intended) of 58 percent of Americans (according to a Gallup poll last year) favoring legalization.

The effects of these new laws have been immediate. One study, which collected data from 2011-12 and 2012-13, showed a 22 percent increase in monthly use in Colorado. The percentage of people there who used daily or almost daily also went up. So have marijuana-related driving fatalities. And so have incidents of children being hospitalized for accidentally ingesting edible marijuana products.

But legalization and our growing cultural acceptance of marijuana have disproportionately affected one group in particular: the lower class.

A recent study by Steven Davenport of RAND and Jonathan Caulkins of Carnegie Mellon notes that “despite the popular stereotype of marijuana users as well-off and well-educated . . . they lag behind national averages” on both income and schooling.

For instance, people who have a household income of less than $20,000 a year comprise 19 percent of the population but make up 28 percent of marijuana users. And even though those who earn more than $75,000 make up 33 percent of the population, 25 percent of them are marijuana users. Having more education also seems to make it less likely that you are a user. College graduates make up 27 percent of the population but only 19 percent of marijuana users.

The middle and upper classes have been the ones out there pushing for decriminalization and legalization measures, and they have also tried to demolish the cultural taboo against smoking pot. But they themselves have chosen not to partake very much. Which is not surprising. Middle-class men and women who have jobs and families know that this is not a habit they want to take up with any regularity because it will interfere with their ability to do their jobs and take care of their families.

But the poor, who already have a hard time holding down jobs and taking care of their families, are more frequently using a drug that makes it harder for them to focus, to remember things and to behave responsibly.

Legalization and our growing cultural acceptance of marijuana have disproportionately affected one group in particular: the lower class.

The new study, which looked at use rates between 1992 and 2013, also found that the intensity of use had increased in this time. The proportion of users who smoke daily or near daily has increased from 1 in 9 to 1 in 3. As Davenport tells me, “This dispels the idea that the typical user is someone on weekends who has a casual habit.”

Sally Satel, a psychiatrist and lecturer at Yale, says that “it is ironic that the people lobbying for liberalized marijuana access do not appear to be the group that is consuming the bulk of it.” Instead, it’s “daily and near-daily users, who are less educated, less affluent and less in control of their use.”

In fact, the typical user is much more likely to be someone at the bottom of the socioeconomic ladder, whose daily life is driven, at least in part, by the question of how and where to get more marijuana. Just consider the cost. Almost a third of users are spending a tenth of their income on marijuana. And 15 percent of users spend nearly a quarter of their income to purchase the drug. The poor have not only become the heaviest users, but their use is making them poorer.

To all the middle-class professionals out there reading this: Do you know anyone who spends a quarter of their income on pot? Of course not. But these are the people our policies and attitudes are affecting.

As the authors of the study note, marijuana use today actually more closely resembles tobacco use than alcohol use. Cigarette smoking has completely fallen off among the educated and well-off, while the poor and working class have continued their habits. Even as far back as 2008, a Gallup poll found that the rate of smoking among people making less than $24,000 a year was more than double that of those making $90,000 or more.

But at least the rates have been going down for everyone. Thanks to a cultural shift on the acceptability of smoking, awareness campaigns about its dangers and a variety of legal measures regarding smoking in public facilities, smoking is significantly less popular. You could object to some of these public policies on the grounds that the government should mind its own business. But the truth is that Americans across all incomes are now less likely to suffer from the harmful effects of smoking.

Maybe the upper classes in this country have some romantic notion of what marijuana can do to the mind (though we once thought cigarettes were terribly classy too). But it is time to get over such silliness and consider the real effects of our attitudes.

As Manhattan Institute fellow and psychiatrist Theodore Dalrymple says, this is like the 1960s all over again. He tells me, “I’m afraid I can’t hear all that stuff about ‘tune in, drop out’ without being infuriated because the people affected really deleteriously [are] people at the bottom.”

Source: http://nypost.com/2016/08/20/legalized-pot-is-making-americas-lower-class-poorer-and-less-responsible/

Hard-partying Baby Boomer parents are more tolerant of drugs and alcohol, and their liberal attitudes may be paying off in an unexpected way.

There’s something terribly wrong with kids these days: a series of major surveys, conducted by the government every two years, suggest that they might just be the most well-behaved generation in recent memory. Teens are increasingly swearing off alcohol, cigarettes, drugs likesynthetic marijuana, and prescription painkillers, according to the latest survey of of more than 50,000 8th, 10th, and 12th graders from the National Institute on Drug Abuse’s Monitoring the Future (MTF) survey. For some illicit substances, such as cocaine and heroin, consumption has dropped to its lowest point since the MTF’s inception in 1975 (fading stigmas around marijuana consumption may be responsible for its relatively consistent popularity amid this decline). The most recent Youth Risk Behavior Survey (YRBS) shows that cigarette smoking is at its lowest level in 24 years—11 percent in 2015, down from 28 percent in 1991. Rates of underage sex, teen pregnancy, HIV, and other sexually transmitted diseases have also declined according to a survey of 16,000 students by the Centers for Disease Control and Prevention (CDC). The kids, apparently, are all right.

But why? Conventional wisdom suggests this shouldn’t be the case. This is a generation that’s taking its cues from their Baby Boomer parents, those 76 million Americans born roughly between 1946 and 1964 who are veterans of the sexual and psychedelic revolutions of the 1960s and 70s and launched the modern trends in risky behaviors measured by surveys like the MTF and YRBS. According to the Substance Abuse and Mental Health Services Administration (SAMHSA), Baby Boomers havemaintained their hard-partying ways more than any other generation. Parental attitudes towards addiction matter. Research suggests that children of addicted parents are more likely to develop substance abuse problems themselves—due to both modeling and lax oversight. A recent longitudinal study of adolescents between 1994 and 2008 confirms that parents with permissive attitudes tend to breed self-destructive behaviors in their children; by contrast, the children of authoritative parents (or were even connected to authoritative adults through friends) were “40 percent less likely to drink to the point of drunkenness, 38 percent less likely to binge drink, 39 percent less likely to smoke cigarettes, and 43 percent less likely to use marijuana.”

So why are today’s young people resisting the allure of binge-drinking and illicit drugs that ensnared their Boomer parents? Perhaps it is precisely due to Baby Boomers’ libertine drug experiences that their children are inclined to avoid substance abuse. This may not just be out of disgust with their parental cautionary tales. Thanks to theirenthusiastic embrace of coddling- and self-esteem-focused helicopter parenting—Boomer parents may actually be better equipped to preemptively (and subsequently) engage their children in the type of interventions that help inoculate their kids against the risks of substance abuse.

Part of that progress is due to our increased knowledge about just what kind of interventions are effective in deterring drug use. Nancy Reagan’s famous “Just Say No” campaign in the 1980s catalyzed concern around adolescent drug use, but interventions that focused purely on abstinence or punishment (like, say, the armed police officer at the front of a D.A.R.E. session) tended to be ineffective. Programs centered on the threat of discipline — you’re going to get arrested, suspended or labeled a criminal in some other way — tend to alienate young people from seeking help from authority figures by perpetuating the stigma surrounding drug addiction, creating a gulf between young people and their parents. A 2014 examination of “just say no” programs by Scientific American found that the most effective substance abuse regimes focused on positive interactions between instructors and students that worked on developing social skills and behavioral norms. Skill development, including communication, goal setting, and negotiation, are the most important tools young people can learn regarding substance abuse, says Dr. Stephanie Zaza, the director of the CDC’s Division of Adolescent and School Health (DASH) which oversees the YRBS. “When students are confronted with an environment that has a lot of temptations, they need to be able to ask questions, talk things through, and stand up for themselves,” she says.

In other words, the same impulse that inspired Baby Boomers’ enthusiastic rebellion—the desire to push back against the strict traditions and institutions of their parents—led to a shift in parenting styles that incorporated their relatively lax views of alcohol and drug consumption with a less authoritative mode of parenting than they experienced as children themselves. More productive interventions (think “talk to your kids about drugs)” emerged as parenting methods of choice. These were widely embraced among open-minded Boomer parents with first-hand experience in the risky behavior they want to prevent. After all, the Boomers have always been “less moralistic about drug use” and more likely to blame society for their ills than their parents, as sociologist Robert Putnam observed in 2001; drugs are a problem to be addressed, not a behavior to be punished. Hell, Boomer parents are more likely to worry about bullying and depression than drug abuse, according to 2015 data from the Pew Research Center. This change in approach seems to be paying off: A 2010 longitudinalexamination of parenting practices across three generations (Gen X and older Millennial children, their Boomer parents and their “Greatest Generation” grandparents) published in Developmental Psychologyfound that the harsh discipline and overbearing monitoring Boomers experienced tended to catalyze externalized behavior problems like “poor

impulse control and oppositional, aggressive, or delinquent behavior.” When harsh discipline was in turn handed down by Boomers, it also spurred bad behavior among their children. But Boomers, by contrast, also engaged in other forms parental monitoring (observing behavior, frank conversations and the like) that lacked harsh behavioral consequences. These more gentle interventions tended to have a mediating effect between Baby Boomers and their children, a unique relationship absent from Boomers and their own discipline-happy parents.

For Boomers, “parental monitoring” takes the form of openness and trust, a propensity to engage with their children rather than merely discipline or alienate them with the likes of D.A.R.E. or Scared Straight. According UC Berkeley psychologist Diana Baumrind’s landmark 1991 research published in The Journal of Early Adolescence, it’s this balance between being demanding (focused on discipline and control) and being responsive (focused on fostering individuality and self-regulation) that both deters children from substance abuse and engenders them with the important social skills that help them avoid risky behaviors without constant parental supervision. Though we often write off this type of engagement as intrusive helicopter parenting and debilitating condescension, this style also comes with a level of empathy, openness, and engagement that helps children fully absorb and comprehend the consequences of substance abuse.

“What [the CDC] knows about parental and school engagement is simple: the more you talk with children about these issues, the less likely they are to do things,” says Dr. Zaza.

It takes more than a bad trip (or a really, really good one) at college to induce parents to change how they communicate to their kids about youth attitudes about illicit substances. The high expectations of overachieving established by Boomer parents certainly help ward kids away from addiction. According to SAMHSA, fear of disappointing ones parents is an increasingly common disincentive to experiment with illicit substances. But those parents who were either less demanding (i.e. permissive parents) or less responsive (authoritarian parents) were less likely to keep their children drug-free. By ensuring interventions are staged by emotional peers and not merely authority figures, parents are more likely to impart the social skills designed to help their children avoid developing a drug problem.

Of course, not every Boomer parent is immediately equipped to stage an in-home intervention just because they smoked a few joints at Woodstock. While a 2001 study found that some 94 percent of parents claimed to have discussed the consequences of substance abuse with their kids, 39 percent of their teenagers said the conversations never actually took place. And too much leniency can be a serious problem: a lack of boundaries and rules in an overly-permissive parent can increase the risk of drug or alcohol abuse, a reminder that “letting kids drink in a safe space” like your home probably isn’t the best idea.

But as far as today’s kids are concerned, actually talking with their once-wild and crazy parents may be the best cure for the scourge of drug addiction. Growing up, I knew that no matter what I did in the way of drugs and alcohol, I could always turn to my own Boomer parents for help and support if I was in trouble, an unspoken agreement that was, in some ways, the foundation of our relationship during my turbulent teen years—all because I knew they would actually understand what I was talking about. While the Boomers have their own issues with illicit substances, they have the experience and compassion to help future generations prepare for the dangerous world of drugs and alcohol better than any previous one. It may have been a long strange trip for the Boomers, but it needn’t go on forever.

Source: http://www.thedailybeast.com/articles/2016/08/07/your-kids-are-better-behaved-than-you.html     7th August 2016 

Filed under: Social Affairs (Papers) :

Even in a culture that puts safety above all else, pilots aren’t properly educated about the potential dangers of common drugs such as antihistamines and sleeping pills. That’s the conclusion from a new National Transportation Safety Board report on rising drug use among aviators, which largely mirrors trends of greater use of prescription, over-the-counter, and illicit drugs by Americans in general.

About 40 percent of the 6,667 pilots killed in accidents since 1990 had prescription, over-the-counter, or illicit drugs in their bodies, according to a study of nearly 6,600 accidents from 1990 to 2012. Over-the-counter antihistamines such as Benadryl and Claritin were the most common. Antihistamine use rose to almost 10 percent between 2008 and 2012, up from 5.6 percent in the 1990s.

The vast majority of those killed in the period of the study—96 percent—were general aviation pilots typically flying small, one-engine planes; less than 1 percent of incidents involved major airlines. The study focused on evidence of drug use, not on whether the effects of the drug led to impairment while flying. Alcohol was not included in the study because toxicology screenings often detect ethanol the body creates naturally after death.

Use of illicit drugs such as marijuana and cocaine increased to almost 4 percent in the 2008-12 span, up from 2.3 percent in the 1990s. Most of the illicit drugs in the study resulted from greater use of marijuana among the pilots who died, the agency said.

The NTSB, which recommends safety improvements, called on the Federal Aviation Administration to better educate pilots about the potential dangers of some common drugs and develop a policy on marijuana use by pilots. Colorado and Washington have legalized marijuana for adult use, and almost two dozen other states allow marijuana for medical uses. More states are also likely to vote on legalizing recreational and medical marijuana use.

Dr. Mary Pat McKay, the NTSB’s chief medical officer, said more research is needed to determine how drugs can interact with each other and lead to pilot impairment. Sleep aids and pain medications, for example, can hurt pilot performance and yet there aren’t guidelines on how pilots might safely use those drugs.

Source: www.businessweek.com  10th Sept. 2014

If medical marijuana is a step toward legalization, just make it legal — or at least decriminalize it — and don’t dump it all on doctors. Making physicians the gatekeepers of legal marijuana is not fair to doctors and is not conducive to public health.

The problem is that marijuana has been prescribed by the courts, not by health-care professionals.

“Dried marijuana is not an approved drug or medicine in Canada,” says the Health Canada website. “The Government of Canada does not endorse the use of marijuana, but the courts have required reasonable access to a legal source of marijuana when authorized by a physician.” Many physicians are reluctant to take on that responsibility.

“We have Health Canada telling us that marijuana is not a medicine, we have our malpractice insurance company telling us to be very cautious because nobody is taking responsibility for the safety of it,” says Dr. Chris Simpson, a Queen’s University cardiologist and incoming president of the Canadian Medical Association.

Simpson doesn’t dismiss marijuana — he says “many compelling anecdotes” indicate that marijuana can help patients with HIV, hard-to-treat seizures and other conditions. But, he adds, “we have people out there saying marijuana can cure cancer, which seems quite improbable.”

“Somewhere in between those two extremes is the truth, and I think we need to find the truth, and the way to do that is with the appropriate research.” Testifying before a parliamentary health committee in May, Dr. Meldon Kahan, medical director of the substance-use service at Women’s College Hospital in Toronto, detailed a long list of harmful effects from cannabis use. They included impairments in attention, increased anxieties, psychosis and cancer.

“Widespread cannabis prescribing by physicians will increase the social and psychiatric harms of cannabis,” Kahan said, calling for the development of evidence-based guidelines for prescribing smoked marijuana.

“Guidelines will give physicians solid grounds on which to make prescribing decisions. Physicians are facing a deluge of requests to prescribe cannabis, and guidelines will give them the support they need to refuse to prescribe cannabis when medically unnecessary or unsafe.”

Because Health Canada allows marijuana to be prescribed by physicians, that enhances the public perception that marijuana is not only harmless, but therapeutic.

“The evidence suggests otherwise,” Kahan said. “Smoked cannabis has negligible therapeutic benefits.” Would marijuana pass the scrutiny of the University of B.C.’s Therapeutics Initiative, established to examine the effectiveness of prescription drugs? It uses solid evidence and rigorous scientific research, and it has saved lives. Marijuana should undergo the same scrutiny as to its potential benefits and harms.

But medical marijuana is not treated the same as other drugs. Science has little to do with it.

“The current means of ‘prescribing’ violates all of the usual practices of medicine,” wrote Maryland psychiatrists Dinah Miller and Anette Hanson in a 2012 Baltimore Sun commentary. “What other medication do we authorize for a year, with no stipulation as to frequency, dose or certainty that there has been a positive response without side effects?”

If marijuana can relieve the agony of someone with severe chronic pain or terminal cancer, who would withhold it? But let’s face it, the biggest demand for pot is as a recreational drug, like alcohol and tobacco. It should be handled the same, with regulations as to its production and distribution. We should not clog our courts and jails with pot-smokers.

By all means, investigate its potential for good, but let’s not pretend it does no harm.

Source: http://www.timescolonist.com/opinion/editorials/editorial-don-t-pretend-pot-is-harmless-1.1304417#sthash.8ubjqn0w.dpuf 9th August 2014

The proportion of marijuana-positive drivers involved in fatal motor vehicle crashes in Colorado has increased dramatically since the commercialization of medical marijuana in the middle of 2009, according to a study. The study raises important concerns about the increase in the proportion of drivers in a fatal motor vehicle crash who were marijuana-positive since the commercialization of medical marijuana in Colorado, particularly in comparison to the 34 non-medical marijuana states. 

ShapeThe proportion of marijuana-positive drivers involved in fatal motor vehicle crashes in Colorado has increased dramatically since the commercialization of medical marijuana in the middle of 2009, according to a study by University of Colorado School of Medicine researchers.

With data from the National Highway Traffic Safety Administration’s Fatality Analysis Reporting System covering 1994 to 2011, the researchers analyzed fatal motor vehicle crashes in Colorado and in the 34 states that did not have medical marijuana laws, comparing changes over time in the proportion of drivers who were marijuana-positive and alcohol-impaired.

 The researchers found that fatal motor vehicle crashes in Colorado involving at least one driver who tested positive for marijuana accounted for 4.5 percent in the first six months of 1994; this percentage increased to 10 percent in the last six months of 2011. They reported that Colorado underwent a significant increase in the proportion of drivers in a fatal motor vehicle crash who were marijuana-positive after the commercialization of medical marijuana in the middle of 2009. The increase in Colorado was significantly greater compared to the 34 non-medical marijuana states from mid-2009 to 2011. The researchers also reported no significant changes over time in the proportion of drivers in a fatal motor vehicle crash who were alcohol-impaired within Colorado and comparing Colorado to the 34 non-medical marijuana states.

Stacy Salomonsen-Sautel, Ph.D, who was a postdoctoral fellow in the Department of Pharmacology, is the lead author of the study, which is available online in the journal Drug and Alcohol Dependence. Christian Hopfer, MD, associate professor of psychiatry, is the senior author. 

Salomonsen-Sautel said the study raises important concerns about the increase in the proportion of drivers in a fatal motor vehicle crash who were marijuana-positive since the commercialization of medical marijuana in Colorado, particularly in comparison to the 34 non-medical marijuana states. While the study does not determine cause and effect relationships, such as whether marijuana-positive drivers caused or contributed to the fatal crashes, it indicates a need for better education and prevention programs to curb impaired driving.

Source:. Trends in fatal motor vehicle crashes before and after marijuana commercialization in Colorado. Drug and Alcohol Dependence, 2014; DOI: 10.1016/j.drugalcdep.2014.04.008

Many of the Op-Eds on the subject of the legalisation or otherwise of cannabis are written by journalists or protagonists of one or other point of view. The following links give scientific evidence from scientist and medics in the USA, and do not support the use of cannabis.

 

Medical organisations in the USA do not support smoked pot or edibles

   
   

Authoritative organisations which do not support smoked pot or edibles as a legitimate form of medication, listed by:

Rethinkpot.org:

American Medical Association,

American Cancer Society,

National Multiple Sclerosis Society, 

American Glaucoma Society,

American Academy of Pediatrics, 

National Institute of Drug Abuse (NIDA),

Substance Abuse and Mental Health Service Association (SAMHSA),

Food and Drug Association  (FDA),

American Academy of Ophthalmology,

Drug Enforcement Agency (DEA),

American Society of Addiction Medicine,

Epilepsy Foundation.

 

However the following information shows this substance is far from harmless and more and more users are seeking treatment to help them give up.     NDPA  March  2015

The emerging cannabis treatment population:

http://www.emeraldinsight.com/doi/abs/10.1108/DAT-01-2014-0005?journalCode=dat 

From:

Advisory Council on the Misuse of Drugs

First published: 27 November 2014

Last updated: 25 March 2015 , see all updates

Part of: Drug misuse and dependency

Report presented to the crime prevention minister recommends a revised generic description, designed to control a broad-range of ‘third generation’ synthetic cannabinoids.

 

Documents

‘Third generation’ synthetic cannabinoids    –  PDF, 611KB, 29 pages

Addendum to report on ‘third generation’ synthetic cannabinoids   –  PDF, 21.1KB, 2 pages

Between January 1, 2015 and April 22, 2015, the American Association of Poison Control Centers reported getting 1900 calls related to synthetic cannabinoid exposure, proving that the popularity of this alternative to natural marijuana has been steadily increasing. Synthetic cannabinoids, when smoked or ingested, act on the endocannabinoid receptors, similar to delta-9 tetrahydrocannabinol, the primary psychoactive ingredient in marijuana.  While dyspnea related to synthetic cannabinoid use is common, other pulmonary adverse effects have rarely been reported, specifically inhalation fever which is discussed in a recent case published in the American Journal of Case Reports.

The patient, a 29-year-old male, presented to the emergency department with severe agitation after smoking the synthetic cannabinoid K2. Medical history included a diagnosis of schizoaffective disorder for which he was not receiving treatment. To sedate him, multiple doses of lorazepam and haloperidol were used. Physical examination of the patient showed the following:

* Temperature: 100.2º F

* Blood pressure: 110/50 mmHg

* Heart rate: 109/min

* Respiratory rate: 18/min

* Oxygen saturation: 95%

* Chest exam: No crackles, wheeze, rhonchi on auscultation; chest radiograph: diffuse reticular-nodular and interstitial infiltrates

* Cardiovascular exam: JVP not elevated, S1 and S2 heard, no additional heart sounds, murmurs, rubs; rate/rhythm regular

* Lab tests: Leukocytosis with predominant neutrophilia (83.4%); blood culture samples showed no growth after 5 days

* Urine toxicology: Negative for cannabinoids, benzodiazepine, phenycyclidine, opiates, cocaine, barbiturates

The patient was given ceftriaxone 1g IV, azithromycin 500mg IV, magnesium sulfate 2g IV (for hypomagnesemia), potassium phosphate 22mEq IV (for hypophosphatemia), famotidine 40mg daily for GI prophylaxis and heparin 500 Units SC twice daily for prophylaxis of venous thromboembolism. His mental status improved and his fever dissipated 24 hours after admission; repeat chest radiograph showed resolution of the pulmonary infiltrates. Clinicians were unable to re-evaluate his blood levels, as the patient refused repeat blood draws.

Once in stable condition, he was discharged with a diagnosis of inhalation fever due to synthetic cannabinoid and was told to abstain from use of this substance. For empirical treatment of pneumonia, he was given levofloxacin 750mg daily for seven days; he was also given a prescription for risperidone 1mg twice daily for two weeks for his schizoaffective disorder. Though an outpatient appointment was scheduled, the patient did not follow-up and so his long-term outcome is uncertain.

In the United States, there are over 50 types of synthetic cannabinoids; the substances are typically available in herbal blends, potpourri, and incense.  In this patient, given the fever and transient pulmonary infiltrates, inhalation fever is believed to have developed as a consequence to K2 inhalation. Symptoms associated with inhalation fever may include cough, dyspnea, headache, malaise, myalgia and nausea, however, this patient did not experience any of these, apart from leukocytosis which is a feature of this condition.

Treatment generally includes supportive care and avoidance of the causative agent. Other diagnoses considered for this patient included acute hypersensitivity pneumonitis (which may present in a similar manner), chemical pneumonitis (an inflammatory reaction to a particulate), or bacterial pneumonia (given the fever, tachycardia, leukocytosis, and pulmonary infiltrates). Infection, however, was not considered likely given a repeat chest radiograph 24 hours later showed resolution of the pulmonary infiltrates and blood culture was negative.

Given this is the first case to report on inhalation fever as a side effect of synthetic cannabinoid inhalation, further research is needed to understand the mechanism by which this reaction occurred. In the meantime, the authors warn that “as the Emergency Department visits by synthetic cannabinoid abusers are increasing, the importance of physicians being aware of these adverse effects cannot be overstated.”

Source:   Thiru Chinnadurai, Srijan Shrestha, Raji Ayinla. A Curious Case of Inhalation Fever Caused by Synthetic Cannabinoid. American Journal of Case Reports. 2016, doi: 10.12659   6th July 2016    http://www.empr.com/

Knowing what to say or do can be tough, but your help can make a huge difference

Helping a friend or family member through an alcohol or drug addiction is by no means easy, but with the right help and knowledge it can be incredibly successful (and rewarding). First things first, there’s no perfect way to behave and it’s rare that the recovery process is understood by anyone except for the individual, but that doesn’t mean you shouldn’t try. Ian Young founder of Sober Services says,

“When someone begins (or even continues or returns to) their addiction recovery journey, the love and support of friends and family is often crucial to their success. This begins with their acceptance of the addictive illness and then continues with sensitivity around the recovery seeking addict’s requirements, such as not visiting bars initially and not socialising with friends who are still using.”

So here are some of the most helpful things you can do to help a loved one tackle addiction…

1. Speak up and offer support

Just the act of offering support alone goes a long way towards helping recovery (whether it’s taken up or not), says Deirdre Boyd, founder of DB Recovery Resources. And to know that people have offered it means a lot. There’s a few different ways you can do this, for example:

“If they attend Alcoholics or Narcotics Anonymous, ask them if they would like you to accompany them to an ‘open’ meeting.”

2. Focus on the replacement rather than sacrifice

Remember that recovery is not about sacrificing something but about replacing it with something healthier (and happier), advises Deirdre. Suggest meeting friends in a coffee bar or even a recovery café instead of the pub, or in a restaurant instead of a night club. There’s now a growing trend of recovery cafes and dry bars, with more people trying to curb their drinking completely. If you’re going out, arrange to meet in the company of ‘safe’ friends instead of old drinking companions, advises Deirdre.

“Don’t replace drinks only with water but with sparkling flavoured waters offered by many supermarkets and interesting drinks, such as those from Schloer. This is especially important on celebratory occasions where others might use champagne to toast, so that they don’t miss out on the ‘ritual’ and sense of belonging.”

You could also suggest a physical activity: perhaps go for a walk. The combination of the natural environment acts as a calming backdrop to any issues up for discussion. Events are also a good option.

“Music and comedy are also often the best anchors for this as they naturally offer a good time to the recovering addict without the requirement for alcohol or drugs, though maybe avoid rave parties or rock concerts,” advises Ian.

3. Be sure they know you’re not judging

Deirdre says:

“People that are in their active addiction can be ashamed of themselves, and they feel that everyone else feels that way. But it is not always the case. A lot of times, good friends and healthy friends are just worried about the person and want them to be the best they can be.”

Understand that an addict is not responsible for their addiction, but when they learn about recovery, they are accountable for their actions.

4. Listen

If you’re helping a friend, listening is the best thing you can do. Deirdre says,

“You can’t always fix someone but you can always say, ‘Have you gone to your meeting?’, ‘Have you spoken to your sponsor?’.”

5. Educate yourself on addiction

There are plenty of resources available for those that want to learn about addiction. The most important part of the family or friends role in the addict’s early recovery will be their own education to what’s appropriate and what isn’t, says Ian.

“For instance, the addict will know it’s not a good idea to visit a pub where their friends may be drinking. But if the family or friend is unaware of this then the simple invitation could be enough to trigger their obsession to drink. Or maybe the suggestion that the recovering addict visits an ex-girlfriend whom the family/friend thinks is a safe person for them to be around, could be bringing up deep emotions that could destabilise the newly recovering addict.”

7. Know that it’s not your job to ‘fix them’

If you notice that your friend is struggling or they tell you that they are, Deirdre says to listen and ‘echo’ what they have said – you don’t have to fix them, just be there for them and advise them to share also at an AA or NA meeting.

In most cases, if the recovering addict is serious about their recovery, they’ll inform the family and friends of their boundaries, but they may not think to speak of everything, or they may be more introverted or shy about specifics, and so sensitivity is encouraged here by the loved ones, says Ian.

Source:  http://www.netdoctor.co.uk/   17th June 2016

 

Addiction Science & Clinical Practice

Katherine A Belendiuk1, Lisa L Baldini2 and Marcel O Bonn-Miller345*

Author Affiliations

1Institute of Human Development, University of California, 1121 Tolman Hall #1690, Berkeley 94720, CA, USA

2Palo Alto University, 1791 Arastradero Road, Palo Alto 94304, CA, USA

3Center of Excellence in Substance Abuse Treatment and Education, Philadelphia VA Medical Center, 3900 Woodland Avenue, Philadelphia 19104, PA, USA

4Center for Innovation to Implementation and National Center for PTSD, VA Palo Alto Health Care System, 795 Willow Road (152-MPD), Menlo Park 94025, CA, USA

5Department of Psychiatry, University of Pennsylvania Perelman School of Medicine, 3440 Market Street, Philadelphia 19104, PA, USA

For all author emails, please log on.

Addiction Science & Clinical Practice 2015, 10:10 doi:10.1186/s13722-015-0032-7

The electronic version of this article is the complete one and can be found online at:http://www.ascpjournal.org/content/10/1/10

Received:

29 August 2014

Accepted:

15 April 2015

Published:

21 April 2015

© 2015 Belendiuk et al.; licensee BioMed Central.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Abstract

The present investigation aimed to provide an objective narrative review of the existing literature pertaining to the benefits and harms of marijuana use for the treatment of the most common medical and psychological conditions for which it has been allowed at the state level. Common medical conditions for which marijuana is allowed (i.e., those conditions shared by at least 80 percent of medical marijuana states) were identified as: Alzheimer’s disease, amyotrophic lateral sclerosis, cachexia/wasting syndrome, cancer, Crohn’s disease, epilepsy and seizures, glaucoma, hepatitis C virus, human immunodeficiency virus/acquired immunodeficiency syndrome, multiple sclerosis and muscle spasticity, severe and chronic pain, and severe nausea. Post-traumatic stress disorder was also included in the review, as it is the sole psychological disorder for which medical marijuana has been allowed. Studies for this narrative review were included based on a literature search in PsycINFO, MEDLINE, and Google Scholar. Findings indicate that, for the majority of these conditions, there is insufficient evidence to support the recommendation of medical marijuana at this time. A significant amount of rigorous research is needed to definitively ascertain the potential implications of marijuana for these conditions. It is important for such work to not only examine the effects of smoked marijuana preparations, but also to compare its safety, tolerability, and efficacy in relation to existing pharmacological treatments.

Keywords:

Cannabis; Medical marijuana; Marijuana; Medicine; Treatment; Alzheimer’s disease; ALS; Cachexia; Cancer, Crohn’s disease; Epilepsy; Seizures; Glaucoma; Hepatitis C virus; HCV; HIV; AIDS; Multiple sclerosis; MS; Pain; Nausea; Vomiting; Post-traumatic stress disorder; PTSD

Introduction

National estimates suggest that 5.4 million people in the United States above the age of 12 have used marijuana daily or regularly within the past year [1]. This represents an increase of approximately 74.2 percent since 2006 [1]. Similar increases have also been noted among vulnerable populations in the U.S. (e.g., veterans and adolescents) [2],[3].

Marijuana is currently illegal in every country in the world. In 2012, Uruguay voted to legalize state-controlled marijuana sales but implementation of the law has been postponed until 2015. The policy in the Netherlands is mixed, with permissible retail sale of marijuana at coffee shops, but restrictions on production and possession. Notably, as the concentration of THC in marijuana has increased, Dutch coffee shops have begun to close, as perception of marijuana as a “soft” drug transitions to perceptions of marijuana as a “hard” drug.

Like the Netherlands, the United States currently has a mixed drug policy; marijuana is an illegalSchedule I drug under U.S. Federal law. However, marijuana policies vary by state, with some states (e.g., Colorado and Washington) legalizing the use of recreational marijuana (i.e., allowing the legal possession and use of marijuana under state law), and other states decriminalizing marijuana (i.e., reducing the penalties for possession and/or use of small amounts of marijuana to fines or civil penalties). Furthermore, as of this review, 23 states and the District of Columbia have passed legislation allowing medical marijuana (i.e., individuals can defend themselves against criminal charges related to marijuana possession if a medical need is documented) for the treatment of a variety of medical and psychological conditions. Though the list of conditions for which medical marijuana has been allowed varies at the state level, the majority of states agree on its use for Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), cachexia/wasting syndrome, cancer, Crohn’s disease (CD), epilepsy and seizures, glaucoma, hepatitis C virus (HCV), human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), multiple sclerosis (MS) and muscle spasticity, severe and chronic pain, severe nausea, and post-traumatic stress disorder (PTSD).

The aim of the present review is to provide a summary of the existing empirical literature regarding the effects of marijuana/cannabinoids on each of the above-noted conditions. Though some recent work has reviewed the adverse effects of marijuana [4] or the efficacy of marijuana for certain conditions (e.g., neurologic) [5], there has yet to be a comprehensive review of the effects of marijuana for each of the medical and psychiatric conditions for which it is currently used.

Methods

The list of all conditions for which medical marijuana is allowed, according to the legislation of each U.S. state for which medical marijuana has been approved, was obtained and examined [6]. From this list, common conditions for which medical marijuana is allowed (i.e., those conditions shared by at least 80 percent of medical marijuana states) were identified as: AD, ALS, cachexia/wasting syndrome, cancer, CD, epilepsy and seizures, glaucoma, HCV, HIV/AIDS, MS and muscle spasticity, severe and chronic pain, and severe nausea. Though not presently a qualifying condition in at least 80 percent of states with medical marijuana laws, PTSD was also included in the review, as it is rapidly gaining attention and recognition as the sole psychological disorder for which medical marijuana is allowed.

Studies for this narrative review were included based on a literature search in the following databases: PsycINFO, MEDLINE, and Google Scholar. Within each database, each combination of the following key marijuana terms and the above-listed conditions were used to conduct a search: cannabis, marijuana, marihuana, cannabinoid, delta-9-tetrahydrocannabinol, THC, cannabidiol, CBD, cannabinol, cannabigerol, Marinol, dronabinol, Sativex, Nabilone, and Nabiximols. References within each obtained article were also examined to assure that no studies were overlooked. Only published, English-language studies were included in this review.

Though the primary focus of this review is on studies of marijuana plant effects, as these are most relevant to recent medical marijuana legislation, synthetic or plant-derived cannabinoids (e.g., dronabinol, Nabilone) were also included due to the general dearth of marijuana plant studies for a number of conditions. Indeed, for purposes of the review, references to oral administrations of marijuana constitute a pharmaceutical grade extraction administered in tablet or liquid form (e.g., dronabinol, Nabilone, Nabiximols), while references to smoked administration of marijuana constitute the inhalation of smoke from burned marijuana leaves and flowers. Finally, the present review is organized alphabetically by condition for which marijuana is allowed, rather than in order of disorder for which it is most to least commonly recommended, or strength of the evidence. We chose this approach as there is currently only state-level data [7]-[9], rather than national, representative data on the primary conditions for which medical marijuana is used or recommended, and the existing literature and state of the evidence for many conditions remains relatively poor.

Results

Alzheimer’s disease

AD, the leading form of dementia in the elderly, is a progressive, age-related disorder characterized by cognitive and memory deterioration [10]. AD has several neuropathological markers, including neuritic plaques and neurofibrillary tangles [11]. Although several researchers have suggested dronabinol and Nabilone may act on these mechanisms to confer therapeutic effects for patients with AD [12],[13], a recent Cochrane systematic review found no evidence that dronabinol was effective in reducing symptoms of dementia [14]. The authors of a placebo-controlled crossover study of 15 patients with AD who were refusing to eat suggest that dronabinol increases weight gain and decreases disturbed behavior [15], but there is insufficient quantitative data to support this conclusion [14], and one study participant had a grand mal seizure following dronabinol administration [15]. Another pilot study of two patients with dementia found that dronabinol reduced nocturnal motor activity [16]. No studies have examined the effects of smoked marijuana in patients with AD. In sum, there is insufficient evidence to recommend marijuana for the treatment of AD. Future directions should include conducting randomized controlled trials (RCTs) comparing both smoked and oral marijuana to placebo and existing treatments, with sample sizes large enough to detect treatment effects and the safety and tolerability of marijuana.

Amyotrophic lateral sclerosis

ALS is a fatal neurological disease with symptoms that include weakness, spasticity, and respiratory difficulties. Cannabinoids are hypothesized to act in the regions of established pathophysiology for ALS [17] and could be used for symptom management (e.g., pain, spasticity, wasting, respiratory failure, dysphagia, negative mood, and dysautonomia) [18]. Although there is limited evidence from a survey of patients with ALS that marijuana consumed in a variety of forms (i.e., oral, smoked, vaporized, and eaten) improves speech and swallowing [19], the anti-salivatory components of marijuana may reduce the risk of aspiration pneumonia, while also increasing patient comfort [18],[19]. These survey findings indicate that up to 10 percent of patients use marijuana for symptom management, and these self-reports suggest efficacy in increasing appetite and mood and decreasing pain, spasticity, and drooling. However, as is consistent with the half-life of smoked marijuana, the beneficial effects of marijuana on symptoms of ALS were fewer than 3 hours in duration [19]. The only randomized, double-blind, placebo-controlled crossover trial of marijuana in patients with ALS has a small sample size (N = 27) and indicates that while 5 mg of dronabinol is well-tolerated, there was no effect on number or intensity of cramps, quality of life, appetite, sleep, or mood [20]. There is currently insufficient clinical evidence in humans with ALS to recommend cannabinoids as primary or adjunctive therapy.

Cachexia/wasting syndrome

Cachexia is the general wasting and malnutrition that occurs in the context of chronic diseases such as HIV/AIDS and cancer. In patients with HIV or cancer, smoked marijuana and dronabinol have been shown to increase weight gain [21],[22] and food intake [22],[23] compared to placebo. In a within-subject, double-blind, staggered, double-dummy study of nine individuals with muscle mass loss, dronabinol resulted in significantly greater calorie consumption than smoked marijuana [24]. A within-subject, double-blind, placebo-controlled trial with seven HIV-positive marijuana smokers taking antiretroviral medications found that compared to placebo, dronabinol increased caloric intake [25]. Additional studies indicate that dronabinol administration increases appetite, decreases nausea, and protects against weight loss [26], with effects on appetite and weight stability enduring in long-term follow-up [27].

Both dronabinol and smoked marijuana increase the number of eating occasions [22],[25], and smoked marijuana may also affect weight gain and calorie intake by modulating appetite hormones [28]. Importantly, weight gain in one study was greater than would have been expected based on increased calorie consumption alone [23], which may be particularly relevant for those who have impaired food intake and/or nausea. These studies demonstrate that marijuana has positive effects on cachexia resulting from a medical condition, but are largely limited by small sample sizes. Additionally, studies comparing THC to FDA-approved medication (i.e., megestrol) indicate that THC is less effective in promoting appetite and weight gain [29]. In sum, there is moderate support for the use of cannabinoids for cachexia/wasting, and dronabinol has been FDA-approved for anorexia associated with weight loss in individuals with AIDS. Additional studies with larger sample sizes that examine the efficacy of marijuana compared to nutritional support/calorie augmentation in the treatment of cachexia are indicated.

Cancer

Cancer is a qualifying medical condition in every state that has approved marijuana for medical use [30]. The majority of clinical research examining the relation between THC and cancer has evaluated the effect of smoked THC on the risk for cancer, or the palliative effects of THC on chemotherapy-related nausea and emesis, chronic pain, and wasting (reviewed in respective sections); few studies have studied the effect of marijuana in any form on the treatment of primary cancer pathology. In vitro and in vivo research suggests that cannabinoids inhibit tumor growth [30] via several proposed mechanisms (e.g., suppression of cell proliferation, reduced cell migration, increased apoptosis) [31]; however, in vitro and in vivo studies also have shown that THC increases tumor growth due to reduced immune response to cancer [32]. The only clinical trial of THC on cancer examined intracranial administration of THC to nine patients with recurrent glioblastoma multiforme who had failed surgical- and radiotherapy, and results indicated that THC decreased tumor growth, while being well-tolerated with few psychotropic effects [33]. This study is limited by lack of generalizability, and clinical trials with larger representative samples that examine oral or smoked administration of THC are essential to elucidate the effects on cancer pathology. There is currently insufficient evidence to recommend marijuana for the treatment of cancer, but there may be secondary treatment effects on appetite and pain.

Crohn’s disease

CD is an inflammatory bowel disease (IBD) that has no cure; treatment targets include reducing inflammation and secondary symptoms. Between 16 percent and 50 percent of patients use marijuana to relieve symptoms of IBD [34]-[36], and patients using marijuana for 6 months or longer are five times more likely to have had surgery for their IBD [34]; whether marijuana exacerbates disease progression or more severe disease results in self-medication is unclear. Only one placebo-controlled study of the effects of marijuana in patients with CD has been conducted[37]. This study found that there was no difference between placebo and smoked marijuana on CD remission (defined as a CD Activity Index (CDAI) of less than 100), and that marijuana was superior to placebo in promoting clinical response (a decrease in CDAI score greater than 100), reducing steroid use, and improving sleep and appetite [37]. Importantly, this study did not include objective measurement of inflammatory activity, and there was no significant difference in placebo and treatment groups 2 weeks after treatment cessation [37]. Until clinical trials with objective measurement of treatment effects over an extended period of time are conducted to examine the safety and efficacy of marijuana for the treatment of IBD, there is insufficient evidence for the use of marijuana for the treatment of IBD.

Epilepsy and seizures

The known effects of cannabinoids on epilepsy and seizures are largely from animal studies, surveys, and case studies. Several animal studies indicate that marijuana and its constituents exhibit anticonvulsant effects [38]-[41] and reduce seizure-related mortality [39], but there is also evidence that cannabinoids can lower the threshold for seizures [42], and THC withdrawal increases susceptibility for convulsions [42]. Cross-sectional surveys indicate that 16–21 percent of patients with epilepsy smoke marijuana [43],[44], with some reporting positive effects (e.g., spasm reduction) and a belief that marijuana is an effective therapy [44], and others reporting increased seizure frequency and intensity [43]. Based on a Cochrane review, the few RCTs that have been conducted in humans include a total of 48 participants [45] and only examine treatment with cannabidiol. These trials exhibited heterogeneity of effects: some indicated a reduction in seizure frequency [46],[47], while others demonstrated no effect compared to placebo [48]. In addition, none of the studies examined response at greater than 6-month follow-up [45]. Systematic reviews of the literature have concluded that there is insufficient clinical data to support or refute the use of cannabinoids for the treatment of epilepsy and seizures [5],[45].

Glaucoma

Glaucoma is a neurodegenerative eye disease that can cause blindness by damaging retinal ganglion cells and axons of the optic nerve. Intraocular pressure (IOP) can influence both onset and progression of glaucoma and is often a target for intervention. Small samples have demonstrated reduced IOP following smoked marijuana [49],[50], but the effect is only present in 60–65 percent of individuals [51] and lasts for 3–4 hours, requiring repeated dosing throughout the day [52]. Furthermore, patients discontinue marijuana use due to side effects (e.g., dizziness, anxiety, dry mouth, sedation, depression, confusion, weight gain, and distortion of perception[53]), and this treatment discontinuity may exacerbate optic nerve damage and obviate the benefits of reduced IOP [54]. Limited research and documented toxicity have resulted in the American Glaucoma Society [54], Canadian Opthalmological Society [55], and the American Academy of Ophthalmology’s Complementary Therapies Task Force [52] determining that there is insufficient evidence to indicate that marijuana is safer or more effective than existing pharmacotherapy or surgery for the reduction of IOP. Development of eye drops for topical application of THC would minimize psychoactive and other side effects but is complicated by the high lipophilicity and low water solubility of cannabinoids [52],[56]. Additionally, the distance from the application site to the retina may be too great to afford neuroprotective benefits [52], given that only 5 percent of an applied dose penetrates the cornea to the intraocular space [56].

Hepatitis C virus

There have been no RCTs examining the use of cannabinoids on HCV infection. Of the studies that have been conducted, one longitudinal study demonstrates that smoked marijuana has no effect on HCV progression in individuals with HIV [57]. In contrast, individuals with HCV who smoke marijuana have a higher fibrosis progression rate [58] and more severe steatosis [59], with daily smokers having a more rapid rate of progression and greater severity [60] than occasional marijuana users [58],[59]. Marijuana may have independent negative effects on steatosis [59], but because none of these findings were in the context of a clinical trial, these correlations are not causal and it is possible that individuals who use marijuana do so to manage greater symptom severity [60].

There may be secondary effects of cannabinoids on HCV treatment side effects: dronabinol and Nabilone stabilized treatment-induced weight-loss [61]; and dronabinol, Nabilone, and marijuana procured from a marijuana club (dose and method of administration unspecified) increased HCV treatment duration and reduced post-treatment virological relapse [61],[62]. However, there is also a potential drug-drug interaction between ribavirin, a traditional HCV treatment, and marijuana due to shared cytochrome 450 metabolism [63]. Because 90 percent of HCV infections are the result of injection drug use [64], treatment of symptoms with marijuana may be contraindicated for this subpopulation, particularly because marijuana use in the context of other substance use (i.e., alcohol) has multiplicative effects on the odds of fibrosis severity [60]. Given that newer treatments for HCV (e.g., sofosbuvir) are replacing ribavirin, there will likely be less need for use of marijuana in management of treatment-related side effects. In sum, there is currently insufficient empirical support to recommend marijuana for the treatment of HCV.

HIV/AIDS

Marijuana use in HIV-infected patients is typically for the management of side effects (e.g., nausea) of older antiretroviral treatments and AIDS-related symptoms, including weight-loss and HIV-associated neuropathy (covered in cachexia and pain sections, respectively). Survey studies indicate that 23 percent of patients with HIV/AIDS smoked marijuana in the past month and do so largely to improve mood and appetite and reduce pain [65]; these patients may exhibit tolerance and need higher doses of THC than are currently approved by the FDA for use in clinical trials [25] to experience treatment effects. The few RCTs that have been conducted in a small number of patients with HIV/AIDS largely examined the effects of marijuana (synthetic or natural marijuana that is smoked or ingested) on symptoms (e.g., nausea and appetite) over a short treatment window (21–84 days; see [66] for systematic review). Studies examining the effects of marijuana on the pharmacokinetics of antiretroviral medication demonstrated that neither smoked marijuana nor dronabinol affects short-term clinical outcomes (e.g., viral load, CD4 and CD8 counts [67]), influences the efficacy of antiretroviral medication [68], or indicates that dose adjustments for protease inhibitors are necessary [21]. However, individuals who are dependent on marijuana have demonstrated poorer medication adherence and greater HIV symptoms and side effects than nonusers and nondependent users [69]. Furthermore, while some studies have no participant withdrawal due to adverse events [21],[70],[71], others reported treatment-limiting adverse events [26],[72],[73]. Finally, because drug use is a risk factor for HIV infection [74], treatment of symptoms with marijuana may be contraindicated for this subpopulation. In sum, there is variability in short-term outcomes and insufficient long-term data addressing the safety and efficacy of marijuana when used to manage symptoms of HIV/AIDS and its role in those also using newer, better-tolerated antiretroviral agents.

Multiple sclerosis and muscle spasticity

Muscle spasticity, a common feature of MS, is disordered sensorimotor control that leads to involuntary muscle activation [75] that results in pain, sleep disturbance, and increased morbidity[76]. The majority of studies examining spasticity have compared oral or sublingual forms of cannabinoids to placebo and found reduced spasm severity [77]-[84], with symptom improvement enduring at long-term follow-up [85]-[87], and also reduced spasm frequency and spasm-related pain and sleep disturbances [77],[88],[89]. With regard to smoked marijuana, one study found reductions in muscle spasticity [90]; however, another study showed that smoking marijuana impaired posture and balance in individuals with spasticity [91], so there is currently insufficient evidence to determine the efficacy of smoked marijuana on spasticity [5].

Surveys of patient populations show that between 14 and 16 percent of patients with MS report using marijuana for symptom management [92],[93] and that compared to non-marijuana-using individuals with MS, marijuana-using individuals with MS have decreased cognitive functioning[90],[94],[95]. Because cognitive dysfunction is present in 40–60 percent of individuals with MS before marijuana administration [96], marijuana use may further compromise impaired cerebral functioning in a neurologically vulnerable population. Additionally, future studies should carefully consider outcome assessment. The primary methods of measuring spasticity, the Ashworth Scale and patient self-report, may not be appropriate measures because antispastic drugs do not decrease Ashworth ratings, and patient-reported spasticity severity may be poorly correlated with patient functioning (i.e., a patient whose spasticity compensated for motor weakness may be unable to ambulate with reduced spasticity) [97]. Importantly for both MS and other neurological disorders, the American Academy of Neurology does not advocate the use of marijuana for the treatment of neurological disorders, due to insufficient evidence regarding treatment efficacy [98].

Post-traumatic stress disorder

There has been a recent emergence of empirical studies of the effects of marijuana on symptoms of PTSD, borne primarily out of the observation that individuals with PTSD report using marijuana to cope with PTSD symptoms; specifically, hyperarousal, negative affect, and sleep disturbances[99]-[101]. Empirical work has consistently demonstrated that the endocannabinoid system plays a significant role in the etiology of PTSD, with greater availability of cannabinoid type 1 receptors documented among those with PTSD than in trauma-exposed or healthy controls [102],[103]. Though the use of marijuana and oral THC [104],[105] have been implicated as a potential mechanism for the mitigation of many PTSD symptoms by way of their effects on the endocannabinoid system, some researchers caution that endocannabinoid activation with plant-based extracts over extended periods may lead to a number of deleterious consequences, including receptor downregulation and addiction [102].

There have been no RCTs of marijuana for the treatment of PTSD, though there has been one small RCT of Nabilone that showed promise for reducing nightmares associated with PTSD [106]. One unpublished pilot study of 29 Israeli combat veterans showed reductions in PTSD symptoms following the administration of smoked marijuana, with effects seen up to one year post-treatment[107]. Remaining studies have been primarily observational in nature, documenting that PTSD is associated with greater odds of a cannabis use disorder diagnosis [108] and greater marijuana craving and withdrawal immediately prior to a marijuana cessation attempt [109]. Indeed, sleep difficulties (a hallmark of PTSD) have been associated with poor marijuana cessation outcomes[110],[111], while cannabis use disorders have been associated with poorer PTSD treatment outcomes [112]. Given the lack of RCTs studying marijuana as a treatment for PTSD, there is insufficient scientific evidence for its use at this time.

Severe and chronic pain

Clinical trials have examined smoked and oral administration of cannabinoids on different types of pain (e.g., neuropathic, post-operative, experimentally induced) in multiple patient populations (e.g., HIV, cancer, and fibromyalgia). Two meta-analyses have been conducted examining the association between marijuana and pain. In the first, 18 RCTs demonstrated that any marijuana preparation containing THC, applied by any route of administration, significantly decreased pain scores from baseline compared to placebo [113]. The second examined 19 RCTs of smoked marijuana in individuals with HIV, which also indicated greater efficacy in reducing pain (i.e., sensory neuropathy) compared to placebo [114]. Importantly, the first meta-analysis showed that marijuana increased the odds of altered perception, motor function, and cognition by 4 to 5 times[113], and the second study did not recommend marijuana as routine therapy [114]. Dosage is an important factor to consider for administration of cannabinoids for pain management, as some studies have found that higher doses of smoked marijuana are associated with improved analgesia[115], whereas other studies show that higher doses of smoked marijuana increase pain response[116]. Because the analgesic effects of marijuana are comparable to those of traditional pain medications [117], future research should aim to identify which analgesics provide the lowest risk profile for the management of severe and chronic pain. Although there is preliminary support to suggest that marijuana may have analgesic effects, there is insufficient research on dosing and side effect profile, which precludes recommending marijuana for the management of severe and chronic pain.

Severe nausea

The majority of research related to the effects of marijuana on severe nausea has involved oral administration of marijuana to individuals with chemotherapy-induced nausea and vomiting (CINV). Oral marijuana (i.e., THC suspension in sesame oil and gelatin) has been shown to be more effective in reducing CINV than placebo [118], including the number and volume of vomiting episodes, and the severity and duration of nausea [119]. When compared to traditional anti-emetics, some meta-analytic reviews indicate that oral THC is more effective in reducing CINV[120]-[123], others find no significant difference [122],[124]-[126], and another suggests that combining both is the most effective at reducing the duration and severity of CINV than either alone [127]. Recent advances in both anti-emetic agents and the mechanisms of cannabinoid administration (i.e., sublingual application) warrant future research.

Importantly, patients receiving cannabinoids for severe nausea reported toxicities, including paranoid delusions (5%), hallucinations (6%), and dysphoria (13%) [122]. Additionally, cannabinoid hyperemesis syndrome has been documented, in which persistent and regular marijuana use (i.e., daily or weekly use for more than 1 year) is associated with cyclic vomiting (i.e., episodic nausea and vomiting) [128] and nonresponse to treatment for cyclic vomiting [129]. Dronabinol has been FDA-approved for CINV in individuals who have not shown a treatment response to traditional anti-emetics, but in line with recommendations from the American Society of Clinical Oncology [130] and the European Society for Medical Oncology [131], cannabinoids should not be utilized as a first-line treatment for nausea and vomiting.

Conclusions

The reviewed literature highlights the dearth of rigorous research on the effects of marijuana for the most common conditions for which it is currently recommended. It is paramount that well-designed RCTs with larger sample sizes be conducted to determine the actual medical benefits and adverse effects of marijuana for each of the above conditions. Indeed, recent reviews [4],[132] comprehensively discuss adverse events associated with marijuana use, and while it is beyond the scope of the current paper to review these effects in-depth, they are important to consider when evaluating whether or not to recommend marijuana for a medical or psychiatric disorder in place of other existing treatment options.

Given the extensive literature speaking to the harms associated with marijuana use, research on the comparative safety, tolerability, efficacy, and risk of marijuana compared to existing pharmacological agents is needed. The present literature also illuminates the need for research into the effects of isolated cannabinoids (e.g., THC, CBD) as well as species of smoked marijuana (e.g., indica and sativa), as the majority of medical marijuana users ingest marijuana by smoking the marijuana plant [133],[134], which contains a wide variety of phytocannabinoids at varying potencies [135],[136]. Furthermore, improved and objective measurement of clinical outcomes should be implemented in clinical trials to determine treatment efficacy. Finally, little research has considered the issues of dose, duration, and potency. If research identifies a therapeutic effect of marijuana for medical or psychiatric conditions, there will need to be revisions in marijuana policy to increase quality control so that dose and potency are valid and reliable. Additionally, risk of abuse and diversion can be decreased by developing prescribing practices with continued supervision of a medical professional, creating prescription monitoring programs to reduce the risk of “doctor shopping”, and identifying provisions for the safe disposal of unused cannabinoids. In sum, the current literature does not adequately support the widespread adoption and use of marijuana for medical and psychiatric conditions at this time.

Source: :http://www.ascpjournal.org/content/10/1/10 21st April 2015

Abbreviations

THC: Δ9-tetrahydrocannabinol

HIV: Human immunodeficiency virus

AIDS: Acquired immunodeficiency syndrome

RCTs: Randomized controlled trials

IOP: Intraocular pressure

MS: Multiple sclerosis

CINV: Chemotherapy-induced nausea and vomiting

HCV: Hepatitis C virus

ALS: Amyotrophic lateral sclerosis

CD: Crohn’s disease

IBD: Inflammatory bowel disease

AD: Alzheimer’s disease

PTSD: Post-traumatic stress disorder

CB1: Cannabinoid type 1

CBD: Cannabidiol

Competing interests

Dr. Belendiuk holds stock in Shire Pharmaceuticals.

Authors’ contributions

Dr. KAB synthesized the literature and authored sections of the manuscript. Ms. LLB assisted with the literature search and synthesis. Dr. MOB-M conceived the review, assisted in the search and synthesis of existing literature, and authored sections of the manuscript. All authors read and approved the final manuscript.

Acknowledgements

Dr. Belendiuk’s salary was supported by National Institute of Mental Health R01 MH40564.

Dr. Bonn-Miller’s salary was supported by the VA Center of Excellence for Substance Abuse Treatment and Education.

Literature review and synthesis was supported by a grant from the VA Substance Use Disorder Quality Enhancement Research Initiative (SUDQ-LIP1410).

The above funding agencies played no role in the writing of the manuscript or decision to submit the manuscript for publication. The expressed views do not necessarily represent those of the Department of Veterans Affairs.

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Do manualized psychosocial interventions help reduce relapse among alcohol-dependent adults treated with naltrexone or placebo? A meta-analysis.

Agosti V., Nunes E.V., O’Shea D. et al.

Unable to obtain a copy by clicking title? Try asking the author for a reprint by adapting this prepared e-mail or by writing to Dr Agosti at agostiv@pi.cpmc.columbia.edu.

Supplementing the medication naltrexone with psychosocial relapse-prevention therapies has not helped prevent relapse among alcohol-dependent patients. However, these therapies have elevated outcomes among placebo patients to the level of those prescribed naltrexone.

SUMMARY Medications such as naltrexone and acamprosate are used in the treatment of alcohol dependence to combat frequent relapse to heavy drinking, but their impact has overall been modest, and many patients leave treatment early or do not take medication as intended. Researchers have tried to address these shortcomings by supplementing medication with psychosocial interventions. The featured review assessed whether these attempts have been successful by conducting a meta-analytic synthesis of results from studies which used psychosocial relapse-prevention interventions (typically cognitive-behavioural in approach) to support adult, alcohol-dependent patients who had achieved abstinence, and then randomly been allocated either to naltrexone or a placebo. Relapse was defined as a return to drinking at least 70g alcohol a day for men or 56g for women.

Key points

The review synthesised results from relevant studies to test whether supplementing the medication naltrexone with psychosocial relapse-prevention therapies helps prevent relapse among adult, alcohol-dependent patients.

It concluded this was not the case, though one finding suggested that psychosocial therapies can elevate outcomes for patients prescribed a placebo to the level of those prescribed naltrexone.

The implications of this and of other studies are that naltrexone can be a valuable supplement to medical counselling of dependent drinkers, especially when specialist therapies such as cognitive-behavioural therapy are refused or unavailable.

In some situations these therapies also work better when naltrexone is added. But if the core treatment is naltrexone, good quality medical care or counselling will on average be as effective as specialist structured psychosocial therapies.

Four of the 18 studies which met these criteria had also randomly allocated patients to cognitive-behavioural therapies versus a different approach – specifically either medical management or supportive psychotherapy. These direct tests of the impact of a cognitive-behavioural approach were analysed separately from the remaining 20 studies, in which all the patients were offered the same psychosocial therapies, either cognitive-behavioural or one typical of that type of service.

All 18 studies had recruited nearly 2,600 patients on average about 42 years old. Where this was known, three-quarters were men, 71% were employed, and about half were married.

Main findings

Within each of the four studies which had randomly allocated patients to these therapies, generally the proportions who relapsed when supported by cognitive-behavioural therapies were about the same as those who relapsed when supported in other ways. This was the case both among patients given naltrexone and those allocated to a placebo. When results from these studies were pooled, relapse rates among patients allocated to naltrexone or placebo were virtually the same regardless of the type of psychosocial support.

Among the remaining studies which each allocated all their patients to the same form of psychosocial support, results were available from seven in which this was a structured, manualised programme, usually cognitive-behavioural in nature. Across these studies, virtually the same proportion of patients (about half) relapsed whether prescribed naltrexone or placebo. In contrast, when support took a typical, less structured form such as counselling, fewer naltrexone patients relapsed (33%) than did patients prescribed a placebo (43%). This contrast was statistically significant, and was largely due to results from older studies published between 1992 and 1997. Another unexpected finding was that whether prescribed naltrexone or a placebo, fewer patients relapsed when the treatment was a typical approach than when it was a structured psychosocial therapy.

The authors’ conclusions

Results show that relative to other approaches, cognitive-behavioural therapy did not significantly decrease the likelihood of relapse to heavy drinking among patients prescribed naltrexone or among those prescribed a placebo, and did not augment the impacts of naltrexone relative to an inactive placebo. In the four studies which made direct comparisons, supportive psychotherapy and medical management interventions worked as well. Among the remaining studies, overall those which used a manualised programme such as cognitive-behavioural therapy actually recorded higher rates of relapse than studies which used a more typical, less structured approach.

These results should be viewed in the light of several major limitations. No adjustments could be made for important factors related to the chance of successful treatment such as severity of dependence, and relapse to heavy drinking was the only drinking outcome sufficiently commonly reported to be amalgamated across the studies. Also, the results derived from studies that required initial abstinence and excluded patients with major comorbid disorders, diminishing their applicability to routine practice.

Source: American Journal on Addictions: 2012, 21(6), p. 501–507. April 2015

COMMENTARY The weight of the evidence in respect of treating alcohol or drug dependence is that despite the prominence of cognitive-behavioural therapies, their theoretical pedigree, and an extensive research effort which has distilled them in to expert manuals (for example, 1 2), overall the advantage they confer over alternatives is minor, and especially so when added to a drug-based treatment. In respect of alcohol problems, an analysis has concluded that any variation in outcomes across different psychosocial therapies is likely to have been due to chance or to the allegiance of the researchers.

However, the large US COMBINE trial did find that supplementing inactive placebo pills with psychological therapy incorporating cognitive-behavioural elements raised outcomes to the level of patients prescribed naltrexone. A similar message emerged from another US study which found that as long as naltrexone was prescribed, primary care-style consultations were as effective as specialist cognitive-behavioural therapy in initiating and sustaining recovery from alcohol dependence. Without the medication, cognitive-behavioural therapy was the more effective option. A similar result emerged from the featured review’s analysis of studies which offered the same psychosocial support to all patients; when this was a structured therapy (generally cognitive-behavioural), it helped raise outcomes for placebo patients to the level of those prescribed naltrexone.

All these results suggest that structured therapies can elevate the outcomes of patients not prescribed an active medication to the level of those prescribed naltrexone – that either medication or structured therapy help relative no medication plus typical care. Combining the two does not augment the drug’s impacts – a surprise, since relapse-prevention therapies would be expected to have their own impacts and to give medication greater leverage by persuading more patients to complete treatment and take the pills as intended.

Even if adding structured cognitive-behavioural therapy to naltrexone does not help, the reverse may still be the case – that supplementing cognitive-behavioural therapy with naltrexone makes a more effective package. In several studies (described in these notes) this has indeed been the case. The findings are in line with guidance from the UK’s National Institute for Health and Clinical Excellence (NICE) that in addition to evidence-based psychological interventions, patients whose alcohol dependence is moderate or severe should also be able to access relapse prevention medication, including naltrexone.

Practice implications seem to be that naltrexone can be a valuable supplement to the medical counselling (by GPs or nurses) of dependent drinkers of the kind who might be treated in primary care, especially when specialist therapies such as cognitive-behavioural therapy are refused or unavailable. In some situations these therapies also work better when naltrexone is added. But if the core treatment is naltrexone, a good quality medical care approach or counselling will on average be as effective as specialist structured psychosocial therapies.

Last revised 17 April 2015. First uploaded 10 April 2015

THE methadone programme has failed drug addicts in Clydebank, a leading addictions worker said this week.

methadone-is-a-monsterDonnie McGilveray is the manager of Alternatives, a West Dunbartonshire charity that helps reform drug addicts, many of them methadone users.

He told the Post the methadone programme used to treat heroin addicts has gone unregulated — and described the green liquid as a “monster” that keeps people hooked for good.

His comments come after shock statistics were released last week showing that Clydebank pharmacies claimed £153,000 for methadone prescriptions in 2014.

Donnie told the Post: “I think methadone is helpful for a small cohort of people, the five to ten per cent of people who are chaotic, suicidal or maybe sex workers being used and abused by people. There is a small group of people who need to be made safe.

But that’s not what is happening. We’ve got this monster, a jolly green giant, that many, many addicts are stuck on. And again, it’s not just them who are stuck in this it’s the doctors and nurses who have an obligation to keep them safe.”

National data obtained by BBC Scotland showed pharmacists were paid £17.8 million for handling nearly half a million prescriptions of methadone in 2014. In Clydebank, £153,000 was paid to eight pharmacies to deliver 3,165 prescriptions of the heroin substitute. In Dalmuir Lloyds, £31,671 was claimed for prescribing and supervising methadone to addicts in 2014. But topping the chart was Lloyds Pharmacy on 375 Kilbowie Road which received £38,207 in payments. Pharmacists are paid around £2.32 for dispensing every dose of methadone and about £1.33 for supervising addicts while they take it. Chemists pay the wholesale cost of buying methadone from the government money they claim.

Around 60 per cent of the cash they are paid is made up of their handling fee for the drug and their charges for dishing it out to addicts. In 2013, pharmacies claimed back more than £17.9 million from the Scottish Government for handling 470,256 prescriptions of methadone — 22,980 prescriptions more than in 2014.

Donnie also told the Post he believes West Dunbartonshire, which has a long history of drug problems, is making progress tackling addiction. He said: “At the end of the day, the statistics don’t tell you how many people are on methadone or any details of the prescription, but what we can tell is the drug companies are making a killing from it.”

Figures released by the NHS in 2012 revealed that methadone-implicated deaths increased dramatically in cases where the individual had been prescribed the drug for more than a year.

The addictions worker told the Post he believes methadone should be reserved for the chaotic drug users and other substitutes such as Buprenorphine, Subutex and Dihydrocodiene should be implemented. He continued: “Methadone is not just a medical or pharmaceutical matter but a human rights issue. “The dilemma is that if you reduce someone’s methadone they become unstable and could relapse. Some of the people we work with at Alternatives have relapsed, it’s a regular situation.

If you start to reduce this person they could relapse and relapse significantly, and they might think they can go back onto heroin and inevitably could end up overdosing.”

He added: “That’s my position and I don’t envy the medical side of it in trying to square this problem.”

Top researcher Dr Neil McKeganey, from the Centre for Drug Misuse Research, said the methadone programme “is literally a black hole into which people are disappearing”.

The statistics of methadone prescriptions can be viewed online at:    www.marcellison.com/bbc/methadone

Alternatives is an organisation funded by West Dunbartonshire Council that helps bring recovering addicts back into society. The project has been around since January 1995, firstly covering Dumbarton and the Vale of Leven, latterly broadening out to Clydebank.

Source: http://www.archive.clydebankpost.co.uk/ 7th April 2015

Increasing numbers of Belgian teenagers are seeking help for cannabis use, De Standaard reported on Monday.

According to a report by the Flemish Association of Addiction Treatment Centres Care (VVBV), in 2013 495 boys and 78 girls aged between 15 and 19 sought assistance over continued use of the drug.

In addition, 36 children under the age of 15 also asked for help.

The report also found that more and more women are seeking help for heroin and cocaine use.

Counselling services are now been targeted at the young.

“Young men with a cannabis addiction used to be all in their twenties before they took the step to recovery.

In recent years, more and more 15- to 19-year olds are added, and they became a separate group in health care,” said VVBV Chairman Dirk Vandevelde.

“Based on these figures, it is difficult to estimate whether it is youth who are experimenting or already have an advanced addiction, and how long they remain in counselling,” he said.

Last week, a law allowing for the sale of medical marijuana was published in Belgium.

The law will come into effect at the beginning of July.

Amongst the drug’s medical properties is the alleviation of pain for sufferers of conditions such as multiple sclerosis.

Source:

http://news.xinhuanet.com/english/2015-06/15/c_134328368.htm  15th June 2015

Scientific studies increasingly suggest marijuana may not be the risk-free high that teens — and sometimes their parents — think it is, researchers say. Yet pot is still widely perceived by young smokers as relatively harmless, said Dr. Romina Mizrahi, director of the Focus on Youth Psychosis Prevention clinic and research program at the Centre for Addiction and Mental Health.

She cites a growing body of research that warns of significantly higher incidence of hallucinations, paranoia and the triggering of psychotic illness in adolescent users who are most predisposed.

“When you look at the studies in general, you can safely say that in those that are vulnerable, it doubles the risk.”  Such fallout is increasingly evident in the 19-bed crisis monitoring unit at the Children’s Hospital of Eastern Ontario in Ottawa.

“I see more and more cases of substance-induced psychosis,” said Dr. Sinthu Suntharalingam, a child and adolescent psychiatrist. “The most common substance that’s abused is cannabis.” One or two cases a week are now arriving on average. “They will present with active hallucinations,” Suntharalingam said. “Parents will be very scared. They don’t know what’s going on. They’ll be seeing things, hearing things, sometimes they will try to self-harm or go after other people.”

She and Mizrahi, an associate professor in psychiatry at University of Toronto, are among other front-line professionals who say more must be done to help kids understand potential effects.

“They know the hard drugs, what they can do,” Suntharalingam said. “Acid, they’ll tell us it can cause all these things so they stay away from it. But marijuana? They’ll be: ‘Oh, everybody does it.”‘  Mizrahi said the message isn’t getting through.

“Teenagers think that cannabis is harmless. It is not. And for some people, it’s particularly dangerous.” She stressed that risk depends on many factors. “Not every 14-year-old who smokes marijuana will have schizophrenia,” she said in an interview. Genetics, social issues, marijuana strength and frequency of use are among complex variables along with how young a person starts using the drug. “We are starting to see this as a very important issue,” Mizrahi said. “I think we have to start to talk about this.”

Brain development in childhood continues through teenage years and into the early 20s, she explained. Cannabis affects how the brain’s regulator — called the endocannabinoid system — controls things like mood and memory, she said. “You’re kind of tampering with or altering the system that’s there to regulate other things.”

Mizrahi said she typically gets feedback when she discusses this topic from people who say they’ve used marijuana for decades with no psychotic effect. There are also those who point out myriad medical benefits. But psychotic episodes, when they occur, could be short-lived or trigger a longer-term illness.

The Centre for Addiction and Mental Health says marijuana use in Canada is most common among teens and young adults. It estimates past-year use in Ontario at 23 per cent for students in Grade 7 to 12, and 40 per cent for those aged 18 to 29.

Amir Englund of King’s College London specializes in the effects of cannabis on the brain and behaviour. Pot with higher THC or tetrahydrocannabinol content, the ingredient that induces most psychological effects, can pack the punch of three shots of scotch versus a pint of beer, he said.  Studies of frequent adolescent users suggest those who start smoking earlier have a higher tendency to develop psychotic illnesses, he said in an interview. “People who get an illness much earlier, their likelihood of having a bad prognosis is higher.”

In Canada, pot is often more accessible to under-agers than alcohol but with no content controls. The Centre for Addiction and Mental Health, the country’s largest teaching hospital of its kind, called last fall for legalization with strict regulation to reduce harm.

Mizrahi advises all young people to avoid pot until they’re at least in their early 20s. “Certainly don’t do it when your brain is developing,” she said. “Don’t put yourself at risk.”

Source:  http://www.ctvnews.ca/health    5th May 2015

 

Marijuana use for medical conditions is an issue of growing concern. Some Veterans use marijuana to relieve symptoms of PTSD and several states specifically approve the use of medical marijuana for PTSD. However, controlled studies have not been conducted to evaluate the safety or effectiveness of medical marijuana for PTSD. Thus, there is no evidence at this time that marijuana is an effective treatment for PTSD. In fact, research suggests that marijuana can be harmful to individuals with PTSD.

Epidemiology

Marijuana use has increased over the past decade. In 2013, a study found that 19.8 million people reported using marijuana in the past month, with 8.1 million using almost every day (1). Daily use has increased 60% in the prior decade (1). A number of factors are associated with increased risk of marijuana use, including diagnosis of PTSD (2), social anxiety disorder (3), other substance use, particularly during youth (4), and peer substance use (5).

Cannabis Use Disorder among Veterans Using VA Health Care

There has been no study of marijuana use in the overall Veteran population. What we do know comes from looking at data of Veterans using VA health care, who may not be representative of Veterans overall. When considering the subset of Veterans seen in VA health care with co-occurring PTSD and substance use disorders (SUD), cannabis use disorder has been the most diagnosed SUD since 2009. The percentage of Veterans in VA with PTSD and SUD who were diagnosed with cannabis use disorder increased from 13.0% in fiscal year (FY) 2002 to 22.7% in FY 2014. As of FY 2014, there are more than 40,000 Veterans with PTSD and SUD seen in VA diagnosed with cannabis use disorder (6).

trends-inptsd

 

Problems Associated with Marijuana Use

Marijuana use is associated with medical and psychiatric problems. These problems may be caused by using, but they also may reflect the characteristics of the people who use marijuana. Medical problems include chronic bronchitis, abnormal brain development among early adolescent initiators, and impairment in short-term memory, motor coordination and the ability to perform complex psychomotor tasks such as driving. Psychiatric problems include psychosis and impairment in cognitive ability. Quality of life can also be affected through poor life satisfaction, decreased educational attainment, and increased sexual risk-taking behavior (7). Chronic marijuana use also can lead to addiction, with an established and clinically significant withdrawal syndrome (8).

Active Ingredients and Route of Administration

Marijuana contains a variety of components (cannabinoids), most notably delta-9-tetrahydrocannabinol (THC) the primary psychoactive compound in the marijuana plant. There are a number of other cannabinoids, such as cannabidiol (CBD), cannabinol (CBN), and cannabigerol (CBG). Marijuana can vary in cannabinoid concentration, such as in the ratio of THC to other cannabinoids (CBD in particular). Therefore, the effects of marijuana use (e.g., experience of a high, anxiety, sleep) vary as a function of the concentration of cannabinoids (e.g., THC/CBD). In addition, the potency of cannabinoids can vary. For example, the concentration of THC in the marijuana plant can range in strength from less than 1% to 30% based upon strain and cultivation methods. In general, the potency of THC in the marijuana plant has increased as much as 10-fold over the past 40 years (9,10). Recently, cannabis extract products, such as waxes and oils, have been produced and sold in which the concentration of THC can be as high as 90%. Thus, an individual could unknowingly consume a very high dose of THC in one administration, which increases the risk of an adverse reaction.

Marijuana can be consumed in many different forms (e.g., flower, hash, oil, wax, food products, tinctures). Administration of these forms also can take different routes: inhalation (smoking or vaporizing), ingestion, and topical application. Given the same concentration/ratio of marijuana, smoking or vaporizing marijuana produces similar effects (11); however, ingesting the same dose results in a delayed onset and longer duration of effect (12). Not all marijuana users may be aware of the delayed effect caused by ingestion, which may result in greater consumption and a stronger effect than intended.

Neurobiology

Research has consistently demonstrated that the human endocannabinoid system plays a significant role in PTSD. People with PTSD have greater availability of cannabinoid type 1 (CB1) receptors as compared to trauma-exposed or healthy controls (13,14). As a result, marijuana use by individuals with PTSD may result in short-term reduction of PTSD symptoms. However, data suggest that continued use of marijuana among individuals with PTSD may lead to a number of negative consequences, including marijuana tolerance (via reductions in CB1 receptor density and/or efficiency) and addiction (15). Though recent work has shown that CB1 receptors may return after periods of marijuana abstinence (16), individuals with PTSD may have particular difficulty quitting (17).

Marijuana as a Treatment for PTSD

The belief that marijuana can be used to treat PTSD is limited to anecdotal reports from individuals with PTSD who say that the drug helps with their symptoms. There have been no randomized controlled trials, a necessary “gold standard” for determining efficacy. Administration of oral CBD has been shown to decrease anxiety in those with and without clinical anxiety (18). This work has led to the development and testing of CBD treatments for individuals with social anxiety (19), but not yet among individuals with PTSD. With respect to THC, one open trial of 10 participants with PTSD showed THC was safe and well tolerated and resulted in decreases in hyperarousal symptoms (20).

Treatment for Marijuana Addiction

People with PTSD have particular difficulty stopping their use of marijuana and responding to treatment for marijuana addiction. They have greater craving and withdrawal than those without PTSD (21), and greater likelihood of marijuana use during the six months following a quit attempt (17). However, these individuals can benefit from the many evidence-based treatments for marijuana addiction, including cognitive behavioral therapy, motivational enhancement, and contingency management (22). Thus, providers should still utilize these options to support reduction/abstinence.

Clinical Recommendations

Treatment providers should not ignore marijuana use in their PTSD patients. The VA/DoD PTSD Clinical Practice Guideline(2010) recommends providing evidence-based treatments for the individual disorders concurrently. PTSD providers should offer education about problems associated with long-term marijuana use and make a referral to a substance use disorder (SUD) specialist if they do not feel they have expertise in treating substance use.

Individuals with comorbid PTSD and SUD do not need to wait for a period of abstinence before addressing their PTSD. A growing number of studies demonstrate that that these patients can tolerate trauma-focused treatment and that these treatments do not worsen substance use outcomes. Therefore, providers have a range of options to help improve the lives of patients with the co-occurring disorders.

Marcel O. Bonn-Miller, Ph.D. and Glenna S. Rousseau, Ph.D.

For more information, see PTSD and Substance Use Disorders in Veterans.

References

  1. (2014). Results from the 2013 National Survey on Drug Use and Health: Summary of National Findings.(Vol. NSDUH Series H-48, HHS Publication No. (SMA) 13-4795). Rockville, MD: Substance Abuse and Mental Health Services Administration.
  2. Cougle, J.R., Bonn-Miller, M. O., Vujanovic, A. A., Zvolensky, M. J., & Hawkins, K. A. (2011). Posttraumatic stress disorder and cannabis use in a nationally representative sample. Psychology of Addictive Behaviors, 25,554-558. doi: 10.1037/a0023076
  3. Buckner, J.D., Schmidt, N. B., Lang, A. R., Small, J. W., Schluach, R. C., & Lewinsohn, P. M. (2008). Specificity of social anxiety disorder as a risk factor for alcohol and cannabis dependence. Journal of Psychiatric Research, 42,230-239. doi: 10.1016/j.jpsychires.2007.01.002
  4. Butterworth, P., Slade, T. & Degenhardt, L. (2014). Factors associated with the timing and onset of cannabis use and cannabis use disorder: Results from the 2007 Australian National Survey of Mental Health and Well-Being. Drug and Alcohol Review, 33,555-564. doi: 10.1111/dar.12183
  5. von Sydow, K., Lieb, R., Pfister, H., Höefler, M., & Wittchen, H. U. (2002). What predicts incident use of cannabis and progression to abuse and dependence? A 4-year prospective examination of risk factors in a community sample of adolescents and young adults. Drug and Alcohol Dependence, 68,49-64.
  6. Program Evaluation and Resource Center, V.A., 2015.
  7. Volkow, N. D., Baler, R. D., Compton, W. M., & Weiss, S. R. B. (2014). Adverse health effects of marijuana use. New England Journal of Medicine, 370,2219-2227. doi: 10.1056/NEJMra1402309
  8. Budney, A. J., Hughes, J. R., Moore, B. A., & Vandrey, R. (2004). Review of the validity and significance of cannabis withdrawal syndrome. American Journal of Psychiatry, 161,1967-1977.
  9. Mehmedic, Z., Chandra, S., Slade, D., Denham, H., Foster, S., Patel, A. S., Ross, S. A., Khan, I. A., & ElSohly, M. A. (2010). Potency trends of Δ9-THC and other cannabinoids in confiscated cannabis preparations from 1993 to 2008.Journal of Forensic Sciences, 55,1209-1217. doi: 10.1111/j.1556-4029.2010.01441.x
  10. Sevigny, E. L., Pacula, R. L., & Heaton, P. (2014) The effects of medical marijuana laws on potency. International Journal of Drug Policy, 25,308-319. doi: 10.1016/j.drugpo.2014.01.003
  11. Abrams, D. I., Vizoso, H. P., Shade, S. B., Jay, C., Kelly, M. E., & Benowitz, N. L. (2007). Vaporization as a smokeless cannabis delivery system: A pilot study. Clinical Pharmacology & Therapeutics, 82,572-578.
  12. Grotenhermen, F. (2003). Pharmacokinetics and pharmacodynamics of cannabinoids. Clinical Pharmacokinetics, 42,327-360.
  13. Neumeister, A., Normandin, M. D., Pietrzak, R. H., Piomelli, D., Zheng, M. Q., Gujarro-Anton, A., Potenza, M. N., Bailey, C. R., Lin, S. F., Najafzaden, S., Ropchan, J., Henry, S., Corsi-Travali, S., Carson, R. E., & Huang, Y. (2013). Elevated brain cannabinoid CB1 receptor availability in post-traumatic stress disorder: A positron emission tomography study. Molecular Psychiatry, 18,1034-1040. doi: 10.1038/mp.2013.61
  14. Passie, T., Emrich, H. M., Brandt, S. D., & Halpern, J. H. (2012). Mitigation of post-traumatic stress symptoms by Cannabis resin: A review of the clinical and neurobiological evidence. Drug Testing and Analysis, 4,649-659. doi: 10.1002/dta.1377
  15. Kendall, D.A. & Alexander, S.P. H. (2009). Behavioral neurobiology of the endocannabinoid system.Current topics in behavioral neurosciences. Heidelberg: Springer-Verlag.
  16. Hirvonen, J., Goodwin, R. S., Li, C-T., Terry, G. E., Zoghbi, S. S., Morse, C., Pike, V. W., Volkow, N. D., Huestis, M. A., & Innis, R. B. (2012). Reversible and regionally selective downregulation of brain cannabinoid CB1 receptors in chronic daily cannabis smokers. Molecular Psychiatry, 17,642-649. doi: 10.1038/mp.2011.82
  17. Bonn-Miller, M. O., Moos, R. H., Boden, M. T., Long, W. R., Kimerling, R., & Trafton, J. A. (in press). The impact of posttraumatic stress disorder on cannabis quit success. The American Journal of Drug and Alcohol Abuse.
  18. Crippa, J. A., Zuardi, A. W., Martín-Santos, R., Bhattacharyya, S., Atakan, Z., McGuire, P., & Fusar-Poli, P. (2009). Cannabis and anxiety: a critical review of the evidence. Human Psychopharmacology, 24,515-523. doi: 10.1002/hup.1048
  19. Bergamaschi, M. M., Queiroz, R. H. C., Hortes, M., Chagas, N., de Oliveira, C. G., De Martinis, B. S., Kapczinski, F., Quevedo, J., Roesler, R., Schröder, N., Nardi, A. E., Martín-Santos, R., Hallak, J. E. C., Zuardi, A. W., & Crippa, J. A. S. (2011). Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naïve social phobia patients. Neuropsychopharmacology, 36,1219-1226. doi: 10.1038/npp.2011.6
  20. Roitman, P., Mechoulam, R., Cooper-Kazaz, R., & Shalev, A. (2014). Preliminary, open-label, pilot study of add-on oral Δ9-tetrahydrocannabinol in chronic post-traumatic stress disorder. Clinical Drug Investigation, 34,587-591. doi: 10.1007/s40261-014-0212-3
  21. Boden, M. T., Babson, K. A., Vujanovic, A. A., Short, N. A., & Bonn-Miller, M. (2013). Posttraumatic stress disorder and cannabis use characteristics among military Veterans with cannabis dependence. The American Journal on Addictions, 22,277-284. doi: 10.1111/j.1521-0391.2012.12018.x
  22. Roffman, R. A. & Stephens, R. S. (2006). Cannabis dependence: its nature, consequences, and treatment.International research monographs in the addictions. Cambridge, UK; New York: Cambridge University Pres

Source:  http://www.ptsd.va.gov/   May 2015

Using marijuana and alcohol together greatly increases the amount of THC, marijuana’s active ingredient, in the blood, a new study concludes. Using the two substances together raises THC levels much more than using marijuana by itself.

The researchers say using alcohol and marijuana together considerably increases the risk of car crashes, compared with using marijuana alone.

The study included 19 people who drank alcohol or a placebo in low doses 10 minutes before they inhaled vaporized marijuana in either a low or high dose, Time reports. When a person drank alcohol, their blood concentration of THC was much higher.  The findings are published in Clinical Chemistry.

A  study published last year  found teenagers who use marijuana and alcohol together are more likely to engage in unsafe driving, compared with those who use one of those substances alone.

Teens who used alcohol alone were 40 percent more likely to admit they had gotten a traffic ticket and 24 percent more likely to admit involvement in a traffic crash, compared with teens who didn’t smoke marijuana or drink. Teens who smoked marijuana and drank were 90 percent more likely to get a ticket and 50 percent more likely to be in a car crash, compared with their peers who didn’t use either sub

Source:   http://www.drugfree.org/join-together     28th May2015

Two years ago, the Georgia Legislature tried but failed to legalize artisanal cannabidiol (CBD) oils for children suffering from epilepsy. Artisanal CBD oils are products marijuana growers are making in states that have legalized marijuana for medical use. No grower in these states has submitted its CBD product to FDA for approval as a safe or effective medicine.

In contrast, two pharmaceutical companies, GW Pharmaceuticals of Great Britain and Insys Therapeutics of the US, are developing pharmaceutical-grade CBD oils. GW’s version, Epidiolex, is in FDA Phase III clinical trials and Insys Therapeutics is about to undergo FDA testing. The Insys drug is 100% synthesized CBD, meaning it is an exact chemical duplicate of cannabidiol found in the marijuana plant but is made of pure chemicals to eliminate impurities and contaminants. Epidiolex is an extract of marijuana that has been purified to remove impurities and contaminants and is 98% CBD with trace amounts of THC and other cannabinoids. Both drugs must be tested in animals to ensure safety before companies can apply to FDA for permission to test their drugs in humans.

Artisanal CBD oils offer no such protections to patients. Random tests have shown that many contain THC, which can cause seizures, contaminants, and in some cases little to no CBD.

When the Georgia bill failed last year, Governor Nathan Deal formed a partnership with GW to conduct clinical trials of Epidiolex in Georgia as well as a statewide FDA expanded access program for children not able to enroll in the clinical trials. Both programs are up and running.

Despite this, the legislature came back with a bill this year to legalize artisanal CBD oils not only for childhood epilepsy but also for seven other diseases. Moreover, this bill permits possession of up to 20 ounces of CBD oil containing up to 5% THC. The bill passed and the governor signed it in April. It provides immunity from prosecution to those who possess CBD and calls for a special commission to recommend how best to grow marijuana, process it into CBD oils, and distribute it to patients.

Like the researchers whose work is published in JAMA today, specialists who treat epilepsy also are beginning to speak out. The NBC-TV affiliate in Atlanta interviewed several this week. Dr. Yong Park, who is helping run the clinical trials in Georgia, says doctors don’t know what the drug interactions are or what the side effects might be because they don’t have the evidence yet. Nor do they know how many pesticides artisanal CBD oils may contain nor what the long-term effects of daily exposure on the brain might be.

Under the new state law, when doctors sign a letter approving patients for the state registry that allows them to possess CBD oils, says Atlanta pediatrician Cynthia Wetmore, M.D., Ph.D., “they are required to keep track of the patients. But how do we know what dose to recommend? The oil patients have access to is not standardized. Each batch can be different. There’s a lot of variability in each batch. What side effects is it causing, if any? We have to report to the state on each patient, quarterly. It will be hard to know if it’s helping or hurting.”

Perhaps the most haunting concerns come from Dr. Amy Brooks-Kayal, a Colorado pediatric neurologist and president of the American Epilepsy Society. The Atlanta NBC-TV affiliate published her letter to a Pennsylvania representative who held hearings a few months ago on a similar bill in his state. In part, she writes:

The families and children coming to Colorado are receiving unregulated, highly variable artisanal preparations of cannabis oil prescribed, in most cases, by physicians with no training in pediatrics, neurology, or epilepsy. As a result, the epilepsy specialists in Colorado have been at the bedside of children having severe dystonic reactions and other movement disorders, developmental regression, intractable vomiting, and worsening seizures that can be so severe they have to put the child into a coma to get the seizures to stop. Because these products are unregulated, it is impossible to know if these dangerous adverse reactions are due to the CBD or because of contaminants found in these artisanal preparations. The Colorado team has also seen families who have gone into significant debt, paying hundreds of dollars a month for oils that do not appear to work for the vast majority. For all these reasons not a single pediatric neurologist in Colorado recommends the use of artisanal cannabis preparations. Possibly of most concern is that some families are now opting out of proven treatments, such as surgery or the ketogenic diet, or newer antiseizure medications because they have put all their hope in CBD oils.

All three epilepsy specialists want parents to know that giving artisanal CBD oils to children exposes them to risks that cannot be defined. They urge parents instead to enroll their children in clinical trials or expanded access programs that are testing pharmaceutical-grade CBD where doctors can monitor the children closely.

Read Atlanta story and full text of Dr. Brooks-Kayal’s letter here

Source:

http://us2.campaign-archive2.com/?u=2138d91b74dd79cbf58e302bf&id=71df2f126e&e=7ee41d6c49

Evidence does not support medical marijuana use for most of the diseases and conditions states are permitting, says an editorial in this week’s issue of the Journal of the American Medical Association (JAMA).

“First, for most qualifying conditions, approval has relied on low-quality scientific evidence, anecdotal reports, individual testimonials, legislative initiatives, and public opinion,” say the editorial’s authors. “The US Food and Drug Administration (FDA) requires evidence from at least two adequately powered randomized clinical trials before approving a drug for any specific indication,” and evidence for most conditions fails to meet FDA standards.

Second, there are inconsistencies between states about which conditions qualify for medical marijuana. Some states legalize medical marijuana for PTSD or sickle cell anemia, for example, while others do not. Such differences reflect inconsistencies in applying current evidence to legislative decision-making.

Third, most FDA-approved  drugs have just one or two active ingredients. Marijuana contains more than 400 compounds whose interactions with each other are poorly understood. In addition, the amounts of some marijuana compounds in various strains vary so widely that precise dosing is difficult, which means doctors cannot give patients proper guidance.

Fourth, some individual marijuana components are available commercially (dronabinol and nabilone) and published data exists to guide dosing. Few data exist to guide dosing of smoked [or eaten] marijuana for medical use.

Fifth, while short-term adverse effects of marijuana are quite well known, the effects of long-term use need further study. Tolerance and dependence occur with repeated exposure to marijuana, meaning that dosages will have to be increased when the drug is used medically to be effective, increasing the risk of addiction and other problems.

Finally, “there is also a small but definite risk of psychotic disorder associated with marijuana use, as well as a significant risk of symptom exacerbations and relapse in patients with an established psychotic disorder,” say the authors. Those with schizophrenia, bipolar disorder, or substance dependence must be identified and measures must be taken to protect them from medical marijuana.

“Perhaps US states should establish clinical follow-up programs to monitor long-term outcomes prospectively, especially negative outcomes (e.g. new cases of psychosis) in patients with contraindications.”

In addition to this editorial, JAMA also publishes several research articles concerning medical marijuana this week.

Read editorial here.
Read “Medical Marijuana for Treatment of Chronic Pain and Other Medical and Psychiatric Problems, A Clinical Review” here.
Read “Cannabinoids for Medical Use, A Systematic Review and Meta-Analysis” here.
Read “Cannabinoid Dose and Label Accuracy in Edible Medical Cannabis Products” here.

Source:  The MarijuanaReport.org.   June 24th 2015

A stressed rat will seek a dose of cocaine that is too weak to motivate an unstressed rat. The reason, NIDA researchers report, is that the stress hormone corticosterone increases dopamine activity in the brain’s reward center. When an animal is stressed, the cocaine-induced dopamine surge that drives drug seeking rises higher because it occurs on top of the stress-related elevation.

Graduate student Evan N. Graf, Dr. Paul J. Gasser, and colleagues at Marquette University in Milwaukee, Wisconsin, traced the physiological pathway that links stress and corticosterone to increased dopamine activity and heightened responsiveness to cocaine. Their findings provide new insight into cocaine use and relapse, and point to possible new medication strategies for helping people stay drug free.

Stress Increases Sensitivity to Relapse Triggers

Former drug users who relapse often cite stress as a contributing factor. The Marquette researchers observed that when stress figures in relapse, other relapse promoters are almost always present as well. Dr. Gasser explains, “It’s never one single event that triggers relapse. It’s the convergence of many events and conditions, such as the availability of the drug, cues that remind people of their former drug use, and also stress.” On the basis of this observation, the researchers hypothesized that stress promotes relapse by making a person more sensitive to other relapse triggers.

To test their hypothesis, the researchers put stressed and unstressed rats through an experimental protocol that simulates regular drug use in people followed by abstinence and exposure to a relapse trigger. As the stressor, they used a mild electric foot shock; as the relapse trigger, they administered a low dose of cocaine (2.5 milligrams per kilogram).

The results confirmed the hypothesis. The stressed rats, but not the stress-free animals, responded to the small cocaine dose with a behavior that parallels relapse in people: They resumed pressing a lever that they had previously used to self-administer the drug (see Figure 1, top graph).

stress_hormone

 

Text Description of Graphic

A Stress Hormone Underlies the Effect

Mr. Graf and colleagues turned their attention to the question of how stress sensitizes animals to cocaine’s motivational effect. One likely place to start was with the hormone corticosterone. In stressful situations, the adrenal glands release corticosterone into the blood, which carries it throughout the body and to the brain. Among corticosterone’s physiological roles is that it affects glucose metabolism and helps to restore homeostasis after stress. The Marquette researchers demonstrated that increasing cocaine’s potential to induce relapse also belongs on the list of corticosterone’s effects. Reprising their original experimental protocol with a couple of new twists, they showed that:

  • Corticosterone is necessary for stress to promote relapse to cocaine seeking: The researchers removed rats’ adrenal glands, which prevented the animals from producing corticosterone. In this condition, the animals did not exhibit relapse behavior when exposed to the stressor and low-dose cocaine.
  • Corticosterone in the brain reward center is sufficient by itself to increase cocaine’s potency as a relapse trigger:The researchers injected these same rats with corticosterone, bringing the hormone concentration up to stress levels in the brain reward center (nucleus accumbens, NAc). Now the animals exhibited relapse behavior when exposed to cocaine, even without the stressor (see Figure 1, middle graph).

Enhanced Dopamine Activity…

The researchers next took up the question: What does corticosterone do in the NAc to increase cocaine’s potency to induce relapse? A hypothesis that suggested itself immediately was that the hormone enhances dopamine activity. Dopamine is an important neuromodulator in the NAc, and all addictive drugs, including cocaine, produce their motivating effects by increasing dopamine concentrations in the NAc.

The Marquette team showed that, indeed, stress-level concentrations of corticosterone enhance the cocaine-induced rise in extracellular dopamine in the NAc. In this experiment, the researchers exposed two groups of rats to low-dose cocaine, then measured their NAc dopamine levels with in vivo microdialysis. One group, which was pretreated with corticosterone injections, had higher dopamine levels than the other, which was not pretreated.

The Marquette team firmed up their hypothesis with a further experiment. They reasoned that if corticosterone promotes relapse behavior by increasing dopamine activity, then preventing that enhancement should prevent the behavior. This indeed turned out to be the case. When the researchers injected animals with corticosterone but also gave them a compound (fluphenazine) that blocks dopamine activity, exposure to low-dose cocaine did not elicit relapse behavior.

…Due To Reduced Dopamine Clearance

So far the Marquette team had established that the stress hormone corticosterone promotes relapse behavior by increasing dopamine activity in the NAc. Now they moved on to the next question: How does corticosterone enhance dopamine activity?

To address this question, the researchers considered the cycle of dopamine release and reuptake. In the NAc, as elsewhere in the brain, dopamine activity depends on the concentration of the neurotransmitter in the extracellular space (space between neurons): the higher the concentration, the more activity there will be. In turn, the extracellular dopamine concentration depends on the balance between two reciprocal ongoing processes: specialized neurons releasing dopamine molecules into the space, and specialized proteins drawing molecules back inside the neurons.

Mr. Graf and colleagues discovered that corticosterone interferes with the removal of dopamine molecules from the extracellular space back into cells. It shares this effect with cocaine, but achieves it by a different mechanism.

In this experiment, the researchers measured real-time changes in dopamine concentration in the NAc in response to electrical stimulation of dopamine release in the area. This technique allowed the team to measure both A) the rate of increase in dopamine concentration, indicating the amount of dopamine released; and B) the rate of decrease in dopamine concentration, indicating the rate of dopamine clearance. The scientists measured stimulation-induced increases and decreases in extracellular dopamine concentrations under three conditions: at baseline, after giving the animals a compound that blocks the dopamine transporter (DAT), which is the mechanism whereby cocaine inhibits dopamine removal; and, last, after injecting the animals with corticosterone. They found that:

  • As happens with cocaine, the clearance of extracellular dopamine decreased after DAT blockade.
  • Clearance of extracellular dopamine decreased further after corticosterone.

 

A Candidate Mechanism

One question remained outstanding to complete the picture of how stress potentiates the response to cocaine: What is the mechanism whereby corticosterone reduces dopamine clearance?

Mr. Graf and colleagues noted that previous research provides a likely answer: Corticosterone has been shown to inhibit the functioning of the organic cation transporter 3 (OCT3), which is another of the specialized proteins that, like DAT, remove dopamine from the extracellular space. To confirm this hypothesis, the researchers resorted again to their initial experimental protocol. This time, they injected rats with a compound (normetanephrine) that blocks OCT3, followed by low-dose cocaine. The animals responded by resuming their previously abandoned lever pressing  behavior, proving that OCT3 blockade is sufficient to potentiate the response to cocaine (see Figure 1, bottom graph).

The Marquette researchers say that further studies will be required to definitively establish that OCT3 plays the role their evidence points to. Taken together, however, their experiments trace a complete pathway connecting stress to an animal’s enhanced responses to cocaine (see Figure 2):

  • Stress raises corticosterone levels.
  • Corticosterone blocks OCT3, inhibiting dopamine clearance and thereby raising dopamine activity in the NAc.
  • When a stressed animal is exposed to cocaine, the resulting dopamine surge builds on the foundation of this already higher-than-normal level of dopamine activity.
  • The added elevation of the dopamine surge increases the animal’s motivation to seek the drug.

 

streee_relapse

Figure 2. Stress Amplifies Cocaine’s Effect on Dopamine Release in the Nucleus Accumbens (NAc) The schematic illustrates how stress may enhance cocaine’s motivational effect and increase the risk for relapse. A) Cocaine binds to the dopamine transporter (DAT) on dopamine-releasing neurons in the NAc, reducing dopamine (DA) clearance and, in turn, increasing extracellular dopamine. B) Stress causes release of corticosterone, which inhibits the OCT3 transporter, further reducing dopamine clearance and increasing extracellular dopamine. The resulting heightened dopamine stimulation of medium spiny neurons (MSNs) enhances drug seeking.

Text Description of Graphic

Stress–Relapse Connection Unraveled

“Our findings show that stress doesn’t just cause relapse behavior by itself, but interacts with other ongoing behaviors to influence relapse,” Dr. Gasser says. “This insight provides a better picture of how stress can affect addiction. It helps us understand why treating cocaine addiction is so difficult and will help in designing therapies whether they be based on pharmacotherapy or counseling.” The researchers believe—and are testing as a hypothesis—that stress increases the power of environmental drug-associated cues to trigger relapse, just as it does the power of low-dose cocaine.

Although researchers have long known that stress plays an important role in relapse, pinning down its role experimentally has been a challenge, says Dr. Susan Volman, program officer and health science administrator at NIDA’s Behavioral and Cognitive Science Research Branch. “This study provides a perspective of stress as a stage-setter or modulator for relapse, and it gets all the way down to the molecular mechanism. Based on this team’s findings, OCT3 offers a potential new target for developing pharmacological therapies to help with treating addiction,” Dr. Volman says.

This work was supported by NIH grants DA017328, DA15758, and DA025679.

Source:

Graf, E.N.; Wheeler, R.A.; Baker, D.A. et al. Corticosterone acts in the nucleus accumbens to enhance dopamine signalling and potentiate reinstatement of cocaine seeking. Journal of Neuroscience 33(29):11800-11810, 2013. Full text

An interactive mobile texting aftercare program has shown promise as a means to help teens and young adults engage with post-treatment recovery activities and avoid relapse, researchers report. In a NIDA-supported pilot study, the program, called ESQYIR (Educating & Supporting Inquisitive Youth in Recovery), reduced young people’s odds of relapsing by half compared with standard aftercare.

Dr. Rachel Gonzales and colleagues at the University of California, Los Angeles (UCLA), designed ESQYIR to teach and reinforce wellness self-management in a manner that fits young people’s attitudes and communication styles. The researchers cite numerous advantages of the mobile texting approach: It is inexpensive and features personalization of content, convenience of use, ease of assessment and monitoring, and flexibility in the time and location of delivery.

The Need

Many young people comply poorly with aftercare interventions and resist involvement in 12-step programs and other post-treatment recovery activities. Dr. Gonzales says, “Teens and young adults don’t want to be stigmatized as having a disease or as still being in recovery. In their minds, after the primary treatment, they are done.” Young people often don’t view addiction as a disease, she adds. Instead, they regard substance use as a matter of lifestyle and personal choice. As a result, as many as 85 percent of teens and young adults relapse within 1 year.

Dr. Gonzales and her research team reckoned that young people might engage more readily with aftercare built on text messaging. This mode of communication is ubiquitous among young people, surpassing most other forms of social interaction. Messages can be personalized and can be accessed and responded to privately, when and where youths find it convenient or feel a need for help. Text messaging interventions are already used to treat maladies including obesity, sexually transmitted diseases, and tobacco dependence in young adults.

“The most effective programs take into consideration the users, their needs, their desires, and their way of connecting,” Dr. Gonzales says. Accordingly, when she and her team composed the text messages for Project ESQYIR, they solicited input from young people in recovery from substance use disorders (SUDs). “The program’s text messages are based on their voices, parallel their views of recovery, and speak to their recovery needs,” Dr. Gonzales says.

Keeping Tabs With Texts

The participants in the ESQYIR pilot study were 80 volunteers, ages 14 to 26, who had been treated in outpatient and residential community treatment centers in the Los Angeles area. The drugs that had caused them problems included marijuana (55 percent), methamphetamine (30 percent), cocaine (15 percent), heroin (11 percent), prescription drug (6 percent), and other substances including alcohol (4 percent). Half of the participants received the mobile texting ESQYIR program, the other half received the standard aftercare offered by their treatment facilities, which consisted of referral to 12-step programs.

Figure 1. Daily Mobile Texts Prompt Self-Monitoring, Give Recovery Advice and Encouragement

The participants in the text messaging program received daily text messages with tips to self-monitor their recovery- and substance use–related behaviors and with alerts to aftercare services in their community.

Each weekday at 12 noon, the participants in the ESQYIR group received a text that reminded them about being in recovery and provided a wellness tip for the day. The reminder portion of the text said, “Today’s a new day in ur recovery! Think about the change ur working towards.” The wellness tip promoted personal, social, physical, or emotional health. For example, one message read, “Write down the top 3 stressors that u need to avoid or deal with for helping u not use.”

Weekdays at 4 p.m., the participants in the ESQYIR group received a text that prompted them to self-monitor and text back numerical ratings of their abstinence confidence, wellbeing, substance use, and recovery behaviors (see Figure 1). The participants then received a feedback text, automatically selected from more than 600 possible messages, which provided motivational/inspirational encouragement, coping advice, or positive appraisal tailored to the participants’ self-rating. For example, motivational feedback texts encouraged participants to keep on track with recovery and attend therapy or self-help meetings when needed.

Dr. Gonzales says, “The self-monitoring texts helped participants remain mindful and aware of potential relapse triggers, particularly in risky situations.” With that awareness and the feedback provided by the program, the young people were able to generate strategies for coping with such situations without drugs, the researchers suggest.

On weekends, the participants received personalized texts with educational information adapted from NIDA reference materials and resource information on local support services.

Less Relapse, More Engagement

Figure 2. Text-Based Delivery of Aftercare Content Decreases Relapse

Teens and young adults receiving daily text messages had lower relapse rates than peers receiving only standard aftercare.

The UCLA researchers monitored the participants’ urine for alcohol and drugs monthly during the program. The results indicated that with passing time, the text-based aftercare participants’ odds of relapsing to their primary substances rose only half as fast as those of the standard aftercare group. Compared with the participants in standard aftercare, those assigned to the ESQYIR group were less likely to have relapsed 1 month (8.6 percent vs. 30.3 percent), 2 months (3.6 percent vs. 39.3 percent), and 3 months (14.7 percent vs. 62.9 percent) after the end of their substance abuse treatment (see Figure 2).

The researchers followed up with 55 of the original 81 study participants 180 days after the end of treatment (90 days after the end of the aftercare programs). Those who had received the ESQYIR mobile wellness aftercare intervention were still less likely to have relapsed (21.4 percent vs. 59.3 percent).

The ESQYIR and standard aftercare participants both attended on average ten 12-step meetings per month during their last month in substance abuse treatment. Both groups reduced their 12-step attendance in the aftercare period, but the ESQYIR participants did so to a lesser degree (8.9 vs. 2.9 meetings in the final month). The two groups no longer differed significantly in 12-step attendance during the third month post-aftercare (7.0 vs. 4.6 days per month). However, during that month the ESQYIR participants were more involved in other recovery-related extracurricular activities (e.g., exercise, walking, and community/volunteer service) than those who received the standard aftercare.

Text and Thrive

Dr. Gonzales and colleagues are planning a larger, stage II efficacy trial of the mobile-based ESQYIR aftercare wellness intervention. For this trial, they are enhancing the program with new features, including text messages to foster HIV awareness and prevention.

“We look forward to further research in this line of work and to learning more about the efficacy of this intervention,” says Dr. Jessica Campbell Chambers, health science administrator at NIDA’sBehavioral and Integrative Treatment Branch. “This work is extremely important given the high rates of relapse among recovering adolescents.”

Dr. Campbell Chambers concurs with Dr. Gonzales that although the pilot nature of the study and its relatively small cohort size make its results only preliminary, the findings are very promising. The UCLA study team will soon publish a report on the ESQYIR program’s effects at 6- and 9-months post-participation.

This study was supported by NIH grant DA027754.

Source

Gonzales, R.; Ang, A.; Murphy, D.A. et al. Substance use recovery outcomes among a cohort of youth participating in a mobile-based texting aftercare pilot program. Journal of Substance Abuse Treatment 47(1):20-26, 2014.

Neuroscientist Woody Hopf opens a cabinet in his alcohol research laboratory at the University of California, San Francisco. Inside is a cage containing a rat that is being taught addictive behaviours. The rat has been conditioned to press a lever to release a squirt of alcohol when it hears a beep. Hopf closes the cabinet so that the rat will not be distracted by the sights and sounds of human visitors. Just as it takes time for people to undergo the characteristic brain changes that enforce addiction, he says, it will take time for his rat to become dependent on alcohol.

Researchers such as Hopf view addiction as a disease of the brain circuits responsible for pleasure, stress and decision-making. “Addictive substances come at the brain in different ways,” says George Koob, director of the US National Institute on Alcohol Abuse and Alcoholism (NIAAA) in Bethesda, Maryland. “But in the end, they’re activating some of the same circuitry and patterns of behaviour.”

For decades, researchers have been mapping the electrical and chemical circuits that underlie addiction. Now they are working on strategies for healing these neural pathways. Imaging studies show how the brain rewires during recovery from addiction. When combined with studies of how the brain develops during adolescence, the work could help researchers to understand how the brain changes that are characteristic of addiction occur, as well as who is most vulnerable and why. This work is rapidly being translated into treatments. By using electrodes and fibre-optic cables, researchers can intervene in neural circuits with great precision, causing animals to lose their taste for alcohol or their interest in cocaine, not just for days but for weeks or months. This work is now being tested in people. Researchers hope that therapies to heal damaged brain circuits will improve the odds of people overcoming addictions.

Crossed wires

Koob divides addiction into three stages, each with its own brain circuit — groups of neurons or larger structures that interact in a characteristic way (see page S46). Addiction starts with the feel-good binge stage, which is fuelled by the brain’s reward circuit, particularly at the nucleus accumbens. Withdrawal brings stress, centred in the emotional amygdala. Finally, craving and compulsion circuits extending from the prefrontal cortex keep someone using a drug, regardless of negative consequences. Impulsive bingeing leads to habits as the user needs the drug to feel normal.

The changes to the brain’s circuitry are long-lasting, so people trying to give up will often relapse. Even years after recovery, people often start using again when some cue, such as the smell of alcohol or the site of an old hangout, retriggers old patterns. But the changes are not permanent. “The brain can enjoy some recovery, probably through remodelling to override the broken parts,” says Edith Sullivan, an experimental psychologist at Stanford University in California.

Some of the physical damage caused by alcohol misuse can be undone. For example, says Sullivan, the brains of people who have misused alcohol for a long period shrink, but some of that brain volume can be regained by sustained sobriety. There is also some functional recovery — even if the pathways are not fully restored, the recovering brain starts to find workarounds.

Sullivan’s group has been using functional magnetic resonance imaging (fMRI) to study cognition in those recovering from alcoholism. A cognitive skill the researchers focused on is spatial working memory — the thinking that helps you to remember where you parked your car, for example. Poor spatial working memory is characteristic of alcohol misuse.

Sullivan’s research suggests that people recovering from alcohol addiction manage to work around brain damage; in other words, their brains find ways of accomplishing tasks by avoiding using damaged areas and they start to regain their working memory1. The group found that alcohol-dependent people who had been sober for at least a month performed as well as non-alcohol-dependent controls on spatial working-memory tasks, but used a different part of the brain to do it. Sullivan gave them a more abstract task than looking for a lost object or a parked car, but like those tasks it required visual processing, which can take one of two broad neural paths. Patients without brain damage typically rely on a ‘where’ pathway to do the task, whereas those in recovery from alcohol dependence activate a ‘what’ pathway, which tends to be used for recognizing and identifying what we see.

“The next step is to find out how to train a person with brain damage to use these new pathways,” says Sullivan. Encouraging the natural recovery process could help people who are dependent on alcohol to make faster progress. Sullivan compares the brain damage from alcohol addiction to that caused by stroke. “Recovery won’t take three days, it may take three or six months, or a year,” she says. It takes time for changes to occur in the brain when someone develops a dependence on alcohol, and it takes time to undo that.

Sullivan is currently investigating whether there is a cost to this rewiring. She suspects that people in recovery are performing the cognitive steps needed for these tasks sequentially, so they take longer than people without addictions who do the steps rapidly in parallel. The damaged brain has fewer circuits to use, so the brain finds it harder to multitask.

Early start

“There is a lot of debate about how harmful substance abuse is for brain development.”

Our understanding of the addicted brain comes from animal studies and from research on people who are already addicted or are in recovery, such as Sullivan’s participants. Researchers can only guess at how these changes develop in people. Henning Tiemeier, a psychiatric epidemiologist at Erasmus Medical Center in Rotterdam, the Netherlands, says that the only way to see these changes is to follow people over time. “There is a lot of debate about how harmful substance abuse is for brain development, and you cannot prove it with one brain image,” he says.

Two studies, one planned in the United States and one already underway in the Netherlands, could provide some answers. Both will follow adolescents. The adult brain is already formed, although it is still plastic, which is why alcoholism and drug addiction become so engrained, and why the resulting damage cannot be fully repaired. The worry, says Koob, is that the developing brain may not form properly under the influence of drugs and alcohol. Children do not have the cognitive skills to make good choices, making them particularly vulnerable. “Young people have a well-developed reward system but they don’t have a good executive control centre,” says Koob. The key part of that centre, in the brain’s prefrontal cortex, does not finish developing until about the age of 25.

The US National Institutes of Health (NIH), a federal agency that includes the NIAAA and the National Institute on Drug Abuse (NIDA), is currently accepting proposals for the Adolescent Brain Cognitive Development study, which will enrol 10,000 children aged 10 and follow them into adulthood, using neuropsychological tests, brain imaging and surveys, focused specifically on addiction.

Tiemeier is working on the Generation R study in the Netherlands, which has a broader focus on fetal and childhood development and has been following 10,000 children from before birth. The youngest are now aged 9, and the oldest are 12, a stage when some will begin experimenting with cigarettes and alcohol.

Generation R is collecting the first set of brain MRI scans from children in the study, and has about 3,300 so far. By continuing to collect them as the children grow, changes over time will become clear. This is by far the largest brain-imaging study on adolescents in the world, says Tiemeier, so it should provide evidence about how substance use affects the developing organ. He does not expect to see major developmental changes associated with the occasional substance use likely to be found in Generation R because it is a general population study, rather than being focused on people who are addicted to a substance. For this reason, such studies need to be as large as possible if they are to find out what damage drug use does, and how it interacts with puberty, when surges of hormones affect behaviour and brain development.

More information will be available when the Generation R data are combined with results from the NIH study, says Nora Volkow, director of NIDA. These studies will provide a better understanding of the brain changes that reflect what she calls “the skeleton of addictive behaviours”. Addiction to cigarettes is different from addiction to heroin, for example, but all addictions have a common neurological framework. These studies will show how it grows. They should also yield insight into who is vulnerable and why, and how they might be helped sooner.

But as further research deepens our understanding of addiction as a disease characterized by changes in the brain, researchers and policymakers need to think about better ways to evaluate medications and therapies, says Volkow. Currently, any pharmaceutical treatment for addiction needs to show that the patient is now completely free of their addiction, which is difficult to prove and takes a long time (see page S53). “Rather than ask for an outcome of complete abstinence, shouldn’t we evaluate these treatments on their ability to counteract these brain changes?” she asks.

Painful realities

This focus on reversing changes to the addicted brain is leading to therapy ideas that are showing promising early results in animals. Hopf’s rat studies, for example, have led to a potential therapy for alcoholism that is focused on countering the compulsion to use despite negative consequences such as the loss of relationships with family and friends, employment or health. Because rats do not fear these outcomes, Hopf uses simpler analogues. In some experiments, alcohol-dependent rats are given extremely bitter alcohol instead of the expected normal flavour, or in the lever-pressing test they occasionally receive a painful electric shock to their paw. “The rats want the alcohol but they are not happy about it,” Hopf says.

After years of painstaking research and some luck, Hopf found that a particular group of neurons in the reward-centred nucleus accumbens has a key role in promoting compulsive drinking. This year, he found that an approved drug called D-serine binds to receptors on these neurons, causing them to fire less often, leading the alcohol-dependent rats to drink less2. It seems to work by disabling the compulsive behaviour — by turning off the power to deny painful realities. Rats that experience bitter or painful consequences drink less when given the drug. Rats have no such negative consequences to fear and are not affected by the drug and drink as normal.

The nucleus accumbens and a denial of the reality of the situation are involved in multiple stages of addiction, according to Koob, and have a role in both intoxication and the withdrawal process. Hopf is now writing up a plan for a clinical trial of D-serine.

Other techniques target addiction circuits by using physical interventions, rather than drugs. Researchers at the University of Geneva in Switzerland led by neurologist Christian Lüscher have used a method called optogenetics to target a particular group of cells and receptors involved in cocaine addiction in mice. Optogenetics allows researchers to turn off gene expression precisely by shining light into the brain through implanted optical fibres. When Lüscher’s group used the method to calm a group of overactive dopamine-receptor neurons in the nucleus accumbens, the mice stopped seeking cocaine3.

However, optogenetics cannot be used to treat people. The method first requires genetic engineering to render the target cells sensitive to light, and it is not yet possible to safely implant optical fibres in the human brain.

Stimulating recovery

Instead, Lüscher’s team is attempting to emulate the effects of optogenetics by using methods that translate better to the clinic. They are developing a variation on deep-brain stimulation (DBS), a technique that uses an electric current to silence overactive neurons, which is commonly used to treat movement disorders such as Parkinson’s disease. By careful placement of the electrodes, clinicians can target DBS to a particular region in the brain. Researchers have tried using it to treat addiction in people, but results have been mixed.

Lüscher is combining DBS with drugs to block particular receptors in the rat brain, making it possible to silence specific cell types. First they implant an electrode in the nucleus accumbens. Then they use a drug that blocks the neurons’ dopamine receptors. Finally, they switch on the electrode for ten minutes. The effects of DBS for treating Parkinson’s are transient: when the electric field is turned off, the tremor returns. But Lüscher’s combined therapy had a longer-lasting effect4. After 10 minutes of stimulation, the rats exhibited normal behaviour for the following 21 days. Lüscher thinks this means that the treatment may be repairing part of the circuit that was damaged by addiction. He says that the group’s next step will be to test this approach in primates, or possibly take it to clinical trials.

This demonstration of an apparently long-term reversal of drug-related behaviour is “a miracle”, says Jessica Wilden, a neurosurgeon at the Louisiana State University Health Center in Shreveport. Could this lead to a therapy in which you give a patient a pill and a day of brain stimulation and then they are drug free? “In a small way that’s what they’re showing,” she says. But doing it in people will be harder, she warns.

Wilden is investigating whether DBS can be used to treat methamphetamine (meth) addiction. Meth affects dopamine receptors (see ‘Methamphetamine misuse’) and is a growing problem, particularly in Iran and in the southern United States, often for military veterans. Unlike other drugs, which tend to be misused mostly by men, meth use is equally common in women, and has a burden on children because women tend to be the primary caretakers, says Wilden.

“I’m trying to set up a stable model of meth abuse, abstinence and relapse in rats, and then try DBS treatment,” says Wilden. It is a huge challenge. The drug is a potent stimulant, with effects lasting for 16–20 hours in the rats; the animals become agitated and stressed, and get tangled up in the equipment used to administer the drug and the cables that connect them to the DBS system.

Although DBS is a helpful research tool, Wilden and Lüscher both doubt whether it can be widely used to treat addiction — and Wilden’s work with meth illustrates the difficulties. The therapy is expensive, invasive and requires patients to care for the implants and to return to the clinic for regular follow-ups. Those motivated to overcome alcoholism might be able to do it. But people with more destructive addictions, particularly to meth, are less cooperative and have high rates of homelessness, making the treatment even less suitable. “The deep-brain stimulator is a pacemaker, with wires going under the skin into the chest where they connect to a battery,” says Wilden. “That’s a lot of metal, especially in people who are fragile. There’s no way I can implant this in someone living on the streets.”

Lüscher and Wilden plan to validate their interventions with optogenetics and DBS in animals, and then adapt the results to clinically realistic techniques. The most likely candidate is transcranial magnetic stimulation (TMS), which uses a magnetic field to stimulate electrical activity in neurons deep in the brain. One advantage is that TMS is non-invasive: treatment simply involves wearing a magnetic helmet for a few minutes. It is currently used to treat depression and migraines.

So TMS is more patient friendly, but it is also more mysterious — researchers do not know why it works. Furthermore, it has poor spatial precision, which frustrates neuroscientists who want to target specific brain locations. But this might not matter, says Antonello Bonci, a clinical neurologist and scientific director at NIDA.

In 2013, Bonci published a paper describing how his team had used optogenetics to reactivate an area of the prefrontal cortex that was abnormally quiet in cocaine-addicted rats5. The treated rats lost interest in pressing a lever to get cocaine. A few months later, Luigi Gallimberti and Alberto Terraneo at the University of Padova in Italy started using TMS to target the equivalent area in the brains of people addicted to cocaine. They have since been successfully using the technique to treat such people.

“It’s up to us to figure out who’s getting better and why, and how many sessions it takes.”

Bonci says that the results are anecdotal, but exciting: most people who stuck with the treatment for a few weeks have now been clean for several months, and testify that they do not even think about cocaine any more, he says. With this black cloud lifted, they are able to enjoy food, sex, reading, family time and all the other good things in life. Bonci is now working with the Italian group to design a double-blind clinical trial, and is collaborating with another group to work out how the TMS works. “It’s up to us now to figure out who’s getting better and why, and how many sessions it takes,” he says.

In addition to TMS, the Italian patients also received supportive medical care and psychological therapy. Even with brain stimulation or medication, people still need emotional support, as well as therapy “to identify triggering cues and memories, and practise making new grooves of thought”, says Hopf. But with tools such as DBS and TMS, neuroscientists’ deepening understanding of the circuitry of addiction is now being translated to the clinic much more rapidly than ever before.

“For the first time in the history of neuroscience, we can think about translating basic science to the clinic in months, as opposed to the 15 years it can take for drug development,” says Bonci. Thanks to the new technologies, he says, “we’re close to a treatment”.

Source:   Nature 522, S50–S52(25 June 2015) doi:10.1038/522S50a

Marijuana Use: Detrimental to Youth

ABSTRACT: Although increasing legalization of marijuana has contributed to the growing belief that marijuana is harmless, research documents the risks of its use by youth are grave. Marijuana is addicting, has adverse effects upon the adolescent brain, is a risk for both cardio-respiratory disease and testicular cancer, and is associated with both psychiatric illness and negative social outcomes. Evidence indicates limited legalization of marijuana has already raised rates of unintended marijuana exposure among young children, and may increase adolescent use. Therefore, the American College of Pediatricians supports legislation that continues to restrict the availability of marijuana except in the context of well controlled scientific studies which demonstrate medicinal benefit together with evidence-based guidelines for optimal routes of delivery and dosing for specific medical conditions.

Introduction

Federal Law has prohibited the manufacture, sale, and distribution of marijuana for more than 70 years. However, with the discovery of potential medicinal properties of marijuana and the increasing misperception that the drug is harmless, there have arisen increased efforts to achieve its broad legalization despite persistent problems of abuse. Medical use of marijuana has prompted many states to establish programs for sale of medically-prescribed marijuana. As public perception of marijuana’s safety has grown, some states have also passed voter-approved referenda legalizing recreational use of marijuana by adults. The result has been the same: limited legalization has led to greater availability of marijuana to youth.

How is Marijuana Used?

Whether used licitly or illicitly, marijuana is smoked or ingested. It may be smoked in hand-rolled cigarettes (joints), pipes or water pipes (bongs), and cigars that have been refilled with a mixture of marijuana and tobacco (blunts). Marijuana emits a distinctive pungent usually sweet-and-sour odour when it is smoked. Marijuana is not so easily detectable, however, when ingested in candy, other foods or as a tea.

 

Has Legalization Escalated Youth Exposure to Marijuana?

There is evidence legalization of marijuana limited to medical dispensaries and/or adult recreational use has led to increased unintended exposure to marijuana among young children. By 2011, rates of poison center calls for accidental paediatric marijuana ingestion more than tripled in states that decriminalized marijuana before 2005. In states which passed legislation between 2005 and 2011 call rates increased nearly 11.5% per year. There was no similar increase in states that had not decriminalized marijuana as of December 31, 2011. Additionally, exposures in decriminalized states where marijuana use was legalized were more likely than those in non-legal states to present with moderate to severe symptoms requiring admission to a paediatric intensive care unit. The median age of children involved was 18-24 months.1

Marijuana use by adolescents has grown steadily as more states enact various decriminalization laws.2 According to CDC data, more teens now smoke marijuana than cigarettes.3 It is unclear, however, whether this trend indicates a causal relationship or mere correlation. There is some evidence legalization may encourage more youth to experiment with the drug. A national study of 6116 high school seniors, prior to legalization of recreational use in any state, found 10% of nonusers said they would try marijuana if the drug were legal in their state. Significantly, this included large subgroups of students normally at low risk for drug experimentation, including non-cigarette smokers, those with strong religious affiliation, and those with peers who frown upon drug use. Among high school seniors already using marijuana, 18% said they would use more under legalization.

There is also evidence of medical marijuana diversion having a significant impact upon adolescents. For example, researchers in Colorado found that approximately 74% of adolescents in substance abuse treatment had used someone else’s medical marijuana. After adjusting for sex, race and ethnicity, those who used medical marijuana had an earlier age of regular marijuana use, and more marijuana abuse and dependence symptoms than those who did not use medical marijuana.4-5 Conclusions from this study may not apply to adolescents as a whole due to the select population surveyed. There are broader adolescent population studies suggesting no significant increase in use due to enactment of medical marijuana laws.6-10 These authors, however, caution that their results may not be definitive for five reasons: not all states with medical marijuana laws are represented in the various studies; the studies rely upon survey data from a voluntary survey (the Youth Risk Behavior Survey) which has the potential for reporting bias; there are gaps in the annual youth risk behavior data; the primary outcome measure was obtained from a single survey item; and the research is not long-term relative to when medical marijuana laws were implemented. Consequently, while all reported their data did not find medical marijuana laws to significantly increase teen use, they also advised continued long-term observation and research.

 

Is Marijuana Medicine?

A recent article in the Journal of the American Medical Association noted there is very little scientific evidence to support the use of medical marijuana. Authors Samuel Wilkinson and Deepak D’Souza explain that medical marijuana is considerably different from all other prescription medications in that “evidence supporting its efficacy varies substantially and in general falls short of the standards required for approval of other drugs by the US Food and Drug Administration (FDA).”11 The FDA requires carefully conducted studies consisting of hundreds to thousands of patients in order to accurately assess the benefits and risks of a potential medication.

Although some studies suggest marijuana may palliate chemotherapy-induced vomiting, cachexia in HIV/AIDS patients, spasticity associated with multiple sclerosis, and neuropathic pain, there is no significant evidence marijuana is superior to FDA approved medications currently available to treat these conditions. Additionally, support for use of marijuana in other conditions, including post-traumatic stress disorder, Crohn’s disease and Alzheimer’s, is not scientific, relying on emotion-laden anecdotes instead of adequately powered, double-blind, placebo-controlled randomized clinical trials.11

Also, to be considered a legitimate medicine, a substance must have well-defined and measurable ingredients that are consistent from one unit (such as a pill or injection) to the next. This consistency allows researchers to determine optimal dosing and frequency. Drs. Samuel Wilkinson and Deepak D’Souza state:

Prescription drugs are produced according to exacting standards to ensure uniformity and purity of active constituents … Because regulatory standards of the production process vary by state, the composition, purity, and concentration of the active constituents of marijuana are also likely to vary. This is especially problematic because unlike most other prescription medications that are single active compounds, marijuana contains more than 100 cannabinoids, terpenoids, and flavonoids that produce individual, interactive, and entourage effects.”11

 As a consequence, there are no dosing guidelines for marijuana for any of the conditions it has been approved to treat. And finally, there is no scientific evidence that the potential healthful effects of marijuana outweigh its documented adverse effects.11 Sound ethics demands that physicians “First do no harm.” This is why a dozen national health organizations, including the College, presently oppose further legalization of marijuana for medicinal purposes.12 If and when rigorous research delineates marijuana’s true benefits relative to its hazards, compares its efficacy with current medications on the market, determines its optimal routes of delivery and dosing, and standardizes its production and dispensing (to match that of schedule II medications like narcotics and opioids), then medical opposition will dissipate.

 

The Extent of Marijuana Abuse

In the United States, marijuana is the most frequently used illicit drug,13-14 with 23.9 million of those at least 12 years old having used an illegal drug within the past month in 2012.15 The National Institute on Drug Abuse (NIDA)-funded 2013 Monitoring the Future study of the year 2012 showed that 12.7 percent of 8th graders, 29.8 percent of 10th graders, and 36.4 percent of 12th graders had used marijuana at least once in the year prior to being surveyed. They also found that 7, 18 and 22.7 percent respectively for these groups used marijuana in the past month.13

Figure 1. Long-Term Trends in Annual Marijuana Use by Grade14

After a period of decline in the last decade, marijuana use has generally increased among young people since 2007, corresponding with both its increased availability through limited legalization and a diminishing perception of the drug’s risks. The number of current (past month) users aged 12 and up increased from 14.5 to 18.9 million.15

In 2010, 7.3 percent of all persons admitted to publicly funded treatment facilities were aged 12-17. Marijuana is the leading illicit substance mentioned in adolescent emergency department admissions and autopsy reports, and is considered one of the major contributing factors leading to violent deaths and accidents among adolescents.16

Figure 2.  Emergency Department Visits by Type of Substance Abuse16

 

Such data indicate that marijuana use in adolescents is a major and growing problem. Given the widespread availability and abuse of marijuana, and its increasing decriminalization, it is important to examine the adverse clinical consequences of marijuana use.

Marijuana and Addiction

Marijuana is addictive. While approximately 9 percent of users overall become addicted to marijuana, about 17 percent of those who start during adolescence and 25-50 percent of daily users become addicted. Thus, many of the nearly 6.5 percent of high school seniors who report smoking marijuana daily or almost daily are well on their way to addiction, if not already addicted.13 In fact, between 70-72% of 12-17 year olds who enter drug treatment programs, do so primarily because of marijuana addiction.18,13

Long-term marijuana users trying to quit report various withdrawal symptoms including irritability, sleeplessness, decreased appetite, anxiety, and drug craving, all of which can make it difficult to remain abstinent.  These withdrawal symptoms can begin within the first 24 hours following cessation, peak at two to three days, and subside within one or two weeks follow drug cessation. Behavioral interventions, including cognitive-behavioral therapy and motivational incentives (i.e., providing vouchers for goods or services to patients who remain abstinent) have proven to be effective in treating marijuana addiction.19 Although no medications are currently available, recent discoveries about the workings of the endocannabinoid system offer promise for the development of medications to ease withdrawal, block the intoxicating effects of marijuana, and prevent relapse.20

Is Marijuana a Gateway Leading to the Abuse of Other Illicit Drugs?

An additional danger associated with marijuana use observed in adolescents is a sequential pattern of involvement in other legal and illegal drugs. Marijuana is frequently a stepping stone that bridges the gap between cigarette and alcohol use and the use of other more powerful and dangerous substances like cocaine and heroin. This stage-like progression of substance abuse, known as the gateway phenomenon, is common among youth from all socioeconomic and racial backgrounds.19, 21 Additionally, marijuana is often intentionally used with other substances, including alcohol or crack cocaine, to magnify its effects. Phencyclidine (PCP), formaldehyde, crack cocaine, and codeine cough syrup are also often mixed with marijuana without the user’s knowledge.21

 

Other Effects of Marijuana on the Brain

The main active chemical in marijuana is delta-9-tetrahydrocannabinol (THC). When marijuana is smoked, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to the brain and other organs throughout the body. It is absorbed more slowly when ingested in food or drink.13 In all cases, however, THC acts upon specific molecular targets on brain cells, called cannabinoid receptors. These receptors are ordinarily activated by chemicals similar to THC called endocannabinoids, such as anandamide. These receptors are naturally occurring in the body and are part of a neural communication network (the endocannabinoid system) that plays an important role in normal brain development and function. The highest density of cannabinoid receptors is found in parts of the brain that influence pleasure, memory, thinking, concentration, sensory and time perception, and coordinated movement. Marijuana over activates the endocannabinoid system, causing the high and other effects that users experience. These effects include distorted perceptions, psychotic symptoms, difficulty with thinking and problem solving, disrupted learning and memory, and impaired reaction time, attention span, judgment, balance and coordination.21 Chronic exposure to THC may also hasten the age-related loss of nerve cells.22

 Numerous mechanisms have been postulated to link cannabis use, attentional deficits, psychotic symptoms, and neural desynchronization.23 The hippocampus, a component of the brain’s limbic system, is necessary for memory, learning, and integrating sensory experiences with emotions and motivations. THC suppresses neurons in the information-processing system of the hippocampus, thus learned behaviors, dependent on the hippocampus, also deteriorate.24 Brain MRI studies now report that in young recreational marijuana users, structural abnormalities in gray matter density, volume, and shape occur in areas of the brain associated with drug craving and dependence. There also was significant abnormality measures associated with increasing drug use behavior. In addition to the regions of the nucleus accumbens and amygdala, the whole-brain gray matter density analysis revealed other brain regions that showed reduced density in marijuana users compared with control participants, including several regions in the prefrontal cortex: right/left frontal pole, right dorsolateral prefrontal cortex, and right middle frontal gyrus (although another small region in the right middle frontal gyrus showed higher gray matter density in marijuana users). Countless studies have also shown that prefrontal cortex dysfunction is involved with decision-making abnormalities and functional MRI and magnetic resonance spectroscopy studies have shown that cannabis use may affect the function of this region.25 Brain imaging with MRI was used to map areas of working memory in the brain and showed similar findings in normal and schizophrenic subjects who did not use marijuana, but decreases in the size of the working memory areas of the striatum and thalamus for those who had a history of cannabis use, that was more marked in those who used marijuana at a younger age and in users with schizophrenia.26

 In chronic adolescent users, marijuana’s adverse impact on learning and memory persists long after the acute effects of the drug wear off. A major study published in 2012 in Proceedings of the National Academy of Sciences provides objective evidence that marijuana is harmful to the adolescent brain. As part of this large-scale study of health and development, researchers in New Zealand administered IQ tests to over 1,000 individuals at age 13 (born in 1972 and 1973) and assessed their patterns of cannabis use at several points as they aged. Participants were again IQ tested at age 38, and their two scores were compared as a function of their marijuana use.

The results were striking: Participants who used cannabis heavily in their teens and continued through adulthood showed a significant drop in IQ between the ages of 13 and 38—an average of eight points for those who met criteria for cannabis dependence. Those who started using marijuana regularly or heavily after age 18 showed minor declines. By comparison, those who never used marijuana showed no declines in IQ.27 This is the first prospective study to test young people before their first use of marijuana and again after long-term use (as much as 20+ years later) thereby ruling out a pre-existing difference in IQ. This means the finding of a significant mental decline among those who used marijuana heavily before age 18, even after they quit taking the drug, is consistent with the theory that drug use during adolescence—when the brain is still rewiring, pruning, and organizing itself—has long-lasting negative effects on the brain.

Other studies have also shown a link between prolonged marijuana use and cognitive or neural impairment. A recent report in Brain, for example, reveals neural-connectivity impairment in some brain regions following prolonged cannabis use initiated in adolescence or young adulthood.28

 

Effects on Activities of Daily Living

Consistent with marijuana’s impact upon the brain, research demonstrates marijuana has the potential to cause difficulties in daily life and/or worsen a person’s existing problems. Heavy marijuana users generally report lower life satisfaction, reduced mental and physical health, more relationship problems, and less academic and career success compared to their peers who come from similar backgrounds. Marijuana use is also associated with a higher likelihood of dropping out of school, workplace tardiness and absence, more accidents on the job with concomitant workman compensation claims, and increased job turnover.29-30

A 2014 study combined the data of 3 investigations from Australia and New Zealand which compared a series of outcome measures of young adults according to their marijuana use at age 17. The researchers found a significant dose-response effect for each of these.  After adjusting for co-variables, compared to those who never used cannabis prior to age 17 (OR 1.0), the odds of graduating from high school by age 25 dropped to 0.78 (95% CI,0.67-0.90) for those who used cannabis less than monthly to 0.61 (95% CI,0.45-0.81) for those using it monthly or more to 0.47 (95% CI,0.30-0.73) for those using it weekly or more to 0.37 (95% CI,0.20-0.66) for daily users.  The decrease in attaining a university degree was almost identical.  The odds of dependence on cannabis between the ages of 17 and 25 rose progressively from 2.06 (95% CI,1.75-2.42) for less than monthly users to 17.95 (95% CI,9.44-34.12) for daily users, and the odds of other illicit drug use between the ages of 23-25 rose from 1.67 (95% CI,1.45-1.92) for less than monthly users to 7.80 (95% CI,4.46-13.63) for those who were daily users prior to age 17.  The odds of a making a suicide attempt between the ages of 17 and 25 were increased from 1.62 (95% CI,1.19-2.19) for less than monthly users to 6.83 (95% CI,2.04-22.9) for daily users.  While unadjusted odds ratios were progressively higher for progressively higher amounts of cannabis used before age 17 for both depression (between ages 17-25) and for welfare dependence (at ages 27-30 depending on the study), these differences were no longer significant after adjusting for co-variables.31Although the greatest harm was among heavier users, it is most concerning that even less than monthly usage prior to age 17 was associated with a significantly lower educational achievement, and significantly higher rates of drug dependence and suicide attempts.

 Marijuana and Mental Illness

Figure 3.  Mood and Anxiety Disorders Among Users and Non-Users of Marijuana32

 A number of studies have shown an association between chronic marijuana use and mental illness. People who are dependent on marijuana frequently have other comorbid mental disorders including but not limited to anxiety, depression, suicidal ideation, and personality disturbances, including amotivation and failure to engage in activities that are typically rewarding (see figure 3).13 Marijuana use is associated with a 7-fold increased risk of depression (OR 7.10, 95% CI,4.39-11.73) and a 5-fold increased risk of suicidal ideation (OR 5.38, 95% CI,3.31-8.73) when used alone, and with a 9-fold increased risk of depression (OR 9.15, 95% CI,4.58-18.29) and nearly 9 fold increased risk of suicidal ideation when marijuana plus other drugs are involved (OR 8.74, 95% CI 4.29-17.79).17 Daily marijuana use in young women has been associated with a five-fold increase in depression and anxiety.33

Population studies also reveal an association between cannabis use and increased risk of schizophrenia. In the short term, high doses of marijuana can produce a temporary psychotic reaction involving hallucinations and paranoia. There is also sufficient data indicating that chronic marijuana use may trigger the onset or relapse of schizophrenia in people predisposed to it, perhaps also intensifying their symptoms .13,34,32A series of large prospective studies showed a link between marijuana use and the later development of psychosis with genetic variables, the amount of drug used, and the younger the age at which use began increasing the risk of occurrence.13 Although it is possible that pre-existing mental illness may lead some individuals to self-medicate with (abuse) marijuana and other illicit drugs, further prospective studies similar to those examining psychosis, will more firmly establish marijuana as a causative factor for other forms of mental illness.

 Marijuana and Driving

Marijuana contributes to accidents while driving due to its significant impairment of judgment and motor coordination. Data from several studies was analyzed and documented that use of marijuana more than doubles a driver’s risk of involvement in an accident.13 Because they impede different driving functions, the combination of even low levels of marijuana and alcohol is worse than either substance alone.35 Studies have shown a statistically significant increase in non-alcohol drugs detected in fatally injured drivers in the past decade. The most commonly detected non-alcohol drug was cannabinol, the prevalence of which increased from 4.2% in 1999 to 12.2% in 2010 (Z = -13.63, P < 0.0001).  The increase in the prevalence of non-alcohol drugs was observed in all age groups and in both sexes. In this study, increases in the prevalence of narcotics and cannabinol detected in fatally injured drivers were particularly apparent.36

 Other Health Effects of Marijuana

Since marijuana contains many of the same compounds as tobacco, it has the same adverse effects on the respiratory system when smoked as tobacco. These include chronic cough, respiratory infections, and bronchitis.19 In the longer term emphysema and lung cancer are also among its effects.21In fact, smoking marijuana is more harmful than tobacco for two reasons: first, because it contains more tar and carcinogens than tobacco, and secondly, because marijuana smokers tend to inhale more deeply and for a longer period of time as compared to tobacco smokers.

Marijuana use also has a variety of adverse, short- and long-term effects, especially on the cardiopulmonary system. Marijuana raises the heart rate by 20-100 percent shortly after smoking; this effect can last up to three hours. In one study, it was estimated that marijuana users had a 4.8-fold increase in the risk of heart attack in the first hour after smoking the drug. This elevated risk may be due to increased heart rate as well as the effects of marijuana on heart rhythms, causing palpitations and arrhythmias. This risk may be greater in older individuals or in those with cardiac vulnerabilities. Marijuana use has been found to increase blood pressure and heart rate and to decrease the oxygen-carrying capacity of the blood.37

 Chronic smoking of marijuana and its active chemical THC has consistently been shown to increase the risk of developing testicular cancer, in particular a more aggressive form of the disease. One study compared 369 Seattle-area men aged 18-44 with testicular cancer, to 979 men in the same age bracket without the disease. The researchers found that current marijuana users were 1.7 times more likely to develop testicular cancer than nonusers, and that the younger the age of initiation (below 18) and the heavier the use, the greater the risk of developing testicular cancer.38,39,40 A similar study of 455 men in Los Angeles found that men with testicular germ cell tumors were twice as likely to have used marijuana as men without these tumors.41 THC can also cause endocrine disruption resulting in gynecomastia, decreased sperm count, and impotence.42

 

Effects of prenatal exposure to marijuana

The risk of using marijuana during pregnancy is unrecognized by the general public, but infants and children exposed prenatally to marijuana have a higher incidence of neurobehavioral problems. THC and other compounds in marijuana mimic the human brain’s cannabinoid-like chemicals, thus prenatal marijuana exposure may alter the developing endocannabinoid system in the fetal brain, which may result in attention deficit, difficulty with problem solving, and poorer memory.13 Evidence especially suggests an association between prenatal marijuana exposure and impaired executive functioning skills beyond the age of three. Specifically, children with a history of exposure are found to have an increased rate of impulsivity, attention deficits, and difficulty solving problems requiring the integration and manipulation of basic visuoperceptual skills.43

 

Rising Potency and Contaminants

The potency of marijuana has been increasing for decades, with THC concentrations rising from 4% in the 1980s to 14.5% in 2012 in samples confiscated by police.  Some strains now contain as much as 30% THC.19 For a new user, this may mean exposure to higher concentrations of THC, with a greater chance of an adverse or unpredictable reaction. Increases in potency may account for the rise in emergency department visits involving marijuana use. For experienced users, it may mean a greater risk for addiction if they are exposing themselves to high doses on a regular basis. However, the full range of consequences associated with marijuana’s higher potency is not well understood, nor is it known whether experienced marijuana users adjust for the increase in potency by using less. Since the legalization in Colorado, one certified lab there has reported that much of the marijuana they have studied and tested has been found to be laced with heavy metals, pesticides, fungus and bacteria.44

 

Health Risks Underestimated

 Health risks associated with marijuana use are often underestimated by adolescents, their parents, and health professionals. As explained above, there are newer, stronger forms of marijuana available than that which existed in 1960; current forms of marijuana are known to be three to five times more potent. Parents underestimate the availability of marijuana to teens, the extent of their use of the drug, and the risks associated with its use. In a 1995 survey, the Hazelden Foundation found that only 40 percent of parents advised their teenagers not to use marijuana, 20 percent emphasized its illegal status, and 19 percent communicated to their teenagers that it is addictive.45

 

Parental Monitoring Important

 Research shows that appropriate parental monitoring can reduce drug use, even among those adolescents who may be prone to marijuana use, such as those with conduct, anxiety, or affective mood disorders.45

Columbia University’s National Center on Addiction and Substance Abuse (CASA) found that adolescents were much less likely to use marijuana if their parents stated their disapproval. “Parents who do not want their kids getting drunk and using drugs should begin by sending a strong message to their kids about the importance of avoiding alcohol. Our survey results this year show how important it is for teens to get a clear anti-use message from their parents, especially from Dad. Teens who get drunk monthly are 18 times more likely to report marijuana use than teens who do not drink; those who believe their father is okay with them drinking are two and a half times more likely to get drunk in a typical month.  Therefore, parents who do not want their kids getting drunk and using drugs should begin by sending a strong message to their children about the importance of avoiding alcohol.”45

 

In 2011, past month use of illicit drugs, cigarettes, and binge alcohol use were lower among youth aged 12 to 17 who reported that their parents always or sometimes engaged in monitoring behaviors compared to youths whose parents seldom or never engaged in monitoring behaviors. The rate of past month use of any illicit drug was 8.2 percent for youths whose parents always or sometimes helped with homework compared with 18.7 percent among youth who indicated that their parents seldom or never helped.

Columbia Center for Alcohol and Substance Abuse found that teens who have frequent family dinners (five to seven per week) were less likely to have used marijuana.46

Compared to teens who had infrequent family dinners (2 or fewer per week), teens who had frequent family dinners were almost 1.5 times likelier to have said they had an excellent relationship with their mother and their father. The report also found that compared to teens who said they had an excellent relationship with their fathers, teens that had a less than very good relationship with their father were:

o    Almost 4 times likelier to have used marijuana

o    Twice as likely to have used alcohol

o    2.5 times as likely to have used tobacco

 

Compared to teens who said they had an excellent relationship with their mothers, teens who had a less than very good relationship with their mother were:

o    Almost 3 times likelier to have used marijuana

o    2.5 times as likely to have used alcohol

o    2.5 times likelier to have used tobacco

 

Consequently, the College encourages parents to take advantage of the “family table,” and to become involved in drug abuse prevention programs in the community or in the child’s school in order to minimize the risk of their children experimenting with drug use.

In Conclusion

In summary, marijuana use is harmful to children and adolescents.  For this reason, the American College of Pediatricians opposes its legalization for recreational use and urges extreme caution in legalizing it for medicinal use.  Likewise, the American Academy of Child and Adolescent Psychiatry (AACAP) recently offered their own policy statement opposing efforts to legalize marijuana. They similarly pointed out that “marijuana’s deleterious effects on adolescent brain development, cognition, and social functioning may have immediate and long-term implications, including increased risk of motor vehicle accidents, sexual victimization, academic failure, lasting decline in intelligence measures, psychopathology, addiction, and psychosocial and occupational impairment.”

Thus the AACAP (a) opposes efforts to legalize marijuana, (b) supports initiatives to increase awareness of marijuana’s harmful effects on adolescents, (c) supports improved access to evidence-based treatment, rather than emphasis on criminal charges, for adolescents with cannabis use disorder, and (d) supports careful monitoring of the effects of marijuana-related policy changes on child and adolescent mental health.47  The College agrees with this position on marijuana.

 

The College urges parents to do all they can to oppose the legalization of marijuana, such as working with elected officials against the drug’s legalization and scrutinizing a candidate’s positions on this important children’s issue when making voting decisions. The College encourages legislators to consider the establishment and generous funding of more facilities to treat marijuana addiction. Children look to their parents for help and guidance in working out problems and in making decisions, including the decision to not use drugs. Therefore, parents should be role models, and not use marijuana or other illicit drugs. Finally, these reports strikingly emphasize the need for parents to recognize and discuss these serious health consequences of marijuana use with their children and adolescents. They also point to the requirement for medical experts and legislators to seriously discuss and review these observations prior to promoting any state or federal effort considering legalization.

For more information on this topic, the National Clearinghouse for Alcohol and Drug Information (NCADI) offers an extensive collection of publications, videotapes, and educational materials to help parents talk to their children about drug use. For more information on marijuana and other drugs, contact: National Clearinghouse for Alcohol and Drug Information, P. O. Box 2345, Rockville, MD 20847; 1-800-729-6686. Additional helpful information is provided at the following websites: www.drugabuse.gov, www.marijuana-info.org, and www.teens.drugabuse.gov.

Primary Author: Donald Hagler, MD, FCP

Original: January 2007

Revised March 2015

Revised September 2015

 

ADDENDUM added September 2015:

The Legalization of Marijuana in Colorado: The Impact”48 is a compilation of data by the Rocky Mountain High Intensity Drug Trafficking Area that analyzes the effects of marijuana legalization in the state. This third volume allows readers to compare and contrast statistics observed from 2006 – 2009 during Colorado’s early medical marijuana era with those from 2009 to 2013 as medical marijuana commercialization grew, and also with those from the current legalized recreational marijuana era from 2013 to the present. The statistics reveal that between 2013 and 2014 there was a 45% increase in marijuana-associated impaired driving, a 32% increase in marijuana-related motor vehicle deaths (with a 92% increase from 2010 to 2014), as well as 29% and 38% increases in emergency room visits and hospital admissions secondary to marijuana use. By 2013, marijuana use in Colorado was 55% above the national average among teens and young adults, and 86% higher among those over age 25. Diversion of marijuana from Colorado to other states has also increased several fold. This new data further supports the College Position Statement above emphasizing concerns that marijuana legalization will result in increased adolescent usage, addiction and its associated risks for them.

 A downloadable web source for parents can be found at this link, Marijuana Talk Kit, from Partnership for Drug-free Kids.

The American College of Pediatricians is a national medical association of licensed physicians and healthcare professionals who specialize in the care of infants, children, and adolescents. The mission of the College is to enable all children to reach their optimal physical and emotional health and well-being.

A PDF copy of this statement is available here: Marijuana Use Detrimental to Youth

 

Source: http://www.acpeds.org/marijuana-use-detrimental-to-youth  Sept.2015

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14. What is the Scope of Marijuana Use in the United States? National Institute on Drug Abuse. http://www.drugabuse.gov/publications/research-reports/marijuana/what-scope-marijuana-use-in-united-states. Published July 2012.

 

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16. National Survey on Drug Use and Health. Center for Behavioral Health Statistics and Quality. http://www.samhsa.gov/data/2K13/CBHSQ128/sr128-typical-day-adolescents-2013.htm. Published 2013.

 

17. Hallfors DD, Waller MW, Ford CA, Halpern CT, Brodeish PH, and Iritani B. Adolescent depression and suicide risk: Association with sex and drug behavior. American Journal of Preventive MedicineVolume 27, Issue 3, October 2004, Pages 224–231, Tables 3 and 4.

18. Hall W, Degenhardt L. Adverse health effects of non-medical cannabis use.Lancet. 2009 Oct 17;374(9698):1383-91.

 

19. Want to know more? Some FAQs about marijuana. National Institute on Drug Abuse. http://www.drugabuse.gov/publications/marijuana-facts-parents-need-to-know/want-to-know-more-some-faqs-about-marijuana. Updated March 2014. Accessed July 10, 2012.

 

20. Available treatments for marijuana use disorders. National Institute on Drug Abuse. http://www.drugabuse.gov/publications/research-reports/marijuana/available-treatments-marijuana-use-disorders. Updated March 2014.

 

21. Nistler C, Hodgson H, Nobrega FT, Hodgson CJ, Wheatley R, Solberg G. Marijuana and adolescents. Minn Med. 2006 Sept:49-51.

22. How Does Marijuana Affect Your Brain and Body? National Institute on Drug Abuse. http://www.drugabuse.gov/publications/research-reports/marijuana/how-does-marijuana-use-affect-your-brain-body. Accessed September 23, 2014. Brain. 2012 Jul;135(7):2245-55. Accessed June 4, 2012. http://www.ncbi.nlm.nih.gov/pubmed?term=effect of long-term cannabis use and zalesky.

 

23. Ashton CH. Pharmacology and effects of cannabis: A brief review. Brit Jrnl Psych. 2001;178: 101-106.

 

24.   Iowa Department of Public Safety. Division of Narcotics Enforcement.http://www.dps.state.ia.us/DNE/marijuana.shtml. Accessed September 23, 2014.

 

25. Gilman JM, Kuster JK, Lee S, et al. Cannabis use is quantitatively associated with nucleus accumbens and amygdala abnormalities in young adult recreational users. J Neurosci. 2014;34(16): 5529-5538.

 

26. Smith MJ, Cobia DJ, Wang L, et al. Cannabis-related working memory deficits and associated subcortical morphological differences in healthy individuals and schizophrenia subjects. Schizophr Bull. 2014 Mar;40(2):287-99.

 

27. Meier MH, Caspi A, Harrington H, et al. Persistent cannabis users show neuropsychological decline from childhood to midlife. ProcNatlAcadScie 2012 Oct 2;109(40):E2657-64.Available at http://www.ncbi.nlm.nih.gov/pubmed?term=persistent%20cannabis%20users%20and%20meier. Accessed on August 27, 2012.

 

28. Zalesky A, Solowji N, Yucel M, et al. Effect of long-term cannabis use on axonal fibre connectivity. Brain. 2012 Jul;135(7):2245-55. Accessed June 4, 2012. http://www.ncbi.nlm.nih.gov/pubmed?term=effect of long-term cannabis use and zalesky.

 

29. How does marijuana use affect school, work, and social life? National Institute of Drug Abuse. http://www.drugabuse.gov/publications/research-reports/marijuana/how-does-marijuana-use-affect-school-work-social-life. Published July 2012.

30. Polen, MR, Sidney, S, Tekawa, IS, Sadler, M, Friedman, GD. Health care use by frequent marijuana smokers who do not smoke tobacco. West J Med. 1993;158(6):596–601.

 

31. Silins E, Horwood LJ, Patton GC, Ferguson DM, Olsson CM, Hutchinson DM, et.al. Young adult sequelae of adolescent cannabis use: an integrative analysis The Lancet Psychiatry, Volume 1, Issue 4, Pages 286 – 293, September 2014 http://www.thelancet.com/journals/lancet/article/PIIS2215036614703074/table?tableid=tbl2&tableidtype=table_id&sectionType=red.

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34. Caspi, A, Moffitt, TE, Cannon, M, et al. Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-Omethyltransferase gene: Longitudinal evidence of a gene X environment interaction. Biol Psych. 2005;57(10):1117–1127. Cited inhttp://www.drugabuse.gov/publications/research-reports/marijuana/there-link-between-marijuana-use-mental-illness.

 

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37. Mittleman MA, Lewis RA, Maclure M. Triggering myocardial infarction by marijuana. Circ. 2001;103(23): 2805-9.

 

38. Daling JR, Doody DR, Sun X. Association of marijuana use and the incidence of testicular germ cell tumors. Can. 2009; 115: 1215–1223.

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41. Lacson JCA, Carroll JD, Tuazon E, Castelao EJ, Bernstein L, Cortessis VK. Population-Based Case-Control Study of Recreational Drug Use and Testis Cancer Risk Confirms an Association Between Marijuana Use and Nonseminoma Risk. Cancer. 2012 September:5374-5383.http://onlinelibrary.wiley.com/doi/10.1002/cncr.27554/pdf. Accessed September 30, 2014.

 

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47. AACAP Marijuana Legalization Policy Statement. American Academy of Child & Adolescent Psychiatry. https://www.aacap.org/AACAP/Policy_Statements/2014/aacap_marijuana_legalization_policy.aspx. Published April 15, 2014.

48.   The Legalization of Marijuana in Colorado: The Impact. http://www.rmhidta.org/html/2015%20PREVIEW%20Legalization%20of%20MJ%20in%20Colorado%20the%20Impact.pdf. Accessed 9/22/15.

DENVER (CBS4) – The results of a new study about the impact of Colorado’s marijuana legalization is raising troubling questions for parents. The study cites a significant increase in marijuana-related traffic deaths, hospital visits and school suspensions. The parents CBS4’s Melissa Garcia spoke with say they’re concerned about their children seeing messages promoting pot all over town. Activists say it’s the way pot is marketed and sold that has started to create some serious problems.

“I never dreamed in a million years that this would happen to my son,” said parent Kendal, who didn’t want to use his last name.

Kendal came home one evening to find his 13-year-old son unconscious from what he says was a marijuana overdose.

He was grey. His heart wasn’t beating and he wasn’t breathing,” he said.

Kendal used CPR to resuscitate him and later talked to his son’s high school peer and supplier.

“I had heard from kids that there was 60 percent of this particular high school using drugs, and she shook her head and said, ‘That’s way low,’” Kendal said.

“Kendal’s story breaks my heart, but I’ve got to tell you we have heard that from hundreds and hundreds and hundreds of parents throughout the state,” said Diane Carlson, Smart Colorado co-founder.

Carlson says Colorado’s child and teen use of marijuana has become an epidemic.

“Kids have no idea how dangerous or harmful Colorado’s pot is,” she said.Carlson says Colorado’s child and teen use of marijuana has become an epidemic.

According to a report released this month by the Rocky Mountain High Intensity Drug Trafficking Area, Colorado saw a 29 percent increase in emergency room visits, and a 38 percent increase in hospitalizations during retail marijuana’s first year.

The study states that over 11 percent of Colorado’s 12 to 17 year-olds use pot — 56 percent higher than the national average. It also cites a 40 percent increase in drug-related suspensions and expulsions — the vast majority from marijuana.

Carlson says the culprit is its commercialization. “Marijuana might have been legalized in our state; it did not have to mean massive commercialization and promotion of marijuana use,” she said.

Source: http://denver.cbslocal.com/2015/09/20/smart-colorado

Posh Spectator and Sunday Times journalist James Delingpole has got his Y-fronts in a twist over outing the PM as former closet stoner. His former mates in the PM’s inner circle don’t approve and have been letting him have it. I can imagine why he’s felt such an urgent need to justify breaking this public school ‘omerta’. He hadn’t anticipated the fall out, he says, in a mea culpa in the Sunday Times. He hadn’t anticipated the impact his revelation to Cameron biographer Isabel Oakeshott would have because he thought that ‘puffing on a reefer’ at Oxford  was no big deal. It was barmy that it was ever a criminal act, he argues in self defence. And he still thinks so.

So since the law’s an ass, what was wrong with putting up two fingers to it? Nor does he see any reason to change his mind about dope now, thirty years later:

“Marijuana is being decriminalised across the world. Quite soon we’ll find the idea that (it) was ever a criminal act about as barmy and illiberal as the notion, that, not so long ago, a man could be imprisoned for sleeping with another man.”

So ‘me lud’, he effectively argued in mitigation, under the impression that we all (not least Dave and his inner sanctum) share liberal views about dope smoking, his and the future PM’s casual disregard for the law (then) was OK.

And besides what was the worst that could have happened as a result of his revelation in today’s modern and progressive world? Dave looking a hypocrite if he ever votes against the decriminalisation of cannabis or Barack Obama cracking a few retro Cheech and Chong jokes next time he meets our PM for a hamburger/baseball love in?

Ho, ho – all very amusing and just about how flippant Mr Delingpole perceives drug use. He really didn’t need to tell us of the state of arrested adolescence he says he is in.

The irony of this self observation is that arrested development is indeed one of the effects of cannabis on the brain. It affects normal maturity (as any drug counsellor will tell you) and specifically the brain development of adolescents. It affects attention, memory and executive functions in the brain. Its use risks worse effects  – from psychotic episodes to full blown schizophrenia for those with a genetic vulnerability. Its victims often do not know until it too late.

Delingpole, although a journalist, seems blissfully unaware of these research findings. It is also hard to believe he is unaware of cases where this apparently ‘innocent’ activity has destroyed the lives of children from affluent families similar to those he and his former friend Dave hail from.

It is hard too to believe as a journalist he’s remained oblivious to the crisis of NHS mental health and psychiatric units, which are bursting at the seams with young male psychotic cannabis addicts –  many incurable.

Maybe it’s a matter of I’m all right Jack. Maybe, he has no children of his own to worry about. Maybe, he’s naive enough to think by some magic of making cannabis freely available these cases would not exist. I have no idea.

As a journalist he should, at the very least, acknowledge that cannabis is a dangerous and for young people, in particular, a very undesirable and addictive drug.

His self-serving attempt to claim the moral high ground (he is not a slave to anyone you’ll be pleased to hear; he does not ingratiate himself with the powerful and he deplores those who do and have compromised themselves to benefit from the Cameron regime) is no substitute for responsible  journalism.

Before he so blithely downplays this drug again and so casually assumes its eventual legalisation is a world wide done deal, I suggest he first acquaint himself with a few more facts and then attend this debate where Dr Kevin Sabet, author of Reefer Sanity: Seven Great Myths About Marijuana, President of Smart Approaches to Marihuana (SAM) and a former advisor on drug policy to President Obama will be speaking.

Source: By Kathy Gyngell www.conservativewoman.co.uk  Sept.2015

The lobby calling to decriminalise drugs focuses too much on gang violence. This overlooks death and health destruction among drug users. Photograph: Lawrence Lawry/Science Photo Library
The real horror of drugs stems not from gangs selling them, but from their effects on users, writes Chris Luke.

The wonderfully mischievous Mae West memorably skewered the perennial dilemma surrounding illicit intoxication when she quipped, “To err is human, but it feels divine!” And of course, it is a truth – almost universally acknowledged – that humans love to self-medicate, to seek oblivion and respite from the “grim predicament of existence”, with whatever mind-altering substance they can get hold of, be it 21st century psychotropic or ancient herbal concoction.
It seems equally likely that a debate has raged for ever between those who fret about the effects of such intoxicants on humanity, and those who see them as divine anaesthetics, soporifics and tonics.

The problem with contemporary substance misuse is mainly to do with its sheer scale and unnatural geography. These can be attributed to the global trading which took off in the 17th century, and to modern chemistry which led in the mid-19th century to the refining of organic produce into powders and liquids. These could be conveniently consumed by wealthy Europeans and Americans in a variety of oral, smoke-able and injectable formulations.

The acceleration, since Victorian times, of mechanised global trading and the dissemination of simplified chemistry kits now means that all sorts of chemical contraband are routinely transported thousands of miles from their source, and are easily and universally available for a small sum.

The illicit drug trade is arguably the most successfully globalised of all. Unfortunately, this enormous commercial success for “drug barons” (and sometimes the difference between life and death for dirt-poor drug-cultivators) has created a global pandemic of substance misuse with immensely problematic consequences.

For the most part, these tend to be viewed through the prisms of crime control and drug addiction treatment, and a remarkable number of commentators are now arguing – as did Dr Paul O’Mahony recently in these pages – for “decriminalisation” as the solution. Their central thesis is that it is the violent drug gangs which cause the main problems associated with substance misuse, and that legalisation would squeeze these menacing middlemen out of the equation.

Sadly, I think that this is extraordinarily naive and completely misses the point.
As a doctor who has been on the “receiving end” of industrial levels of substance misuse for many years (in inner-city hospital emergency departments in Dublin, Edinburgh, Liverpool, and now Cork), I am convinced that the question of “legality” of drugs is largely irrelevant in terms of the hazards of drugs to society in general and people’s health in particular.

Putting it very simply, the criminality of users is almost never an issue. It is the deaths, destruction of health and communities and the distraction from the primary function of the emergency department, due to substance misuse, that are of interest to me.

And as for Fintan O’Toole’s recent assertion, in The Irish Times, that “there is no great evidence that the demand is actually higher now . . . than it was a century ago”, I would point out that there is no funding for research into the healthcare frontline workload. So he will have to take my word that, while the appetite for them may not vary much over time, the intoxicants du jour in Ireland are much more worrisome than they were, say, in the post-war period, adding incalculably as they do, in terms of complexity and labour-intensity, to the existing tobacco and alcohol burdens.

The notions of “legalising”, “purifying” and “controlling” once-illegal drugs are frankly laughable in today’s risk-averse society. But drug users (including those who consume alcohol and tobacco) are prone to utter hypocrisy and self-delusion when it comes to their own prescriptions.

The fact is that people are no longer prepared to accept even minimal levels of risk when it comes to existing, legal and fastidiously purified pharmaceuticals (thalidomide is notorious but all medicines carry a risk of occasionally tragic adverse effects) and patients eagerly litigate, even after rare and unpredictable complications from the medications they have been prescribed.

The same would immediately apply to consumers of (hypothetically) legalised “hard drugs” like cocaine and heroin – and even cannabis – whose natural (ie “pure”) effects will always be unpredictably catastrophic for some individuals and inevitably disastrous for society, as dysphoric or delirious people interact with their hazard-ridden environment, as well as with other individuals who may often be less than sympathetic to their drug-addled fellow citizens. In addition, just because a commodity is legal doesn’t mean that it won’t be of interest to criminal gangs: think petrol, tobacco and alcohol and simply look North, after all.

Setting aside such specious reasons for “decriminalising” drugs, it is vital that people grasp the pivotal reality about drug misuse: the hideous and worsening global epidemic of violence – be it in British and Irish cities or Caribbean hotel rooms – is primarily fuelled by the effects of alcohol, cannabis and cocaine on the human psyche, and not by the illegality of the drugs. Drugs (including drink) derange. That is the whole point of taking them, and those who are easily or already deranged will do terrible things to the people around them as a direct result.

Sadly, “anti-prohibitionists” continue wilfully to forget that before drugs (like cocaine, cannabis or opium) were illegal, they were legal – with violent, woeful consequences. My greatest fear is that the ignorance of this seems invincible.

Chris Luke is consultant in emergency medicine in Cork University Hospital and Mercy University Hospital, Cork.

Source 2008 The Irish Times Monday, August 4, 2008

Abstract

Smoking cannabis daily doubles an individual’s risk of developing a psychotic disorder, yet indicators of specific vulnerability have proved largely elusive. Genetic variation is one potential risk modifier. Single-nucleotide polymorphisms in the AKT1 and catechol-O-methyltransferase (COMT) genes have been implicated in the interaction between cannabis, psychosis and cognition, but no studies have examined their impact on an individual’s acute response to smoked cannabis. A total 442 healthy young cannabis users were tested while intoxicated with their own cannabis—which was analysed for delta-9-tetrahydrocannbinol (THC) and cannabidiol content—and also ±7 days apart when drug-free. Psychotomimetic symptoms and working memory were assessed on both the sessions. Variation at the rs2494732 locus of the AKT1 gene predicted acute psychotic response to cannabis along with dependence on the drug and baseline schizotypal symptoms. Working memory following cannabis acutely was worse in females, with some suggestion of an impact of COMT polymorphism on working memory when drug-free. These findings are the first to demonstrate that AKT1 mediates the acute response to cannabis in otherwise healthy individuals and implicate the AKT1 pathway as a possible target for prevention and treatment of cannabis psychosis.

Discussion

To our knowledge, this study provides the first evidence that the acute psychotic effects of cannabis are predicted by variation at the rs2494732 locus of the AKT1 genotype. No evidence was found for an interaction of the COMT Val158Met genotypes with cannabis use, in producing psychotomimetic symptoms in this group of healthy cannabis users. Cannabis dependence predicted non-intoxicated schizotypal symptoms, but neither genotype had any impact on these. COMT Val158Met genotype had a marginal impact on performance on a working memory task when non-intoxicated and when memory load was low; however, at higher load, schizotypy was the only emerging predictor of performance. When intoxicated with cannabis, gender was the only predictor of working memory performance, with poorer performance in females at a high working memory load.

In the current study, which is the largest ever to be conducted on the acute response to cannabis, psychotomimetic symptoms while intoxicated were found to be predicted by variation at the rs2494732 locus of the AKT1 genotype in healthy young cannabis smokers, increasing with C allele dosage. These data are very important as acute psychotic response to cannabis is thought to be a marker of the risk of developing psychosis from smoking the drug.1 Two previous studies have implicated this polymorphism in the interaction with cannabis and psychosis,9, 18 but this work concentrated on individuals who were at familial risk of schizophrenia. This study is the first to demonstrate that the acute response to cannabis is modulated by AKT1 in otherwise healthy cannabis smokers. The mechanism for this modulation of acute effects may be through the interaction of AKT1 with dopamine.2, 9Our sensitivity analyses suggested that these effects may be confined to dependent cannabis smokers but further investigation of these data with larger samples is required.

AKT1 codes for a protein that is a serine/threonine kinase, which has a variety of functions, one of which is as a signalling molecule downstream of the dopamine D2 (DRD2) receptor. Decreased AKT1 functionality may result in enhanced responses to DRD2 receptor stimulation.19 THC has been found to acutely induce dopamine release in

rats20, 21 and in humans,22, 23 although not in all studies.24 Dopamine release is thought to occur via the blockade of cannabinoid 1 (CB1) receptors on GABAergic neurons that target pyramidal cells. These neurons normally exert an inhibitory effect on the firing of dopamine neurons that project back to the nucleus accumbens, so agonism of CB1 receptors by THC may produce increased dopamine release. This THC-mediated increase in dopamine release may be further exacerbated by decreased AKT1 functionality. Elevated levels of mesolimbic dopamine are known to have a role in the development of psychotic symptoms, potentially through disrupted salience attribution.25

In contrast to the role of variation at the rs2494732 locus of AKT1, this study found no support for the direct involvement of the functional polymorphism of the COMT gene in mediating acute psychotic response to cannabis. This is in contrast to one previous small-scale acute laboratory study giving acute THC to patients with schizophrenia,26 and other work that suggested that COMT may mediate the psychotomimetic risk of cannabis3 but in agreement with subsequent larger studies that failed to replicate these findings.4, 27 There was a marginal effect of COMT on working memory performance at a low load when not intoxicated. This polymorphism of COMT initially caused some excitement as several studies emerged demonstrating its association with working memory,28, 29 but this finding was not confirmed by meta-analyses,30 which suggested that this may be a case of publication bias.

Greater schizotypal symptoms predicted in poorer working memory performance on the more difficult section of the task among drug-free cannabis users. This echoes recent findings of poorer working memory in individuals high in schizotypy31 and indeed of the relationship between working memory performance and transition to psychosis.32 Working memory impairment is considered a central cognitive impairment in schizophrenia, and there is some evidence that such impairments are related to symptoms, particularly to negative symptoms.33, 34

Only gender predicted acute working memory impairment from cannabis, with greater impairment in females. Very few studies have examined gender differences in neurocognitive acute response to THC, with those that have using very small samples and in finding little evidence of gender differences.35 However, this study examined the acute effects of cannabis in over 400 cannabis smokers. There is an emerging preclinical literature that might explain this effect. CB1 density has been found to vary by gender, with animal studies reporting greater CB1 receptor density among males across several brain regions.36, 37 However, across their lifetime, adult female brains show increases in CB1 receptor density, with levels eventually surpassing those observed in males.38 Furthermore, greater CB1 de-sensitization after exposure to THC in the prefrontal cortex, hippocampus, striatum, amygdala and midbrain is seen in female adolescent rats.36, 37 Preclinical studies have also demonstrated that female rats preferentially metabolize THC to its most highly active metabolite, while male rats metabolize THC to multiple compounds.39 In combination, these findings may in part explain the finding of greater acute working memory impairment from cannabis in females. This also may partly be driven by gender differences in frequency of cannabis use. Users who smoked cannabis less frequently experienced stronger effects, and as there was a higher proportion of low frequency female cannabis users compared to males this may have contributed to the observed gender differences in working memory following the drug.

Strengths of this study include the large sample size for assessing acute cannabis effects. We also used independent verification of the cannabinoid content of the cannabis consumed and drug history. Further, the hypothesis-driven approach we took to genetic analysis was a strength, examining only loci implicated in previous studies and, therefore, circumventing some of the problems of type I error that have dogged earlier research. However, inevitably there are several limitations of the study. For the cannabis use data, while verifying past 3 months use with hair analysis, we inevitably relied on retrospective self-reports of drug use, which are particularly complicated as cannabis is known to acutely impair episodic memory. However, we opted to use years of cannabis use in this model as this was considered the most reliable to estimate. As we purposely recruited a young group of cannabis users, there was restricted variation in years used and future studies may investigate this further. We used a predominantly white Caucasian sample. However, it is unlikely that ethnic differences in allele frequency at rs2494732 biased the outcome of the study, as there was no difference between the frequency of rs2494732 alleles across the dichotomized ethnic groups. In addition, analyses with only Caucasian participants gave the same results to the analysis containing all ethnicities.

In summary, we found that the AKT1 rs2494732 C allele was associated with increased psychotomimetic symptoms after smoking cannabis. The other factor impacting on acute psychotomimetic response to cannabis was baseline schizotypy. Gender was the only factor to predict acute working memory impairment, with poorer performance in females. When drug free, cannabis dependence weakly predicted schizotypal symptoms and COMT genotype had a marginal impact on working memory, along with ethnicity. The findings of this study contribute to a recent and growing body of evidence suggesting that variation at the AKT1 locus confers details of the risk of cannabis smoking for schizophrenia. This is likely to be in the context of numerous other genetic variants, so the clinical utility at the moment is unclear. It is nonetheless encouraging that there is concordance between genetic influences on acute effects of cannabis and those mediating risk of psychosis. However, the fact that AKT1 is relevant to the biology of psychotic symptoms suggests that this might be a promising direction for novel therapeutics for cannabis-induced psychosis.

Source:  Citation: Translational Psychiatry (2016) 6, e738; doi:10.1038/tp.2015.219 Published online 16 February 2016 

For complete paper log on to: http://www.nature.com/tp/journal/v6/n2/full/tp2015219a.html

Editor’s note: This commentary is by Patrick J. Kennedy, who is a former member of Congress from Rhode Island and an honorary adviser to SAM, Smart Approaches to Marijuana.

The epidemic of drug addiction and overdoses gripping Vermont, and our country at large, cries out for reform. We must change the perception that jail is an effective treatment for the disease of drug addiction, and give mental health issues the attention and funding they deserve, an opinion I know many Vermonters share.

But the legalization and commercialization of another addictive drug — marijuana — is precisely the wrong way to address this critical problem. Legalization has nothing to do with whether we lock up pot users, and everything to do with making money. Marijuana industry lobbyists that are pushing legalization to the Vermont Legislature disingenuously conflate the two issues, claiming that the only way to stop imprisoning marijuana users is to legalize the drug. They also make sweeping claims about how commercialization will control the black market and make the drug “safer.”

But both claims are demonstrably false. First of all, we can stop jailing marijuana users without letting big business sell marijuana at corner stores. Vermont has already decriminalized marijuana use for adults, and will not arrest or jail you if you possess an ounce or less of marijuana for personal use. And our Congress is already debating broader criminal justice reforms that may reduce the burden of arrests and imprisonment for drug offenses, especially on minority and low-income communities.

Second, and more broadly, we know from other states’ experiences that the billion-dollar marijuana industry — the folks behind the legalization effort — is more interested in profits than our health and safety. Legalization means inviting a powerful lobby into Vermont that pushes hard against regulations. Pot lobbyists in Colorado defeated restrictions on pot ads aimed at children. They have opposed restrictions on marijuana potency. And they are fighting laws keeping pot shops away from schools, parks, and day care centers in Oregon. Vermont legislators may think they have cracked the code on how to implement legalization “safely,” but it will not be long until industry forces expose and exploit any openings they see for the sake of profits.

Now, I put the call out to the Vermont Legislature: Please learn from the experiences of other states, and heed the warning signs — marijuana legalization does not reduce the toll drug addiction takes on our communities.

In other words, commercial marijuana behaves just like another large American industry peddling addiction — Big Tobacco. It may surprise Vermonters to know that the large tobacco companies have been studying the marijuana business since the 1960s, seeing it as a natural extension of their product line. And like tobacco, the marijuana business can only profit when it creates and cultivates heavy users. Just 20 percent of pot users consume 80 percent of all marijuana. Those heavy users, many of whom are addicts, are the target market for the pot industry, not the casual smoker.

This profit motive is why legalization and commercialization has yielded more pot use, not less, among children and adults. After legalizing pot, Colorado took the dubious honor of having the highest past-month marijuana use rates in the country in both age groups. A host of related problems have accompanied this dubious honor, including a surge in marijuana poisonings — up 148 percent overall, and up a shocking 153 percent

among children 0 to 5 years old — and a 32 percent spike in marijuana-related traffic fatalities. Even without legalization, Vermont already ranks No. 2 in past-month consumption. Commercialization will only push those numbers higher.

Moreover, legalization has not blunted Colorado’s black market. The state’s attorney general told the press last February that “The criminals are still selling on the black market. … We have plenty of cartel activity in Colorado. …” Colorado law enforcement officers have even indicated that black market activity may have increased, as people illegally export pot to other states.

Finally, like the tobacco companies, who once boasted that they targeted “the young, the poor, the black, and the stupid,” the marijuana industry has had an outsized impact on poor and minority communities in Colorado. A recent exposé showed that Denver’s pot business was highly skewed towards poor areas, with one neighborhood having one marijuana business for every 47 residents. A strategy of “profits before public health” is not the way to serve socioeconomic and racial justice.

Now, I put the call out to the Vermont Legislature: Please learn from the experiences of other states, and heed the warning signs — marijuana legalization does not reduce the toll drug addiction takes on our communities. It represents burning down the village in order to save it, by handing Vermont’s public health over to Wall Street and the marijuana lobby. Rather, I urge you to focus on solutions we know will work — sensible criminal justice reform and serious investments in drug prevention.

Source:   http://vtdigger.org/2016/02/03/patrick-kennedy-say-no-to-marijuana-legalization/

As Colorado “celebrates” its third year of marijuana legalization, reporters and marijuana enthusiasts gloat of the state’s sweeping success. “Live and let live,” they naively remark, with all the wisdom of a 1970s hippie fresh out of Woodstock. But perhaps the cannabis devotees should pause and ask themselves by what metric success ought be measured.

Most accounts of Colorado’s triumph extol the vast revenue accrued via legalization and subsequent taxation (see here, here, and here). These heralds, however, neglect to tell you the rest of the story.

Just off 15th and Little Raven Streets in Denver, Colorado is a place called “Stoner Hill.” At Stoner Hill, Colorado’s homeless youth, who are ever-growing in number, congregate and smoke in what a Denver news site, Westword, describes as “a perpetual party, a misdemeanor micro-economy and a meeting ground for Denver’s youngest homeless and assorted travelers.” Westword reports, “The grassy hilltop is where a housing crisis meets legal cannabis, and it just happens to have a panoramic view of booming downtown Denver.”

Stoner Hill is emblematic of the growing crisis Colorado and other legalization states like Washington, Oregon, and Alaska face. Coincidentally – or perhaps not so coincidentally – both Colorado and Washington, the first two states to legalize, were among the top three states with the largest increases in youth homelessness from 2013 to 2014. In each state, the youth homelessness rate grew by 27 and 13.3 percent respectively in just one year.

The youth-related marijuana numbers are no less concerning and should be alarming to anyone concerned with the betterment of America’s youth. Just this month, the U.S. Department of Health and Human Services released a survey showing that Colorado now ranks number one for regular marijuana use among youth. This proud achievement only came incrementally, though; Colorado once ranked a distant 14th in the country for youth usage. Once again, this jump in the rankings coincided with Colorado’s 2012 passage of Amendment 64, which legalized marijuana for recreational use.

These numbers are unsurprising, though, since Colorado’s “edibles” often intentionally resemble candy or cookies. Much like the big tobacco advertising campaigns geared toward young people, big marijuana is marketing its drug as an innocuous or appealing snack, sure to garner youth attention. Stanford Law Professors Rob MacCoun and Michelle Mello have dubbed it an “attractive nuisance.”

The distrusting naysayer would retort that Colorado is just one state and should not be a bellwether for the nation. Colorado, however, is not alone in its marijuana accolades. When you consider “average past month use of marijuana by those 12 to 17 years old” – the main metric for youth usage – the cynic has a lot of explaining to do. Average youth use among teens in recreational/medical marijuana states rests at 10.5 percent compared to 8.9 percent in states where it is only legal for medicinal purposes and 6.1 percent in states were the drug is banned altogether. In other words, there is a direct correlation between availability of marijuana and teen usage.

Teenage use numbers alone do not fully capture the impending crisis Colorado and other states face. According to Arapahoe House Treatment network in Colorado, teenage admissions for marijuana addiction in Colorado increased by 66 percent between 2011 and 2014, again correlating with the 2012 passage of Amendment 64. This phenomenon is entirely predictable by science. Dr. Christian Thurstone of the University of Colorado explains the epidemic this way:

I’m interested in this subject because 95 percent of the teenagers treated for substance abuse and addiction in my adolescent substance-abuse treatment clinic at Denver Health are there because of their marijuana use,

and because nationwide, 67 percent of teens are referred to substance treatment because of their marijuana use. Marijuana is the No. 1 reason why adolescents seek substance-abuse treatment in the United States.

Citing a study by Wayne Hall and Louisa Degenhardt, Dr. Thurstone points out that two-thirds of new marijuana users annually are under the age of 18, and one in six of those new users will go on to use regularly or become dependent on the substance. For Colorado, this is a troubling finding.

Marijuana usage is not only detrimental for its addictive characteristics but also for its long-term effects on the adolescent brain. Marijuana has “acute (meaning up to six hours), subacute (6 hours to 20 days) and long-term (more than 20 days) effects.” Where the subacute effects of alcohol can be the annoyance of a brief hangover, marijuana can have substantial lingering effects, especially for young people. Charles Stimson of the Heritage Foundation reports that, while alcohol is broken down quickly, THC – the main active chemical in marijuana – is stored in the body, where it can remain for days or weeks and impair cognitive ability for enduring periods of time. Consequently, using the drug is associated with “lower test scores and lower educational attainment.”

The long-term effects are most worrisome. A comprehensive New Zealand study of 1,000 individuals over many years found that participants who used cannabis heavily in their teens had an astonishing average loss of eight IQ points. Accordingly, Dr. Michelle Cretella, President of the American College of Pediatricians, notes that “[m]arijuana’s impact on the teen brain leads to an increased risk of motor vehicle accidents, sexual victimization, academic failure, permanent loss of IQ, psychopathology, addiction, and psychosocial and occupational impairment.”

Sadly, youth usage is not the only devastating impact legalization has had. In Colorado, “pot-positive traffic fatalities” have increased 100 percent, emergency room visits related to marijuana have increased 57 percent, and infant exposure has increased 268 percent since legalization.

But the adverse impact on America’s youth should be enough by itself to trigger scrutiny and reform. Former Drug Czar William Bennett remarked: “We know we have a problem, and we have not managed to keep those

things from kids. Colorado was supposed to eliminate the marijuana black market, but it did not.”

While supporters applaud America’s new cash cow – marijuana – perhaps we should ask ourselves whether this newfound flow of revenue should be hoarded at the expense of America’s youth – the marijuana martyrs.

Source:  http://abovethelaw.com/2015/12/americas-youth-the-marijuana-martyrs/

CNN– Last week, the government released its National Survey on Drug Use and Health. It didn’t make much of a news splash, but it should have — and in years past, it would have.

When a serious war is taking place, officials throughout the administration hold press conferences and issue statements while print and televised media across the country report on it. Almost none of this happened, although the reasons for talking and reporting are greater than they have been in a very long time.

Here’s the takeaway: Illicit drug abuse is seriously affecting our children, our schools, our workplaces and our society. And it is on the rise. In 2009, nearly 22 million Americans were regularly abusing illicit drugs: a rise of 1.5 million abusers of marijuana from 2008 and a rise of 2.3 million users from 2007, a rise of 205,000 abusers of Ecstasy from 2008, a rise of 188,000 abusers of methamphetamine from 2008 and a rise of 800,000 abusers of prescription drugs from 2008.

Then there’s the death toll. Nearly 40,000 Americans are killed each year by drug overdoses — not drug-related car accidents, not drug-related gang violence or homicide; those are an entirely different and eye-popping set of numbers. By overdose alone, we lose the equivalent of more than one 9/11 a month and almost eight times as many Americans as have been killed in Iraq and Afghanistan since 2001 (deaths the national media reports on weekly, if not daily).

There are more people dying from drug overdose in America than people dying from gun violence. In several states, drug overdose deaths outnumber deaths caused by car crashes. But these drug-death statistics receive almost no media attention.

Who, outside those that toil in the fields of addiction and recovery, knows these numbers? And how many people caught this in another recent report: Almost 30 percent of public school students ages 12-17 attend schools that are both “gang and drug-infected.” This accounts for almost 6 million children attending schools where drugs and violence dominate their campuses. Places of learning, places once known as safe.

Keeping drugs from children should be our main focus and concern. As Joseph Califano, the founder of the Center on Addiction and Substance Abuse, points out, a child who gets to age 21 without using illegal drugs “is virtually certain never to do so.” But fewer and fewer children are getting the message they need about the dangers and toxicity of illegal drugs, both from our national leaders and our culture. The message the dominant culture in America does send on drug use and abuse is the wrong one.

President Obama may be struggling to find an issue on which leaders from both sides of the aisle can come together. We suggest the growing drug abuse epidemic as ideal. But our president, a man popular with the youth of America, a man children look up to and listen to, has been silent on the issue, the very one with which he could make a dramatic difference in the lives of young people.

As for the popular culture, the message has been even more damaging. Where once television shows actively promoted the dangers of drug use, several of our more popular shows, from “Weeds” to “Entourage” to “Mad Men,” make drug use a laugh line.

Back when our country was making a serious assault on drug abuse, a show like “Weeds” would never be aired. Today it is promoted in full page ads in our nation’s most popular magazines. This, for a comedy about the life and times of a marijuana-growing and -dealing family.  As the head of the network that produces and airs “Weeds” put it, “Our ratings were va-va-va-voom! Who said hedonism is passé?” This, for a show where one is lured to root for a family responsible for the death of a DEA agent, children dropping out of school, gang violence and rape.

In the meantime, the state of California has certified a proposition for November’s ballot that would legalize the individual possession of dozens of joints of marijuana, even as more and more studies come out revealing the connection between marijuana use, psychosis and psychotic symptoms, among other ill-health effects; even as a recent Rand Corp. study found that such a legalization scheme in California could increase use by as much as 50 to 100 percent. Just what California needs. The most recent polling shows this proposition has an even chance of passing.

With all this, it should be no real surprise the drug numbers are on the increase. Our national leaders are silent, our culture makes laugh lines of drug use and serious numbers of serious people are advocating further legalization.

Legalization, however, is a siren song that truly will shipwreck more of our youth. Even with marijuana as prevalent and accessible as it is to young people, there is a reason the numbers for alcohol and tobacco use are higher than illicit drug abuse. When one talks to children, they give the answer: It is found in the word “illegal.” Legalization removes stigma, is the handmaiden of availability and, as Joe Califano has pointed out, “availability is the mother of use.”

The verbal and cultural detoxification of the dangers of drugs has shown its cost in the cultural message that has been sent out. The only question that remains is how much higher a price do we want our children to pay with the further verbal, cultural and legal detoxification of the toxic?

Once upon a time, our national and popular cultural leaders took a strong stand against drug use, and a unified, concerted message was disseminated to help reduce drug use in America. It worked. In the late 1980s and early 1990s, use was reduced by more than 50 percent. But it took effort from our political leaders, our cultural leaders, television, movies and schools — everyone got involved to help create a “sobriety chic” where drug use was not glamorized, and the media gave intense coverage to the devastation wrought by drugs.

That is exactly what is needed again, and now. We know how to do this. There is a rare group of actors and entertainers who have been lucky, fortunate, rare enough to overcome their addictions. Society has cheered for them and repaid them for their recovery at the box office. We should find a way for them to convey to the public their cautionary stories as to what it was like thinking they were going to die, or waking up in a cold jail cell, about their ruined relationships and the time they wish they had back.

At the same time, let’s start a national campaign with those who have not had drugs ruin their lives. Let them be the new national role models for young people. We should see public service announcements and ads from the likes of Beyonce, Reese Witherspoon, Jennifer Lopez, Taylor Swift, Tim McGraw, the Jonas Brothers; from the likes of the Williams Sisters and the Manning brothers; from Jimmy Johnson and Danika Patrick.

This issue needs such a campaign. In drug recovery circles, there is a popular saying: If you do the same thing over and over again, you will get the same result. This message has a very helpful converse however, if we repeat the strategies we used that worked once before, i.e., in the late 1980s and early 1990s, we can also get the same result.

This is our plea to the country’s national and cultural leaders: Address it, talk to our youth about it, make a campaign of it and, as for Hollywood and the rest of California: Stop with the drug use and legalization “chic.” Such a national campaign worked before, it can work again.

Source:  By William J. Bennett, Alexandra Datig and Seth Leibsohn, Special to CNN September 24, 2010   http://edition.cnn.com/2010/OPINION/09/24/bennett.drug.abuse/

There is, naturally, a hope amongst parents whose child is desperately ill with seizures that a new treatment will help.  Many parents in the USA have been convinced that medical marijuana may be the answer – and some have even moved home in order to be able to legally purchase this substance.  Sadly however, it has been shown that whilst this substance may be able to help some patients it can also have disastrous effects on others.  There is much research going on with a purified and uniform preparation of cannabidiol (CBD) called Epidiolex to see if this can indeed become a genuine treatment for epileptic seizures.  Until then, parents should be advised not to use the products available in ‘medical marijuana dispensaries’ – which are not regulated for purity or uniformity and could be dangerous for their children. (see letter below).

This situation has come about because of the shameful way so called medical marijuana has been used as a wedge to introduce the recreational use of the substance – dating from the statement made in the seventies  by Keith Stroup in a post debate encounter at Emory University in the USA when he said “we’ll be using the issue as a red herring to give marijuana a good name’.

This is the current position of the American Epilepsy Society, as written in a letter from Dr. Brooks-Kayal to a Pennsylvania legislator:

March 22, 2015

Dear Representative,

As Pennsylvania considers enacting new cannabis legislation (HB 193), I write to offer the perspective of the American Epilepsy Society (AES), the leading U.S. organization of clinical and research professionals specializing in the treatment and care of people with epilepsy.

Epilepsy is the most common and potentially devastating neurological disease that affects people across the lifespan. In America, one in 26 people will be diagnosed with epilepsy at some time in the course of their life – more will experience an isolated seizure. Epilepsy is associated with significant morbidity and mortality and is associated with many co-morbidities including depression, cognitive dysfunction, and autism. Today between 2.2 and 3 million Americans, including almost 400,000 children, live with epilepsy, with one third living with treatment-resistant seizures that do not respond to current medications.

The American Epilepsy Society position on medical marijuana as a treatment option for people with epilepsy is informed by the current research and supported by the position statements from the American Academy of Neurology, the American Academy of Pediatrics and the American Medical Association. Additionally, a 2014 survey of practitioners published in the journal Epilepsy Currents found that the majority of epilepsy practitioners agreed with and supported the AES position.

Specifically, AES has called for more research, for the rescheduling of marijuana by the DEA to ease access for clinical studies, and has supported the compassionate use program of GW Pharmaceuticals, where a is being administered under the guidance and close monitoring of an appropriate medical professional. AES has also been highly supportive of the double-blind clinical trial now underway by GW Pharmaceuticals and of the forthcoming clinical trial by INSYS Therapeutics.

These clinical trials utilize a vastly different substance than the artisanal cannabis products that are being considered for use in Pennsylvania, and that have been used in Colorado. As you likely know, medical marijuana and its derivatives are legal in Colorado, but you may not realize that the content of these products is not regulated for purity or uniformity. A study by a team from Children’s Hospital Colorado that was presented during the AES Annual Meeting in December 2014 and has recently been accepted for publication in the journal Epilepsy & Behavior, found that artisanal “high CBD” oils resulted in no significant reduction in seizures in the majority of patients and in those for whom the parents reported improvements, these improvements were not associated with improvement in electroencephalograms (EEGs), the gold standard monitoring test for people with epilepsy.

Additionally, in 20% of cases reviewed seizures worsened with use of cannabis and in some patients there were significant adverse events. These are not the stories that you have likely heard in your public hearings, but they are the reality of practitioners at Children’s Hospital Colorado who have cared for the largest number of cases of children with epilepsy treated with cannabis in the U.S.

The families and children coming to Colorado are receiving unregulated, highly variable artisanal preparations of cannabis oil prescribed, in most cases, by physicians with no training in pediatrics, neurology or epilepsy. As a result, the epilepsy specialists in Colorado have been at the bedside of children having severe dystonic reactions and other movement disorders, developmental regression, intractable vomiting and worsening seizures that can be so severe they have to put the child into a coma to get the seizures to stop. Because these products are unregulated, it is impossible to know if these dangerous adverse reactions are due to the CBD or because of contaminants found in these artisanal preparations. The Colorado team has also seen families who have gone into significant debt, paying hundreds of dollars a month for oils that do not appear to work for the vast majority. For all these reasons not a single pediatric neurologist in Colorado recommends the use of artisanal cannabis preparations. Possibly of most concern is that some families are now opting out of proven treatments, such as surgery or the ketogenic diet, or newer antiseizure medications because they have put all their hope in CBD oils.

AES is sympathetic to the desperation parents of children with severe, treatment-resistant epilepsy feel, and understand the need for compassionate or promising new therapies in in appropriate and controlled circumstances. We are however opposed to the use of artisanal preparations of unregulated compounds of cannabis that contain unverified content and are produced by people with no experience in pharmaceutical production. That is what is currently happening in Colorado and may soon be happening in multiple states across the county as they legalize the use of medical marijuana products.

The products currently provided in Colorado do not meet the FDA definition of expanded or compassionate use. The FDA requires compassionate use therapies to meet the same criteria as an investigational new drug which require standard purity, content and content uniformity testing of the product. None of these criteria are met in the products being given to people with epilepsy in Colorado and we are seeing the distressing results noted above. And yet, these and other similar products are being considered for use in Pennsylvania.

It is also worth noting that in late February 2015, the FDA issued several warning letters to firms that claim that their products contain CBD. The FDA has tested those products and, in some of them, did not detect any CBD as claimed on the label. Because there is no standard for these products, the market is increasingly flooded with a wide variation of products and states which approve access to these preparations will bear the burden of monitoring for quality and controlling for the continuity of supply.

In sum, there simply is no clinical, controlled research to support the adoption of new CBD legislation for epilepsy such as your state is considering. The anecdotal results of a few families in Colorado, shared in the media, should not be the basis for law making. The rush by states to pass CBD legislation has created an unusual situation where people with epilepsy and their families are demanding access to a highly variable homegrown substance that may or may not be beneficial and the medical and scientific community lacks the necessary efficacy and safety data to make good treatment decisions regarding cannabis for people with epilepsy, especially in children.

The new legislation in most states places epilepsy practitioners in an untenable situation where they are expected, or in some states directed by law, to respond to requests for these highly variable artisanal products with no protocols, no research and no clinical guidelines regarding dosing or side-effects, and no assurance that the cannabis products that are to be recommended are pure, safe or uniform, making it nearly impossible to know if we are truly “Doing No Harm.”

We need to accelerate the clinical research and wait to act until we have results to support decisions. If there are components of cannabis with specific therapeutic values we need to know this and we need to develop pharmacy grade compounds that utilize these components to help the nearly one million people living with drug resistant epilepsy. And if the harmful aspects of cannabis outweigh the therapeutic benefits, we need to find out now, before more medically fragile children have been exposed to cannabis products that are not effective and may risk damage to vital organs, brain development, or worse.

We urge you and your fellow committee members to delay adoption of new cannabis legislation and to continue to support and encourage new research. If we can be of additional help please contact our Executive Director, Eileen Murray, at emurray@aesnet.org.

Thank you for your consideration of our position.

Sincerely,

Amy Brooks-Kayal, MD,  President, American Epilepsy Society.  Chief and Ponzio Family Chair, Children’s Hospital Colorado,  Professor of Pediatrics and Neurology, University of Colorado School of Medicine

One evening in April, Ethan Darbee, a 24-year-old paramedic in Syracuse, responded to a call on the city’s south side: unknown man down. Rolling up to the scene, he saw a figure lying motionless on the sidewalk. Darbee raked his knuckles across the man’s sternum to assess his level of consciousness. His eyelids fluttered. Inside the ambulance, Darbee hooked him up to a heart monitor, and he jerked involuntarily. The odd reaction puzzled Darbee. Why would the guy recoil from an electrode sticker but not a sternal rub? The driver started for the hospital. Darbee sat in the captain’s chair in the back of the rig, typing on a laptop. Then he heard a sound no paramedic ever wants to hear: the click of a patient’s shoulder harness unlatching. Swivelling around, he found himself eyeball to eyeball with his patient, who was now crouched on all fours on top of the stretcher, growling.

That same evening, Heather Drake, a 29-year-old paramedic, responded to a call at an apartment complex on the west side. When she arrived, four firefighters were grappling with a 120-pound woman who was flailing and flinging vomit at anyone who came near her. A bystander shouted that the woman was high on ‘‘spike’’ — the prevailing local term for synthetic marijuana, which is more commonly known around the country as spice. But Drake didn’t believe it. Spike didn’t turn people into violent lunatics. Phencyclidine (PCP) or synthetic cathinones (‘‘bath salts’’) could do that, maybe even a joint soaked in formaldehyde — but not spike. Drake sprayed a sedative up the woman’s nose and loaded her into the ambulance. A mayday call from another crew came over the radio. In the background static of the transmission, Drake could hear Ethan Darbee yelling.

Darbee’s patient had sprung off the stretcher and knocked him to the floor of the ambulance, punching him repeatedly in the face. Darbee grasped the side-door handle and tumbled into the street. Within moments, the police arrived and quickly subdued the man. Two days later, 19 more spike overdoses would swamp local emergency rooms, more in one day in Syracuse than the number of overdoses reported statewide in most states for all of April.

Syracuse, where I’ve lived almost my entire life, has struggled with synthetic drugs before. William Harper, a local businessman and two-time Republican candidate for City Council, moonlighted as the kingpin of bath salts in New York for two years before the Drug Enforcement Administration took him down in 2011. Was there a spike kingpin out there now, flooding the street with a bad batch? Perhaps, but similar outbreaks occurred in several states along the Gulf of Mexico in April, and the American Association of Poison Control Centers reports that between January and June, the nationwide number of synthetic marijuana ‘‘exposures’’ — that is, reported contact with the substance, which usually means an adverse reaction —

had already surpassed totals for 2013 and 2014, and that 15 people died from such exposure. Maybe there was a larger cause.

Every state has banned synthetic cannabinoids, the chemicals in spike that impart the high. Although the active ingredients primarily come from China, where commercial labs manufacture them to order like any other chemical, spike itself is produced domestically. Traffickers spray the chemicals on dried plant material and seal the results in foil pouches; these are then sold on the Internet or distributed to stores across the country, which sell them sometimes under the counter, as in Syracuse, or sometimes right by the cash register, depending on local laws. Unlike marijuana, cocaine and other naturally occurring drugs, synthetic cannabinoids can be tweaked on a molecular level to create novel, and arguably legal, drugs.

Since 2008, when authorities first noted the presence of synthetic cannabinoids in ‘‘legal marijuana’’ products, periodic surges in overdoses have often coincided with new releases, and emergency doctors have had to learn on the fly how to treat them. This latest surge is notable for the severity of symptoms: seizures, extreme swings in heart rate and blood pressure, kidney and respiratory failure, hallucinations. Many patients require such enormous doses of sedatives that they stop breathing and require intubation, and yet they still continue to struggle violently. Eric Kehoe, a shift commander at the Rural Metro ambulance company that employs Darbee and Drake, said bath-salts overdoses are easier to deal with. ‘‘You might find them running naked down the middle of the street,’’ he said, but ‘‘you could talk them down. These people here — there’s no point. You can’t even reason with them. They’re just mute. They have this look about them that’s just like a zombie.’’

Syracuse is one of the poorest cities in America — more than a third of the people here live below the poverty line. After I made a few visits to Upstate University Hospital’s emergency department, where most spike cases in the area end up, it became clear to me that the vast majority of serious users here don’t resemble the victims typically featured in reefer-madness-type stories about the dangers of ‘‘designer drugs.’’ They aren’t curious teenagers dabbling in what they thought was a legal high dispensed from a head shop. They’re broke, often homeless. Many have psychiatric problems. They’ve smoked spike for months, if not years. They buy it from rundown convenience stores and corner dealers in the city’s worst neighborhoods, fully aware that it’s an illegal drug with potentially severe side effects. Doctors could tell me what happened when people overdosed on spike, but they couldn’t tell me why anyone would smoke it in the first place, given the possible consequences.

‘‘It’s crazy,’’ was all that one overdose patient could tell me. ‘‘Syracuse is Spike Nation, man. I don’t know who called it that, but that’s what they’re saying.’’

Slide Show | Syracuse’s Spike Epidemic One of the poorest cities in America has become a hotbed for synthetic marijuana.

The visible center of Syracuse’s spike epidemic is the Mission District, a three-block wedge bounded by treeless boulevards and a red railroad trestle with the pronouncement LIVES CHANGE

HERE painted on it in huge white letters. Before urban renewal gutted the neighborhood in the 1960s, it was home to a typewriter factory and a rail yard surrounded by blue-collar homes and fringed by mansions that have long since been bulldozed or carved up into boarding houses. The sprawling Rescue Mission campus, which includes a men’s shelter and a soup kitchen, lends the district its name. The shelter explicitly forbids spike, along with alcohol and other drugs. But at any time during the day, a knot of people can be found under the trestle, dealing and smoking spike, and sometimes passing out from it. One unseasonably hot May afternoon, while I was combing a creek bank for discarded spike packets, a man shouted at me from a bridge: ‘‘That’s a lot of spike down there!’’

He introduced himself as Kenneth, a 44-year-old barber and spike addict with fingertips stained highlighter-yellow by spike resin. He had thin, expressive lips, and when he spoke, his words flowed in multiple stanzas. We sat in the shade under the trestle to talk. Kenneth was in prison when he first smoked spike, which he praised as a ‘‘miracle drug’’ because it didn’t show up on a drug test. ‘‘An addict is always trying to get slick, always trying to get over, always trying to beat a urine, always trying to beat a parole officer, always trying to get high without getting in trouble,’’ he said. ‘‘So I’m loving this drug! I come home, and it’s all over the place.’’

That was a year ago, after Kenneth got out of prison. For a time, he said, he considered dealing spike but decided that smoking it was all the trouble he could afford. Now he hated the stuff. Nobody he knew would choose it over real weed — if real weed were legal. In this way, spike was less a drug of choice than one of necessity. Now he was hooked, he said, and trying to quit. ‘‘It’s an annoying drug,’’ he said, comparing it to crack. ‘‘It’s great in the first two minutes. But then you got to keep lighting up, and lighting up, and lighting up. It’s not like marijuana, smoking a blunt and you’re high for two or three hours.’’

I asked him if he was afraid of landing in the hospital with a tube in his throat, or even dying. The risk of death isn’t a deterrent to an addict, he said — it’s a selling point. Take Mr. Big Shot, for example, a brand of spike that had a reputation on the street for knocking people unconscious. That’s the one everybody wanted, including Kenneth: ‘‘One joint lasted me six hours! I would light it up, take about three lungs, and turn it off. It was that strong. Even the guy in the store where I bought it from said, ‘Listen, smoke this in your house, don’t go into the street with this.’ ’’ If there was a spike dealer in the city selling bad stuff, Kenneth wasn’t aware of it, or he wouldn’t say. In his opinion, people were losing control on spike because they were smoking way too much of it. It was that simple.

‘‘That’s what all these guys do all day long,’’ he said, pointing to a group of loud-talking men hanging out at the other end of the trestle. ‘‘That’s what they’re doing right now.’’ (Kenneth, now 45, recently told me he had kicked his spike habit.)

Other spike users I spoke to in the Mission District made the same argument. One of them was Tyson, a 27-year-old drifter with shaggy brown hair who affected an air of party-dude bonhomie. He’d shot up, smoked, swallowed or snorted just about every drug there is, he said. Last fall, he started using spike for the same reason Kenneth did — to foil mandatory drug tests. Now he was living on the street, waiting for a bed to open up in a rehab facility. I bought him an iced coffee and a wedge of poundcake at the Starbucks in Armory Square, an upscale neighborhood of shops and restaurants three blocks from the Mission District. We sat on a sun-dappled bench, watching lawyers and insurance executives come and go. When I

asked him why so many people were overdosing on spike in Syracuse, Tyson blamed novice smokers.

‘‘The first week or so of smoking spike, there’s no control over it,’’ he said. ‘‘I’d smoke it and black out and come to three hours later, hugging a pole.’’

They can’t all be novices, I pointed out. Many of the spike users I talked to at Upstate University Hospital were plenty experienced, and they had ended up in the emergency room regardless. Tyson slurped a blob of whipped cream from his cup and reconsidered the question. His answer was rambling and profane, but it gave me deeper insight into how the spike economy works in Syracuse.

Spike, Tyson said, is a ‘‘poverty drug.’’ A five-gram bag goes for $10 in the store, but it is often subdivided and resold on the street as $1 ‘‘sticks,’’ or joints, and $2 ‘‘freestyle’’ portions — spike poured directly from the bag into the hand of the buyer. Many of the users I spoke to claimed that, in addition to being dirt-cheap, spike was addictive. There are no studies to back up this claim. Toxicologists know only that synthetic cannabinoids bind to certain receptors in the brain, and they understand nothing about the drug’s long-term health effects. Scientific proof aside, Tyson said he knew spike users who performed sex acts for a few dollars. ‘‘That’s how you know that spike is definitely addictive,’’ he said. ‘‘People are out tricking for it.’’

Tyson also explained how easy spike is to get in Syracuse. He ticked off the names of corner stores that sold it from behind the counter. Some required users to know code words — ‘‘Skittles,’’ for example — while others sold spike to anybody who asked for it, including children. Along with the stores, and the entrepreneurs peddling sticks to subsidize their own habits, street dealers offered bags of spike purchased in bulk from distributors in New York City.

‘‘That dude over there, with the headphones on?’’ Tyson said. ‘‘He does it.’’ He pointed his chin toward a young man in a leather coat crossing the street. ‘‘He’s got bags on him right now, but he does that pop-top.’’

‘‘Pop-top’’ is slang for the local spike sold in resealable pouches, the cheapest of the cheap. ‘‘You don’t know where it’s been, who did what with it,’’ Tyson said. No brand of spike is tested for its pharmacological effects, but pop-top spike doesn’t even have the benefit of a street rep. It’s the ditch weed of Spike Nation: rank, wet and worst of all, weak — unless you get a ‘‘hotspot,’’ an unpredictably powerful batch. ‘‘Seventeen joints, you might be fine. Eighteenth joint might put you down for six hours,’’ Tyson said. ‘‘That’s probably going to be what’s going to give somebody a heart attack.’’

Tyson said he’d seen a pop-top operation once, in a dingy basement on Syracuse’s north side. Potpourri was spread atop silk screens on Ping-Pong tables, then doused with unknown chemicals from a spray bottle. What pop-top manufacturers lacked in quality control, they made up for in marketing talent. Their spike was even cheaper than the store-bought variety, and new brands hit the street every month. They also produced clever knockoffs, stuffing their inferior spike into pouches identical to popular store brands. ‘‘That’s the name of the game right now, dude,’’ Tyson said. ‘‘Who can have the best-looking bag.’’

Since the attack on Ethan Darbee, the number of spike overdoses in Syracuse has fallen by half, just as mysteriously as it rose. Maybe spike smokers are being more careful, or doctors are reporting overdoses less frequently. Maybe a bad batch of spike finally ran its course. The answer doesn’t really matter. In a year, or a month, or perhaps tomorrow, the chemicals will be completely different, and we’ll be talking about another surge in emergencies.

The problem is resistant to criminal prosecution, or even basic police work. The Syracuse Police Department has a cellphone video of a spike overdose that they use for training purposes. It was taken in the first week of the outbreak, when the police were responding to as many as 20 overdoses a day. A lieutenant played the video for me one afternoon on a computer at the police station. It starts with a man writhing on the floor in a corridor of an apartment building. The man isn’t under arrest, but his hands are cuffed behind his back, for his own safety, until an ambulance can get there. The man screams the same unintelligible words over and over in a hysterical falsetto. He bangs the back of his head against the wall and hammers his bare heels against the floor. Ragged flaps of pink skin hang off his kneecaps. His bottom lip is literally chewed away. The video ends abruptly with the man in mid-scream. The lieutenant jerked his thumb toward the computer screen. ‘‘Now,’’ he said to me, ‘‘try to get his name and phone number.’’

When the bath-salts outbreak peaked in 2012, the city passed an ordinance equating possession of synthetic drugs with minor infractions like loitering. It also gives the police the authority to confiscate spike from users and, with probable cause, from stores as well. But the ordinance, which pushed spike sales onto the street, did little to prevent the surge of overdoses that hit the city in April. Bill Fitzpatrick, the Onondaga County district attorney, responded to the recent ‘‘crisis,’’ as he put it, by notifying store owners in May that he would charge them with reckless endangerment if they were caught selling spike, a misdemeanor punishable by up to a year in prison. That was the extent of his authority. ‘‘What I would ask from the federal government is some sort of sanction against China,’’ a frustrated Fitzpatrick told me. ‘‘Forget about the doctrines of Mao Zedong or Karl Marx — what

better way to subvert American society than by shipping this garbage over here and making it attractive to our future generations?’’

In March, the D.E.A. did arrest one Chinese national, a suspected manufacturer who made the mistake of traveling to the United States on business. For the most part, though, federal prosecutors have focused on arresting United States distributors under the controlled-substance-analogue statute, which was designed specifically to target synthetics. According to the statute, prosecutors must prove that the cannabinoids are ‘‘substantially similar’’ to previously banned cannabinoids both chemically and pharmacologically, and that they’re meant for human consumption. That’s why every bag of spike carries the disclaimer ‘‘Not for Human Consumption’’ as a legal fig leaf.

Carla Freedman, assistant United States attorney for the Northern District of New York, has successfully prosecuted many synthetic-drug cases under the statute. She won convictions against not just Syracuse’s bath-salts kingpin but also the owner of a chain of upstate head shops and the members of a Syracuse family who cranked out 200 pounds of spike a month in a rented house with the aid of a cement mixer. ‘‘If you keep taking out smoke shop after smoke shop, you’re putting your finger in the dike,’’ Freedman said. ‘‘If you take out the manufacturer and shut his business down, you stop production for a while.’’

Her current case concerns three associates of a Los Angeles-based organization called Real Feel Products Inc., who are charged with conspiring ‘‘to distribute one or more controlled-substance analogues.’’ Real Feel has done its business in the open, and indeed claims on its website to rank as ‘‘the Top 5 counter culture distribution company in North America.’’ Since Freedman charged the defendants under the analogue statute, their most likely defense will be to argue that they have changed their products frequently enough to keep them within the realm of legality. It’s Freedman’s job to prove that they didn’t. If they had sold heroin instead of spike, they’d already be in jail, and none of this would be an issue. As if more evidence were necessary to prove that synthetic drugs are the new frontier, Real Feel was also at one point developing a reality television show about growing its business.

Neither Fitzpatrick nor Freedman nor Syracuse’s mayor, Stephanie Miner, had any idea who, or what, was causing the overdoses. In Miner’s view, spike was just the drug of the moment, as heroin was last year and bath salts the year before that. She said she believes the real problem is centered on ‘‘undiagnosed trauma’’ that drives people to use drugs — any drugs — in the first place.

‘‘You can’t arrest your way out of these problems,’’ Miner said. ‘‘If somebody thinks that you can use the law to correct behavior that results from mental health issues? Not gonna happen.’’

The next day I went for a ride along with Police Officer Jacob Breen. Just four years out of the academy, Breen still enjoyed patrolling a beat and showed a keen interest in the social fabric of the city’s tough south- and west-side neighborhoods. After decades of economic decline, Syracuse has become one of the most segregated cities in the country, with a predominantly black underclass trapped in the urban core and middle-class whites living in the suburbs. Onondaga County, where Syracuse is the largest city, also has the third-highest rate of ‘‘zombie homes’’ — abandoned by their owners but not yet reclaimed by the banks — in the state. Cruising from block to block, Breen glanced back and forth between the road and a laptop wedged between our seats that displayed mug shots of felons on open warrants, the majority of them young black men. We passed a dilapidated two-story house, its boarded-up windows tagged with graffiti. The front door was ajar. ‘‘Open for business,’’ Breen said, craning his head around to get a glimpse through the door.

What bothered Breen most about the spike problem was how little he could do about it. Dealers, he knew, didn’t care about being hit with an appearance ticket for violating the city ordinance. He had to spend much of his time running around the city to protect ambulance crews from being attacked by freaked-out spike heads — ‘‘a waste of police resources,’’ he said. Sure enough, around 5 p.m., dispatch put out a call regarding a spike overdose. Four officers were already on the scene when we arrived. They stood in the yard of a tidy white house, trying to coax a man down from a set of stairs. The man was in his 40s, with a shaved head and a scraggly beard. Oblivious to the officers, who seemed to know him, he stared at the sky, rolling his eyes.

‘‘Hey, Will, c’mon,’’ one officer said. ‘‘You want to crawl down?’’ Paramedics wheeled a gurney to the stairs, and the situation escalated quickly. When the police laid hands on him, Will began jerking spastically and didn’t stop, even after he was strapped to the gurney and loaded into the ambulance.

Nurses at the hospital discovered three bags of spike on Will. But there was also a sandwich bag filled with what appeared to be small stones. Breen took the spike and the ‘‘moon rocks,’’ as he called them, to the Public Safety Building downtown. While he went to fetch a drug-test field kit, the supervising officer, Sergeant Novitsky, examined the haul. The moon rocks baffled him. ‘‘I just don’t want to touch it,’’ he said.

Whatever it was, it certainly wasn’t spike. The kit returned negative results for amphetamines, cocaine, LSD, marijuana, MDMA, methadone, methamphetamine and PCP as well. Breen and Novitsky weren’t sure what to do next. Toss the rocks into an evidence locker? Send them to the crime lab? Neither possibility appealed to Breen. ‘‘The lab’s not testing anything we’re sending,’’ he complained. ‘‘They won’t unless it’s a criminal case.’’ Novitsky shrugged. Overdoses weren’t criminal cases. At my suggestion, Breen decided to take it to Ross Sullivan, an emergency-room doctor at Upstate who has been investigating the toxicology of synthetic drugs.

We parked outside the entrance of Upstate’s emergency department and waited in the dark for the handoff. This was how knowledge of synthetic drugs was being advanced — an ersatz drug deal between a rookie cop and a toxicologist, with a reporter acting as middleman. It was absurd, but it was also somehow fitting. The synthetic-drug industry, and the response to it, are based on improvisation. A molecule is tweaked in a Chinese lab, triggering a chain reaction that goes all the way down the line from dealers to users to paramedics and the police to doctors and lawyers. Just when everybody seems to have a handle on it, the molecule gets tweaked again, and the cycle begins anew. Whatever these rocks were, Upstate’s doctors might very well see a flood of overdoses on it next year.

For what it’s worth, the “moon rocks” described at the end of this article are likely methylone, an analog of MDMA that acts as a CNS stimulant and empathogen. User’s have described methylone’s effects as variously being similar to MDMA or LSD. A 2012 paper from The Annals of Toxicology describes 3 fatal intoxications:  Pearson JM, et al. Three fatal intoxications due to methylone. J Anal Toxicol. 2012 Jul;36(6):444-51.

Source:Search   http://mobile.nytimes.com/2015/07/12/magazine/spike-nation.html?referrer=

So much has been said and written about addiction, much of it so wisely put by individuals in and out of recovery. One popular adage is “the definition of insanity is doing the same thing over and over again and expecting a different outcome.” In clinical terms, one of the most distinguishing diagnostic features of addictive disorders is that those affected continually and repeatedly revert to their addictive behaviors, despite the devastating negative and adverse consequences.

In my own career and investigative studies as an addiction specialist spanning many decades, I have emphasized that a primary factor that contributes to repeated abuse is that addictive substances temporarily relieve emotional pain and suffering that otherwise feel unmanageable or intolerable. That is, those who endure such distress self-medicate, and they wittingly or unwittingly provide support for the self-medication hypothesis (SMH) of addictive disorders, a theory that has received much endorsement and at least an equal amount of criticism and rejection.

On occasion, I somewhat satirically comment that I believe in the SMH more on some days than others. Although I continue to believe that it is a powerful paradigm to explain addictive disorders, today was one of those times when I found myself thinking it does not satisfy the complexities (or perhaps the subtleties) involved in the bedevilling, repetitious, self-harming behaviors associated with addictions. An e-mail from a former patient with whom I had parted ways because I relocated my office to another community, stimulated my thoughts about the irrationality of addiction and doubt and curiosity about the SMH aspect of addiction.

CASE VIGNETTE

Matthew is a 55-year-old gifted author and college professor of English studies. After struggling for many years as a heavy drinker, he sought out professional help with only modest progress in obtaining control over his drinking. He finally established abstinence and a protracted period of sobriety (5 years) before he started treatment with me. He then immersed himself in AA meetings where he felt supported and found a caring sponsor to work with him.

For reasons not entirely clear but at least to some extent related to recent stressors (some related to chronic musculoskeletal pain), he resorted to periodically drinking large amounts of alcohol. The following e-mail typified that pattern, in this case indicating that his current drinking was in part celebratory:

Dear Dr K,

I finally felt okay physically last week, when my class began. I had a great week, so much so that I wanted to celebrate/prolong and drank a bottle and a half of wine Friday night. Saturday was a total loss, but I managed to get out and buy one bottle of wine, which I consumed. Feel okay now and am ready for 4 straight days of classes.

Not worried about drinking during the class, but certainly when it ends. The whole thing is very strange. I guess my life was turned upside down by the pain in recent months, not able to go to early morning meeting, etc. But something has to give . . . haven’t quite figured it out. Don’t feel committed to sobriety.

Thanks so much for your text. Would love to come see you, but obviously I need to find someone in the area, sooner than later.     Best,Matt

I responded to his e-mail as follows:

Dear Matt,

Get back to basics. That should include someone to work with you on the insanity of addiction. You know what to do as well as anyone else, and that is to get a safety net of others who care about and love you. YOU CAN’T DO THIS ALONE.

I would also add that I am not entirely surprised about your notion that when you complete your course, you will be more apt to drink. Perhaps success creates the illusion that you can control the uncontrollable and be immune to the consequences of drinking.

And should you continue to delay in finding someone, come see me in the interval for a sanity check.    EJK

I was reminded that persons addicted to substances find countless reasons to drink and drug—to grieve, to celebrate, to heighten feelings, to reduce or drown feelings, to get a job done, to drink when a job is done, and so on. Obviously, the reasons to self-medicate are myriad and the motives, seemingly contradictory.

My response to Matt was guided in part by my unyielding, evolving curiosity and interest in what it is that governs and drives the needs and issues that perpetuate addictions. So notwithstanding the criticisms of self-medication motives, the repetitious nature of the “insanity of addiction” does not necessarily contradict. Rather, it begs the question whether addictive behaviors accomplish or fix anything for those who repeatedly resort to it.

To Matt’s credit, he followed up with several e-mails and a phone call to indicate that he was more aggressively seeking out an addiction counsellor locally to obtain support and to regain control of the drinking.

Discussion

When addicted persons in recovery speak of the puzzling sense of powerlessness and inability to control their drinking, as Matthew suggests in his e-mail, they also often indicate how the irrationality of it is so painful and bedevilling. As I indicated, the irrational component challenges me as well, on some days more than others, including whether the ideas and theories of addiction psychiatry are sufficient to address and explain what seems so unexplainable and confusing. I offer a few thoughts here, drawing on my clinical experiences and ideas about addiction, which might shed light on what often can seem irrational and incomprehensible. Although modern neuroscience research has yielded important findings on how substances alter the brain and contribute to addictive patterns of use and misuse, such brain changes and mechanisms alone are insufficient to explain the complexities of dependence on alcohol and addictive drugs. I do not suggest that I have all the answers, but I believe that clinical study and treatment of addiction offer valuable insights into repetitious, self-harm behaviors, as unreasonable as they may seem.

In treatment, my patients consistently reveal their life-long difficulties in dealing with their feelings. They have been plagued by issues of poor sense of self and low self-

esteem. Their relationships with others suffer, and they find it difficult to practice self-care. Often they fail to appreciate very real danger—in their surroundings and especially those associated with addiction. I refer to these issues as the human challenge of self-regulation. Persons at risk for addiction are underdeveloped or deficient in some or all of these areas.

In my experience, in the context of experimenting with addictive substances, some people discover (italics for emphasis) that addictive substances provide short-term relief from the pain, suffering, and dysfunction associated with their problems in regulating their emotions, low self-esteem, and difficulties with interpersonal relationships. These factors then malignantly interact with deficits in self-care to make addictive attachments more likely.

Thinking about addiction as a self-regulation disorder “helps” in part to explain how addictive substances assist in regulating a wide range of challenges. Considering addiction from such a perspective provides some measure of understanding for what seems so unreasonable, irrational, and incomprehensible.

Returning to Matthew and his dilemma: he knows that resorting to alcohol will be devastating, but he nevertheless feels powerless to avoid that prospect. As we so often say in our work as psychiatrists and mental health professionals, people have their reasons for what they believe, say, and do, as unreasonable and irrational as it may seem. Addicted individuals, including my patient Matthew, do not have exclusive claim to this aspect of human existence.

See more at:    http://www.psychiatrictimes.com/addiction/insights-insanity-addiction?GUID=8CCBBF2C-6541-4A09-A30A-3E72BFE8C975&rememberme=1&ts=04062015#sthash.YRB4VlwK.dpuf

Source:   http://www.psychiatrictimes.com/    3rd March 2015

Filed under: Addiction (Papers) :

Legalization keeps rolling ahead. But because of years of government roadblocks on research, we don’t know nearly enough about the dangers of marijuana—or the benefits

Yasmin Hurd raises rats on the Upper East Side of Manhattan that will blow your mind.

Though they look normal, their lives are anything but, and not just because of the pricey real estate they call home on the 10th floor of a research building near Mount Sinai Hospital. For skeptics of the movement to legalize marijuana, the rodents are canaries in the drug-policy coal mine. For defenders of legalization, they are curiosities. But no one doubts that something is happening in the creatures’ trippy little brains.

In one experiment, Hurd’s rats spent their adolescence getting high, on regular doses of tetrahydrocannabinol (THC), the psychoactive compound in marijuana. In the past, scientists have found that rats exposed to THC in their youth will show changes in their brain in adulthood. But Hurd asked a different question: Could parental marijuana exposure pass on changes to the next generation, even to offspring who had never been exposed to the drug?

So she mated her rats, but only after she had waited a month to make sure the drug was no longer in their system. She raised the offspring, along with another group of rats that shared the same life experiences except for the THC. She then trained the children to play a game alone in a box. The prize: heroin.

Press one lever to get a shot of saline into the jugular vein. Press the other to get a rush of opiates. Initially, the rats with THC-exposed parents performed about the same as the rats with sober parents. But when Hurd’s team changed the rules, requiring the rats to work harder for the drug, differences emerged. The rats with drug-using parents pushed the lever more than twice as much. They wanted the heroin more.

When she analyzed the brains of the rats, she also found differences in the neural circuitry of the ones with drug-using parents. Even the grandkids have begun to show behavioral differences in how they seek out rewards. “This data tells us we are passing on more things that happen during our lifetimes to our kids and grandkids,” Hurd explains, though it remains unclear how those changes manifest in humans. “I wasn’t expecting these results, and it’s fascinating.”

Welcome to the encouraging, troubling and strangely divided frontier of marijuana science. The most common illicit drug on the planet and one of the fastest-growing industries in America, pot remains–surprisingly–something of a medical mystery, thanks in part to decades of obstruction and misinformation by the federal government. Potentially ground breaking studies on the drug’s healing powers are being done to find treatments for conditions like epilepsy, posttraumatic stress disorder (PTSD), Alzheimer’s disease, Parkinson’s disease, sickle-cell disease and multiple sclerosis. But there are also new discoveries about the drug’s impact on recreational users.

The effects are generally less severe than those of tobacco and alcohol, which together cause more than 560,000 American deaths annually. Unlike booze, marijuana isn’t a neurotoxin, and unlike cigarettes, it has an uncertain connection to lung cancer. Unlike heroin, pot brings almost no risk of sudden death without a secondary factor like a car

crash. But science has also found clear indications that in addition to short-term effects on cognition, pot can change developing brains, possibly affecting mental abilities and dispositions, especially for certain populations. The same drug that seems relatively harmless in moderation for adults appears to be risky for people under age 21, whose brains are still developing. “It has a whole host of effects on learning and cognition that other drugs don’t have,” says Jodi Gilman, a Harvard Medical School researcher who has been studying the brains of human marijuana users. “It looks like the earlier you start, the bigger the effects.”

Beyond Reefer Madness

That relatively measured tone is a far cry from the shrill warnings of Harry J. Anslinger, the first commissioner of the Federal Bureau of Narcotics, who in the 1930s set the standard for America’s fraught debate over marijuana with wild exaggerations. “How many murders, suicides, robberies, criminal assaults, holdups, burglaries and deeds of maniacal insanity it causes each year, especially among the young, can only be conjectured,” he wrote as part of a campaign to terrify the country. As recently as the 1970s, President Richard Nixon talked about the drug as a weapon of the nation’s enemies. “That’s why the communists and the left-wingers are pushing the stuff,” he was recorded saying in private. “They’re trying to destroy us.”

The official line today is better grounded in data and research. And the new focus is squarely on brain development. “I am most concerned about possibly harming the potential of our young people,” says Dr. Nora Volkow, the head of the National Institute for Drug Abuse (NIDA), which funds Hurd’s and Gilman’s work. “That could be disastrous for our country.”

But decades of prohibition and official misinformation continue to shape public views. “The government did not spend as much effort in finding out the facts about marijuana,” says Hurd. “That strategy of scaring people rather than provide knowledge has made people sceptical now when they hear anything negative.”

As states now rush to legalize pot and unwind a massive criminalization effort, the federal government is trying to play catch-up on the science, with mixed success. The only federal marijuana farm, at the University of Mississippi, has recently expanded production with a $69 million grant in March, and Volkow has expressed a new openness to studies of marijuana’s healing potential. In the coming months, Uncle Sam will begin a 10-year, $300 million study with thousands of adolescents to track the harm that marijuana, alcohol and other drugs do to the developing brain. High-tech imaging will allow researchers for the first time to map the effects of marijuana on the brain as humans age.

But scientists and others point out that a shift to fund the real science of pot still has a long way to go. The legacy of the war on drugs haunts the medical establishment, and federal rules still put onerous restrictions on the labs around the country that seek to work with marijuana, which remains classified among the most dangerous and least valuable drugs. “We can do studies on cocaine and morphine without a problem, because they are Schedule II,” explains Fair Vassoler, a researcher at Tufts University who has replicated Hurd’s rat experiment with synthetic pot. “But marijuana is Schedule I.”

That means that under the law, marijuana has “no medical benefit,” even though 23 states have legalized pot as medicine and NIDA acknowledges that “recent animal studies have shown that marijuana can kill certain cancer cells and reduce the size of others.” And marijuana researchers face barriers even higher than those faced by

scientists studying other Schedule I drugs, like heroin and LSD. Pot studies must pass intensive review by the U.S. Public Health Service, a process that has delayed and thwarted much research for more than 15 years. The result is sometimes a catch-22 for scientists seeking to understand the drug. “The government’s research restrictions are so severe that it’s difficult to find and show the medical benefit,” says neurobiologist R. Douglas Fields, the chief of the nervous-system-development section at the National Institutes of Health (NIH).

That all may change soon. On Capitol Hill, a left-right coalition of Senators Kirsten Gillibrand of New York, Rand Paul of Kentucky and Cory Booker of New Jersey introduced a bill in March to federally legalize medical marijuana in states that have already approved it. “For far too long,” said Paul, a Republican candidate for President, “the government has enforced unnecessary laws that have restricted the ability of the medical community to determine the medicinal value of marijuana.”

The Cannabinoid System

Harm researchers and neuroscientists aren’t completely deadlocked. They agree on at least one thing. Marijuana’s positive and negative effects both spring from the same source: the body’s endocannabinoid system. First discovered in the late 1990s, it’s a complex neural system that researchers are only beginning to fully comprehend.

A little Brain Science 101: Human grey matter contains around 86 billion neurons, a type of cell that essentially talks to other cells in the brain through electrochemical processes. Neurons talk to each other through chemical messengers known as neurotransmitters–including dopamine, serotonin, glutamate and compounds called endocannabinoids–which in turn send instructions to your body about what to do.

Researchers now know the body produces endocannabinoids, which activate cannabinoid receptors in the brain. Interestingly, one plant on earth produces a similar compound that hits those same receptors: marijuana. Just as poppy-derived morphine mimics endorphins, marijuana-derived cannabinoids like THC and cannabidiol (CBD) mimic endocannabinoids, which impact feelings of hunger and pleasure. Cannabinoid receptors are especially widespread in the brain, where they play a key role in regulating the actions of other neurotransmitters.

“The more we investigate the hidden recesses of the brain, the more it seems like practically every neuron either releases endocannabinoids or can sense them using cannabinoid receptors,” explains Gregory Gerdeman, a neuroscientist and endocannabinoid researcher at Florida’s Eckerd College. Neurotransmitters carry out brain communication through synapses. “But too much synaptic excitation is poisonous–it damages cells,” says Gerdeman. “Endocannabinoids are a mechanism for putting on the brakes when that toxic level of excitation is approached.”

Cannabinoids like CBD may be thought of as neuro-protectants–that is, brain protectors. In fact, the NIH actually owns a patent (No. 6630507) on cannabinoids as neuro-protectants, based on the work of researcher Aiden Hampson and his mentor, Nobel Prize–winning neuroscientist Julius Axelrod. They found that CBD showed particular promise in limiting neurological damage in patients with Alzheimer’s disease and Parkinson’s disease and in those who have suffered a stroke or head trauma.

Endocannabinoids also play a role in the regulation of pain, mood, appetite, memory and even the life and death of individual cells. Curiously, cannabinoid receptors aren’t

densely packed in the medulla (within the brain stem), which controls breathing and the cardiovascular system. That’s why a heroin overdose can be fatal–the drug shuts down the respiratory control center – but a marijuana overdose generally can’t. PTSD researchers are keen to crack the cannabinoid code because the compounds appear to play a role in extinguishing unpleasant memories. “Part of what happens with PTSD is that the brain’s stress buffers have been blown out by trauma,” says Gerdeman. “Endocannabinoids within the amygdala”–the brain region important for emotional learning and memory–“act as a key mechanism for what we call memory extinction.”

But what accounts for the potentially healing effects of pot in some can cause harm in others. That’s because endocannabinoids appear to play a critical role in the development of the adolescent brain. If the brain were a house, the childhood years would be spent pouring the foundation and framing up the walls. Adolescence is when the wiring and plumbing get finished. Neural networks are refined and strengthened through pruning. The strong synapses, axons and dendrites are preserved, the weak culled.

Researchers now believe the cannabinoid system plays a critical role in this neural fine-tuning. This is where the worries about teenage pot use come to the fore. At the precise moment when the brain relies on a finely calibrated dose of endocannabinoids, the adolescent weed smoker floods the system. “If you actively and repeatedly overload the endogenous cannabinoid system,” says Volkow, “you are going to disrupt that very well-orchestrated system.”

That disruption may lie at the heart of still inconclusive science about marijuana’s impact on human behavior, especially among younger users. Early studies suggest that there may be long-lasting impacts on mental acuity, higher brain function and impulse control for younger users. There is also a well-documented connection between pot smoking and schizophrenia, a condition that affects about 1% of the U.S. population. Scientists have been aware of the link since the 1970s. Among those with a family history of mental illness, marijuana can hasten the emergence of schizophrenia.

Researchers are trying to identify the mechanisms in play. “Many genes are undoubtedly involved in risk for schizophrenia,” says Dr.Michael Compton, a professor at Hofstra North Shore–LIJ School of Medicine and the head of psychiatry at New York City’s Lenox Hill Hospital. “But there are also a host of social or environmental influences at work.” For a subset of the population, the earlier the initiation of marijuana use, the earlier the onset of psychosis.

Here’s why that matters: The later schizophrenia emerges, the greater the likelihood of recovery. Schizophrenia onset in a 15-year-old is often permanently life-altering. In a 24-year-old, it can be less damaging, because the person has had the chance to accomplish more psychological and social-developmental milestones. But that doesn’t mean all teenage pot users are smoking themselves into mental illness. Darold Treffert, the Wisconsin psychiatrist who first documented the marijuana-schizophrenia link in the 1970s, puts it this way: “Perhaps some persons can safely use marijuana, but schizophrenics cannot.” A test or a clear genetic marker to identify kids who are vulnerable to schizophrenia is likely years away.

The Healing Possibilities

While American research on the potential harms from marijuana is booming, the U.S. continues to lag in funding investigations into the possible benefits. In the late 1990s, the U.S. and British governments commissioned separate studies of medical marijuana.

The U.K. study was spurred by multiple-sclerosis patients’ using pot to calm spasticity. The U.S. study, done by the Institute of Medicine, was in response to California’s 1996 legalization of medical marijuana.

Both studies reached a similar conclusion: medical pot wasn’t a hippie’s delusion. The research showed that the stuff held real therapeutic potential for specific conditions, including epilepsy, chronic pain and glaucoma. The British responded by treating marijuana as a plant with biotech prospects. U.K. officials licensed GW Pharmaceuticals, a start-up lab in Salisbury, England, to grow weed and develop cannabinoid drugs, some of which U.S. scientists like Hurd use in their research.

The Americans, meanwhile, doubled down on the war on drugs. Barry McCaffrey, Bill Clinton’s drug czar, was outraged at the Institute of Medicine’s results. “I think what the IOM report said is that smoked marijuana is harmful, particularly for those with chronic conditions,” he said–pretty much the opposite of the report’s conclusions. Nonetheless, he and then Attorney General Janet Reno vowed to prosecute medical-marijuana patients and doctors who prescribed the drug. Shortly thereafter, the U.S. Department of Health and Human Services adopted even tougher strictures against the study of marijuana as a medicine.

The federal anti-pot policies resulted in a strange kind of scientific trade deficit. The U.S. leads the world in studies of marijuana’s harm, but we’re net importers of data dealing with its healing potential. THC discoverer Raphael Mechoulam runs the world’s leading cannabinoid lab at the Hebrew University of Jerusalem. Spanish biologist Manuel Guzmán is doing cutting-edge work on the potential of cannabinoids to retard the growth of glioblastoma, one of the deadliest forms of brain cancer. Canada’s health agency may soon approve the world’s first clinical trial to test medical marijuana on military and police veterans with PTSD.

There are signs of change at home, though. This year, the Colorado department of public health awarded $9 million in grants for medical-marijuana research, funded with tax revenue from state-licensed pot stores. They will be among the first U.S. clinical trials to look into the effectiveness of marijuana for childhood epilepsy, irritable-bowel disease, cancer pain, PTSD and Parkinson’s disease. Dr.Kelly Knupp, a paediatric-epilepsy specialist at Children’s Hospital in Denver, will track children using high-CBD marijuana strains to calm seizures. “Some of these children can have 100 to 200 seizures a day,” Knupp says. “We’re hoping we can measure seizure frequency to see if there’s any improvement” among kids trying the cannabinoid medicine.

This Is a Rat on Drugs

Back at Hurd’s Upper East Side lab, the rats have begun to show the way. In a separate experiment, she gave heroin-addicted rats doses of CBD and found that it decreased their willingness to work hard for more heroin, suggesting that parts of marijuana could help human drug addicts stay clean. She is now testing that hypothesis by giving CBD tablets, made in England, to recovering human addicts in New York City.

She is also continuing to study the behavior of rats whose only exposure to marijuana’s active ingredients came through the DNA passed on to them from their parents or grandparents. That research suggests that THC may have epigenetic effects, which have been found in other drugs like cocaine and heroin, changing the way genes express themselves in the brains of offspring. This doesn’t necessarily mean that parents who smoked weed in high school have damaged their kids, because those changes may be

overrun by other behaviors. The science is too new to know for sure. “It’s not a given that this is going to happen,” Hurd explains of her rats. “They tell us the potential.”

That word–potential–still qualifies much of what is known about pot, but it won’t be that way for long. The science of pot is likely to expand in the coming years, and it could boom if federal restrictions are lifted. What the government once dismissed as a communist plot that prompted murderous rages has turned out to be a window into the very workings of the human mind. In the years to come, researchers may yet find genetic markers that predispose people to pot-induced psychotic reactions, map out the specific ways in which THC changes the brain and find new medicines for some of the most intractable illnesses. Until then, the great marijuana experiment will continue in a country where 1 in 10 adults–and 35% of high school seniors–admit to conducting their own, mostly recreational, research.

Barcott is a journalist who has contributed to the New York Times, National Geographic and other publications. Scherer is TIME’s Washington bureau chief. Portions of this article were adapted from Barcott’s new book Weed the People: The Future of Legal Marijuana in America, published by TIME Books.  the Future of Legal Marijuana in America,” is now available wherever books are sold, including Amazon.com, Barnes & Noble and Indiebound.

Source:  May 25, 2015 issue of TIME.

CLEARING THE HAZE

….The ugly truth is that Colorado was suckered. It was promised regulation and has been met by an industry that fights tooth and nail any restrictions that limit its profitability.”  Ben Cort, Director of Professional Relations for the Center for Additction Recovery and rehabilitation at the University Of Colorado Hospital

Source:   http://gazette.com/clearingthehaze

 

REGULATION STILL INEFFECTIVE

But how it would work was described only in general terms and sound bites before voters headed to the polls to make a decision Gov. John Hickenlooper later would call “reckless” and “a bad idea” and new Colorado Attorney General Cynthia Coffman declared “not worth it” to dozens of state attorneys general last month.

Source:http://www.washingtonexaminer.com/regulation-still-ineffective/article/2562323?custom_click=rss

 

NO APPROVED MEDICINE IN MARIJUANA

Dr. Stuart Gitlow, a physician serving as president of the American Society of Addiction Medicine, does not mince words: “There is no such thing at this point as medical marijuana,” he said. It’s a point he has made routinely for the past decade, as advocates for marijuana legalization have claimed the drug treats an array of serious illnesses, or the symptoms of illnesses, including cancer, depression, epilepsy, glaucoma and HIV, the virus that causes AIDS.

Source:http://www.washingtonexaminer.com/no-approved-medicine-in-marijuana/article/2562336

 

LEGALIZATION DIDN’T UNCLOG PRISONS

Of all the misunderstandings about marijuana’s impact on the country, perhaps none is greater than the belief that America’s courts, prisons and jails are clogged with people whose only offense was marijuana use. This is the perception, but statistics show few inmates are behind bars strictly for marijuana-related offenses, and legalization of the drug will do little to affect America’s growing incarceration numbers.

Source:http://www.washingtonexaminer.com/legalization-didnt-unclog-prisons/article/2562326

 

DRUG USE A PROBLEM FOR EMPLOYERS

“This is a very troublesome issue for our industry, but I do not see us bending or lowering our hiring standards,” Johnson said. “Our workplaces are too dangerous and too dynamic to tolerate drug use. And marijuana? In many ways, this is worse than alcohol. I’m still in shock at how we (Colorado) voted. Everyone was asleep at the wheel.”

Source:http://www.washingtonexaminer.com/drug-use-a-problem-for-employers/article/2562334

 

MEDICAL MARIJUANA INDUSTRY STILL GROWING

And amid all the hoopla around legalized recreational pot, its older cousin, the medical marijuana (MMJ) industry — with 505 stores throughout Colorado — quietly continued to grow, adding patients by the thousands who seemingly had no problem finding physicians willing to diagnose what critics say are often phantom medical conditions. Statewide, the number of people on the Medical Marijuana Registry grew 4 percent in 2014 — the first year of legal recreational sales — from 111,030 to 115,467 by year’s end.

Source:http://www.washingtonexaminer.com/medical-marijuana-industry-still-growing-in-colorado/article/2562335

Some good news, some not-so-good news about brain recovery from alcohol use disorders

According to a recent review article on recovery of behavior and brain function after abstinence from alcohol[1], individuals in recovery can rest assured that some brain functions fully recover; but others may require more work. In this article, authors looked at 22 separate studies of recovery after alcohol dependence, and drew some interesting conclusions.

First, the good news; studies show improvement or even complete recovery to the performance level of healthy participants who had never had an alcohol use disorder in many important areas, including short-term memory, long-term memory, verbal IQ, and verbal fluency. Even more promising, not only behavior, but the structure of the brain itself may recover; an increase in the volume of the hippocampus, a brain region involved in many memory functions, was associated with memory improvement.

Another study showed that after 6 months of abstinence, alcohol-dependent participants showed a reduction in a “contextual priming task” with alcohol cues; in day to day terms, this could mean that individuals in early recovery from alcohol dependence may be less likely to resume drinking when confronted with alcohol and alcohol-related cues in their natural environment because these alcohol-related triggers are eliciting less craving.- a good thing for someone seeking recovery!

Still other studies showed that sustained abstinence was associated with tissue gain in the brain; in other words, increases in the volumes of brain regions such as the insula and cingulate cortex, areas which are important in drug craving and decision-making, were seen in abstinent alcoholics. This increase is a good thing, because more tissue means more recovery from alcohol-induced damage. A greater volume of tissue in these areas may be related to a greater ability to make better decisions.

Now, the not-so-good news: these studies reported no improvement in visuospatial skills, divided attention (e.g. doing several tasks at once), semantic memory, sustained attention, impulsivity, emotional face recognition, or planning.  This means that even after abstinence from alcohol, people in recovery may still experience problems with these neurocognitive functions, which may be important for performing some jobs that require people to pay attention for long periods of time or remember long lists of requests. These functions may also be important for daily living (i.e. assessing emotions of a spouse, planning activities, etc.).

Importantly, there were many factors that influenced the degree of brain recovery; for example, the number of prior detoxifications. Those with less than two detoxifications showed greater recovery than those with more than two detoxifications.  A strong family history of alcohol use disorder was associated with less recovery. Finally, cigarette smoking may hinder recovery, as studies have shown that heavy smoking is associated with less recovery over time.

So what does all this mean? Recovery of brain function is certainly possible after abstinence, and will naturally occur in some domains, but complete recovery may be harder in other areas. Complete recovery of some kinds of behavior (e.g. sustained attention, or paying attention over long periods of time) may take more time and effort! New interventions, such as cognitive training or medication (e.g. modafinal, which improved neurocognitive function in patients with ADHD and schizophrenia, as well as in healthy groups), may be able to improve outcomes even more, but await further testing.

[1] Recovery of neurocognitive functions following sustained abstinence after substance dependence and implications for treatment

Source:  Mieke H.J. Schulte et al., Clinical Psychology Review 34 (2014) 531–550   October 2014

 

When you smoke marijuana, there’s an almost immediate effect on your brain, sense of perception, and heart rate. There may be long-term effects as well.

 

The Effects of Marijuana on the Body

Marijuana comes from the Cannabis plant. The flowers, seeds, leaves, and stems of the plant must be shredded and dried before they can be used. Most people who use marijuana smoke it, but it can be mixed into food, brewed into tea, or even used in a vaporizer. One of the ingredients in marijuana is a mind-altering chemical called delta-9-tetrahydrocannabinol (THC).

When you inhale marijuana smoke into your lungs, it is quickly released into your bloodstream on its way to your brain and other organs. It takes a little longer to be absorbed when you eat or drink it.

The effects of marijuana on the body are immediate. Longer-term effects may depend on how you take it, how much you take, and how often you use it. Since its use has long been illegal in the United States, large-scale studies have been difficult to manage.

In recent years, the medicinal properties of marijuana are gaining acceptance in mainstream America. Medical marijuana is now legal in 23 states and the District of Columbia. THC and another ingredient called cannabidol (CBD) are the main substances of therapeutic interest. National Institutes of Health-funded research into the possible medicinal uses of THC and CBD is ongoing.

In addition to medicinal use, recent legislation has made marijuana a legal recreational drug in Colorado and Washington State. With the potential for increased recreational use, knowing the effects that marijuana can have on your body is as important as ever.

Respiratory System

 

Much like tobacco smoke, marijuana smoke is made up of a variety of toxic chemicals that can irritate your bronchial passages and lungs. If you’re a regular smoker, you’re more likely to wheeze, cough, and produce phlegm. You’re also at increased risk of bronchitis and lung infections. Marijuana may aggravate existing respiratory illnesses like asthma and cystic fibrosis.

Marijuana smoke contains carcinogens. It has the potential to elevate your risk of developing lung cancer. However, studies on the subject have had mixed results. According to the National Institute of Drug Abuse(NIDA), there is no conclusive evidence that marijuana smoke causes lung cancer. More research is needed.

Circulatory System

THC moves from your lungs into your bloodstream and throughout your body. Within minutes, your heart rate may increase by 20 to 50 beats per minute, according to the NIDA. That rapid heartbeat can continue for up to three hours. For people with heart disease, this faster heartbeat could raise the risk of heart attack.

One of the telltale signs of recent marijuana use is bloodshot eyes. They look red because marijuana causes blood vessels in the eyes to expand or dilate. Marijuana may help stop the growth of blood vessels that feed cancerous tumors.

 Central Nervous System

 

When you inhale marijuana smoke into your lungs, it doesn’t take long for THC to enter your bloodstream. From there, it is quickly transported to your brain and the rest of your organs. When you get marijuana from food or drink, it is absorbed a little more slowly.

THC triggers your brain to release large amounts of dopamine, a naturally occurring “feel good” chemical. That’s what gives you a pleasant “high.” It may heighten your sensory perception, as well as your perception of time. In the hippocampus, THC changes the way you process information, so your judgment may be impaired. It may also be difficult to form new memories when you’re high.

Changes also take place in the cerebellum and basal ganglia, upsetting your balance, coordination, and reflex response. All those changes mean that it’s not safe to drive.

Very large doses of marijuana or high concentrations of THC can cause hallucinations or delusions. According to the NIDA, there may be an association between marijuana use and some mental health problems like depression and anxiety, but more research is needed to understand the connection. In people who have schizophrenia, marijuana use can make symptoms worse.

When you come down from the high, you may be tired or feel a bit depressed. In some people, marijuana can cause anxiety. About nine percent of marijuana users develop an addiction, according to the NIDA. Symptoms of withdrawal may include irritability, insomnia, and loss of appetite.

In young people whose brains are not yet fully developed, marijuana can have a lasting impact on thinking and memory skills. If you use marijuana when pregnant, it can affect the brain of your unborn baby. Your child may be more prone to trouble with memory, concentration, and problem-solving skills.

THC can lower pressure in the eyes, which can ease symptoms of glaucoma for a few hours. According to theAmerican Academy of Ophthalmology, more research is needed to understand the active ingredients in marijuana and whether or not it’s a good treatment for glaucoma.

The pharmacologic effect of marijuana extends throughout the central nervous system. It is thought to ease pain and inflammation. It may also be of use in controlling spasms and seizures.

Digestive System

 

Smoking marijuana can cause stinging or burning in your mouth and throat. When you take oral THC, it is processed in your liver. Marijuana can ease nausea and vomiting. It can also increase appetite, which can be useful to people living with cancer or AIDS.

Immune System

Some research indicates that THC affects the immune system. Studies involving animals showed that THC might damage the immune system, making you more vulnerable to illness. Further research is needed.


Source: https://learnaboutsam.org/

Young men who use cannabis may be putting their fertility at risk by inadvertently affecting the size and shape of their sperm, according to new research. In the world’s largest study to investigate how common lifestyle factors influence the size and shape of sperm, a research team found that sperm size and shape was worse in samples ejaculated in the summer months, but was better in men who had abstained from sexual activity for more than six days.

(Stock image) Credit: © milkovasa / Fotolia

In the world’s largest study to investigate how common lifestyle factors influence the size and shape of sperm (referred to as sperm morphology), a research team from the Universities of Sheffield and Manchester also found that sperm size and shape was worse in samples ejaculated in the summer months but was better in men who had abstained from sexual activity for more than six days.

However, other common lifestyle factors reported by men, including smoking cigarettes or drinking alcohol, appeared to have little effect.

The study, published in the medical journal Human Reproduction, recruited 2,249 men from 14 fertility clinics around the UK and asked them to fill out detailed questionnaires about their medical history and their lifestyle. Reliable data about sperm morphology was only available for 1,970 men and so the researchers compared the information collected for 318 men who produced sperm of which less than four per cent was the correct size and shape and a control group of 1,652 men where this was above four per cent and therefore considered ‘normal’ by current medical definitions.

Men who produced ejaculates with less than four percent normal sperm were nearly twice as likely to have produced a sample in the summer months (June to August), or if they were younger than 30 years old, to have used cannabis in the three month period prior to ejaculation.

Lead author Dr Allan Pacey, Senior Lecturer in Andrology at the University of Sheffield, said: “Our knowledge of factors that influence sperm size and shape is very limited, yet faced with a diagnosis of poor sperm morphology, many men are concerned to try and identify any factors in their lifestyle that could be causing this. It is therefore reassuring to find that there are very few identifiable risks, although our data suggests that cannabis users might be advised to stop using the drug if they are planning to try and start a family.”

Previous research has suggested that only sperm with good sperm morphology are able to pass into the woman’s body following sex and make their way to the egg and fertilize it. Studies in the laboratory also suggest that sperm with poor morphology also swim less well because their abnormal shape makes them less efficient. Dr Andrew Povey, from the University of Manchester’s Institute of Population Health, said: “This research builds on our study of two years ago which looked at the risk factors associated with the number of swimming sperm (motile concentration) in men’s ejaculates.

“This previous study also found that there were relatively few risk factors that men could change in order to improve their fertility. We therefore have to conclude again that there is little evidence that delaying fertility treatment to make adjustments to a man’s lifestyle will improve their chances of a conception.”

Although the study failed to find any association between sperm morphology and other common lifestyle factors, such as cigarette smoking or alcohol consumption, it remains possible that they could correlate with other aspects of sperm that were not measured, such as the quality of the DNA contained in the sperm head.

Professor Nicola Cherry, originally from the University of Manchester but now at the University of Alberta, commented on a recent companion paper published by the group in the Journal of Occupational and Environmental Medicine: “In addition to cannabis exposure shown in this paper, we also know that men exposed to paint strippers and lead are also at risk of having sperm with poor morphology.”

Source:

University of Sheffield. “Sperm size, shape in young men affected by cannabis use.” ScienceDaily. ScienceDaily, 4 June 2014. <www.sciencedaily.com/releases/2014/06/140604202946.htm>.

February 24, 2015

Work loads in high school can be extreme, causing some kids to think about cheating or taking study drugs. GSE senior lecturer Denise Pope comments on the problem and possible solutions, such as cutting homework load and ensuring kids get enough “play time, down time and family time.”

In a shifting economy without any assurances of success, there’s a lot of pressure on students to succeed in school. More and more kids are going to college and the application process is competitive. To help stand out, students are taking on tougher course loads, along with extracurricular activities and leadership roles. In order to pack everything in, some kids turn to prescription drugs like Adderall and Ritalin to stay awake and focus on school work and test prep. They can obtain the medication from doctors, peers and sources they find online. However, many of these students, both in high school and in college, don’t know the physical or neurological ramifications of taking drugs that haven’t been prescribed to them by a doctor.

“We live in this culture of excellence,” said Michael McCutcheon, a counseling psychology phD candidate at New York University, on KQED’s Forum, “and if you are at a competitive high school and you know the culture really only celebrates success or money, then everything is riding on this test.” That overwhelming pressure – the feeling that every test and grade matters for ones future – combined with ease of access to these drugs makes their use seductive. Stanford Graduate School of Education senior lecturer Denise Pope found similar experiences among thousands of high school students she has interviewed or observed in her work.

“These kids are completely overloaded,” Pope said. “They come from high achieving schools, but these kids feel like there’s more homework than there is time in a day.” She cited increased pressure to take Advanced Placement or honors classes that require lots of homework, along with the explosion of extracurricular activities and the time students devote to them as some of the reasons for increased stress.

“The kids who cheat in high school, absolutely cheat in college,” Pope said. “My guess would be that if this is negative coping strategy that you are employing, it’s your go-to strategy when you have the stress and overload in college.”

Indeed, study drugs are most often used by high achieving high school students and among college student-athletes and those who participate in the Greek system. A 2009 review of the literature on study drugs found that anywhere between five and nine percent of middle and high school students, and five to 35 percent of college students use prescription drugs to stay awake and focus longer than they would normally.

What Study Drugs Do to the Brain

Drugs like Adderall and Ritalin are prescribed to kids with Attention Deficit Disorder (ADD) or Attention Deficit Hyperactivity Disorder (ADHD). These kids are easily distracted by visual or auditory background noises, which can overwhelm them and

make it hard to focus. People with ADD or ADHD don’t produce enough dopamine in the brain, which the drugs help correct.

“They are meant to increase dopamine in the brain, which regulates two things: executive functioning and the rewards system in the brain,” said Michelle Goldsmith, assistant clinical professor at Stanford. “Both of those things come into play when we talk about attention.”

For kids who actually need Adderall or Ritalin, the brain’s dopamine pathways aren’t strong enough to circulate the neural signals that make certain mental processes go. For those kids the added dopamine can have a huge influence on ability to focus, but also comes with some less desirable side effects when the drug wears off like fatigue, depression and mood-swings. There’s a lot less known about how the drug affects brains that start out with normal dopamine levels because clinicians consider it too risky to conduct a study that would subject “normal” students to the drug.

“The question is do they really help normal people with learning,” Goldsmith said, “There hasn’t been any reason to study them because the risks are so significant.” Those risks include depression, psychosis, mood swings, suicidal thoughts, seizures, decreased appetite and insomnia.

Read the full story at KQED. Denise Pope is a senior lecturer at the Stanford Graduate School of Education and co-founder of Challenge Success(link is external).

Source:   https://ed.stanford.edu/     http://blogs.kqed.org/mindshift/2015/02/teaching-kids-to-learn-without-study-dru. 24th February 2015

Cocaine addicted individuals may continue their habit despite unfavorable consequences like imprisonment or loss of relationships because their brain circuits responsible for predicting emotional loss are impaired, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published today in The Journal of Neuroscience.

The study focuses on the difference between a likely reward (or loss) related to a given behavior and a person’s ability to predict that outcome, a measurement known as Reward Prediction Error, or RPE. Such RPE signaling is believed to drive learning in humans, which guides future behavior. After learning from an experience, we can, in the best case, change our behavior without having to go through it again, and thus maximize rewards and avert expected losses. Past research has determined that prediction of actual reward or loss is managed by shifting levels of the nerve signaling chemical dopamine produced by nerve cells in the midbrain, where changes in dopamine levels accompany unexpected gains and losses.

The Mount Sinai study recorded the brain activity of 75 subjects (50 cocaine users and 25 healthy controls) using EEG, a test that detects electrical activity in the brain, while subjects played a gambling game. Each person had to predict whether or not they would win or lose money on each trial.

Results showed that the group of the 50 cocaine users had impaired loss prediction signaling, meaning they failed to trigger RPE signals in response to worse-than-expected outcomes compared to the 25 healthy people comprising the control group. The results offer insights into the compromised ability of addicted individuals to learn from unfavorable outcomes, potentially resulting in continued drug use and relapse, even after encountering numerous losses.

“We found that people who were addicted to cocaine have impaired loss prediction signaling in the brain,” said Muhammad Parvaz, PhD, Assistant Professor of Psychiatry at the Icahn School of Medicine at Mount Sinai and the lead author of the study. “This study shows that individuals with substance use disorder have difficulty computing the difference between expected versus unexpected outcomes, which is critical for learning and future decision making. This impairment might underlie disadvantageous decision making in these individuals.”

Next, the study looked at individual differences among the 50 cocaine users. Half of the subjects had used cocaine within 72 hours of the study and the other half had abstained for at least 72 hours. The cocaine addicted individuals with the more recent use had higher electrical activity associated with the brain’s reward circuit when they had an unpredicted compared to a predicted win, a pattern that was similar to the 25 healthy controls. The cocaine users who had abstained for at least 72 hours did not show this higher activity in response to an unpredicted win. These findings are consistent with the hypothesis that in addiction the drug is taken to normalize a certain brain function, which in this case is RPE signaling of better-than-expected outcomes.

“This is the first time a study has targeted the prediction of both gains and losses in drug addiction, showing that deficits in prediction error signaling in cocaine addicted individuals are modulated by recent cocaine use,” said principal investigator Rita Goldstein, PhD, Chief of Neuropsychoimaging of Addiction and Related Conditions, Chief of the Brain Imaging Center, and Professor of Psychiatry and Neuroscience at the Icahn School of Medicine. “Direction of results supports the self-medication hypothesis in drug addiction whereby drug self-administration improves response to reward in drug addicted individuals. The reductions in prediction of loss across all cocaine addicted individuals included in this study are also of great interest; they could become important markers that can be used to predict susceptibility for addiction or relapse or to develop targeted interventions to improve outcome in this devastating, chronically relapsing disorder.”

Source:  The Journal of Neuroscience.   3rd Feb 2015

The American Academy of Paediatrics published a policy statement in January about the impact of marijuana use on youth. The AAP is strongly opposed to legalizing marijuana due to the potential impact on child and adolescent health.

Marijuana use is common in the U.S. The Substance Abuse and Mental Health Services Administration estimates that more than 12 percent of those over age 12 years have used marijuana in the last year; the rate of use has been increasing since the 1990s. Statistics show that if this trend continues, marijuana use will overtake cigarette smoking for high school seniors.

The active ingredient in marijuana is a chemical called tetrahydrocannabinol. This chemical stimulates brain receptors and produces hallucinations, illusions, dizziness, altered perception, impaired thinking and sedation.    Currently, 23 states and the District of Columbia permit marijuana to be prescribed by a doctor for medical purposes. Two states, Colorado and Washington, allow its sale for recreational purposes and Alaska, Oregon and the District of Columbia voted in November to legalize marijuana.

There are many actual and potential risks from legalized marijuana. Legalizing marijuana portrays marijuana use as harmless and results in the commercialization and marketing of a proven harmful substance. Even with strictly enforced age restrictions, increased adolescent use would occur.

Commercialization will lead to the production of stronger marijuana products. The concentration of the active ingredient in marijuana has increased four times since the 1980s. The ingestion risk of edible marijuana products such as cookies and chocolates is 10 times higher when compared to smoking marijuana. Smoking effects are seen within seconds, but oral ingestion effects are much slower. This increases the risk of ingesting more of the chemical before feeling satisfied.

Accidental ingestion of marijuana-laced food products has led to young children being admitted to intensive care units for sedation and respiratory failure in the states that have legalized marijuana. Common negative effects in teens include decreased scholastic and sports participation and performance, a loss of interest in outside activities, a withdrawal from peer interactions, increased risk-taking behaviors, decreased driving skills, damaged lung function and increased interpersonal problems with family and friends

Marijuana is an addictive substance. It is estimated that 9 percent of all those who experiment with marijuana will become addicted to it. When this estimate is limited to teens, the addiction risk increases to 17 percent. The 2012 National Survey on Drug Use and Health reported that 2.7 million people in the U.S. over age 12 met the Diagnostic and Statistical Manual criteria for addiction to marijuana.

Addiction symptoms are often overlooked because withdrawal symptoms may be minor or absent. Studies have repeatedly shown that teens who use marijuana several times per week have difficulty quitting, and the younger a child is when marijuana use starts, the greater the deleterious effects and the higher the chance for addiction.

Marijuana legalization poses a monumental risk to children and teens. The history of alcohol misuse by teens proves the limited potential of regulations and penalties to limit access by teens. The answer is clear. Legalizing marijuana is a risk we should not take.

JOE BARBER, M.D., is a pediatrician and child neurologist at Children’s Community Care Pediatrics-Erie Pediatrics. He is division chief of the Department of Pediatrics at Saint Vincent Hospital and is active on social media (www.drjoebarber.com).

 Source: www.goerie.com   6th Feb 2014

Putnam County Circuit Court Judge Joeseph K. Reeder and Putnam County Adult Drug Court Probation Officer LaKeisha Barron-Brown applaud the accomplishment/graduation of Stacy Casto Wednesday at the Putnam County Judicial Building in Winfield. Casto was quoted by Judge Reeder as she was being introduced saying, “Judge, I’m gonna graduate and I want my picture in the paper with you.”

  

Putnam County Drug Court Graduates Lindsey Eddy and Stacy Casto sit relieved and all smiles at their accomplishemnt Wednesday at the Putnam County Judicail Building in Winfield. Bob Wojcieszak/Daily

 

With a picture of his mug shot on the screen before him, Putnam County Drug Court Graduate Craig Owens goes through the circumstances in his life that forced him to take a long look at where he was going and what made him seek out Putnam County Circuit Judge Joeseph K. Reeder to sign up for drug court and change. Having been arrested twenty one times in his past, Owens used the Putnam County Drug Court to change his life. Behind him is Judge Reeder. Bob Wojcieszak/Daily Mail

 

Having been involved with drugs since the age of twelve, twenty-year-old Putnam County Drug Court Graduate Lindsey Eddy looks at a composity picture of who she was when she was arrested and what she looks like clean and sober during Putnam County Drug Court Graduation ceremonies Wednesday at the Putnam County Judicial Building.

A drug addict of more than 30 years, Stacy Casto was facing felony drug charges when she was given a second chance in Putnam County’s new adult drug court program.

Putnam Circuit Court Judge Joseph K. Reeder met with the first class of offenders more than a year ago to explain how intensive drug court would be; constant drug testing, home visits, counselling and curfews.

“(Casto) was the first person who spoke up, and when she did, she said ‘Judge, I’m going to graduate and when I do I want my picture in the paper with you,’” Reeder said.

Casto, of Hometown, was among the first five graduates of Putnam County’s adult drug court program. Casto, Lori Hodges, Craig Owens, Lindsey Eddy and Jacob Pauley were honored during a graduation ceremony Wednesday at the Putnam County Courthouse in Winfield.

Family and friends packed a courtroom as Reeder spoke about each graduate’s transformation. Many admitted they believed they would have been dead today if it weren’t for drug court.

Lindsey Eddy, 21, of Hurricane, starting using heroin when she was 12 years old. She had been through the juvenile court system and was most recently arrested for violating her probation order from felony drug charges she received when she was 18 years old.

As of Wednesday, Eddy had been drug-free for 221 days.

“Before, my life was hectic,” Eddy said. “I was always worried about my next high or what I was going to do for my next high. I never really imagined life without drugs. I tried rehabs and regular probation and I failed at that, and until I was entered into the drug court problem, this was the only thing that’s worked for me and it’s helped me out tremendously. I’m responsible now and I have a full time job, and I’ve been sober.”

Putnam adult drug court probation officer Lakeside Barron-Brown said Putnam’s program began in November 2013. She said candidates for the program have had drug-related charges or convictions, and must be willing to work toward a drug-free life.

“Once accepted into our program, they then come into a very intensive, therapeutic setting within our court system,” Barron-Brown said. “They are placed on home confinement, and the judge determines when they should be released.”

Offenders go through three phases, each lasting at least four months. During the first phase, they’re subjected to multiple drug tests and home visits a week. They attend group and individual counselling, put in community service hours and abide by a curfew.

During the second phase, drug court offenders receive help looking for and obtaining a job. In the third phase, Barron-Brown said offenders are given “a little more room” to become stabilized for society.

Barron-Brown said all five graduates had obtained jobs during the program and are still working those jobs to this day.

“We have five graduates here that when they first started, they were apprehensive about not knowing what to expect — the same as when you go into a college class and the professor says ‘Here’s a syllabus, you have a test’ and not knowing what the test is like until you’ve taken the test,” Barron-Brown said. “I think that’s what drug court has been for our clients. It’s a test of seeing how confident they can become and seeing how much self-esteem and self-worth they can gain. Obviously, all of them have shown they can be successful and they can be drug-free.”

West Virginia Supreme Court of Appeals Justice Brent D. Benjamin congratulated the five men and women for turning their lives around. He pointed out that West Virginia’s adult drug court system is celebrating its 10th anniversary this year, and that 1,000 adults and juveniles have successfully completed drug court programs in West Virginia.

“What you’ve done is something a lot of people can’t do or haven’t done,” Benjamin told the graduates during the ceremony. “Thankfully we have a state in which you have an opportunity to do this.

“You’re in control of your lives now, and you weren’t before. And now you have the opportunity that not many people have; to turn around to the next drug court class and help them,” Benjamin said.

Reeder said offenders can get into the drug court by either entering a hybrid or conditional plea that allows for their charges to be lessened or dropped upon successful completion of the program, or by accepting drug court as a sentence in lieu of prison time. He said drug court is a good alternative to prison, but it takes a lot of work and responsibility for those who go through the program.

“I think it’s very important not just for the graduates involved, but it’s also important for Putnam County and our community because drugs have become such a problem in our society,” Reeder said. “It’s good that a program like this does give these folks a chance to rehabilitate and to get back on track.”

Casto said drug court “completely saved my life” because it gave her the ability to get help to fight her addiction ­— something she says prison time wouldn’t have done. Now that she’s sober, Casto said she would like to help juveniles who are battling addiction problems.

“I knew I had to have something in my life in order to change my life,” Casto said. “They offered counseling, they offered classes on drug prevention, they offered all these different things that I knew prison wouldn’t do for me. I’ve been a drug addict for 30 years, but during this time, I’ve started going to church, I’ve given my heart to the Lord and my whole entire life has changed.

Barron-Brown said the graduates will go through six more months of “supervised release” from the drug court program until they are completely finished with the program. She said there are 19 people in Putnam’s adult drug court program, including the graduates.

There are 24 adult drug court programs in West Virginia serving 40 counties, and 16 juvenile drug court programs serving 20 counties with 581 people actively participating in the programs, the Daily Mail reported earlier this month. As part of the Justice Reinvestment Act, which was passed last year, adult drug courts will be in all of West Virginia’s counties by July 1 of next year.

Contact writer Marcus Constantino at 304-348-1796 or marcus.c@dailymailwv.com. Follow him at www.twitter.com/amtino.

Source: http://www.charlestondailymail.com/article/20150226/DM01/150229485/1276#sthash.TzJh3TEA.dpuf 26th Feb. 2015

This article originally appeared on VICE Romania

Ana Iorga is a Romanian neuromarketing pioneer, who specialises in market research using EEG sensorsbiometric measures and implicit-association testsAttending an advertising conference in Amsterdam last month, Ana staged an impromptu experiment to measure the effect that weed has on the brain using the EEG helmet she tends to carry around in her bag.

“I noticed how quite a few of the attendees grabbed a joint between breaks, and I kept wondering what goes on in their brains during those moments. Because I don’t possess any mind-reading techniques, I thought about comparing their brain activity before and after smoking,” she told me when she got back.

Two of her colleagues were kind enough to sacrifice themselves to the shrine of science; One evening, after dinner, one of them lit a spliff and the other got to munching on a space cookie.

 


The first participant – EEG trajectory before smoking

“Before consuming the products, we went to the hotel bar and I recorded their brain activity. After 15 minutes, I repeated the measures. I was convinced that I’d see a decrease in brain activity, because they said they felt slower, more absent and more relaxed. I was very surprised by the result.”

 


The first participant – EEG trajectory after smoking

Your brain contains billions of cells called neurons, which communicate with each other through electricity. The simultaneous communication between billions of neurons produces a large quantity of electric brain activity, which can be detected and measured through EEG technology. Because these electric impulses are triggered periodically as waves, they’re called “brain waves”.

EEG sensors measure the activity of neurons located on the surface of the cerebral cortex, and in the case of the two subjects, they showed a very high frequency and amplitude after smoking – the cerebral rhythm being visibly changed compared to the initial situation. This translates into a brain activity contrasting heavily with the participants’ mood (in stand-by mode and relaxed mode).

 


The second participant – EEG trajectory before eating the space cookie

Often, studies claim that THC has the effect of slowing down the cerebral rhythm when it is associated with a state of relaxation, and of speeding up when it is associated with visual hallucinations or tripping. With Ana’s two subjects, “it was clear that the cerebral rhythm was faster after smoking and that wave amplitude was larger – which doesn’t mean that things function chaotically, but that the brain is in a higher alert state. Maybe the guy was tripping or had some sort of bizarre feelings,” explains Laura Crăciun – a neurologist.

Crăciun emphasises that in the case of the first subject there is an imbalance standing out between the left hemisphere’s cerebral electricity [which deals with logic, language and math processes] and the right [where creativity, intuition, art and music processes take place] and along the sequence from the wave recording taken before smoking. That means that the imbalance is not exclusively determined by cannabis smoking.

Both subjects had consumed moderate quantities of alcohol at dinner, which didn’t interfere with the process very much. During the experiment, the two weren’t asked to perform any tasks, as their brain activity was measured in stand-by and relaxation mode.

 


The second participant – EEG trajectory after eating the space cookie.

“With the subject who ate a space cookie, the effect was both a slowing down [the basic wave frequency rhythm of both hemispheres went down] and speeding up of the amplitude, which is associated with a state of sleep-like, profound relaxation.”

“On the first recording, the cerebral rhythm is visibly faster – in the right hemisphere, because I can’t see a big difference in the left one – as well as less symmetrical and steady, but I wouldn’t say the effect is a “disturbance” over the brain waves, but more likely a state of awareness,” Crăciun added.

Source: http://www.vice.com/en_uk/ 15th Feb 2015

Teens can’t control impulses and make rapid, smart decisions like adults can — but why?

Research into how the human brain develops helps explain. In a teenager, the frontal lobe of the brain, which controls decision-making, is built but not fully insulated — so signals move slowly.  “Teenagers are not as readily able to access their frontal lobe to say, ‘Oh, I better not do this,’ ” Dr. Frances Jensen tells Fresh Air’s Terry Gross.

Jensen, who’s a neuroscientist and was a single mother of two boys who are now in their 20s, wrote The Teenage Brain to explore the science of how the brain grows — and why teenagers can be especially impulsive, moody and not very good at responsible decision-making. “We have a natural insulation … called myelin,” she says. “It’s a fat, and it takes time. Cells have to build myelin, and they grow it around the outside of these tracks, and that takes years.”  This insulation process starts in the back of the brain and heads toward the front. Brains aren’t fully mature until people are in their early 20s, possibly late 20s and maybe even beyond, Jensen says.

“The last place to be connected — to be fully myelinated — is the front of your brain,” Jensen says. “And what’s in the front? Your prefrontal cortex and your frontal cortex. These are areas where we have insight, empathy, these executive functions such as impulse control, risk-taking behavior.”   This research also explains why teenagers can be especially susceptible to addictions — including drugs, alcohol, smoking and digital devices.

Interview Highlights

On why teenagers are more prone to addiction

Addiction is actually a form of learning. … What happens in addiction is there’s also repeated exposure, except it’s to a substance and it’s not in the part of the brain we use for learning — it’s in the reward-seeking area of your brain. … It’s happening in the same way that learning stimulates and enhances a synapse. Substances do the same thing. They build a reward circuit around that substance to a much stronger, harder, longer addiction.

Just like learning a fact is more efficient, sadly, addiction is more efficient in the adolescent brain. That is an important fact for an adolescent to know about themselves — that they can get addicted faster.

It also is a way to debunk the myth, by the way, that, “Oh, teens are resilient, they’ll be fine. He can just go off and drink or do this or that. They’ll bounce back.” Actually, it’s quite the contrary. The effects of substances are more permanent on the teen brain. They have more deleterious effects and can be more toxic to the teen than the adult.

On the effects of binge drinking and marijuana on the teenage brain

Binge drinking can actually kill brain cells in the adolescent brain where it does not to the same extent in the adult brain. So for the same amount of alcohol, you can actually have brain damage — permanent brain damage — in an adolescent for the same blood alcohol level that may cause bad sedation in the adult, but not actual brain damage. …

Because they have more plasticity, more substrate, a lot of these drugs of abuse are going to lock onto more targets in [adolescents’] brains than in an adult, for instance.

We have natural cannabinoids, they’re called, in the brain. We have kind of a natural substance that actually locks onto receptors on brain cells. It has, for the most part, a more dampening sedative effect. So when you actually ingest or smoke or get cannabis into your bloodstream, it does get into the brain and it goes to these same targets.

It turns out that these targets actually block the process of learning and memory so that you have an impairment of being able to lay down new memories. What’s interesting is not only does the teen brain have more space for the cannabis to actually land, if you will, it actually stays there longer. It locks on longer than in the adult brain. … For instance, if they were to get high over a weekend, the effects may be still there on Thursday and Friday later that week. An adult wouldn’t have that same long-term effect.

On marijuana’s effect on IQ

People who are chronic marijuana users between 13 and 17, people who [use daily or frequently] for a period of time, like a year plus, have shown to have decreased verbal IQ, and their functional MRIs look different when they’re imaged during a task. There’s been a permanent change in their brains as a result of this that they may not ever be able to recover.

It is a fascinating fact that I uncovered going through the literature around adolescence is our IQs are still malleable into the teen years. I know that I remember thinking and being brought up with, “Well, you have that IQ test that was done in grade school with some standardized process, and that’s your number, you’ve got it for life — whatever that number is, that’s who you are.”

It turns out that’s not true at all. During the teen years, approximately a third of the people stayed the same, a third actually increased their IQ, and a third decreased their IQ. We don’t know a lot about exactly what makes your IQ go up and down — the study is still ongoing — but we do know some things that make your IQ go down, and that is chronic pot-smoking.

On teenagers’ access to constant stimuli

We, as humans, are very novelty-seeking. We are built to seek novelty and want to acquire new stimuli. So, when you think about it, our social media is just a wealth of new stimuli that you can access at all times. The problem with the adolescent is that they may not have the insider judgment, because their frontal lobes aren’t completely online yet, to know when to stop. To know when to say, “This is not a safe piece of information for me to look at. If I go and look at this atrocious violent video, it may stick with me for the rest of my life — this image — and this may not be a good thing to be carrying with me.” They are unaware of when to gate themselves.

On not allowing teenagers to have their cellphones at night

It may or may not be enforceable. I think the point is that when they’re trying to go to sleep — to have this incredibly alluring opportunity to network socially or be stimulated by a computer or a cellphone really disrupts sleep patterns. Again, it’s also not great to have multiple channels of stimulation while you’re trying to memorize for a test the next day, for instance.

So I think I would restate that and say, especially when they’re trying to go to sleep, to really try to suggest that they don’t go under the sheets and have their cellphone on and be tweeting people.  First of all, the artificial light can affect your brain; it decreases some chemicals in your brain that help promote sleep, such as melatonin, so we know that artificial light is not good for the brain. That’s why I think there have been studies that show that reading books with a regular warm light doesn’t disrupt sleep to the extent that using a Kindle does.

Source:   http://www.mprnews.org/story/2015/01/28/npr-teen-brains

A case report of the synthetic amphetamine 2,5-dimethoxy-4-chloroamphetamine. Burish MJ1, Thoren KL2, Madou M1, Toossi S1, Shah M1.

Abstract

Although traditional hallucinogenic drugs such as marijuana and lysergic acid diethylamide (LSD) are not typically associated with seizures, newer synthetic hallucinogenic drugs can provoke seizures. Here, we report the unexpected consequences of taking a street-bought hallucinogenic drug thought to be LSD. Our patient presented with hallucinations and agitation progressing to status epilepticus with a urine toxicology screen positive only for cannabinoids and opioids. Using liquid chromatography high-resolution mass spectrometry, an additional drug was found: an amphetamine-derived phenylethylamine called 2,5-dimethoxy-4-chloroamphetamine. We bring this to the attention of the neurologic community as there are a growing number of hallucinogenic street drugs that are negative on standard urine toxicology and cause effects that are unexpected for both the patient and the neurologist, including seizures.

Source:  Neurohospitalist. 2015 Jan;5(1):32-4. doi: 10.1177/1941874414528939.

van Amsterdam J1, Brunt T2, van den Brink W3. Author information

* 1Amsterdam Institute for Addiction Research, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands jan.van.amsterdam@amc.uva.nl.

* 2Trimbos Institute (Netherlands Institute of Mental Health and Addiction), Utrecht, The Netherlands.

* 3Amsterdam Institute for Addiction Research, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Abstract

Cannabis use is associated with an increased risk of psychosis in vulnerable individuals. Cannabis containing high levels of the partial cannabinoid receptor subtype 1 (CB1) agonist tetrahydrocannabinol (THC) is associated with the induction of psychosis in susceptible subjects and with the development of schizophrenia, whereas the use of cannabis variants with relatively high levels of cannabidiol (CBD) is associated with fewer psychotic experiences. Synthetic cannabinoid receptor agonists (SCRAs) are full agonists and often more potent than THC. Moreover, in contrast to natural cannabis, SCRAs preparations contain no CBD so that these drugs may have a higher psychosis-inducing potential than cannabis. This paper reviews the general toxicity profile and the adverse effects of SCRAs with special emphasis on their psychosis-inducing risk.

The review shows that, compared with the use of natural cannabis, the use of SCRAs may cause more frequent and more severe unwanted negative effects, especially in younger, inexperienced users. Psychosis and psychosis-like conditions seem to occur relatively often following the use of SCRAs, presumably due to their high potency and the absence of CBD in the preparations. Studies on the relative risk of SCRAs compared with natural cannabis to induce or evoke psychosis are urgently needed.

Source:  J Psychopharmacol. 2015 Jan 13. pii: 0269881114565142. [Epub ahead of print]

In the 1980s and 90s two successive waves of heroin use swept Britain resulting in massively escalating levels of addiction, deaths, crime, and HIV. At the same time the use of other drugs, cannabis, cocaine, etc was also increasing. There was a widespread sense of crisis with the fear that control of our cities would be lost to drug gangs, drug related crime would continue to grow exponentially, and injecting drug use would become a major route for the transmission of HIV across the population. The drug treatment system was under resourced with lengthy waiting times and high levels of drop out. In 1992 the Major government launched the first national drug strategy “Tackling Drugs Together” to grip these problems.

Fast forward to 2014. Drug use is falling, down from 12% in 2004 to 9% now. The use of heroin peaked at the end of the 1990s at 450,000, it is now 260,000. Young people are shunning heroin with typical users now in their 40s rather than the vulnerable teenagers of popular imagination. Drug related crime has fallen dramatically with investment in treatment initiated during the Blair government enabling offenders and other users to access treatment in days rather than months. The quality of treatment has improved with lower drop out and improved outcomes. The Home Office estimate 30% of the reduction in crime since 2000 is attributable to ready access to treatment which currently prevents 4.9m crimes a year. Levels of HIV among drug injectors is among the lowest in the world, 2% compared to 20% in the USA and 70% in parts of Russia, a legacy of the harm reduction policies pioneered by Norman Fowler as health secretary in the Thatcher government.

None of this featured in last weeks critique in the Huffington Post of the failures of current policy from Caroline Lucas and Julian Huppert, or in their speeches in last Thursdays parliamentary debate. Instead we had a tired unevidenced assertion that policy is a failure, in Nick Clegg’s dramatic language, “on an industrial scale”. Why are outcomes that would have been a cause of celebration in 1992 consistently derided as failure?

The major difference between 1992 and today is that the crisis has abated. There is no longer a plausible argument that drug misuse is spiralling out of control with potentially disastrous consequences for social stability. The absence of crisis frees up ideologues of right and left to posture either about the “failed war on drugs” on the left or the “calamitous consequences of 1960s hedonism” on the right.

The value of the drug debate as a badge of moral and political affiliation is too potent to allow inconvenient truths to intrude. The reality of less use and less harm has to be airbrushed out of the debate if the power of the opposing polemics is to be sustained.

The commentariat’s  self indulgence is buttressed by a political/media culture in which no government policy is allowed to succeed. Ministers are wary of claiming success, fearing charges of complacency today, and ridicule tomorrow if events turn for the worse. Perhaps surprisingly, success is more likely to be buried in Whitehall than failure. Civil servants, policy advocates, and service providers have learned to sidestep inconvenient good news to sustain an ever evolving narrative of failure which is the best route to maintain the high media and political salience on which future funding, policy influence and employment depend.

To highlight the hidden successes of current drug policy is not to deny the continuing challenges and deficits. In England drug related deaths rose alarmingly last year after falling significantly since 2008. The immediate and long term health risks of “legal highs” present an unknown threat. The lack of integration between drug and mental health services is a continuing scandal. Locking people up to protect them from themselves is difficult to justify. But the reality of our drug problem today is that fewer people are using drugs, fewer are becoming addicted, and the social and economic costs of drug use are shrinking.

Any evidence based change to policy needs to acknowledge its successes as well as its deficits. It isn’t enough to dust off arguments from the sixth form debating society as MPs did in the commons this week. The calls for a radical change in policy do not sit well with a significantly shrinking problem. Proponents of change need to explain, not only how reform will prevent imprisonment of users, a laudable aim, but also how they would prevent increases in use and harm arising as a consequence. To steer a sensible pragmatic evidence based route through these policy challenges requires all the evidence to be on the table, including the surprisingly good news that some people would prefer to see ignored.

Source:   http://www.huffingtonpost.co.uk/paul-hayes/drug-policy-uk-untold-success-story  4th Nov 2014

Albert Stuart Reece

Medical School, University of Queensland, Highgate Hill, Brisbane, QLD, Australia

 Introduction 

Cannabis is the most widely used illicit drug worldwide. As societies reconsider the legal status of cannabis, policy makers and clinicians require sound knowledge of the acute and chronic effects of cannabis. This review focuses on the latter.

Methods

Asystematic review of Medline, PubMed, PsychInfo, and Google Scholar using the search terms “cannabis,” “marijuana,” “marihuana,” “toxicity,” “complications,” and “mechanisms” identified 5,198 papers. This list was screened by hand, and papers describing mechanisms and those published in more recent years were chosen preferentially for inclusion in this review. Findings. There is evidence of psychiatric, respiratory, cardiovascular, and bone toxicity associated with chronic cannabis use. Cannabis has now been implicated in the etiology of many major long-term psychiatric conditions including depression, anxiety, psychosis, bipolar disorder, and an amotivational state.

Respiratory conditions linked with cannabis include reduced lung density, lung cysts, and chronic bronchitis.

Cannabis has been linked in a dose-dependent manner with elevated rates of myocardial infarction and cardiac arrythmias. It is known to affect bone metabolism and also has teratogenic effects on the developing brain following perinatal exposure. Cannabis has been linked to cancers at eight sites, including children after in utero maternal exposure, and multiple molecular pathways to oncogenesis exist. Conclusion. Chronic cannabis use is associated with psychiatric, respiratory, cardiovascular, and bone effects. It also has oncogenic, teratogenic, and mutagenic effects all of which depend upon dose and duration of use.

Introduction

According to the United Nations Office of Drugs and Crime, there are some 165 million users of cannabis worldwide, making it the most widely used illicit drug.1 This review examines the psychiatric, respiratory, cardiovascular, and bone effects associated with chronic cannabis use and the neurodevelopmental, genotoxic, mutagenic, and oncogenic effects of cannabis.

Methodology

A systematic review of Medline, PubMed, PsychInfo, Google, Scholar, Scopus, Proquest, Web of Knowledge, and Ebsco- Host using the search terms “cannabis,” “marijuana,” or “marihuana” identified 14,065 papers, excluding duplicates. When the search terms “toxicity,” “complications,” and “mechanisms” were added, the list narrowed to 5,198 papers.

This list was screened by hand, and original papers describing mechanisms and those published in more recent years were chosen preferentially. Review papers are cited where appropriate to introduce a large or detailed field for the interested reader. Few case reports are included and they are specifically flagged where they occur; those that are cited have been included largely because they suggest important pathophysiological mechanisms.

Psychiatric and social disorders

An authoritative meta-analysis of cannabis-related psychopathology has been published,2 with an accompanying editorial.3  Another review found an elevated risk of psychosis in many studies, with an odds ratio (OR) of about 2.3.4 A similar meta-analysis from the Netherlands found a pooled OR for psychosis of 2.1.5 Several studies from diverse cultures have confirmed the elevated risk of psychosis and schizophreniform spectrum disorders5–17 following high levels of cannabis use, particularly when cannabis consumption has commenced at a young age.14,18 Cannabis use has been found to exacerbate pre-existing psychotic disorders.5,15 There is a similar and increasing literature around both bipolar disorder19–21 and depression.22–25 Although the psychoneurological  effects of cannabis are usually stereotypically characterized as a depressant, both its use and the withdrawal state are accompanied frequently by psychomotor agitation, which has been implicated causally with interpersonal violence.26 Interestingly, in a series of forensic examinations of suicide, cannabis use was associated with the most  violent means of death, particularly severe motor vehicle accidents.27

In 1972 Nahas28 drew attention to the devastating effects of cannabis in Egypt as quantified by carefully prepared and formally psychologically documented surveys from that country. Higher levels of anxiety, impaired memory, poor concentration, impaired learning ability, and psychomotor impairment including reduced quality and quantity of work were seen in these users. In addition, a common dependency syndrome was observed, which made exit from the dependent state both difficult and rare.28 Geographical microclustering of cannabis use has been demonstrated, which has the effect of establishing local socially normative use patterns.29 Both  in northern Africa and in New Zealand communities exist where cannabis use is common, and intellectual impairment, psychomotor slowing, poor work capacity, and severe social deprivation are entrenched.30–32 Lee and colleagues33,34 have published several descriptions of heavy, problematic, and refractory cannabis use in remote indigenous communities of the Northern Territory and across northern Australia more generally. A substantial proportion (31–62%) of users’ median weekly income and up to 10% of the total community income were spent on cannabis. Ninety percent smoked cannabis heavily (more than six cones daily) and were not able to cease use. Severe mental illness was commonplace, as were depression, suicidal ideation, auditory hallucinations, and imprisonment. There was less participationin employment, education, or training. Community violence escalated when cannabis supplies from distant centers were interrupted. Most users had not “matured out” of dependent cannabis use even 5 years later. It is particularly noteworthy that these same communities had largely successfully defeated alcohol abuse, primarily by tight restrictive policies aimed at severely curtailing alcohol supply. The authors concluded that cannabis was both an important cause and a consequence of ongoing severe social disadvantage and deprivation.

Respiratory effects

Both the Thoracic Society of Australia and New Zealand35 and the British Lung Foundation4 have issued major statements in recent years acknowledging the known deleterious effects of cannabis on the lungs. Cannabis is smoked differently from tobacco. Users commonly inhale deeply to a  maximal breath and then retain the smoke in the lungs, which generates higher pressures during breath holding and on expiration.35–37 Cannabis smoke stimulates inflammation in the airways so that its long-term use is associated with the development of chronic bronchitis. A New Zealand study38 demonstrated large airway inflammation and obstruction and hyperinflation but was seldom associated with macroscopic emphysema, with a dose equivalence of one cannabis joint to 2.5–5 cigarettes. These findings were supported by an accompanying editorial39 and press release.40 Decreased lung density has also been noted with increased lung volumes, signs of destruction of lung tissue, cyst formation, and emphysematous change with secondary pneumothorax because of bullous rupture.41–43 Cannabis smoke is known to contain several potent carcinogens including anthrocyclines, nitrosamines, polycyclic aromatic hydrocarbons, terpenes, and vinyl chloride.4,35,44–47 As a consequence, cannabis use is associated with cancer of the lung.30–32

Cardiovascular effects

Cannabis exposure is known to cause phasic systemic vasodilation, mild hypertension, and tachycardia often associated with postural hypotension, and a reduced duration and increased heart rate response to exercise.48–51 Some but notall these effects are mediated by the autonomic nervous system. Tolerance to many of these acute effects with time appears. In most young healthy patients such changes are clearly generally well tolerated,48,50 but this is not universally true and several exceptions cited below are of considerable pathophysiological interest. Such generic reassurances cannot be provided to patients with pre-existing coronary or atherosclerotic disease.50,52 Several case reports associate cannabis use with infarctions of kidney,53 brain,54–60 heart61–65, and digits,66,67 and of priapism in humans with sickle cell disease.68 An association between cannabis use and pedal gangrene has also been described in a 27-year old.67 Some 50 cases of cannabis arteritis have been reported in the literature.67 Cannabis use can acutely trigger myocardial infarction,69 which has also been documented in a 25-year-old man with no other cardiac risk factors and normal coronary arteries at angiography.62 Coronary no-flow phenomenon has been observed after acute cannabis use.57 Cardiomyopathy has also been reported in a young man.70 One large study of 1,913 adults conducted in the United States found both a significant association between myocardial infarction and cannabis use, and a dose– response effect, with adjusted hazard ratios of 2.5 and 4.2 for less than weekly and weekly use, respectively.52 Reversible cerebral vasospasm71 as well as slowing and flow reversal in the middle cerebral artery72 has also been documented and attributed to cannabis use. On the contrary, the same authors also reported an increase of blood flow in the cerebral frontal lobes.73 Several case reports have described a cannabis-associated inflammatory angiitis,61,74,75 which can be so severe as to mimic Buerger’s disease (thromboangiitis obliterans or “disappearing artery syndrome”). In a study in 19 patients, alterations of the cardiac pressure cycle were found with a highly significant prolongation of both electromechanical systole (by 17 ms) and left ventricular ejection time, in the context of a reduced pre-ejection period (systolic pressure upstroke), a tachycardia of 132 bpm, and unchanged brachial systemic pressures.76 These more abrupt cardiac pressure changes imply increased cardiac work in the context of a prolonged QTc interval and reduced opportunity for myocardial perfusion (the “Buckberg index”), which is limited to the diastolic phase of the cardiac cycle.77,78 Hence, this scenario combines both an adverse mechanical and electrical profile in the context of reduced coronary perfusion and an altered endothelial, coagulation, angiogenic,79 and inflammatory milieu.

Cannabis has also been linked with elevated rates of cardiac arrhythmias in several case reports.80  Generally, these are supraventricular and trivial,81–83 but well-documented cases of lethal ventricular arrythmias do exist57 and one such was recently reported from a man who survived and whose episode was recorded on his implantable defibrillator.84 Elevated plasma concentrations of the endocannabinoid 2-arachidonylglycerol status have been associated in an Italian study of 62 patients with an exacerbation of the cardiovascularrisk profile with worse concentrations of total  cholesterol, high-density lipoprotein cholesterol, body mass index, intra-abdominal obesity, and adiponectin.85

Bones

Cannabinoid receptors are present on bones. Physiological studies have shown that cannabinoids have an important role in the regulation of bone density86; blockade or modulation of CB1 cannabinoid activity protects from bone loss.87 Heavy cannabis use in humans is associated with substantial bone loss.54 Interestingly, CB2 stimulation appears to be causally associated with stimulation of both endosteal and periostealbone growth by mechanisms involving inhibition of osteoclastogenesis, osteoblast stimulation, and favorable modulation of the RANKL (receptor activated NF-kB ligand) – osteoprotegerin system, matrix metalloproteinase inhibition, inhibition of adrenergic sympathetic signaling to bone, and inhibition of  bone marrow monocyte-directed hemopoiesis88–99 (the bone marrow-derived monocyte is believed to be the immediate precursor of the multinucleate osteoclast). Cannabis use is also known to be associated with profound loss of alveolar bone from the jaws,100–103 often in the context of severe erosive periodontitis.104,105

Maternal cannabis use and fetal development Not all the studies in this field have returned results confirming a link between maternal cannabis use and later deleterious changes in the offspring.106 However, maternal cannabis use has been shown to reduce body weight at birth.107 Many birth abnormalities were identified in a large Hawaiian sample over 6 years. Of 54 birth defects studies, 39% were noted in cannabis-exposed babies.108 Many of these defects were major and involved the brain (encephalocoele, hydrocephaly, microcephaly, anophthalmia/microphthalmia), cardiovasculature (tetralogy of Fallot, ventricular septal defect, atrial septal defect, and right and left heart atretic syndromes), gastrointestinal system (pyloric stenosis, intestinal atresias and stenoses, and gastroschisis), and limbs (polydatyly, syndactyly, and reduction deformities of the upper and lower limbs); oro-facial clefts were also reported. One large American study found a somewhat elevated risk of anencephaly (OR =1.7, CI = 0.9–3.4).109 The association with gastroschisis has been confirmed by other investigators.110

The dominant theme to emerge from studies of perinatal exposure is that of impaired executive cortical functioning reflected in reduced attention and analytical behavior and visuospatial analysis and hypothesis testing;111 parent-rated behavioral problems, language comprehension, and distractibility112; and inattention, hyperactivity, impulsivity, and substance use disorders.113 Indeed, close agreement between human and animal studies of perinatal exposure has been shown.113 Such changes emerge from as early as the first weeks of life and persist in children in longitudinal studies into the school ages. Importantly, cannabis seemed to potentiate other causes of disadvantage such as smoking, low protein nutrition, and early age of first maternal pregnancy,and child sexual abuse implying that cannabis use by disadvantaged groups compounds other functional deficits.112,114 Lower school age child IQ was also noted in another large longitudinal follow-up study.115 It is important to note, however,  that such reductions in intellectual performance, executive function, memory, sustained attention, and verbal ability are also seen in samples of low-risk upper middle class children of school age.116 Equally, it is important to note that careful studies controlling for such pertinent confounding psychosocial variables find strong persistent effects of cannabis exposure.117 Maternal prenatal cannabis use has been found to predict later cannabis use during adolescence both as age of onset and frequency of use, a relationship that persisted after adjustment for many other risk factors.118

Genotoxicity, mutagenicity, and oncogenesis

Cannabis use is associated with cancer of the lung30–32 (OR = 2.3, 4.1, and 5.7), head and neck44,119 (OR = 4.1, 2.6, and 3.1), larynx (OR = 1.7 and 2.3), prostate (OR = 3.1)120, cervix (OR = 1.4),120 testes (OR = 1.7),121 and brain (OR = 2.8).122 Cannabis has also been linked with tumors of the urothelial tracts.123–125 Several authors have also found evidence of a dose–response relationship, either with dose, duration, or the combined lifetime total duration of cannabis consumption. 31,32,44,121 A report from Tunisia showed an eightfold rise in lung cancer risk, but initially did not demonstrate a dose– response relationship; tobacco is frequently mixed with cannabis in that country.30 A later expanded revision of these data from the same area in northern Africa was able to demonstrate a relationship with the total dose duration of cannabis exposure.121 Of great concern is the evidence of inheritable tumors such as childhood neuroblastoma (OR = 1.8, 4.7),126 rhabdomyosarcoma,45 and leukemia (OR = 11), particularly non-lymphoblastic leukemia,127 in cannabis-exposed pregnant mothers. It should be noted that not all epidemiological studies have been positive,128 with some studies failing to demonstrate such a link, possibly because cannabis exposure in the study population was limited.45 For example, a study conducted in Los Angeles did not observe an association with lung cancer, which the authors attributed to the relatively few cases exposed to significant amounts of cannabis.129 Similarly, a New Zealand study of head and neck cancer was recently found to be negative, a finding attributed by the authors to uncontrolled confounding and inadequate sampling of the New Zealand population.128 Cannabinoids liberate radical species both by receptor binding (nitrogen-centered species130–132 ) and by uncoupling mitochondrial oxidative phosphorylation via stimulation of the matrix protein uncoupling protein 2.133,134 Nitric oxide generation at the cell membrane occurs via both CB1130 and non-CB1/2 receptor-mediated131 mechanisms. Indeed, it has been shown that oxidation135 of the DNA base guanosine to oxo-guanosine is a normal part of endocannabinoid signaling. This potentially very serious and inherently mutagenic defect is overcome during normal signaling by activation of the base excision DNA repair pathway within cells. The capacity of such DNA repair pathways is well known to be limited, so the possibility exists that with pathological overstimulation, as might occur during substantial cannabis use, the resulting major genetic defects would become fixed and eventually translated into altered mRNAs, micro-RNAs,genetic expression, and protein sequences. Cannabis is known to stimulate the oncogenic MAP kinase pathway,136 which is potently oncogenic, and to be involved particularly in the genesis of non-lymphocytic leukemias.137 A strongly positive association between cannabis consumption and this tumor has been found.127 Cannabinoids block topoisomerase II, an enzyme that untwists and makes accessible the dominant coding DNA strand and plays a vital role in DNA repair, meiotic chromosomal replication, mRNA transcription, and DNA hypermutation in prelymphocytes.138,139

Cannabinoids also impair RAD-51, another enzyme involved in the accurate repair of DNA breaks. Mice chromosomal studies imply that cannabinoids also interfere with the normal maintenance of the ends of chromosomes.140 Chromosomal ends or telomeres are made up of many copies of a 6-nt repeat structure (T–T–A–G–G–G) and are protected by a complex of proteins collectively called “shelterin.”141,142 Telomeres are maintained by an enzyme called telomerase, which is absent from most cells but is present in stem cells, gonads (testes and ovaries), and cancers. 143,144 The length of the telomeres has been shown recently to be proportional to the age, the health, and the reproductive fitness of stem cells in a variety of in vivo tissue niches.145 It is of concern that the chromosomal damage was shown in mice not only for tetrahydrocannabinol but also for cannabidiol (and cannabinol),140 a non-psychoactive cannabinoid that has been added to commercial cannabis sprays supposedly to confer safety!146

The involvement of cannabinoids with at least three enzymes involved in DNA repair raises questions about their potential genetic toxicity, a subject that remains largely uninvestigated. Gonadal stem cell and genetic toxicity have implications for cell growth inhibition, fetal malformations, and inheritable defects including cancers. Indeed, evidence of cannabis-induced altered DNA expression,147 a higher incidence of 21 birth defects,107 and an 11-fold rise in inherited leukemias in the offspring of cannabis users127 have been documented. Other studies have produced similar findings,148 including tissues of the germ line.149 The presence of such major chromosomal abnormalities in sperm cells but not in circulating white blood cells149 is consistent with the inhibition by cannabinoids of telomerase, which is well known to be present in stem cells, germ cells, and cancer cells but not in the nuclei of normal tissue.150–152

Conclusions

In summary, now there is evidence for the implication of cannabis in various psychiatric, respiratory, cardiovascular, and bone pathologies.153,154 The reports of social disruption, disorganization, and deprivation consequent on widespread heavy cannabis use from a number of communities around the world are of substantial concern. The features associated with chronic cannabis use imply that a clear public health cautionary message is warranted along the lines employed for other environmental intoxicants such as tobacco, which should be targeted strategically to young and otherwise vulnerable populations.

Declaration of interest: There is no conflict of interest to declare.

This article may be used for research, teaching and private study purposes. Any substantial or systematic reproduction, re-distribution, re-selling, loan or sub-licensing, systematic supply or distribution in any form to anyone is expressly forbidden.

Source:  Reece, Albert Stuart(2009)’Chronic toxicology of cannabis’,Clinical Toxicology,47:6,517 — 524

To link to this Article: DOI: 10.1080/15563650903074507

URL: http://dx.doi.org/10.1080/15563650903074507

Background 

Debate continues about the consequences of adolescent cannabis use. Existing data are limited in statistical power to examine rarer outcomes and less common, heavier patterns of cannabis use than those already investigated; furthermore, evidence has a piecemeal approach to reporting of young adult sequelae. We aimed to provide a broad picture of the psychosocial sequelae of adolescent cannabis use.

Methods

We integrated participant-level data from three large, long-running longitudinal studies from Australia and New Zealand: the Australian Temperament Project, the Christchurch Health and Development Study, and the Victorian Adolescent Health Cohort Study. We investigated the association between the maximum frequency of cannabis use before age 17 years (never, less than monthly, monthly or more, weekly or more, or daily) and seven developmental outcomes assessed up to age 30 years (high-school completion, attainment of university degree, cannabis dependence, use of other illicit drugs, suicide attempt, depression, and welfare dependence). The number of participants varied by outcome (N=2537 to N=3765).

Findings

We recorded clear and consistent associations and dose-response relations between the frequency of adolescent cannabis use and all adverse young adult outcomes. After covariate adjustment, compared with individuals who had never used cannabis, those who were daily users before age 17 years had clear reductions in the odds of high school completion (adjusted odds ratio 0·37, 95% CI 0·20–0·66) and degree attainment (0·38, 0·22–0·66), and substantially increased odds of later cannabis dependence (17·95, 9·44–34·12), use of other illicit drugs (7·80, 4·46–13·63), and suicide attempt (6·83, 2·04–22·90).

Interpretation 

Adverse sequelae of adolescent cannabis use are wide ranging and extend into young adulthood. Prevention or delay of cannabis use in adolescence is likely to have broad health and social benefits. Efforts to reform cannabis legislation should be carefully assessed to ensure they reduce adolescent cannabis use and prevent potentially adverse developmental effects.

Funding Australian Government National Health and Medical Research Council.

Source:  Lancet Psychiatry 2014; 1: 286–93

Abstract

To review and summarise the literature reporting on cannabis use within western communities with specific reference to patterns of use, the pharmacology of its major psychoactive compounds, including placental and fetal transfer, and the impact of maternal cannabis use on pregnancy, the newborn infant and the developing child. Review of published articles, governmental guidelines and data and book chapters. Although cannabis is one of the most widely used illegal drugs, there is limited data about the prevalence of cannabis use in pregnant women, and it is likely that reported rates of exposure are significantly underestimated. With much of the available literature focusing on the impact of other illicit drugs such as opioids and stimulants, the effects of cannabis use in pregnancy on the developing fetus remain uncertain. Current evidence indicates that cannabis use both during pregnancy and lactation, may adversely affect neurodevelopment, especially during periods of critical brain growth both in the developing fetal brain and during adolescent maturation, with impacts on neuropsychiatric, behavioural and executive functioning. These reported effects may influence future adult productivity and lifetime outcomes. Despite the widespread use of cannabis by young women, there is limited information available about the impact perinatal cannabis use on the developing fetus and child, particularly the effects of cannabis use while breast feeding. Women who are using cannabis while pregnant and breast feeding should be advised of what is known about the potential adverse effects on fetal growth and development and encouraged to either stop using or decrease their use. Long-term follow-up of exposed children is crucial as neurocognitive and behavioural problems may benefit from early intervention aimed to reduce future problems such as delinquency, depression and substance use.

Introduction

About 3.9% (or 180.6 million) of the world’s population between 15 and 64 years of age use cannabis, making it one of the most widely used illegal psychoactive drugs in the world.[1] In some countries, cannabis has been used by up to 40% of adults at some point during their lives.[2] Cannabis is accepted as a relatively harmless recreational agent in many parts of the world[3] despite gathering evidence of its detrimental impact on both the adult[4] and the developing[5] central nervous system. Severe cannabis use, for example, decreases the metabolism of the prefrontal and temporal cortex,[63] and chronic exposure doubles the risk of psychosis and memory and cognitive dysfunction, most likely from neurotransmitter dysregulation.[7] This risk of neurological impairment is especially pronounced if cannabis is consumed during periods of critical brain development, such as adolescence.[8]

Cannabis, however, is one of the most commonly used illicit drugs in pregnancy and lactation.[1,2] Approximately 2.5% of women admit to continued cannabis use even during pregnancy.[9] This is of great concern because its lipophilic nature[10]allows it to readily cross many types of cell barriers, including the blood/brain and transplacental membranes. Cannabis metabolites are consequently easily detectable in many types of human tissues,[11] including the placenta, amniotic fluid and the fetus.[12] The effects of cannabis on the developing fetus may, however, be subtle and not be detectable for many months to years after birth, as the aetiology of some of the ‘softer’ neurological signs such as aggressive behaviours[5] or other neuropsychological problems[13] are difficult to be attributed unequivocally to cannabis exposure due to frequently concurrent negative environmental influences such as parental drug use, poverty[14] and psychiatric co-morbidity.[15]

Evidence regarding the effects of perinatal cannabis exposure, that is, during pregnancy and lactation, is plentiful but, unfortunately, ambiguous. In this review, we offer an overview of this problem, including discussion about the potential effects of this practice on the unborn, newborn and older child and adolescent. We also discuss some of the pertinent issues associated with perinatal management, including the utility of drug screening and the practical aspects of breast-feeding in the known cannabis user. Our overall aim is to provide the health practitioner with some guidance for advising women who use cannabis in pregnancy, including best available information on the potential effects of cannabis use on their unborn baby and future childhood development.

What Is Cannabis?

Cannabis is a genus of flowering plant with three main varieties: sativa, indica and ruderalis. It has been used for thousands of years for its fibre (hemp) and for its medicinal and psychoactive effects that are mediated through a unique family of at least 85 different compounds called cannabinoids, the most abundant of which are cannabidiol (CBD) and delta-9-tetrahydrocannabinol (THC). THC is the only cannabinoid with psychoactive properties, and plants are categorised according to the amount of THC or ratio of THC/CBD they contain. Hemp-producing cannabis strains are specifically bred, as per the United Nations Convention, to produce low THC levels.[16]

Cannabinoids are most abundant in the floral calyxes of the plant. The forms and strengths of THC obtained are dependent on the part of the plant that is used as well as the process used to extract and manufacture the plant product. Hash oil is the strongest, followed by hashish (resin) and marijuana (dried leaves/flowers). Cannabis may be inhaled by smoking with tobacco or through a water pipe or ingested in foods and drinks.[17] Most countries in the world have criminalised the growing and recreational use of cannabis, but controlled programmes in some countries such as the United States, Holland and Canada allow regulated use of medicinal cannabis, including the synthetic compounds dronabinol and nabiolone, for the management of conditions, such as cancer-related nausea[18] and neuropathic pain.[19]

Pharmacodynamics of Cannabis

Endocannabinoids are naturally occurring arachidonic acid metabolites[20] that are essential for the regulation of movement, memory, appetite, regulation of body temperature, pain and immunity.[21] Endogenous endocannabinoids and plant-derived phytocannabinoids exert their effects by activating the cannabinoid receptors of the endocannabinoid system. To date, five cannabinoid receptors have been identified, including the cloned CB1 and CB2 receptors.[22] The CB1 receptor is predominantly located in the central nervous system while the CB2 receptor is largely confined to immune cells and the retina.[23,24]

Psychoactive drugs, such as cannabis, are generally lipophilic and of small molecular size, enabling them to readily cross the blood–brain or other cellular (for example, placental) barriers. In animal studies, fetal blood and tissue THC concentrations are around 10% lower than maternal blood levels,[25] but in the rat model repeated dosing of the dam, particularly at higher doses, resulted in significantly higher plasma concentrations in the fetus as compared with single acute dosing. This suggests that heavy and chronic cannabis use may result in concentration of active cannabinoids in the developing fetus.[26] No similar human studies exist, but when plasma concentrations were measured in human cord blood samples, THC levels were found to be 3 to 6 times lower than in simultaneously collected maternal blood, with a similar concentration gradient being noted for the metabolite 9-carboxy-THC.[27]

Endogenous cannabinoids and cannabinoid receptors are expressed early in the developing fetal brain. CB1 receptors are identifiable in white matter and cell proliferative regions and are involved in critical neurodevelopmental events, such as neuronal proliferation, migration and synaptogenesis. Endocannabinoids are also pivotal in regulating neural progenitor cell commitment and survival.[28] Cannabis exposure during pregnancy therefore has the potential to induce supra-physiological stimulation of the endogenous cannabinoid system, which may then disrupt the ontogeny of endogenous endocannabinoid signalling and interfere with synaptogenesis and the development of neuronal interconnections. In addition to the possible effects of cannabis use on endocannabinoid-mediated neuronal maturation, it appears that cannabis exposure in pregnancy may also disrupt developing neurotransmitter systems. Dopaminergic neurones are expressed very early in the developing brain and exert trophic effects on neuronal cells.[29] Cannabis exposure during pregnancy disrupts tyrosine hydroxylase activity, the rate-limiting enzyme in dopamine synthesis, which has the potential to impact on the maturation of dopaminergic target cells.[28] Disturbances in dopamine function have consequently been associated with an increased risk of neuropsychiatric disorders, such as drug addiction,[30] schizophrenia[31] and depression.[32] Prenatal THC has also been noted to alter endogenous enkephalin precursor and the expression of opioid and serotonin receptors in animal models.[28]Whether these changes are implicated in the future risk of addictive behaviours and depression in the human is as yet uncertain.

Is There a Genetic Susceptibility to the Effects of Cannabis?

The effect of phytocannabinoids on mature neuronal cells is complex. Both neurotoxic and neuroprotective effects have been described depending on the cannabinoid, the cell type and the stage of cell differentiation.[22] There is evidence that individual susceptibility to cannabis, at least in the adolescent onset user, may be substantially influenced by heredity. Adolescent catechol-O-methyltransferase (COMT) knock-out mice, as compared with wild type, are more vulnerable to cannabinoid-induced modification of expression of schizophrenia-related behaviours.[33] In humans, neuroimaging studies demonstrate that chronic consumption of cannabis beginning before the age of 16 years is associated with alterations in the volume of the caudate nucleus and amygdala in users with specific COMT gene polymorphisms that produce increased copies of the val allele.[34] The presence of the COMT gene polymorphism val158met and the SLC6A4 gene 5-HTTLPR polymorphism in young adult cannabis users, on the other hand, has a moderating effect of decreased performance on executive functioning.[35]Whether genetic susceptibility influences the long-term neuropsychiatric and cognitive outcomes of gestational cannabis-exposed children has not been explored but could lead to individual direction of early intervention and supportive services to ameliorate possible undesirable outcomes.

The Prevalence of Cannabis Use in Pregnant Women

Cannabis is the most frequently used substance in any drug-taking population. In the gravid population, it accounts for >75%,[35] and generally self-reporting from developed Western countries such as Australia[36] and the United Kingdom[37] place the prevalence of cannabis use at up to 5% of all pregnant women. However, the certainty of these estimates is limited due to the variability of self-reporting rates.[37] Although many illicit drug users stop or decrease drug use during pregnancy, cannabis users often continue to use throughout pregnancy and while breast feeding.[38] Persisting cannabis use throughout pregnancy may, in part, be due to widespread societal acceptance of cannabis as a relatively harmless recreational agent compared with other ‘hard’ drugs of dependency such as heroin,[3, 36] and certainly more study into why this occurs is warranted. It must be noted that cannabis use in pregnancy is frequently accompanied by other forms of drug use or abuse. Many women continue to smoke tobacco and/or consume alcohol. Using record linkage data collected over a 5-year period, Burns et al. [39]demonstrated that 12% of cannabis users were concurrently identified as using opioids, 10% as using stimulants and 4% were identified as having an alcohol-related diagnosis during pregnancy. Almost 50% reported that they smoked >10 cigarettes per day. Identifying cannabis use in a pregnant woman therefore should prompt investigation into exposure to other substances.

Detecting Cannabis Use in Pregnancy

Optimal identification of drug exposure has a crucial impact on pregnancy and long-term health outcomes for both the mother and her child.[40] Early detection of drug use allows for timely implementation of harm-reduction strategies designed to moderate drug use as well as to minimise the impact of drug-using lifestyles (for example, unstable home situations, poor nutrition, poverty) on the family. Supportive care may favour changes that alter drug-using behaviours,[41] although it must also be acknowledged that complete cessation or abstinence of drug use is not possible for many women. Nevertheless, early detection facilitates ongoing support and may produce potentially valuable lifestyle changes that go beyond the perinatal period.

Other health issues may be addressed with timely detection of drug use. Ongoing drug use and abuse is frequently associated with psychiatric co-morbidities, and the impact of this on the mother and her family can be further complicated by socioeconomic problems, such as domestic violence and ongoing drug use by co-addicted partners.[42] Reducing drug use may also not be possible without appropriate identification and management of underlying psychiatric co-morbidities, such as anxiety disorders or depression. Evidence suggests that these psychiatric co-morbidities themselves may be a significant trigger for drug use[33] and that the co-existence of mental health problems may independently impact on pregnancy outcomes. Maternal depressive illness, for example, is strongly correlated with an increased risk of preterm delivery,[43–46]and of course, the earlier in pregnancy drug-dependent women have access to psychosocial supports, the higher the likelihood is of them to establish appropriate living conditions for their family and of addressing financial and any associated legal problems.

In addition to specific supports targeting drug use, detection of drug use in pregnancy also permits implementation of strategies that provide drug-using mothers with specific mothercraft and intensive postnatal support, such as intensive home-visiting programmes. Such programmes have been demonstrated to decrease the risk of childhood morbidity and mortality in high-risk disadvantaged adolescent parents.[47] Similarly, targeted education in other aspects of routine parenting, such as safe sleeping practices, may be beneficial as the incidence of night-time Sudden Infant Death Syndrome is significantly higher (for as yet uncertain reasons), in cannabis-exposed infants.[48]

Screening for drug and alcohol use should be considered a normal part of the standard antenatal interview process. Screening tools used in this setting are generally questionnaires that are designed to be administered face-to-face by the provider to the patient. They are not intended to specifically diagnose a substance abuse problem but rather to determine if a patient may be at risk for alcohol or drug problems and would therefore benefit from a more comprehensive evaluation. Ideally, a screening tool should be administered multiple times during each pregnancy, because patients may be more willing to disclose substance abuse problems once they develop rapport with a provider. Screening tests can also provide an opportunity to educate the patient about alcohol and drug abuse and the benefits of addressing these problems while pregnant. Asking every patient relevant but sensitive questions in a health context lessens the stigma associated with the topic. However, administering these screens in the antenatal period can be problematic. Seib et al. [49] demonstrated that while only 15% of the patients being screened were uncomfortable with the process, staff compliance was an issue, with 25% of women not being screened adequately or not being screened at all. All maternity hospitals should therefore encourage staff training to ensure that health providers are comfortable and familiar with screening processes used for their particular local area.

In contrast to the proven effectiveness of specific screening tests for identifying alcohol consumption in pregnancy,[50] the evidence for the efficacy of formal screening tests for drug use in the antenatal period is not as clear. Few screening tools have been directly evaluated for their efficacy in detecting drug, or more specifically cannabis, use in pregnancy. Phillips et al. [102]found that direct questioning by midwives using a structured screening tool facilitated drug use disclosure during early antenatal consults but that the use of some forms of questionnaires, for example, the Drug Abuse Screening Test (DAST-10), had only a sensitivity of 0.47 when self-reporting was validated against positive toxicology screens.[51] Again, we suggest that all staff involved in maternity care be trained to administer (and act on) drug screening tools confidently and without prejudice.

Toxicology screening for drug metabolites is generally carried out with the expectation of increasing the likelihood of detecting undisclosed drug use in pregnancy. Either maternal urine and hair samples or newborn urine, hair and meconium samples can be collected and analysed for the presence of drug metabolites, but only maternal toxicology screening has any value if the intention is to implement harm-minimisation strategies early in pregnancy. Newborn toxicology screening primarily focuses on identifying families at risk of ongoing drug use, to address child protection concerns that may be associated with parental drug use and to provide appropriate treatment for suspected cases of withdrawal or intoxication.[41]

Depending on the locale, toxicology screens may increase the chance of drug detection by up to fivefold,[52] but the general applicability of such screening programmes has often been limited by their selective application to perceived high-risk groups, such as infants of certain racial groups.[51,53] The value of screening maternal urine for drug metabolites is limited by the narrow time frame in which many drugs are excreted after use. Drug testing for cannabis is particularly problematic as there is generally a wide variability in individual excretion profiles.[53] Cannabis metabolites may also be undetectable in the naive user after 48 h. However, they can be potentially detectable in the urine for several weeks in chronic users, making it difficult to determine whether or not a positive urine sample represents past or recent ongoing use.

Maternal hair samples can also be used to detect substance use in pregnancy. However, hair toxicology has not been proven to be of great value in the detection of undisclosed cannabis use in pregnancy. Ostrea et al. [54] compared the sensitivity and specificity of maternal interview, maternal hair analysis and newborn meconium analysis in detecting perinatal exposure to opioids, cocaine and cannabis. Although hair and meconium analysis showed a high sensitivity in detecting opioid and cocaine exposure as compared with interview, hair and meconium analysis demonstrated a sensitivity of only 21% and 23%, respectively, as compared with a sensitivity of 58% for detection by maternal interview. The use of maternal hair samples is further complicated, because results may be affected by passive exposure to environmental cannabis smoke.[55] It is possible to distinguish between environmental contamination and true exposure by assaying for the derivative, Δ9-tetrahydrocannabinolic acid-A (THCA-A), as low concentrations of THCA-A compared with other metabolites suggests environmental contamination,[56] but this increases the complexity and expense of maternal hair analysis and will therefore not be considered suitable in most facilities for routine screening purposes.

Neonatal urine testing by immunoassay provides rapid results but is limited by the short time frame in which an infant will excrete recently used drug metabolites post delivery, resulting in a high rate of false negatives. In contrast, meconium that is collected within the first 2 days of life can be used to detect maternal cannabis use from the second trimester onwards. Neonatal hair samples can also be examined for evidence of exposure during the last trimester of pregnancy, as this is when fetal hair grows. Both meconium and neonatal hair sampling have been shown to be helpful in confirming suspicion of maternal cannabis use, at least in the second and third trimesters of pregnancy. A direct comparison between sensitivity of meconium and neonatal hair testing has found meconium to be more sensitive but is limited by the need to collect a sample within a few days of birth. Hair samples may be useful in confirming prenatal exposure to cannabis for up to 3 months after delivery but facilities for hair analysis remain limited for many care practitioners.

Although both maternal and newborn toxicology screening can increase the likelihood of detecting drug use in pregnancy, most authors do not recommend their routine use because of the expense and the burden on laboratory time constraints. Rather, they suggest toxicology testing be selectively used where there is a suspicion of maternal drug use that can not be confirmed by maternal interview.[41,57]

The Impact on the Fetus and Newborn Infant

It is difficult to determine the direct effects of maternal cannabis use on the developing fetus because of the often high prevalence of other concurrent drug use, including tobacco,[48, 58] and other adverse parenting and lifestyle issues, including poor nutrition, poverty and stress. The endogenous cannabinoid system has a crucial role in maintaining and regulating early pregnancy. Human placental studies have determined that the CB1 receptor is present in all the placental membrane layers[59] and that stimulation of these receptors will impair fetal growth by inhibiting cytotrophoblastic proliferation.[60] In a large population-based prospective cohort study, maternal cannabis use during pregnancy was found to be associated with growth restriction in mid-pregnancy and late pregnancy, with effects on low birth weight being most pronounced if maternal cannabis use continued throughout pregnancy.[61] These growth effects remained significant even after adjustment for potential confounding variables, such as exposure to tobacco and self-reporting of cannabis use (raising the possibility of selection bias). To date, there is no known association between cannabis exposure and spontaneous abortions of either chromosomally normal or abnormal fetuses,[62] and any such links are probably more likely to be related to concomitant stressful life events than to cannabis use per se.[63]

Although some animal studies indicate that cannabis may be teratogenic in very high doses, there is no firm link between gestational cannabis use and congenital malformations in humans.[64] Reports of associations between cannabis use in pregnancy and gastroschisis remain unsubstantiated.[65] A study of almost 420 000 Australian live births over a 5-year period by Burns et al. [39] found that in utero cannabis exposure increased the risk of neonatal intensive care unit admissions, predominantly for prematurity, but there was no relation to any increased risks of perinatal death.

Significant newborn withdrawal or intoxication syndromes requiring pharmacological treatment have not been described with exclusive gestational cannabis exposure, but subtle neurobehavioural disturbances such as exaggerated and prolonged startle reflexes and increased hand–mouth behaviour have been described.[66] High-pitched cries[67] and sleep cycle disturbances with EEG (electroencephalography) changes have been noted,[68] suggesting that prenatal cannabis affects newborn neurophysiological function. Pharmacological treatment for neonatal cannabis withdrawal has not been described, although this may be secondary to a lack of definitive evaluation techniques. Indeed, cannabis withdrawal has been described as a’mild narcotic withdrawal’,[69] and further study into additional treatments, evaluation and long-term outcomes is required.

Long-term Growth and Neurodevelopment

Of greater concern, however, is the increasing evidence that in utero cannabis exposure may impair long-term growth and neurodevelopment, particularly in terms of cognition and behaviour. Evidence from population-based human studies and in vitroanimal data indicates that interference with the endocannabinoid system disrupts normal neurobiological development,[70]particularly of neurotransmitter maturation[5] and neuronal survival.[22]

A longitudinal cohort study of growth parameters in children exposed to cannabis and cigarettes during pregnancy found that cannabis-exposed children have smaller head circumferences at birth, which increase in disparity in adolescence.[71] It must be noted that head growth, especially during the first month of life, is significantly associated with future intelligence quotient.[72]

Most studies, nevertheless, do not support measureable differences in neurodevelopmental outcomes in infants aged <2 years after cannabis exposure, but by early childhood and school age, cannabis-exposed children acquire visual–perceptual tasks and language skills more slowly and show increased levels of aggression and poor attention skills, particularly in girls.[73] The levels of cognitive and intellectual deficits are also related to the timing and degree of in utero exposure. Heavy use (defined as >1 joint per day) during the first trimester was associated with lower verbal reasoning scores in 648 children at 6 years of age when compared with their non-exposed peers, while second trimester use was associated with deficits of composite, short-term memory and quantitative scores.[74]

Problems with tasks requiring visual memory, analysis and integration appear to persist beyond late childhood[75] into adolescence.[76] The long-term effects of in utero cannabis exposure on visuospatial working memory were explored by Smithet al. [78] using functional magnetic resonance imaging. They demonstrated that in 19 to 21-year olds, high levels of maternal prenatal cannabis use was associated with significantly more neural activity in the left inferior and middle frontal gyri, parahippocampal gyrus, middle occipital gyrus and cerebellum and right inferior and middle frontal gyri.[77] The specific learning problems identified in these children appear to significantly interfere with school achievement scores[78] from as early as 6 years of age.

The aetiology of these problems is uncertain. In utero cannabis exposure alters neurotransmitter homeostasis, including ventral striatal dopamine D2 gene regulation[79] and expression,[80] and these changes have been linked to a risk of future neuropsychiatric problems, including disorders of impulse control associated with addiction behaviours.[79] Further, a significantly increased risk of childhood depressive symptoms and attention problems was identified at age 10 years in a large prospective cohort study documenting the use of cannabis in low-income pregnant women.[81] The same group of investigators also demonstrated that the risk of delinquency at 14 years was significantly increased in a prospective longitudinal study of cannabis-exposed children.[82] Other factors, however, are undeniably important in the expression of adverse behaviours during the teenage years. For example, the risk of adverse behaviours, including early initiation of drug abuse, is more likely in an intrauterine drug-exposed child if they are male or simultaneously exposed to other problems such as violence.[83] There is no firm association with prenatal cannabis and future psychiatric problems such as psychosis,[84] but depressive symptoms are increased.[82] Assisting the family unit with moderating adverse environmental influences from as early as possible after birth may have the potential to decrease future problems in young people affected by prenatal cannabis exposure.

The effects of cannabis on future physical growth are still to be determined. CB1 receptors mediate energy incorporation into adipose tissue and reduce energy expenditure. The Ponderal Indices of adolescents exposed to prenatal cannabis are higher than non-exposed children,[85] but further work needs to be done to determine their risk of developing clinically important sequelae such as appetite problems, dyslipidemia and diabetes, which are all common manifestations in chronic adult cannabis users.[86]

Medical Cannabis

In recent years, there has been a re-emergence in the use of medicinal cannabis to treat a variety of conditions, including amelioration of neurogenic pain and management of chemotherapy- and pregnancy-associated hyperemesis.[87] Increasing numbers of states in the United States, for example, have legalised medical marijuana for certain specific indications.[88]However, it is not known whether the long-term effects of prenatal exposure to medicinal cannabis used in a controlled manner differ from the effects of cannabis used as a recreational drug during pregnancy, and urgent study is required. At this point in time, any advice about medicinal cannabis use during pregnancy must take into consideration both the potential benefits of the substance with regards to maternal well being and potential impact of this type of cannabis exposure on the developing fetus.

Lactation

Cannabis and its metabolites readily pass in to breast milk in variable concentrations that depend considerably on the amount of drug ingested by the mother. When cannabis is regularly consumed by breast-feeding mothers, human milk THC concentrations may be up to eightfold higher than simultaneously measured maternal plasma concentrations.[89] Certainly, even bovine consumption of cannabis results in detectable metabolites in at least 30% of children even up to the age of 3 years.[90] There are substantial concerns that continued maternal cannabis use during the first month of life may impede neurodevelopment at 1 year of age,[91] but the effects of postnatal exposure is difficult to delineate from prenatal use as most mothers will not begin using cannabis as a de novo habit after birth.

Delta 9-THC inhibits gonadotropin, prolactin, growth hormone and thyroid-stimulating hormone release and stimulates the release of corticotropin, thereby inhibiting the quantity and reducing the quality of breast milk.[92] The Academy of Breastfeeding Medicine, in line with most professional bodies, recommends against breastfeeding whenever illicit drug use has occurred in the 30-day period before birth. This is especially pertinent if substance abuse is ongoing post delivery or if the mother is not engaged in substance abuse treatment programmes.[93–95] Unfortunately, specific recommendations with respect to breast feeding while using cannabis are hampered by the lack of substantial and definitive studies. In particular, occasional users should be counselled on a case-by-case basis and made aware of the risks of maternal intoxication while caring for an infant and the potential neurodevelopmental sequelae on their child, should cannabis usage become a regular activity.

Recommendations for the Management of Women Using Cannabis in Pregnancy

There are no known ‘safe’ threshold limits for cannabis use in pregnancy, and currently, there are also no specific pharmacological treatments for cannabis dependency. Evidence overwhelmingly indicates that cannabis use during pregnancy and possibly in the postnatal period remains a significantly under-recognised problem that has the potential to cause long-term harm. However, there are a variety of approaches that can facilitate identification of cannabis use in women presenting for pregnancy care that may allow implementation of harm-minimisation procedures to reduce long-term risks for both the mother and her child.

Carefully directed and sensitive histories should be routinely taken to elucidate cannabis and other substance use in pregnancy. In some high-risk cases, toxicological screening may be appropriate where heightened suspicions are not in keeping with maternal history offered. Due to increasing concerns about long-term neurodevelopmental, behavioural and possibly even metabolic consequences of perinatal cannabis exposure, women should be objectively informed of the possible impact of cannabis use during pregnancy and lactation and be strongly advised to stop using cannabis wherever possible. If complete abstinence is not possible, women should be advised to reduce regular cannabis use during pregnancy, as current evidence indicates that daily use of cannabis is most strongly associated with future adverse neurobehavioural outcomes. A harm-reduction approach focusing on minimising risks to the woman and her baby rather than complete cessation may be most effective in this scenario. Engaging women into an antenatal service that provides drug relapse prevention support or referring women to drug and alcohol services should be considered, particularly where an antenatal service cannot offer specific drug and alcohol counselling services itself. Cognitive behavioural therapy centred around drug relapse and prevention support and tobacco cessation education is recommended. Midwives and doctors should ask women about their level of cannabis use and their willingness to change their drug-use behaviours at each antenatal contact. General health education, including the adverse effects from continued cannabis and tobacco exposure and safe sleeping guidelines should be reinforced. Depending on family circumstances, the benefits of breast feeding, even with continued cannabis use, may outweigh the negative side-effects, especially in infrequent cannabis users. Each institution should work towards a policy of ensuring best practices for their particular population of cannabis users.

During the postnatal period, mothers should be advised not to smoke either tobacco or cannabis around their infants and children. They should be educated about the risks of passive smoke exposure as well as the potential effect of cannabis use on a mother’s decision-making ability. Mother-crafting support may be required to ensure best infant care, including safe sleeping practices. Of particular note, counselling cannabis-using fathers is also crucial as continued paternal cannabis triples the risk of Sudden Infant Death Syndrome[96] ( ).

Summary of recommendations

Issue

Detection of maternal use

Recommendations                         

Antenatal drug and alcohol questions best to screen large populations

Maternal and infant toxicology most likely unhelpful unless maternal history is ambiguous56

Early detection may help implement harm-minimisation strategies

Issue

Fetal effects

Recommendations

No definitive link to increased spontaneous abortions97 or congenital abnormalities64, 65  Intrauterine growth restriction, including head size of fetus, common61

Issue

Neonatal effects

Recommendations

Severe withdrawal uncommon but mild symptoms similar to an opioid-type withdrawal is recognised69

Need for pharmacological treatment from cannabis only exposure uncommon

Transient high pitched cry67 and sleep disturbances68 noted

Increased risk of sudden infant death syndrome96

Issue

Effects on childhood and later life

Recommendations

Small head circumference may persist into teenage life

Risk of long-term problems correlated with severity of prenatal exposure,74 particularly on visual memory and executive function74, 75 that may persist to late childhood75 and adolescence76

Aggression and attention problems noted in toddlers (especially girls)73

Issue

Lactation

Recommendations

Cannabis and metabolites cross the milk barrier, and levels in milk may be higher than maternal plasma89

Effects of continued use during lactation may impair early (<1 year) neurodevelopment90

Issue

General

Recommendations

Screen all pregnant women for drug use with a well-validated questionnaire

Cease or decrease use as early as possible—chronic/heavy use (>1 joint per day) increases risk of long-term adverse outcomes for the child

Lactation recommendations must be taken on a case by case basis. Mother must be aware of dangers of breast feeding while intoxicated, of passage of cannabis and metabolites into milk and of possible adverse influence of continued cannabis exposure via breast milk on childhood neurodevelopmental outcomes There is insufficient current evidence to provide definitive recommendations for the use of medicinal cannabis

Conclusion

It is not uncommon for the health-care professional caring for pregnant women to encounter the problem of maternal cannabis use during the antenatal period. Although cannabis is viewed by many as a harmless recreational drug when compared with other illicit drugs, there is mounting evidence to suggest that prenatal cannabis exposure can have a negative effect on fetal growth and that exposure to cannabis during periods of critical brain development, particularly during the fetal and adolescent periods, has the propensity to significantly adversely impact on neurodevelopmental and behavioural outcomes. Ultimately, long-term changes in neurobehaviour, particularly those involving executive functioning, may adversely affect adult educational and vocational outcomes. As health-care professionals, we have a responsibility to seek to actively identify women who use cannabis in the antenatal period and inform them of the possible risks of their cannabis use in a non-threatening and non-judgmental manner. Currently, pregnant and breast-feeding cannabis users should be advised to cease use where possible or substantially decrease their drug use. At this point in time, there remains ongoing uncertainty about both short- and long-term implications of cannabis use during pregnancy and lactation, especially if use is intermittent. Further adequately powered studies are required to resolve this pressing dilemma.

Key Notes

1. Regular cannabis use in pregnancy is a widespread but an under-recognised problem.

2. Fetal growth is possibly affected by gestational cannabis exposure, but the dose-response relationship has not been well defined.

3. There is evidence that regular cannabis use in pregnancy significantly increases the risk of future neurodevelopmental and behavioural problems, with particular effect on executive functioning.

4. Pregnant and breast feeding cannabis users should be identified early and advised to either decrease or where possible cease cannabis use entirely.

Source:  J Perinatol. 2014;34(6):417-424. 

Bertha K. Madras1

Division on Alcohol and Drug Abuse, Harvard University Medical School, McLean Hospital,

Belmont, MA 02478

The current watershed in legal status and rising use of marijuana can be traced to a Cal-ifornia ballot initiative (Prop. 215, its legal successor SB420), that enabled widespread access to smokeable or edible forms of marijuana for self-reported medical conditions. Circumventing the Food and Drug Adminis-tration (FDA) drug approval process, the movement in California was replicated by ballot or legislative initiatives in 23 states and the District of Columbia, and culminated in the legalization of marijuana in 2012 by Washington state and Colorado. The shifting status of marijuana reflects a change in public perception and belief that marijuana is harm-less. Marijuana use in the population over age 12 is escalating; 60% of 12th graders do not perceive marijuana as harmful, and daily or nearly daily use has risen dramatically in this cohort (1, 2). Paradoxically, public perception of marijuana as a safe drug is rising simulta-neously with accumulating evidence that frequent marijuana use is associated with adverse consequences, especially among youth (3). In PNAS, Volkow et al. register compelling new observations that marijuana abusers manifest adaptive behavioral, physiological, and biological responses, which conceivably contribute to marijuana addiction and com-promised function (4). In response to a dopamine challenge (methylphenidate) and compared with non-using controls, marijuana abusers self-reported blunted reward (less “high”) and heightened negative responses (anxiety and restlessness), which were associated with attenuated dopamine responses in brain and cardiovascular responses.

Dopamine, Reward, the Adapted Brain

The role of the neurotransmitter dopamine in drug reward and addiction is the key to understanding the rationale for interrogating dopamine function in long-term marijuana abusers.Thedopaminehypothesisofaddiction was formulated by preclinical observations showing that opiates, cocaine, amphetamine, nicotine, alcohol, and (delta-9)-tetrahydro-cannabinol(THC,thepsychoactiveconstituent of marijuana), raise extracellular dopamine levels in the dopamine-rich nucleus accum-bens, a brain region associated with reward (5, 6). Repeated drug-induced dopamine surges were subsequently shown to engender neuroadaptive changes in brain regions implicated in drug salience, drug reward, motivation, memory, and executive function (7–9). In humans dependent on alcohol, cocaine,  methamphetamine, nicotine, or heroin, adaptation of dopamine signalling is manifest by reduced D2 dopamine receptor availability and blunted dopamine release in cocaine, heroin, and alcohol abusers challenged with a psychostimulant (10–14). In-terrogation of whether marijuana abusers manifest parallel adaptive changes in dopamine signaling has yielded inconsistent results (15).

By integrating behavioral and brain-imaging measures following a dopamine challenge (methylphenidate) in marijuana abusers, Volkow et al. (4) add a new di-mension to clarifying the impact of long-term marijuana use on brain dopamine response. Methylphenidate, a surrogate for dopamine, elevates extracellular levels of dopamine (and norepinephrine) by blocking the dopamine transporter (DAT) in dopa-mine-expressing neurons. As the DAT sequesters dopamine in dopamine-releasing neurons, the blockade raises extracellular dopamine levels in dopamine-rich brain regions. The rapid rise in dopamine triggers self-reports of a “high.” Marijuana abusers self-reported blunted measures of “high,” drug effects, increased anxiety, and rest-lessness. The magnitude and peak behavioral effects of methylphenidate were more robust in controls than marijuana abusers. Cardiovascular responses (diastolic blood pressure, pulse rate) were also attenuated in the abusers. Significantly, the younger marijuana use was initiated, the higher the scores for negative emotionality. These findings reinforce the accumulating evidence that earlier age of initiation of mar-ijuana abuse is associated with worse out-comes (3, 16). Collectively this phase of the study suggests that brain dopaminergic, pos-sibly noradrenergic systems, are significan-tly modified in long-term, heavy marijuana abusers. These changes conceivably contribute to reduced rewarding effects, emotion-ality and motivation, increased propensity for addiction, with early initiators being more vulnerable.

D2/D3 dopamine receptors are critical mediators of the initial responses to drugs of abuse. PET imaging of brain revealed a more complex pattern of change in dopamine signaling than previously reported for other specific drugs of abuse. D2/D3 dopamine receptor availability, measured with the D2/D3 receptor antagonist [11C]raclopride, was not reduced in marijuana abusers, in contrast to reduced dopamine receptor availability observed in subjects with other specific substance use disorders (11–14).

This conclusion remains tentative, as the age of the marijuana-abusing cohort was considerably younger than drug-abusing subjects previously interrogated for D2 dopamine receptor availability.

[11C]Raclopride can also serve as an in-direct measure of dopamine production, release, and extracellular levels (17). Reduced [11C]raclopride binding-site availability is detectable following administration of a psy-chostimulant (e.g., methylphenidate or amphetamine), which elevates the extracellular dopamine by blocking transport or promoting its release from neurons. The dopamine surge competes with [11C]raclopride for binding to the D2/D3 receptor, with [11C]raclopride displacement proportional to extracellular dopamine. In marijuana abusers, diminished dopamine responses were observed in the ventral striatum compared with controls, and were inversely correlated with addiction severity and craving. The attenuated responses to methylphe-nidate are consistent with decreased brain reactivity to dopamine stimulation in marijuana abusers, which conceivably contributes to the increase in stress responses, irritability, and addictive behaviors. Thus, marijuana joins the roster of other abusable drugs in promoting blunted dopaminergic responses in a brain region implicated in drug reward, but deviates from other drugs in that it apparently does not promote a decline in D2/D3 receptor availability.

The study yielded several unanticipated discoveries. Marijuana abusers displayed enhanced dopamine release in the substantia nigra/subthalamic nucleus, which correlated with marijuana and tobacco craving, as well as addiction severity. Because this brain re-gion has relatively high densities of the D3 receptor, this preliminary finding reinforces the need to expand PET imaging to multiple, discrete brain regions, with higher-resolution cameras, and to enlist other probes capable of selective monitoring of each of five dopamine receptor subtypes. Another surprising obser-vationwasthedecreaseindistributionvolume in the cerebellum by methylphenidate in con-trols, but not in marijuana abusers, another manifestationofabluntedresponse.Thisbrain region characteristically is used as a reference region to normalize for nonspecific binding (“baseline”) of PET imaging probes if comparing group differences, possibly resulting in overestimates of the methylphenidate re-sponse in other brain regions of marijuana abusers. This finding, which may reflect vas-cular changes engendered by marijuana, highlights the necessity of heightened scrutiny ofthe cerebellum asa“neutral”baseline region for dopamine receptor monitoring in group comparisons.

Collectively, abnormal behavioral responses to a methylphenidate challenge implicate dopamine signaling adaptation in mari-juana abusers. Even though a decrease in striatal D2 receptor density does not ac-count for the responses, other components of the synapse (e.g., DAT, dopamine syn-thetic capacity, the dopamine signaling cascade, events downstream of dopamine receptors) conceivably contribute to mani-festations of blunted subjective responses.

Future Multidisciplinary Research

The current research (4), providing strong evidence that marijuana abuse is associated with blunted dopamine responses and re-ward, is a major contribution to a growing body of evidence that heavy marijuana use is associated with brain changes that could be detrimental to normal brain function. Numerous other brain-imaging studies have been conducted in heavy adult marijuana users (e.g., ref. 18), with reported changes in brain morphology and density, defor-mation of specific structures, altered con-nectome (e.g., hippocampus), and function.

The current research, which integrates be-havioral and physiological changes within the context of a specific neurochemical substrate, dopamine, provides important leads for in-tegrating with other changes gleaned from MRI technologies. Intriguingly, evidence that dopamine receptor signaling can affect ex-pression of genes encoding axonal guidance molecules that are critical for brain devel-opment and neuroadaptation (19) may pro-vide a link between drug-induced receptor activity and gross and discrete altered mor-phology and circuitry characteristic of the drug-adapted brain.

There remains a compelling need for prospective, integrated longitudinal research in this field, especially in adolescent mari-juana users, as the impact of marijuana on the developing brain is more robust with early age of initiation (3, 16). Imaging studies are predominantly snapshots in time, relying on self-reports of marijuana use, dose, and frequency, with subjects of varying ages, group sizes, differing imaging tech-niques, and other variables that confound meta-analyses or integration of data from different sites to expand study power. A critical longitudinal study showing a signifi-cant IQ decline in early marijuana users is a prime example of the direction in which the field should be going, but with co-ordinated brain-imaging approaches (20).

Preclinical studies can circumvent the limitations of some clinical metrics, and es-tablish causality for specific changes that are not feasible to measure in humans. Yet the divergence of the human brain anatomically and functionally limits unfettered extrapola-tion from animals to humans. Large-scale, multicenter prospective longitudinal human research starting before initiation of drug use and extending for three decades of life is needed to further pursue causal relation-ships of marijuana and adverse consequences reported in numerous shorter-term studies. Research design could include: (i) brain im-aging to document occurrence of, resolution, or persistence of structural, circuitry, vascu-lar, and associated and neuropsychological decrements; (ii) neurocognitive function; (iii) behavioral, emotional assessment; (iv) neural, cognitive, epigenetic, proteomic, and affec-tive markers; and (v) preclinical, relevant parallel studies.

In view of the growing public health con-cerns of escalating high-dose, high-frequency marijuana use, early age of initiation and daily use, high prevalence of marijuana addiction, rising treatment needs, the void of effective treatment, high rates of relapse, association with psychosis and IQ reduc-tion, a rising tide of emergency room epi-sodes, and vehicular deaths, constitute compelling reasons to expand marijuana research and to clarify its underlying biology and treatment targets/strategies. Longitudinal studies that begin before initiation of use, and that integrate brain imaging with behavioral, cognitive, and other parameters, will facilitate shaping of public perception and public policy with more informed scientific evidence.

1 Center for Behavioral Health Statistics and Quality (2013) National

Survey on Drug Use and Health (Substance Abuse & Mental Health Services Administration, Rockville, MD).

2 Johnston LD, et al. (2013) Monitoring the Future: National Survey Results on Drug Use, 1975–2013 — Overview, Key Findings on Adolescent Drug Use. (Institute for Social Research, University of Michigan, Ann Arbor) Avaliable at http://monitoringthefuture.org// pubs/monographs/mtf-vol1_2013.pdf. Accessed July 13, 2014.

3 Volkow ND, Baler RD, Compton WM, Weiss SR (2014) Adverse health effects of marijuana use. N Engl J Med 370(23):2219–2227.

4 Volkow ND, et al. (2014) Decreased dopamine brain reactivity in marijuana abusers is associated with negative emotionality and addiction severity. Proc Natl Acad Sci USA, 10.1073/ pnas.1411228111.

5 Di Chiara G, Imperato A (1988) Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci USA 85(14):5274–5278.

6 Chen JP, et al. (1990) Delta 9-tetrahydrocannabinol produces naloxone-blockable enhancement of presynaptic basal dopamine efflux in nucleus accumbens of conscious, freely-moving rats as measured by intracerebral microdialysis. Psychopharmacology (Berl) 102(2):156–162. 7 Hyman SE, Malenka RC, Nestler E (2006) Neural mechanisms of addiction: The role of reward-related learning and memory. Annu Rev Neurosci 29:565–598.

8 Koob GF, Volkow ND (2010) Neurocircuitry of addiction. Neuro-psychopharmacology 35(1):217–238.

9 Volkow ND, Wang GJ, Fowler JS, Tomasi D (2012) Addiction circuitry in the human brain. Annu Rev Pharmacol Toxicol 52:321–336. 10 Volkow ND, et al. (1997) Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects. Nature 386(6627):830–833.

11 Martinez D, et al. (2005) Alcohol dependence is associated with blunted dopamine transmission in the ventral striatum. Biol Psychiatry 58(10):779–786.

12 Martinez D, et al. (2012) Deficits in dopamine D(2) receptors and presynaptic dopamine in heroin dependence: Commonalities and differences with other types of addiction. Biol Psychiatry 71(3): 192–198.

13 Wang GJ, et al. (2012) Decreased dopamine activity predicts relapse in methamphetamine abusers. Mol Psychiatry 17(9):918–925.

14 Fehr C, et al. (2008) Association of low striatal dopamine d2 receptor availability with nicotine dependence similar to that seen with other drugs of abuse. Am J Psychiatry 165(4):507–514.

15 Ghazzaoui R, Abi-Dargham A (2014) Imaging dopamine transmission parameters in cannabis dependence. Prog Neuropsychopharmacol Biol Psychiatry 52:28–32. 16 Lynskey MT, et al. (2003) Escalation of drug use in early-onset cannabis users vs co-twin controls. JAMA 289(4): 427–433.

17 Seeman P, Guan HC, Niznik HB (1989) Endogenous dopamine lowers the dopamine D2 receptor density as measured by [3H]raclopride: Implications for positron emission tomography of the human brain. Synapse 3(1):96–97.

18 Batalla A, et al. (2013) Structural and functional imaging studies in chronic cannabis users: A systematic review of adolescent and adult findings. PLoS ONE 8(2):e55821.

19 Jassen AK, Yang H, Miller GM, Calder E, Madras BK (2006) Receptor regulation of gene expression of axon guidance molecules: Implications for adaptation. Mol Pharmacol 70(1):71–77.

20 Meier MH, et al. (2012) Persistent cannabis users show neuropsychological decline from childhood to midlife. Proc Natl Acad Sci USA 109(40):E2657–E2664.

Source: www.pnas.org/cgi/doi/10.1073/pnas.1412314111 PNAS Early Edition

 ALASKA Association of Chiefs of Police, Inc.

1.     Legalization will place a significant financial burden on local law enforcement agencies due to the need for special training that will be necessary to identify marijuana users who are driving impaired and to create or enhance youth education programs.

  •  It is estimated that Alaskan police departments will have combined costs of nearly $6,000,000 to respond to immediate needs which will arise from legalization of marijuana. These costs include necessary training of police officers to establish drug impairment based on symptomology because there are no roadside tools like breathalyzers for testing marijuana usage, and for increasing the number of School Resource Officers (SROs) in communities to educate teens about the dangers of drug use. These are expenditures that have been tallied by mostly municipal police departments, therefore the bulk of these costs will likely need to be borne by taxpayers in the impacted communities. Additional costs may exist for the Department of Public Safety.

  • After medicinal marijuana became easy to get in Colorado, seizures of smuggled marijuana quadrupled in roughly 4 years as “legal” marijuana was diverted to other markets . No comparable studies have been found addressing this problem in Alaska, but if legalization in this state results in a similar increase in diversion trafficking, more than 75% of Alaskan police feel they will not have sufficient local resources to combat the potential impact in their community.

  • In 2011, the national average for youth aged 12 to 17 years old and considered “current” marijuana users was 7.64 percent which was the highest average since 1981. The most recent figures found for Alaska teens dates from 2009 and puts the number of students claiming to have used marijuana within the last 30 days at 22.7% and the number who have used the drug  during their lifetime at 44.5% . Only 16 Alaskan chiefs report currently having SROs in their communities. If legalization occurs in Alaska, 64% of police chiefs felt it would be necessary to increase the number of school resource and DARE officers doing youth outreach in their communities to protect against an increase in local teen drug usage.

  •  In 2006, Colorado drivers testing positive for marijuana were involved in 28 percent of fatal vehicle crashes involving drugs. By 2011 that number had increased to 56 percent. These statistics clearly indicate the importance of traffic enforcement, but identification of impairment due to marijuana requires special skills. No figures seem to exist which can illuminate the degree of the problem in Alaska  but the consistency of data from other states would support the assumption that the Alaskan experience would be comparable. Ninety seven percent of Alaskan chiefs responding to the AACOP survey felt their officers needed additional Advanced Roadside Impaired Driving Enforcement (ARIDE) or Drug Recognition Expert (DRE) training to help them properly identify drivers impaired by marijuana. Of more than 950 police officers in the state, less than 100 are estimated to have ARIDE training, and less than 20 now have DRE training.

  • Less than 6% of the AACOP survey respondents felt their local taxpayers would support a sufficient increase in their police budget to meet the anticipated financial implications of marijuana legalization.

  • Seventy five percent of respondents felt their agency would require financial assistance to meet training needs that will be created by legalization. Providing this training for all police officers will not only be costly to local taxpayers and also logistically difficult.

  • ·Unlike alcohol, for which impairment can be reasonably measured using a breathalyzer (and confirmed with a blood alcohol content measurement), valid detection for cannabis is time-consuming, and blood tests cannot definitively determine an approximate degree of impairment. The lack of suitable roadside tests and agreed-upon intoxication levels will make enforcement of impaired driving more difficult.       

  • The necessity of drawing blood for toxicology testing creates another potential problem for police as it will necessitate training officers as phlebotomists, contracting with an independent phlebotomist to be on call, or taking all drivers suspected of impaired driving due to drugs (DUID) to the nearest hospital or clinic to have blood drawn.. In this “post-CSI” era, juries are likely to expect effective prosecution of drug impairment will require a toxicology evaluation combined with the testimony of a trained Drug Recognition Expert.

 

2.     Stoned driving and other dangers would be increased, while the difficulty of proving impairment from marijuana may impact prosecutions, and could make civil settlements more difficult in the case of personal injury lawsuits.

  • Drugged driving impairs one’s motor skills, reaction time, and judgment and  is a public health concern because it puts not only the driver at risk, but also passengers and others who share the road.

  • In other states where there has been an enormous increase in “medical” marijuana cardholders, DUI arrests involving marijuana have skyrocketed, as have traffic fatalities where marijuana was found in the system of one of the drivers. Because toxicology results are not universally reported for Alaskan crashes no definitive data exists which would demonstrate a different result here.

  • In 2011 there were 9.4 million persons aged 12 and older who reported driving under the influence of illicit drugs during the past year. The rate was highest among young adults aged 18 to 25.

  • Drugs that may affect driving were detected in one of every seven weekend night time drivers in California during the summer of 2012. In the first California state wide roadside survey of alcohol and drug use by drivers, 14 percent of drivers tested positive for drugs, 7.4 percent of drivers tested positive for alcohol, and just as many as tested positive for marijuana as alcohol.

  • In a study of seriously injured drivers admitted to a Maryland Level-1 shock-trauma center, 65.7 percent were found to have positive toxicology results for alcohol and/or drugs. Almost 51 percent of the total tested positive for illegal drugs. A total of 26.9 percent of the drivers tested positive for marijuana.

  • The National Organization for the Reform of Marijuana Laws (NORML) has called for a science-based educational campaign targeting drugged driving behavior. In a January 2008 report titled, Cannabis and Driving, it is noted that motorists should be discouraged from driving if they have recently smoked cannabis and should never operate a motor vehicle after having consumed both marijuana and alcoholThe report also calls for the development of roadside, cannabis-sensitive technology to better assist law enforcement in identifying drivers who may be under the influence of pot.

  • In a 2007 National Roadside Survey of alcohol and drug use by drivers, a random sample of weekend nighttime drivers across the United States found that 16.3 percent of the drivers tested positive for drugs, compared to 2.2 percent of drivers with blood alcohol concentrations at or above the legal limit. Drugs were present more than 7 times as frequently as alcohol.

  • Low doses of THC moderately impairs cognitive and psychomotor tasks associated with driving, while severe driving impairment is observed with high doses, chronic use and in combination with low doses of alcohol. The more difficult and unpredictable the task, the more likely marijuana will impair performance.

 

3.     Persons under the influence of marijuana will present a risk on job-sites. If marijuana is legalized, aggressive drug screening and periodic testing of medical personnel, industrial workers, transportation workers. and others will be necessary to insure safety of the public and other workers. 

  • According to the American Council for Drug Education in New York, employees who abuse drugs are 10 times more likely to miss work, 3.6 times more likely to be involved in on-the-job incidents (and 5 times more likely to injure themselves or another worker in the process) and 5 times more likely to file a workers’ compensation claim. They also are said to be 33 percent less productive and responsible for potentially tripling health care costs.

  • The risk that your surgeon, pilot, bus driver, or coworker has used marijuana will increase if the drug is decriminalized.

  • A Rand study suggests drug use leads to about a 25-percent increase in men’s risk of having a workplace injury.

  •  In addition to the acute effects of alcohol and other drug use on judgment and psychomotor skills, substance use that occurs hours before a worker begins his or her shift can cause spillover effects, such as fatigue and hangovers, that may independently increase injury risk. Studies have shown that hangovers affect cognitive skills, including tasks related to driving or piloting aircraft, which may therefore influence the risk of injury in a manner similar to the influences of acute alcohol intoxication.

  • Persons more likely to misuse alcohol and other substances may be more likely to be engaged in other behaviors that increase the risk of injury, a concept termed deviance proneness

 

4.     Marijuana legalization will usher in Drug Commercialization increasing the chances of the drug falling into the hands of kids.

  • Already, private holding groups and financiers have raised millions of start-up dollars to promote businesses that will sell marijuana and marijuana-related merchandise.

  • Cannabis food and candy is being marketed to children and are already responsible for a growing number of marijuana-related ER visits.  Edibles with names such as “Ring Pots” and “Pot Tarts” are inspired by common children’s candy and dessert products such as “Ring Pops” and “Pop Tarts.”

  • Several, profitable vending machines containing products such as marijuana brownies are emerging throughout the country.

  • The former head of Strategy for Microsoft has said that he wants to “mint more millionaires than Microsoft” with marijuana and that he wants to create the “Starbucks of marijuana.”

 

5.     Marijuana use will increase under legalization

  • Because they are accessible and available, our legal drugs are used far more than our illegal ones. According to recent surveys, alcohol is used by 52% of Americans and tobacco is used by 27% of Americans. Marijuana is used by 8% of Americans.

  • When RAND researchers analyzed California’s 2010 effort to legalize marijuana, they concluded that the price of the drug could plummet and therefore marijuana consumption could increase.

  •  The 2011 Monitoring the Future Survey noted that daily or near daily marijuana use, defined as use on 20 or more occasions in the past 30 days rose significantly in the 8th, 10th and 12th grades in 2010 and rose slightly higher again in 2011. This translates to one in every 15 high school seniors smoking pot on a daily or near daily basis, the highest rates that has been seen in thirty years – since 1981.

 

6.     Marijuana is especially harmful to kids and adolescents.

  • Marijuana use that begins in adolescence increases the risk they will become addicted to the drug. The risk of addiction goes from about 1 in 11 overall to 1 in 6 for those who start using in their teens, and even higher among daily smokers.

  • Marijuana contributes to psychosis and schizophrenia , addiction for 1 in 6 kids who ever use it once , and it reduces IQ among those who started smoking before age 18.

  • Regular or daily use of marijuana may be robbing many young people of their potential to achieve and excel. THC, a key ingredient in marijuana, alters the ability of the brain’s hippocampus to communicate effectively with other brain regions. In addition, recent research has shown that marijuana use that begins during adolescence can lower IQ and impair other measures of mental function in adulthood.

 

7.     Today’s marijuana is NOT your Woodstock weed.

  •  In the 1960s and ‘70s, THC levels of the marijuana smoked by baby boomers averaged around 1%, increasing to just under 4% in 1983, and almost tripling in the subsequent 30 years to around 11% in 2011.

 

8.     Marijuana legalization will increase public costs.

  • For every $1 in alcohol and tobacco tax revenues, society loses $10 in social costs, from accidents to health damage .

  • In addition to the costs to law enforcement for training and prevention, the anticipated increase in impaired driving arrests would result in additional court costs including prosecution and public defenders. Even in places where these costs are not borne directly by taxpayers, they will divert funds which might otherwise be used to support other civic needs.

 

9.     People are not in prison for small time marijuana use.

  • Few people are currently in prison for marijuana possession (in fact, only 0.1% of prisoners with no prior offenses ) and current alcohol arrest rates are over three times higher than marijuana arrest rates.

  • Statistics on state-level prisoners around the United States reveal that just 0.3% of all state inmates were behind bars for marijuana possession only (with many of those pleading down from more serious crimes).

  • 99.8% of federal prisoners sentenced for drug offenses were incarcerated for drug trafficking.

  • The risk of arrest for each joint smoked is estimated at 1 in 12,000. 

  • On the most recent prison census date only 4 people were incarcerated in Alaska prisons due to conviction on 6th degree Misconduct Involving Controlled Substance (MICS) which would include possession of less than 1 oz. of marijuana (the amount legalized by the proposed legislation). It is undetermined if these MICS-6 offenders had concurrent convictions for other offenses as well, but it is possible that at least some do.

 

10.  Drug cartels and the black market will continue to function under legalization.

  • A recent RAND report showed that Mexican drug trafficking groups only received a minority of their revenue (15-25%) from marijuana. For them, the big money is found in illegal trade such as human trafficking, kidnapping, extortion, piracy, and other illicit drugs.

  • We know from past experience with other businesses that illegal actors have a lot to do with so called legal industries. These cartels will only be helped with legalization and more addiction, not hurt.

  • Dealers aren’t likely to give up their lucrative income. Legalization of marijuana will lead entrepreneur dealers and cartels to focus their energies on selling harder drugs.

 

11.  The foreign experience is not promising. Neither Portugal nor Holland provides any successful example of legalization.

  • Offenses related to drug use or possession for use continued to comprise the majority of drug law offenses in 2010; between 2005 and 2010, there was an estimated 19 percent increase in the number of offenses related to drug use in Europe.

  • Independent research reveals that in the Netherlands, where marijuana was commercialized and sold openly at “coffee shops,” marijuana use among young adults increased almost 300%. Now, the Dutch are retreated from their loose policies. About 70 percent of Dutch towns have a zero-tolerance policy toward cannabis cafes.

  • There are signs that tolerance for marijuana in the Netherlands is receding. They have recently closed hundreds of coffee shops, and today Dutch citizens have a higher likelihood of being admitted to treatment than nearly all other countries in Europe.

  • In Portugal, use levels are mixed, and despite reports to the contrary, they have notlegalized drugs. In 2001, Portugal started to refer drug users to three person “panels of social workers” that recommend treatment or another course of action. As the European Monitoring Center’s findings concluded: “the country does not show specific developments in its drug situation that would clearly distinguish it from other European countries that have a different policy.”

 

12.   Marijuana is believed by some to have medicinal properties, but we shouldn’t smoke the plant in order to derive those benefits, just like we do not smoke opium to get the benefits of morphineMore widespread use would increase the dangers of secondhand smoke damage to nonsmokers  and children in the homes of users.

  • A 1999 The Institute of Medicine (IOM) study explained that “smoked marijuana . . . is a crude THC delivery system that also delivers harmful substances.” In addition, “plants contain a variable mixture of biologically active compounds and cannot be expected to provide a precisely defined drug effect.” Therefore, the study concluded that “there is little future in smoked marijuana as a medically approved medication.”

  • The principal IOM investigators explicitly stated that using smoked marijuana in clinical trials “should not be designed to develop it as a licensed drug, but should be a stepping stone to the development of new, safe delivery systems of cannabinoids.”

  • In states with medical marijuana laws, the average user is a male in his 30s with no terminal illness and a history of drug abuse. 

  • Less than 2% of users have cancer or AIDS.

  • Residents of states with medical marijuana laws generally have abuse and dependence rates almost twice as high as states with no such laws.

  • ·Research should be conducted to produce pharmacy-attainable, non-smoked medications based on marijuana.

 

13.   The Alaska Initiative is premature. The experience of Colorado and Washington is not promising. It is better to wait to see if predictions of both sides are borne out by hard data rather than rely on speculation and the promise that benefit will outweigh harm.

  • Two independent reports released in August 2013 document how Colorado’s supposedly regulated system is not well regulated at all.

  • Teen use has increased in the past five years. Currently, the marijuana use rate among Colorado teens is 50% above the national average.

  • Drug-related referrals for high school students testing positive for marijuana has increased.

  • Medical marijuana is easily diverted to youth.

  • While the total number of car crashes in Colorado declined from 2007 to 2011, the number of fatal car crashes with drivers testing positive for marijuana rose sharply.

 

14.   Marijuana is often used as a stepping-stone drug, leading to heroin, cocaine, or other harder drugs.

  • Teens who experiment with marijuana may be making themselves more vulnerable to heroin addiction later in life, if the findings from experiments with rats are any indication. Cannabis has very long-term, enduring effects on the brain..

  • Marijuana is a frequent precursor to the use of more dangerous drugs and signals a significantly enhanced likelihood of drug problems in adult life. The Journal of the American Medical Association reported, based on a study of 300 sets of twins, “that marijuana-using twins were four times more likely than their siblings to use cocaine and crack cocaine, and five times more likely to use hallucinogens such as LSD.”

  • Long-term studies on patterns of drug usage among young people show that very few of them use other drugs without first starting with marijuana. For example, one study found that among adults (age 26 and older) who had used cocaine, 62 percent had initiated marijuana use before age 15. By contrast, less than one percent of adults who never tried marijuana went on to use cocaine. 

  • Columbia University’s National Center on Addiction and Substance Abuse (CASA) reports that teens who used marijuana at least once in the last month are 13 times likelier than other teens to use another drug like cocaine, heroin, or methamphetamine and almost 26 times likelier than those teens who have never used marijuana to use  another drug.

  • An estimated 3.1 million persons aged 12 or older – an average of approximately 8,400 per day – used a drug other than alcohol for the first time in the past year according to the 2011 National Survey on Drug Use and Health. More than two-thirds (68 percent) of these new users reported that marijuana was the first drug they tried. 

  • Nearly one in ten high school students (9 percent) report using marijuana 20 times or more in the past month according to the findings of the 2011 Partnership Attitude Tracking Survey.

  • Teens past month heavy marijuana users are significantly more likely than teens that have not used marijuana in the past to: use cocaine/crack (30 times more likely); use Ecstasy (20 times more likely); abuse prescription pain relievers (15 times more likely): and abuse over the counter medications (14 times more likely). This clearly denotes that teens that use marijuana regularly are using other substances at a much higher rate than teens who do not smoke marijuana, or smoke less often.

 

ENDNOTES

AACOP survey of  Alaskan police chiefs conducted April 28-May 5, 2014

The Legalization of Marijuana in Colorado: The Impact Vol. 1/August 2013

AACOP survey of  Alaskan police chiefs conducted April 28-May 5, 2014

MARIJUANA USE BY YOUNG PEOPLE: The Impact of State Medical Marijuana Laws By Karen O’Keefe, Esq, .Director of State Policies, Marijuana Policy Project and Mitch Earleywine, Ph.D., Professor of Psychology University at Albany, State University of New York, Updated: June 2011

AACOP survey of  Alaskan police chiefs conducted April 28-May 5, 2014

The Legalization of Marijuana in Colorado: The Impact Vol. 1/August 2013

AACOP survey of  Alaskan police chiefs conducted April 28-May 5, 2014

AACOP survey of  Alaskan police chiefs conducted April 28-May 5, 2014

AACOP survey of  Alaskan police chiefs conducted April 28-May 5, 2014

http://en.wikipedia.org/wiki/Cannabis_drug_testing

Interview with AK Crime lab director O. Dym, May 27,2014

NIDA Info Facts: Drugged Driving, September 10, 2009, page 1. http://drugabuse.gov/Infofacts/driving.html

Volz, Matt. “Drug overdose: Medical marijuana facing a backlash.” http://www.msnbc.msn.com/id/37282436

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Alaska Department of Corrections prison population census data 2013

Kilmer, B, Caulkins, J.P, Bond, B.M. & Reuter, P.H. “Reducing Drug Trafficking Revenues and Violence in Mexico: Would Legalizing Marijuana in California Help?” Santa Monica, CA: RAND Corporation, 2010.

http://www.rand.org/pubs/occasional_papers/OP325  ___“Annual Report 2012: The State of the Drugs Problem in Europe.” European Monitoring Centre for Drugs and Drug Addiction. Lisbon. November 2012. P. 35.

Annual Report 2012: The State of the Drugs Problem in Europe.” European Monitoring Centre for Drugs and Drug Addiction. Lisbon. November 2012. P. 35.

MacCoun, R. & Reuter, P. (2001). Evaluating Alternate Cannabis Regimes. The British Journal of Psychiatry, 178.

INTRAVAL Bureau for Research & Consultancy. “Coffeeshops in the Netherlands 2004.” Dutch Ministry of Justice. June 2005.http://www.intraval.nl/en/b/b45.html.

MacCoun, R. (2010). What can we learn from the Dutch Cannabis Coffeeshop experience? RAND Drug Policy Research Center.Retrieved from http://www.rand.org/content/dam/rand/pubs/working_papers/2010/RAND_WR768.pdf

European Monitoring Center for Drugs and Drug and Addiction. (2011). Drug Policy Profiles-Portugal. Retrieved fromhttp://www.emcdda.europa.eu/publications/drug–policyprofiles/portugal

Institute of Medicine. “Marijuana and Medicine: Assessing the Science Base.” (1999). Summary http://www.nap.edu/html/marimed   (January 11, 2006).

Benson, John A., Jr. and Watson, Stanley J., Jr. “Strike a Balance in the Marijuana Debate.” The Standard-Times. 13 April 1999.

O’Connell, T.J. & Bou-Matar, C.B. (2007). Long term marijuana users seeking medical cannabis in California

(2001–2007): demographics, social characteristics, patterns of cannabis and other drug use of 4117 applicants. Harm

Reduction Journal, 4(16)

   Colorado Department of Public Health and Environment. (2011)

Cerda, M., et al. (2012). Medical marijuana laws in 50 states: Investigating the relationship between state legalization of medical marijuana and marijuana use, abuse and dependence. Drug & Alcohol Dependence, 120(1-3).

Colorado Office of the State Auditor. (2013). & City of Denver Office of the Auditor. (2013).

 NSDUH, Summary of National Findings, 2012. Retrieved from

 http://www.samhsa.gov/data/NSDUH/2012SummNatFindDetTables/NationalFindings/NSDUHresults2012.pdf

Rocky Mountain HIDTA. (2013). Legalization of Marijuana in Colorado: The Impact. Retrieved from

 http://www.rmhidta.org/html/FINAL%20Legalization%20of%20MJ%20in%20Colorado%20The%20Impact.pdf

Salomonsen-Sautel, S., et al. (2012). Medical marijuana use among adolescents in substance abuse treatment. Journal of American Academic Child & Adolescent Psychiatry, 51(7).

Rocky Mountain HIDTA. (2013). Legalization of Marijuana in Colorado: The Impact. Retrieved from

http://www.rmhidta.org/html/FINAL%20Legalization%20of%20MJ%20in%20Colorado%20The%20Impact.pdf

Harding, Anne. “Pot May Indeed Lead to Heroin Use, Rat Study Shows” Reuters. July 12, 2006. See also: “Why Teenagers Should Steer Clear of Cannabis” Vine, Gaia. www.NewScientist.com

“What Americans Need to Know about Marijuana.” Office of National Drug Control Policy. October 2003.

Gfroerer, Joseph C., et al. “Initiation of Marijuana Use: Trends, Patterns and Implications.” Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. July 2002. Page 71.

“Non-Medical Marijuana II: Rite of Passage or Russian Roulette?” CASA Reports. April 2004. Chapter V, Page 15.

“More Than Two-Thirds of U.S. Residents Who First Started Using Drugs in the Past Year began with Marijuana: 22% Started with Nonmedical Use of Prescriptions.” CESARFAX. Vol. 21. Issue 42. October 22, 2012

“Nearly One in Ten U.S High School Students Report Heavy Marijuana Use in the Past Month: One Third or More of  Heavy Users Also Used Cocaine, Ecstasy, or Other Drugs.” CESARFAX, Vol 21. Issue 21. May 29, 2012

The Partnership Attitude Tracking Study: 2011 Parents and Teens Full Report.” MetLife and the Partnership At Drugfree.org.   May 2, 2012. P7.

Source:

Alaska Association of Chiefs of Police, Inc. – 14 Reasons Against Marijuana Legalization Sept.2014

 

Loyola adolescent medicine expert talks about the potential dangers of marijuana for teens 

Whether states should legalize marijuana for recreational and medical use is a hot topic across the country. As the debates continue a potentially dangerous environment is being created where more preteens, teens and young adult are beginning to use the substance with the feeling that it is safe. In fact, 36 percent of all seniors in high school and 7 percent of eighth-graders report using the drug in the past month, according to a recent study. Though public perception is that marijuana is a harmless drug, research is showing it can have a damaging impact on developing brains and may lead to life-long addiction.

“Teens are seeing marijuana as a safe substance, but its effects on the adolescent brain can be dangerous, especially if there is heavy use. As the stigma of marijuana use becomes less the number of teens using the drug has increased. More high-schoolers in the U.S. now smoke marijuana than they do cigarettes,” said Garry Sigman, MD, director of the adolescent medicine division at Loyola University Health System and professor in the Department of Pediatrics at Loyola University Chicago Stritch School of Medicine.

Marijuana is an addictive substance and, according to Sigman, adolescents are 2-4 times more likely to become dependent on the drug within two years after first use compared with adult users. “Marijuana is the most common substance addiction being treated in adolescents in rehabilitation centers across the country. Like all addictive substances, marijuana is used to lessen uncomfortable feelings like anxiety and depression. Because the type of addiction is seen as less ‘intense’ in comparison to other substances such as cocaine or heroin, many people don’t realize that marijuana can cause dependence and has a withdrawal syndrome,” Sigman said.

Some adolescents use marijuana only occasionally because of peer pressure at a party or in a social setting, but others self-medicate with marijuana to cope with emotions and stress. One of the signs of a substance-use disorder is when drugs are used often to cope with uncomfortable feelings.

Addiction isn’t the only hazard for adolescents when it comes to smoking marijuana. Research shows that heavy use can lead to neurotoxicity and alternations in brain development leading to:
• Impairment in thinking
• Poor educational outcomes and perhaps a lower IQ
• Increased likelihood of dropping out of school
• Symptoms of chronic bronchitis
• Increased risk of psychosis disorders in those who are predisposed.

“Parents should inform themselves about the scientific facts relating to marijuana and the developing brain and be able to discuss the topic calmly and rationally. They need to explain that the dose of the drug in a ‘joint’ is three to four times higher than in years past, and that if the parents occasionally used during their lives, they now know that the risk is present if used before adulthood,” Sigman said.

Source:  http://www.newswise.com/articles/view/623773/?sc=dwtn    Sept. 2014

The fall of the Roman Empire is the subject of much debate, and includes attention to the possible role of their aqueducts, lined with lead. More likely, the decline was the result of lead poisoning caused by the consumption of grape juice boiled in lead cooking pots. The aristocracy of Rome consumed as much as two liters of wine a day — almost three bottles — adding alcoholism to the risk of lead poisoning. 

Lead poisoning has an impact on intelligence, even at concentrations as low as 10 micrograms per deciliter. In the New England Journal of Medicine on April 17, 2003, Richard L. Canfield writes that children between the ages of 3 and 5 suffer a decline of 7.4 IQ points from environmental lead exposure. That figure represents a substantial loss of intellectual capacity. There is no effective treatment for children so exposed. One can be grateful for a dedicated public health campaign to mitigate this powerful yet avoidable toxin in the lives of children.

That said, no one is advocating that pregnant woman splash lead-based paint in their nursery. Unlike another substance that also holds high risk during the prenatal period. Incredibly, it is a substance that for pregnant women is more than permitted, it is encouraged by some advocates. That substance is marijuana. In the life of the developing adolescent, heavy marijuana exposure is associated with brain abnormalities, emotional disruption, memory decline, and yes, loss of IQ; a decline of an estimated 8 points into adulthood, according to research by M. Meier in the Proceedings of the National Academy of Sciences in October, 2012. But what of prenatal exposure, from maternal marijuana use?

The website Cannabis Culture provides an answer in a 1998 article. The opening graphic is of a dreamy, topless woman who is in the late-term of her pregnancy. She is curled around a hookah. Under advice from a “Dr. Kate,” she is told that smoking marijuana while pregnant is not only safe, but that “cannabis can be a special friend to pregnant women in times of need.” It is said to mellow out those periods of morning sickness and to reduce anxiety.

The potential impact of such misinformation is widespread. According to the 2012 National Survey of Drug Use and Health, the rate of illicit drug use in 2012 was 18.3 percent among pregnant women aged 15 to 17. The drug being used is overwhelmingly marijuana.

An article by L. Goldschmidt in Neurotoxical Teratology in April/May 2000 concluded “Prenatal marijuana use was significantly related to increased hyperactivity, impulsivity and inattention syndrome (as well as) increased delinquency.” The marijuana used by pregnant women in this study would almost certainly be seen today as low-potency.

Recent research is even more specific concerning the damage. For instance, Xinyu Wang published on Dec. 15, 2004 in Biological Psychiatry results from examination of foetal brains. It noted, “Marijuana is the illicit drug most used by pregnant women, and behavioral and cognitive impairments have been documented in cannabis-exposed offspring.”

Their results showed “specific alterations of gene expression in distinct neuronal populations of the fetal brain as a consequence of maternal cannabis use.” The reduction was correlated with the amount of maternal marijuana intake during pregnancy, and particularly affected male fetuses. The THC “readily crosses the placenta and can thus affect the fetus,” while “longitudinal human studies have shown motor, social, and cognitive disturbances in offspring who were exposed to cannabis prenatally.” Finally, “school children exposed in utero to marijuana were also weak in planning, integration and judgment skills.”

The authors also note “Depending on the community, 3 percent to 41 percent of neonates born in North America are exposed in utero to marijuana.” Marijuana, the president has assured us in an interview with  David Remnick  (The New Yorker, Jan. 27, 2014), is “no more dangerous than alcohol.” To which he could now add, “and for the newly born, only marginally more dangerous than lead.” With this president, you take your assurances where you may.

In Colorado today, marijuana is treated as a legal recreational indulgence and is hawked as a medicine. Moreover, adolescent use of this substance, in the form of the new, highly potent industrial dope now being produced, is soaring. Included in that population of adolescent users are young females, some of whom are, or shortly will be, pregnant.

Murray is a former White House chief scientist and currently a senior fellow at the Center for Substance Abuse Policy at Hudson Institute in Washington, D.C.

Source:http://www.utsandiego.com/news/2014/sep/25/pregnancy-marijuana/    Sept   2014

 An early onset of drinking is a risk factor for subsequent heavy drinking and negative outcomes among high school students, finds a new study. 

Researchers asked 295 adolescent drinkers (163 females, 132 males) with an average age of 16 years to complete an anonymous survey about their substance use. These self-report questions assessed age at first intoxication – for example, “How old were you the first time you tried alcohol/got drunk?”  They also took stock of the previous month’s consumption of alcohol, including an assessment of the frequency of engaging in binge drinking.

“Teenagers who have their first drink at an early age drink more heavily, on average, than those who start drinking later on,” said Meghan E. Morean, an assistant professor of psychology at the Oberlin College, Ohio and adjunct assistant professor of psychiatry at Yale School of Medicine. The findings also suggest that how quickly teenagers move from having their first drink to getting drunk for the first time is an important piece of the puzzle.

“In total, having your first drink at a young age and quickly moving to drinking to the point of getting drunk are associated with underage alcohol use and binge drinking, which we defined as five or more drinks on an occasion in this study,” Morean noted. We would expect a teenager who had his first drink at age 14, and who got drunk at 15, to be a heavier drinker than a teenager who had his first drink at age 14, and waited to get drunk until age 18, researchers emphasised.

“The key finding here is that both age of first use and delay from first use to first intoxication serve as risk factors for heavy drinking in adolescence,” said William R. Corbin, associate professor and director of clinical training in the department of psychology at Arizona State University

The study is scheduled to be published in the journal Alcoholism: Clinical and Experimental Research.

Source:  www.business-standrd.com  20th Sept 2014

Many people who struggle with alcohol or drugs have a difficult time getting better. There are many reasons why these people do not get the help they need to get better. Many family members who see their loved ones struggle have a very difficult time in getting their loved ones assistance. Here are six suggestions on how to convince a person struggling with alcohol or drugs to get the help they need to get better. 

1. Family Intervention

The most popular way to get someone the help they need is to do a family intervention. This is when family members and an interventionist get together with the addict to tell them how they love them and wish that they get help to get better. Each family member takes a turn and tells the person how special they are and that they need to get help. The person who is struggling listens and hopefully they become convinced to get the help they need.

2. Talk To The Person On What Will Happen If They Do Not Get Help

Another way to convince the person who is struggling with alcohol or drugs is to get someone who is an expert on addiction and have them do a one on one talk with this person. This expert on addiction should explain to the addict what will happen if they do not get the help they need to get better. Basically, the expert should warn the person of the dire consequences of what will happen if they do not change their ways. The expert should be vivid as possible and hold nothing back. The goal is to convince the person to get help or they will suffer and eventually their life will slowly come to an end.

3. Use The Services of A Professional Or A Former Addict

Try to find a professional or even a former addict who has “Been There” to talk to the person. This is similar to Step Two, however instead of warning the person, these professionals can use their skills to talk and try to reason with the person. These experts are usually trained and can use a proactive approach into trying to convince the addict to get help. The goal is to try to reason and talk with the person so they can get professional help.

4. Find Out The Reasons Why The Person Won’t Get Help

Many people overlook this suggestion. Ask the person who is struggling with alcohol or drugs to list 3 reasons why they will not get help. At first, they will say all kinds of things, but continue to engage the person and get the 3 main reasons why they refuse to get help. It might take a couple of tries but listen to what they say. Once you get the answers, WRITE them down on a piece of paper. Note: Fear and Frustration are huge factors for the person not getting help.

5. Determine The Solutions To Those Barriers

Once you get those 3 reasons, get a professional or an expert to find the solutions to those issues. For example, the person says that they will not get help because they tried a few times and they failed and that they will fail again. Ask a few addiction professionals to find a solution to this issue that will help the addict overcome this barrier. One good answer to this example is the following: “Yes, you tried to get better and failed however this time we will do things differently. We will keep a daily diary of everything you do and you or someone else will document what you do each day. If you stumble or fail you will write down your feelings at the time and why you failed. When you recover from a bad episode you can READ your diary and find out what went wrong. Once you know what went wrong you will know why you failed and will find a way to prevent this from happening again.”

Use your list from step three and list every positive thing that will counter those barriers. When you are finished, present this to the person who is struggling and explain what you came up with. This will help reduce the person’s fears and anxieties and may convince them to get help. Developing a plan to counter their reasons of not getting help will go a long way.

6. Talk to the Person Instead of Talking At Them

Nobody wants to be lectured. Be honest with them and tell them that it will require some hard work on their part but that they can get better. If they don’t get help, they will suffer. The person who is struggling is scared and they need help in overcoming their fears and resistance to getting help. Remember to find out those fears, address possible solutions to those fears, and you will have a better chance of getting through to that person. Hopefully, sooner or later, you will be able to get through to the person. The key is to be persistent. Be very persistent.

Source:   www.huffingtonpost.com  25th September 2014

D.A.R.E. America joins every major public health association, including the American Medical Association, the American Psychiatric Association, the American Society of Addiction Medicine, and other groups in opposing the legalization of marijuana. Simply put, legalization would drastically increase marijuana use and use disorder rates, as well as hamper public safety and health at a cost of billions to society in lost productivity, impaired driving, health care, and other costs. 

Of particular concern to D.A.R.E. is the relaxed attitude regarding the use of marijuana, which will lead to increased accessibility and reduced perception of harm. This will undoubtedly contribute to greater youth use and abuse of the drug.

Legalized marijuana means ushering in the next “Big Tobacco.” Already, private holding groups and financiers have raised millions of start-up dollars to promote businesses that will sell marijuana and marijuana-related merchandise.  The former head of Strategy for Microsoft has even said he wants to “mint more millionaires than Microsoft” with marijuana and that he wants to create the “Starbucks of marijuana.” A massive industry has exploded in the legal marijuana states of Washington and Colorado.

Colorado’s experience is already going poorly. Colorado is the first jurisdiction to fully legalize marijuana and sell marijuana in state-licensed stores. And already in its first year, the experience is a disaster. Calls to poison centers have skyrocketed, incidents involving kids coming to school with marijuana candy and vaporizers have soared, and explosions involving butane hash oil extraction have increased. Employers are reporting more workplace incidents involving marijuana use, and deaths have been attributed to ingesting marijuana “edibles.” Open Colorado newspapers and magazines on your web browser (or look at the real thing) on any given day and you will find pages of marijuana advertisements, coupons, and cartoons. Remember Joe Camel and candy cigarettes? The marijuana industry offers a myriad of marijuana-related products such as candies, sodas, ice cream, and cartoon-themed paraphernalia and vaporizers, which are undoubtedly attractive to children and teens.i  As Al Bronstein, medical director of the Rocky Mountain Poison and Drug Center recently told the Denver Post, “We’re seeing hallucinations, they become sick to their stomachs, they throw up, they become dizzy and very anxious.” Bronstein reported that in 2013 there were 126 calls concerning adverse reactions to marijuana. From January to April 2014 alone the center receive 65 calls.ii Dr. Lavonas, also from the Rocky Mountain Poison and Drug Center, said in 2014 that emergency rooms have seen a spike in psychotic reactions from people not accustomed to high potency marijuana sold legally, severe vomiting that some users experience, and children and adults having problems with edibles. iii 

No advocate for marijuana legalization will openly promote making marijuana available to minors. However, it would be unwise to believe that relaxed attitudes about the drug, reduced perceptions of harm and increased availability will not result in increased youth use and abuse of marijuana. Children are the marijuana marketer’s future customers. Just as alcohol and tobacco companies have been charged with promoting their goods to children, so has the Colorado marijuana industry. In March 2014, the Colorado legislature was forced to enact legislation to prohibit edible marijuana products from being package to appeal to children. “Keeping marijuana out of the hands of kids should be a priority for all of us,” said Governor Hickenlooper, before signing the bill.iv But that was not enough.  

As discussed above, Dr. George Sam Wan of the Rocky Mountain Poison and Drug Center and his colleagues compared the proportion of marijuana ingestions by young children who were brought to an emergency room before and after October 2009, when Colorado drug enforcement laws regarding medical marijuana use were relaxed. The researchers found no record of children brought into the ER in a large Colorado children’s hospital for marijuana-related poisonings between January 2005 and September 30, 2009 — a span of 57 months. It is a different story following legalization.v Dr. Bronstein reported twenty-six people have reported poisonings from marijuana edibles this year, when the center started tracking such exposures. Six were children who swallowed innocent-looking edibles, most of which were in plain sight. Five of those kids were sent to emergency rooms, and two to hospitals for intensive care.vi

The scientific verdict is in: marijuana can be addictive and dangerous. Despite denials by legalization advocates, marijuana’s addictiveness is not debatable: 1 in 6 kids who ever try marijuana, according to the National Institutes of Health, will become addicted to the drug. Today’s marijuana is not your “Woodstock weed” – it can be 5-10 times stronger than marijuana of the past.vii More than 400,000 incidents of emergency room admissions related to marijuana occur every year, and heavy marijuana use in adolescence is connected to an 8-point reduction of IQ later in life, irrespective of alcohol use.

Marijuana legalization would cost society in real dollars, and further inequality in America. Alcohol and tobacco today give us $1 for every $10 that we as society have to pay in lost social costs, from accidents to health damage.viii The Lottery and other forms of gambling have not solved our budget problems, either. We also know these industries target the poor and disenchantedix – and we can expect the marijuana industry to do the same in order to increase profits. 

IF THEY SAY…

YOU SAY…

Marijuana is not addictive.

Science has proven – and all major scientific and medical organizations agree – that marijuana is both addictive and harmful to the human brain, especially when used as an adolescent. One in every six 16 year-olds (and one in every eleven adults) who try marijuana will become addicted to it.x

Marijuana MIGHT be psychologically addictive, but its addiction doesn’t produce physical symptoms.

Just as with alcohol and tobacco, most chronic marijuana users who attempt to stop “cold turkey” will experience an array of withdrawal symptoms such as irritability, restlessness, anxiety, depression, insomnia, and/or cravings.xi

Lots of smart, successful people have smoked marijuana. It doesn’t make you dumb.

Just because some smart people have done some dumb things, it doesn’t mean that everyone gets away with it. In fact, research shows that adolescents who smoke marijuana once a week over a two-year period are almost six times more likely than nonsmokers to drop out of school and over three times less likely to enter college.xii In a study of over 1,000 people in 2012, scientists found that using marijuana regularly before the age of 18 resulted in an average IQ of six to eight fewer points at age 38 versus to those who did not use the drug before 18.xiii These results still held for those who used regularly as teens, but stopped after 18. Researchers controlled for alcohol and other drug use as well in this study. So yes, some people may get away with using it, but not everyone.

No one goes to treatment for marijuana addiction.

More young people are in treatment for marijuana abuse or dependence than for the use of alcohol and all other drugs.xiv

Marijuana can’t hurt you.

Emergency room mentions for marijuana use now exceed those for heroin and are continuing to rise.xv

 

IF THEY SAY…

YOU SAY…

I smoked marijuana and I am fine, why should I worry about today’s kids using it?

Today’s marijuana is not your Woodstock Weed. The psychoactive ingredient in marijuana—THC—has increased almost six-fold in average potency during the past thirty years.xvi

Marijuana doesn’t cause lung cancer.

The evidence on lung cancer and marijuana is mixed – just like it was 100 years ago for smoking – but marijuana contains 50% more carcinogens than tobacco smokexvii and marijuana smokers report serious symptoms of chronic bronchitis and other respiratory illnesses.xviii

Marijuana is not a “gateway” drug.

We know that most people who use pot WON’T go onto other drugs; but 99% of people who are addicted to other drugs STARTED with alcohol and marijuana. So, indeed, marijuana use makes addiction to other drugs more likely.xix

Marijuana does not cause mental illness.

Actually, beginning in the 1980s, scientists have uncovered a direct link between marijuana use and mental illness. According to a study published in the British Medical Journal, daily use among adolescent girls is associated with a fivefold increase in the risk of depression and anxiety.xx  Youth who begin smoking marijuana at an earlier age are more likely to have an impaired ability to experience normal emotional responses.xxi

 

The link between marijuana use and mental health extends beyond anxiety and depression. Marijuana users have a six times higher risk of schizophreniaxxii, are significantly more likely to development other psychotic illnesses.

Marijuana makes you a better driver, especially when compared to alcohol.

Just because you may go 35 MPH in a 65 MPH zone versus 85 MPH if you are drunk, it does not mean you are driving safely! In fact, marijuana intoxication doubles your risk of a car crash according to the most exhaustive research reviews ever conducted on the subject.xxiii

 

IF THEY SAY…

YOU SAY…

Marijuana does not affect the workplace.

Marijuana use impairs the ability to function effectively and safely on the job and increases work-related absences, tardiness, accidents, compensation claims, and job turnover.xxiv

Marijuana simply makes you happier over the long term.

Regular marijuana use is associated with lower satisfaction with intimate romantic relationships, work, family, friends, leisure pursuits, and life in general.xxv

Marijuana users are clogging our prisons.

A survey by the Bureau of Justice Statistics showed that 0.7% of all state inmates were behind bars for marijuana possession only (with many of them pleading down from more serious crimes). In total, one tenth of one percent (0.1 percent) of all state prisoners was marijuana-possession offenders with no prior sentences. Other independent research has shown that the risk of arrest for each “joint,” or marijuana cigarette, smoked is about 1 arrest for every 12,000 joints.xxvi

Marijuana is medicine.

 

 

Marijuana may contain medical components, like opium does. But we don’t smoke opium to get the effects of Morphine. Similarly we don’t need to smoke marijuana to get its potential medical benefit.xxvii

The sick and dying need medical marijuana programs to stay alive.

 

Research shows that very few of those seeking a recommendation for medical marijuana have cancer, HIV/AIDS, glaucoma, or multiple sclerosis;xxviii and im most states that permits the use of medical marijuana, less than 2-3% of users report having cancer, HIV/AIDS, glaucoma, MS, or other life-threatening diseases.xxix

Marijuana should be rescheduled to facilitate its medical and legitimate use.

 

Rescheduling is a source of major confusion. Marijuana meets the technical definition of Schedule I because it is not an individual product with a defined dose. You can’t dose anything that is smoked or used in a crude form. However, components of marijuana can be scheduled for medical use, and that research is fully legitimate. That is very different than saying a joint is medicine and should be rescheduled.xxx

 

IF THEY SAY…

YOU SAY…

Smoking or vaporizing is the only way to get the medical benefits of marijuana.

 

No modern medicine is smoked. And we already have a pill on the market available to people with the active ingredient of marijuana (THC) in it – Marinol. That is available at pharmacies today. Other drugs are also in development, including Sativex (for MS and cancer pain) and Epidiolex (for epilepsy). Both of these drugs are available today through research programs.xxxi

Medical marijuana has not increased marijuana use in the general population.

Studies are mixed on this, but it appears that if a state has medical “dispensaries” (stores) and home cultivation, then the potency of marijuana and the use and problems among youth are higher than in states without such programs. This confirms research in 2012 from five epidemiological researchers at Columbia University. Using results from several large national surveys, they concluded, “residents of states with medical marijuana laws had higher odds of marijuana use and marijuana abuse/dependence than residents of states without such laws.xxxii

Legalization is inevitable – the vast majority of the country wants it, and states keep legalizing in succession.

The increase in support for legalization reflects the tens of millions of dollars poured into the legalization movement over the past 30 years. Legalization is not inevitable and there is evidence to show that support has stalled since 2013.

Alcohol is legal, why shouldn’t marijuana also be legal?

Our currently legal drugs – alcohol and tobacco – provide a good example, since both youth and adults use them far more frequently than illegal drugs. According to recent surveys, alcohol use is used by 52% of Americans and tobacco is used by 27% of Americans, but marijuana is used by only 8% of Americans.xxxiii

 

IF THEY SAY…

YOU SAY…

Colorado has been a good experiment in legalization.

 

 

 

Colorado has already seen problems with this policy. For example, according to the Associated Press: “Two Denver Deaths Linked to Recreational Marijuana Use”. One includes the under-aged college student who jumped to his death after ingesting marijuana cookie.

 

The number of parents calling the poison-control hotline to report their kids had consumed marijuana has risen significantly in Colorado.

Marijuana edibles and marijuana vaporizers have been found in middle and high schools.xxxiv

We can get tax revenue if we legalize marijuana.

With increased use, public health costs will also rise, likely outweighing any tax revenues from legal marijuana. For every dollar gained in alcohol and tobacco taxes, ten dollars are lost in legal, health, social, and regulatory costs.xxxv And so far in Colorado, tax revenue has fallen short of expectations.

I just want to get high. The government shouldn’t be able to tell me that I can’t.

 

Legalization is not about just “getting high.” By legalizing marijuana, the United States would be ushering in a new, for-profit industry – not different from Big Tobacco. Already, private holding groups and financiers have raised millions of start-up dollars to promote businesses that will sell marijuana and marijuana-related merchandise. Cannabis food and candy is being marketed to children and are already responsible for a growing number of marijuana-related ER visits.xxxvi

 

Edibles with names such as “Ring Pots” and “Pot Tarts” are inspired by common children candy and dessert products such as “Ring Pops” and “Pop Tarts.” Moreover, a large vaporization industry is now emerging and targeting youth, allowing young people and minors to use marijuana more easily in public places without being detected.xxxvii

 

IF THEY SAY…

YOU SAY…

Legalization would remove the black market and stop enriching gangs.

Criminal enterprises do not receive the majority of their funding from marijuana. Furthermore, with legal marijuana taxed and only available to adults, a black market will continue to thrive. The black market and illegal drug dealers will continue to function – and even flourishxxxviii – under legalization, as people seek cheaper, untaxed marijuana.

 

Patients taking opioid painkillers for chronic pain not associated with cancer — conditions such as headaches, fibromyalgia and low-back pain — are more likely to risk overdose, addiction and a range of debilitating side effects than they are to improve their ability to function, a leading physicians group declared Wednesday.

A leading physicians group has laid out the conditions that should govern the long-term use of opioid painkillers such as OxyContin. (Toby Talbot / Associated Press)

http://www.latimes.com/local/lanow/la-sci-sn-painkiller-deaths-20140916-story.html

The long-term use of opioids may not, in the end, be beneficial even in patients with more severe pain conditions, including sickle-cell disease, destructive rheumatoid arthritis and severe neuropathic pain, the American Academy of Neurologists opined in a new position statement released Wednesday.

But even for patients who do appear to benefit from opioid narcotics, the neurology group warned, physicians who prescribe these drugs should be diligent in tracking a patient’s dose increases, screening for a history of depression or substance abuse, looking for signs of misuse and insisting as a condition of continued use that opioids are improving a patient’s function.

In disseminating a new position paper on opioid painkillers for chronic non-cancer pain, the American Academy of Neurology is hardly the first physicians group to sound the alarm on these medications and call for greater restraint in prescribing them. But it appears to be the first to lay out a comprehensive set of research-based guidelines that outline which patients are most (and least) likely to benefit from the ongoing use of opioids — and what practices a physician should follow in prescribing the medications for pain conditions.

The statement would govern the prescribing of morphine, codeine, oxycodone, methadone, fentanyl, hydrocodone or a combination of those drugs with acetaminophen. It was published Wednesday in the journal Neurology.

The American Academy of Neurology’s position statement also urges physicians to work with officials to reverse state laws and policies enacted in the late 1990s that made the prescribing of opioid pain medication vastly more commonplace.

The position paper notes that despite a national epidemic of painkiller addiction that has claimed more than 100,000 lives in just over a decade, many of the laws and practices adopted in the late 1990s remain unchanged. It adds that prescription drug monitoring programs — online databases that would allow physicians to quickly check on all controlled substances dispensed to a patient — “are currently underfunded, underutilized and not interoperable across state lines or healthcare systems.” The result is that patients’ tendency to develop a tolerance for opioid drugs — and to require ever-higher doses to achieve pain relief — often go unnoticed. The result is not only addiction and misuse, but an escalating risk of accidental overdose, since opioid narcotics depress breathing and, especially when mixed with alcohol or other sedative drugs, can prove deadly.

In the age group at highest risk for overdose — those between 35 and 54 — opioid use has vaulted ahead of firearms and motor vehicle crashes as a cause of death.

The American Academy of Neurology statement cites studies showing that roughly half of patients taking opioids for at least three months are still on opioids five years later. Research shows that in many cases, those patients’ doses have increased and their level of function has not improved.

In addition to screening patients for depression or past or present drug abuse, physicians prescribing a long-term course of opioids to patients with pain should draw up an “opioid treatment agreement” which sets out the responsibilities of patients and physicians. Physicians should track dose increases and assess changes in a patient’s level of function, and if a specific daily dose is reached (a “morphine equivalent dose” of 80-120 mg) and a patient’s pain is not under control, doctors should seek the help of a pain specialist.

The statement also recommends against prescribing any benzodiazepines or other sedating drugs to patients who take opioid painkillers. And it recommends the “prudent use” by physicians of random urine testing for patients taking opioids to detect misuse of the drugs or abuse of other, non-prescribed drugs. When a physician takes on the care of a patient who has taken opioid painkillers for more than three months and has aberrant behaviour or a history of overdose, he or she should consider a trial aimed at weaning the patient off such medication.

Source:   www.laties.com  1st October 2014

Prescription Drugs ‘Orphan’ Children In Eastern Kentucky

Orphaned by prescription drug overdoses .   Story highlights

  • Many children and teens in eastern Kentucky have lost a parent to drug overdose
  • “Without a normal mom and dad, you feel different,” one teen says
  • Kentucky is the fourth most medicated state in the nation and sixth for overdoses
  • A drug task force aims to help children left behind by parents’ addictions

This area of eastern Kentucky is known for lush, green hillsides and white picket fences. It is a place where bluegrass music may be heard trailing off when a car passes by, where “downtown” is a two-block stretch of quaint shops. Life here may seem simple, but a darkness has been quietly nestling itself into the community.

“Rockcastle County is averaging one drug-related death per week,” said Nancy Hale, an anti-drug activist and educator. “When your county is a little over 16,000 people and you’re losing a person a week … you’re losing a whole generation.”

The generation being lost, Hale said, is parents. An inordinate number of children in Rockcastle County — and in neighboring areas in eastern Kentucky — are living without them.

According to 2010 census data, more than 86,000 children in Kentucky are being raised by someone who is not their biological parent — mostly grandparents — and many here blame those fractured families on prescription drugs.

Prescription drugs can be dangerous 

“I know a little girl who found her father dead of a drug overdose, found her uncle dead of a drug overdose, and now she’s living with her aunt,” said Karen Kelly, executive director of Operation UNITE, a community coalition devoted to preventing overdose deaths in Kentucky.

“The kids really are the ones paying the biggest price.”

‘You’re always worried’

“It’s a terrible thing,” said Sean Watkins, 17, a junior at Rockcastle County High. “Especially in our community, it’s really bad.”

When he was 10, Watkins and his family were expecting his mother for dinner, but she never showed up. He and a family friend went looking for her at her home.

They walked into her bedroom and saw her face down, motionless. The friend quickly whisked Watkins out of the room. “I don’t know what was going on, but I knew something was wrong,” said Watkins.

His mother was dead after overdosing on Oxycontin.

At the time, Watkins says that he and his mother had been estranged for years because of her prescription-drug addiction. His father had not been in his life since shortly after his birth.

“Growing up without parents, without a normal mom and dad, you feel different,” said Watkins. “You go to your friend’s house and they have a happy family … you’re jealous. You want that.”

Shortly after his mother’s death, Watkins says his grandmother also became addicted to prescription drugs, and eventually vanished. Now he lives with his grandfather.  “I’m grateful that I have my grandfather who stepped in and takes care of me now,” said Watkins. Still, he calls growing up without parents “horrible.”

Gupta: Let’s end the prescription drug death epidemic

It sometimes feels is as if every student at his school has been touched by the epidemic, he said. “The hardest part of growing up without a dad would be not having that model family that you always see,” said Avery Bradshaw, 16, also a student at Rockcastle County High School.

Bradshaw’s father overdosed on Oxycontin when he was 7. His mother, he said, is in and out of his life, so he is being raised by his great-grandparents.

Avery knows many children at school who are not so lucky. After their parents overdose or abscond because of prescription drugs, the kids go from couch to couch and from home to home — living in a constant state of transience.

For those children whose parents have not overdosed but are deep in their addiction, there is a sense of perpetual wariness about what they might find when they get home from school.

“You’re always worried … if your parents are even going to be there, you know, what’s going on in your house?” said Bradshaw. “A lot of kids have to go through that every day and it definitely wears them down, you know.”

Guardians’ Day

The prescription drug overdose epidemic just recently began appearing on the national radar, so figures concerning the number of children orphaned after a parent overdoses are difficult to assess.

What is known is the high number of overdoses, broadly: In the United States, someone dies of a prescription drug-related overdose about every 19 minutes. The epidemic affects every state in the nation, and has hit hardest in places like Washington, Utah, Florida, Louisiana, Nevada and New Mexico.

Kentucky — and the Appalachian ridge, generally — is one of the regions hit hardest. Kentucky is the fourth most medicated state in the nation and it has the sixth highest rate of overdose deaths, according to the state’s Attorney General.

In Knott County, adjacent to Rockcastle, Kelly said more than half of the children have lost their parents due to death, abandonment or legal removal. Anecdotally, she says, the numbers in other areas could be even higher.

And in nearby Johnson County, so many children have lost parents that school administrators there changed “Parents’ Day” to “Guardians’ Day.”

Addiction and death are common concerns for families here, according to Kelly — too common.

Her voice wavering, Kelly recalled the story of a young girl who realized her mother was overdosing on prescription drugs right in front of her.

“She wanted to call the police and the other adults in the home were so high they wouldn’t allow her to call,” said Kelly. “So she crawled up into her mother’s arms while her mother died. Now she’s just living with a lady she met at the local Boys and Girls Club.

“Those are the situations we’re dealing with in eastern Kentucky.”

Prescription drug deaths: Two stories

“Someone has to take care of these kids, and we simply do not have the facilities to do that,” said U.S. Rep. Hal Rogers, whose district in Kentucky is mired in prescription drug abuse. “So it’s neighbors, it’s churches, other civic groups that are trying to be parents to these kids who are orphaned by drug-abusing parents.

“That’s a huge undertaking, because there’s literally tens of thousands of these young children,” he added.

Rogers started the Operation UNITE drug task force in 2003 as a response to the broader prescription drug abuse epidemic in his state. Initially, he thought, “If we could get the pushers off the streets, that the problem would be solved.”

But years after he launched the task force, groups of children were showing up at community meetings to speak of their struggles after one parent — or both — overdosed.

“That hit me like a ton of bricks in the head,” said Rogers. “These are young people who are now thrown into the streets. So there are some real side effects to these parents using drugs.”

Now, the UNITE program is channeling energy toward the children floundering socially, emotionally and academically after losing parents. They have programs set up at schools across Kentucky.

‘It’s time for it to stop’

Hale, who worked in the local school system for 34 years, started a UNITE chapter at Rockcastle County High.

“It really got to the point where we were sick and tired of going to funerals,” Hale said. “We were tired of having kids come in and not being able to sit through physics class because they were worried about Mom who had overdosed. So we were like, ‘What can we do? How can we help these families?'”

One way UNITE helps is by educating and counseling children who are having problems at home related to addiction. The group also empowers children like Bradshaw to speak out about their own loss.

“I know that a lot of kids deal with drug abuse from their parents,” said Bradshaw. “I don’t know how many have lost parents, but I know a lot of kids definitely deal with that going home every day. I think right now we’re definitely at a point where everybody needs to know about it and how it affects everybody.”

“It’s time for it to stop,” said Kelly. “It’s leaving our communities in shreds and we’re left behind to pick up the pieces from that.”

Advocates such as Hale and Kelly are desperate for an intervention to reach the thousands of children who are not being helped by programs like UNITE.  Watkins said that the pain of having no parents is something that he will deal with for the rest of his life.

“People have to understand that this is a problem,” he said. “It doesn’t affect just the person that uses, it affects the entire family.”

Source:  http://edition.cnn.com/2012/12/14/health/kentucky-overdoses/index.html

 

Pot plants grow at a medical marijuana dispensary in San Jose Photograph by David Paul Morris/Bloomberg

Months after her biotechnology company sold for $40 million, Jessica Tonani is on Seattle’s Highway 99, where Kurt Cobain in his final days shot heroin in cheap motels. She’s scoring a gram of Blueberry Kush.

Tonani doesn’t plan to smoke the pot. Her typical procedure is to isolate some of its DNA and bank it, sequence its genetic profile, and test it for bacteria. After her stop at Choice Wellness, a medical marijuana store in one of the states where pot is newly legal, she buys the same strain in three more places (often collecting a “new-patient gift” of pot-infused gummi bears or goldfish). The goal for her new company, Verda Bio, is to build a database bringing order to billions of potential DNA combinations and, eventually, create stable strains that people can grow like a Red Delicious apple. Right now, Tonani says, people using pot for health conditions—legal in 23 U.S. states—are doing the equivalent of rummaging through their medicine cabinet blindfolded. One day they might get Tylenol; another, mouthwash. Even when they buy the same strain from the same place, it might not have the same effect because of differences in how each plant is grown. The variety Harlequin, for example, is sometimes recommended for children with epilepsy because it’s high in cannabidiol, or CBD, a non-psychedelic pot compound that appears to limit seizures.

Tonani analyzed more than 20 samples of Harlequin along with Analytical 360, a Seattle testing lab, and found that 22 percent were high in the psychedelic tetrahydrocannabinol, or THC, and had almost no CBD. Any kids taking it were likely just getting stoned.

Tonani is also looking at contaminants to determine where they’re introduced and how to control for them. The first two samples turned up a long list of nastiness, including the fecal bacteria Enterobacter asburiae and the vaginal bacteria Gardnerella vaginalis. What this means, politely, is that many people handling pot don’t wash their hands.

The irony of legalization in the U.S. is that recreational users often now have more certainty of their weed’s safety than people with legitimate conditions whose suffering was part of the original justification. Washington State, for example, requires its few dozen recreational stores to test pot for contaminants and to display THC and CBD content. There’s no such rule for the far more numerous medical pot stores—as many as 300 in the Seattle area alone—which are still in a legal gray area after the state legislature failed to pass a bill regulating them this year.

“It’s exactly the opposite of the way it should be,” says Randy Oliver, chief science officer at Analytical 360. Oliver says his lab gives failing grades to about 15 percent of the recreational samples it tests for mold, potentially dangerous to sick people with compromised immune systems. Medical pot stores rarely seek tests of mold and other contaminants, he says.

Some of the latest states permitting medical marijuana, including Florida and Utah, have done so by allowing only a type that’s verified as low in THC and high in CBD. Colorado, the other state to permit recreational use, doesn’t require contaminant testing for medical marijuana centers, though most test on their own, says Natriece Bryant, a spokeswoman for the state’s Marijuana Enforcement Division. Colorado also has rules on hand-washing and sanitation for those locations.

In the dispensaries Tonani visits, there’s little consistency. The waiting room in one place is like a doctor’s office, with plush leather chairs and stacks of manila folders. At another, lit with a harsh bulb over a marijuana plant growing in a converted shower, the guy at the counter says he’s never found that certain strains work any better for ailments. Just find one that gets you really high and numbs the pain, he says. Tonani, 38, who co-founded GnuBIO, a DNA sequencing company sold (PDF) in April to Bio-Rad Laboratories (BIO), has a personal as well as financial interest in pot’s future. She turned to the drug a decade ago for a gastrointestinal condition that led to the removal of part of her stomach, multiple surgeries, and twice-weekly intravenous infusions. Her doctor has since asked her to counsel other patients who think pot might help, and she’s frustrated not to have better answers.

While Colorado is spending $9 million on research into marijuana’s potential medical benefits, there’s little federal funding because of pot’s classification as a Schedule I dangerous drug. Many of the cannabis breakthroughs—like Sativex, a mouth spray for multiple sclerosis sufferers developed by the U.K.’s GW Pharmaceuticals (GWPH)—have occurred overseas. Verda Bio, which may raise money from investors later this year, hopes to eventually generate revenue from licensing or sales of stable plant varieties and cannabis-based treatments, Tonani says.

“I honestly believe it saved my life,” she says of pot. “But it’s just not a medical system right now. Some people get lucky, and some people don’t.” Source: http://www.businessweek.com/ 8th August 2014

CORRESPONDENCE FROM TEN DOCTORS

To the Editor: In their article, Volkow et al. (June 5 issue)1 state that marijuana may have adverse health effects, particularly on the vulnerable brains of young people. Potential mechanisms underlying the effect of marijuana on the cerebrovascular system are indeed complex, although a temporal relationship between the use of marijuana (natural or synthetic) and stroke in young people has recently been described.2,3 Simultaneously, the presence of multifocal intracranial arterial vasoconstriction was observed, which was reversible in some cases after cessation of cannabis exposure.3 Thus, stroke, which is still underdiagnosed, may potentially play a role in neuronal damage related to marijuana use, even in young people without cardiovascular risk factors. Furthermore, tetrahydrocannabinol (THC), a major component of cannabis, has been shown experimentally to impair the function of the mitochondrial respiratory chain and to increase the production of reactive oxygen species in the brain.4 Both of these processes are key events during stroke,5 suggesting that THC may also increase a patient’s vulnerability to stroke. In the ongoing shift toward marijuana legalization, physicians should probably inform marijuana users, whether they are using it for recreational purposes or therapeutic indications, about the risk of stroke with potential severe disability.

Valérie Wolff, M.D. Olivier Rouyer, M.D., Ph.D. Bernard Geny, M.D., Ph.D. Fédération de Médecine Translationnelle de Strasbourg, Strasburg, France bernard.geny@chru-strasbourg.fr

To the Editor:

Volkow et al. focus primarily on the neurocognitive and societal effects of marijuana use. We wish to note the known and potentially unknown infectious risks of marijuana, which were not discussed.

Recreational use of marijuana has been associated with a multistate outbreak of salmonellosis, illustrating the potential for widespread exposure through either inadvertent contamination during growing and storage or purposeful adulteration.1 More worrisome are the risks of marijuana use for medical purposes, particularly by the population of immunocompromised patients. Prior reports have documented the frequent contamination of marijuana with fungal organisms and the potential for severe complications, including death.2-4 These risks are not well studied and thus are poorly defined.

To date, 23 states allow the medical use of marijuana; however, dispensaries are currently not subject to regulation or quality control. We believe that the infectious risks need to be better defined, which would allow for appropriate regulatory oversight. The current approach places patients (unknowingly) at undue risk for acquisition of severe, and often lethal, infections.

George R. Thompson, III, M.D. Joseph M. Tuscano, M.D. University of California, Davis, Medical Center, Sacramento, CA grthompson@ucdavis.edu

To the Editor:

One safety aspect that is not discussed by Volkow et al. is the potential for interactions between marijuana and medications. Cannabis sativa Linnaeus products contain more than 700 distinct chemical entities. The relative abundance of these chemical entities in marijuana products and in human plasma can vary considerably depending on numerous factors, including the geographic location of cultivation, the method of preparation or administration, and the cultivar administered.

In vitro studies have shown that constituents of cannabis are potent and broad-spectrum inhibitors of key drug-metabolizing enzymes and transporters, including CYP2C9, CYP2C19, CYP2D6, CYP2E1, CYP3A4, and P-glycoprotein.1-4 Other data from in vitro studies suggest the potential for enzyme induction, especially of CYP1A2.

Case reports support the risk of pharmacokinetic interactions; however, clinical studies have been equivocal. Notably, these studies have not replicated the long-term high potency and high dose achieved by some marijuana users (e.g., hashish users). Health care providers need to maintain a high level of suspicion for drug interactions in their patients who use marijuana products.

Carol Collins, M.D. University of Washington, Seattle, WA carolc3@u.washington.edu

The authors reply: We thank Wolff et al., Thompson and Tuscano, and Collins for their correspondence regarding potential adverse consequences of marijuana use that were not explicitly highlighted in our recent review. Given the shifting landscape of marijuana use, it is critically important that we be on the lookout for the emergence of predictable or unexpected health effects. This is particularly important when it comes to the potential of marijuana to negatively affect persons with various medical conditions, to interact with specific medications, or to influence the course of heretofore unstudied conditions. It will also be important to support the targeted research needed to understand the effects, both positive and negative, that may result from patients experimenting with marijuana in an attempt to relieve their specific symptoms. These studies should also focus on the possibility that such patients may forego evidence-based treatments while chasing after the purported therapeutic benefits of marijuana. Finally, we encourage particular attention to research targeting the effects of marijuana and other substances on adolescents, whose actively developing brains make them a particularly vulnerable population.1,2

Nora D. Volkow, M.D. Wilson M. Compton, M.D. Susan R.B. Weiss, Ph.D. National Institutes of Health, Bethesda, MD nvolkow@nida.nih.gov

Since publication of their article, the authors report no further potential conflict of interest.

Source:  Adverse Health Effects of Marijuana Use N Engl J Med 2014; 371:878-879 August 28, 2014 DOI: 10.1056/NEJMc1407928

A brief look at the confusing messages emerging from current ‘prevention’ application in Australian drug policy.

Shane Varcoe – Executive Director “Will the real ‘Drug policy’ please stand up!”

Dalgarno Institute | www.dalgarnoinstitute.org.au 2

QUIT – MODERATE – ACCOMMODATE? WHICH EMPHASIS ARE WE FOLLOWING?

What is going on with Australian Drug Policy Prevention application? It appears to be struggling with, what can only be described, as a Dis-associative Identity Disorder (D.I.D). The current interpretation continues to baffle the average Australian, and leaves many of us who are active in the Alcohol and Other Drug (AOD) field scratching our heads in bewilderment and sometimes utter disbelief!

SMOKING – The new leprosy?

The growing and relentless assault against tobacco via the QUIT campaign is something only ‘mushrooms’ would know little of. This vital and effective demand-reduction and education ‘war’ has been clear from its inception, and has continued to burgeon, evermore aggressively to the crusade we now see today.

The message is at the very least unambiguous, at times, bombastic! There is no guessing what the outcome of this endeavour is to be. The message and mandate is not ‘slow down’, it is not ‘moderate’ it is QUIT. The end game is the only game. There are no illusions about the time it may take to reach that goal, but that goal is the only target to aim at and as a consequence measures and outcomes are effective – more and more Australians are quitting!

Let’s commence by acknowledging the following principle, which is all but irrefutable… accessibility, availability and permissibility all increase consumption. When you reduce these, you reduce consumption. For example, the following details shows how education and legislation all reduced demand. Accessibility, availability and permissibility are all restricted and consumption drops.

In 1945 approximately 72% of Australian men smoked. The rate has been dropping ever since then. In 2007 only 18% of Australian males were daily smokers. In 1945 26% of Australian women smoked…In 2007 women were smoking at a lower rate than men with 15.2% still smoking daily. 1

• increases in getting help to quit smoking, especially use of the Quitline (2% to 4%) and nicotine replacement therapy (7% to 10%);

• increase in one year quit rate from 8% to 11% among smokers and recent quitters;

• a statistically significant reduction of about 1.5% in the estimated adult prevalence of smoking. 2

However, as successful as this message has been, the fight is not over yet, as the following excerpt so irrefutably affirms…

“ANTI-SMOKING campaigners have far from finished their battle with the tobacco industry, with some pushing for a ”license to smoke” and many predicting that cigarettes could be outlawed within a decade.” 3

Well so was the bold opening statement in recent article ‘Now butt out: new push seeks to outlaw cigarettes’ in The Age Newspaper.

Fascinating…outlawing cigarettes, even though around 17% of Australians are still smoking – outrageous! The article went on to note that if such a ban were to take place the government would stand to lose around $6 billion dollars in tax revenue, but save an estimated $31 billion dollars currently spent per annum on smoking related health problems.

No doubt to everyone who is not a smoker this makes good health and fiscal sense…maybe even to some smokers too?    So how is that we have managed to convince a society that a ban could actually be possible on a legal drug – tobacco, that in its boom era (during the 40’s, 50’s and 60’s) was a key social accessory, that a legal ban be actually possible? A quick inventory of the processes engaged may give us some insight…

§ A clear and uncompromising acknowledgement from health, government and fiscal sectors that cigarette smoking was damaging our community.

§ The ensuing resolve that this must change for both fiscal, but more importantly, health reasons.

§ The continuing single voice of disapproval of cigarettes from academics, politicians and health professionals. (Stopped the propaganda of the pro-smoking academics/doctors and started the recognition of the undeniable facts that ‘every cigarette is doing you damage’.)

§ The sustained political will to create and implement policies to bring about change, including increased taxation, total advertising ‘blackouts’ and bans on smoking in defined places.

§ These have been followed by the creation and implementation of Demand Reduction strategies that only grow in number and intensity and the relentless public education campaign on the dangers of smoking.

It would appear from both empirical data that such resolute policies work…even with a once widely accepted and socially palatable ‘legal drug’ like tobacco.   In a recent war of words over the zealous, if not poorly thought through, ‘plain packaging’ strategy, the Federal Minister for Health Nicola Roxon was quoted as saying…. “Big tobacco are fighting to protect their profits, but we are fighting to save lives.” 4 If that vitriol wasn’t enough, she was also quoted in the Australian Newspaper, again in regard to challenges to the plain packaging strategy …‘”We’re Australians. We can make laws in Australia to protect Australians…” 5     Feisty! I like it! However, comes the question… protect Australians from what? Well, Captain Obvious may answer that in this context it would be protection from the health and health budget destroying wrecking ball that is tobacco.

But is ‘health’ the real motivator that is underpinning this zeal for the wellbeing of Australians? I hope it is, but the utter inconsistency of this focused passion belies another agenda. Or is it that some people just can’t see the utter inconsistencies or, at worst, hypocrisies of this unbalanced policy focus?

“We’re Australians. We can make laws in Australia to protect Australians…” 

Nicola Roxon – Federal Minister for Health

If ‘health’ was the sole or main issue, then wouldn’t that same zeal, that same passion for justice of Aussie’s Health be mirrored in other areas of drug policy too? I mean, Roxon is pursuing a policy – plain packaging – that has a number of downsides to it, and only small possibility of a reduction in smoking – But that was enough, it seems, for her to implement the policy! Great I say, go for it, but why doesn’t this same ‘doggedness’ apply to the two other big monsters in the drug arena?

The Federal minister seems passionate about the anti-smoking message, passionate enough to make those sweeping statements we just read – ‘fighting to save lives!’ – ‘Making laws to protect Australians!’ and pursuing every possible vehicle to STOP people killing themselves (and our health budgets)on the way.

In a very recent interview published by the Financial Review, we get a glimpse into some of the motivators behind Roxon’s campaign against tobacco – ‘This is a defining moment for Roxon one that transcends politics and is deeply personal. Her father, a one-time smoker, died of oesophageal cancer at the age of 42…“All of us girls keenly felt the loss of not having our father as we grew up but that is not the same as being out on the street as some families are…it has made me very aware of the impact that smoking can have,” Said Roxon. This mother of a 6 year old daughter went on in the interview to declare that, ”This fight is about the past and the future. “We might be making the world a healthier place for our children, and that is very motivating. I don’t think the political gains will be very high or very quick, but the long-term health impact and feeling [that] you are in government to do some good is rewarding.”’*

I have no issue at all with this motivation from Roxon, I mean it is the personal encounter with tragedy and/or the grief of loss/dysfunction that adds undisputable weight to the abundance of health-destroying evidence that exists. But again, why isn’t this same passion for health/safety/future of children applied to the other life and health destroying drugs in the ‘recreational’ arena? Nicola would do well to spend time at Rehabilitation clinics, with families of alcohol and other drug using individuals who have not only shattered their lives but their families. Countless stories of lives and potential ruined at young ages because a drug was accessible, permissible, available and cheap. This very powerful evidence should also inform the prevention focused emphasis of alcohol and other drugs policy platform. All measures including high volumetric tax, plus clear and powerful warning labels should also be taken immediately to further ensure that children and families have the greatest protection from the damage of these drugs.

Alcohol – The protected substance? 

When it comes to the other ‘legal drug’ the (it would appear) culturally entrenched alcohol – options for management have one glaring omission. Can you guess what it might be? No prizes if you said ‘QUIT’. The conspicuousness of the absence of this goal in the strategy is probably the noisiest of all elephants in the ‘Drug policy’ room. So, why is that?

*’Where there’s smoke there’s fire’ – Financial Review 29/7/2011 http://afr.com/p/home/where_there_smoke_nFtdXlsglhsibzQQCzgyDM 

The Globe, Issue 2, 2011 

 

We seem to have no problems creating what ‘defenders of the right to self destruct’ call a ‘Nanny State’ posture when it comes to cigarette smokers or our indigenous communities for that matter – But when it comes to the rest of the population quitting or abstaining from alcohol, then howls of derision chanting anti-‘Nanny State’ mantras are deafening!

James Campbell in his article ‘wowsers enough to drive you to drink’ featured in Herald-Sun 6 drew out, in his classic libertine framework article, some of the same inconsistencies we are bringing to attention in this paper – but I’m quick to add, for very different reasons. (Of course James would never have used the term ‘wowser’ in his title if he had even an inkling of what it stands for – We Only Want Social Evils Rectified – This of course is what all socially responsible people want. Yes, a free society, but a freedom that doesn’t disregard a) the liberty, safety and wellbeing of others b) the protection of the young, and c) bestowal of dignity on every human being… all of which are casualties when the imbibing begins.)

In his article he noted the data and subsequent recommendations recently released by the Cancer Council, but also what he has interpreted their seeming ‘double standard’ on the ‘drink’ issue. Professor Olver was quoted in the Age as saying… ”If you want to reduce your cancer risk as far as possible [abstinence] would be the option you have.” 7     yet in his article, Campbell states they stopped short of recommending abstinence from alcohol and settled for NHRMC recommendations of ‘a couple of standard drinks at any time’.   ‘The point now is what do we do with that information? Certainly promoting abstinence as an option should be absolutely imperative, but that’s the problem, the ‘A’ word isn’t permitted, even in the ‘optional’ category!’

Now whilst I can see the point of incongruence, I would like to challenge Campbell’s ‘framing’ of the response. It is clear that not all cancers are caused or even added to, by alcohol, but it is equally clear, through evidence based science, that alcohol is carcinogenic.*  The point now is what do we do with that information? Certainly promoting abstinence as an option should be absolutely imperative…but that’s the problem… the ‘A’ word isn’t permitted, even in the ‘optional’ category!

Our culture is either so deeply addicted to this drug or so completely gripped by fear at being labeled something less than human because they don’t drink, that they actually cannot see the option of saying ‘No Thank you!’

Now if this was just, fully developed ‘grown ups’ who don’t care about their health or even worse, are self-medicating the vicissitudes of life with the grog, and never venture into the public space and expose others in the community to their less than sober persona, I suppose it would make less difference if one ‘partook’ (except for the medical and health bills the tax payer will have to fund)! However, it is the vulnerable in our society – the young (under 25 – still developing brains), the mentally ill, the socially and relationally isolated, the violent, the elderly, children and often women, who end up casualties of not only their own drinking, but that of others!

Whilst the link between cigarettes and disease is clear, it is no less clear with alcohol…

Alcohol consumption is the world’s third largest risk factor for disease and disability; in middle-income countries, it is the greatest risk. Alcohol is a causal factor in 60 types of diseases and injuries and a component cause in 200 others. Almost 4% (1 in 25) of all deaths worldwide are attributed to alcohol, greater than deaths caused by HIV/AIDS, violence or tuberculosis. 8

 

A couple of questions that are often conspicuous by their absence, when it comes to the inconsistencies in drug policy when dealing with tobacco and alcohol, are to do with impact on others. Yes, it is good to have gone to considerable lengths to minimise ‘passive smoking’, but what of the impact of what Professor Rob Moodie calls ‘passive drinking’? A couple of quick questions to ponder…

The real tragedy in all this ‘cultural reinforcement’ is that the imperative message for this demographic of abstinence, and delayed onset of drinking as long as possible, has completely disappeared.

When was the last time a cigarette caused a man to beat his wife to death?

When was the last time a cigarette caused an automobile accident killing two and disabling one for life?

When was the last time a cigarette caused a pub brawl or ‘glassing’ incident?

 

For the sake of brevity (and being seen to be too merciless on the sensibility of the Aussie imbiber) the following are just some of the long known, but only recently quantified data on this so called ‘social lubricant’….

 

a) Fiscal Cost: The research by the Australian Education and Rehabilitation Foundation (AER Foundation) has now put the total economic impact of alcohol misuse at $36 billion per annum which is over double 2005 estimates. This comprises $24.7 billion in tangible costs, which include out-of-pocket expenses, forgone wages or productivity and hospital and childcare protection costs. There are a further $11.6 billion in intangible costs, which includes lost quality of life from someone else’s drinking

b) Consumption: Drinking more than ever before, at least 10.2 litres pure alcohol per person per annum 10  , mouth, pharynx and larynx. 1 in 5 cases of breast cancer are linked to alcohol”. 11

c) Cancer: “Alcohol use has been linked to thousands of cases of cancers including bowel 9

d) Violence: There are more than 70,000 Australians who are victims of alcohol related assaults each year

e) Emergency Services: Ambulance Call outs in Greater Melbourne alone, for predominantly alcohol abuse have increased almost 600%: 1998-99: 1043 by 2008-09 it was 6924 13

f) Crime – In just one State alone, alcohol-related crime in Queensland has increased by 30 per cent, and public disorder offences by 65 per cent just in the past few years alone…Alcohol abuse in Queensland is now responsible for 100,000 crimes annually, or one-quarter of all offences.14

…alcohol-fuelled violence and abuse affects one in five people 12 You get the point! This is, if not worse, then at the very least as bad as the smoking issue…. So, why aren’t all zeal, all passion and all strategies being implemented to prevent or stop the impact of alcohol on the Australian people and the economy?

So entrenched is the alcohol culture that according to the Australian Drug Foundation, parental supply has eclipsed all other sources of supply of alcohol to children aged 12-17. Now the excuses  tabled for this kind of outrageous conduct are as follows…

a) Parents want to either, initiate their child into alcohol ‘wisely’ or at least ‘know’ how much they are drinking.

b) Parents want to be friends with their child and not parents. Believing they are avoiding stress at home by giving in to negative social influences.

c) Parents believe that if their children are going to ‘experiment’ then it’s better to do so with the legal drug.

d) ‘It’s part of being Aussie, it’s gunna happen, so might as well try and be ‘responsible’ and give them a hand in using this legal drug ‘properly’.’     So, how has that been working for us as a community? Well the evidence seems to correspond with the mindset. Again an Australian Drug Foundation recent release shows that by 16, one in five teenagers regularly binge drinks; by 18 it is 50 per cent.    It would appear this level of permissibility has only added to accessibility and availability and thus consumption has increased. I mean… ‘after all Mum and Dad are giving it to me and they use it, so it must be ok?’        The real tragedy in all this ‘cultural reinforcement’ is that the imperative message for this vulnerable demographic of abstinence and delayed onset of drinking as long as possible, has completely disappeared. All the scientific evidence reveals that their vulnerable developing brains need this option to be aggressively promoted as best practice and their parents, above all, need to get this reality check too.     Again, what continues to generate this disconnect between policy emphasis around the legal drugs of tobacco and alcohol? Both drugs are legal, but perhaps smoking an easy target now that fewer Australians do it, and is marginalised so much that scathing vitriol and uncompromising legislation will have little opposition?

But, not so with alcohol – Whilst approximately 14% of Australians who are legally permitted to drink, don’t, the amount of alcohol being consumed per person, per annum is near record highs. It would seem that challenging this second ‘monster’ can prove a difficulty, if a) votes matter b) the power brokers themselves are unable to say NO to alcohol; c) It has become the central and often sole ‘social amenity’ or even worse, d) it becomes the medication of choice for the ever growing epidemic of community wide psycho-social dysthymia.

Whatever the reason, a clear gulf exists in zeal, attention and endeavour when we juxtapose tobacco and alcohol. A gulf that screams, at best inconsistency, but at worst hypocrisy!

A quick recap… 

When it comes to tobacco the policy aim for smoking is ‘quit’, and we have no problem aggressively challenging ‘smoking’ as a reckless act that needs stronger management. We have used Prohibition in its legal context to prevent smoking in a number of places and breaches of such prohibitions have met with not only social censure, but a fiscal punitive response – fines. And in this framework there appears no fear about attracting the pejorative ‘nanny state’ label.

 

When it comes to Alcohol, the policy aim (at the moment at least) is to avoid the ‘nanny state’ label, calling instead for management, more like a caring friend provoking a peer to a healthier choice. So the push seems to be toward ‘moderation’.

 

But what is happening in the arena of current illicit drug policy?

We appear to be losing the plot – the pro-drug lobby is trying to take over the judiciary, if not legislature!

When it comes to illicit drugs there appears to be a departure from all regulatory sanity. The ‘State’, on whose advice we can easily guess (George Soros funded propagandists) works ruthlessly to assassinate, mutilate and bury all processes that are focused on prevention or abstinence. Such processes the patronizingly dump into the ‘Nanny-State’ model/basket . Nor, would it seem are they interested in a Good Parent model, or even the ‘caring friend’ model… No, it would appear from all current debate this confederacy has opted for the ‘go with whatever feeling grabs you; it’s your ‘right’ and let the State clean up the mess’ approach!

 

There appears little to no censure, no label of ‘bad’ or ‘harmful’ or ‘destructive’ to the conduct that is illicit drug using. In fact great pains are taken to remove all terms from public documents that could potentially ‘marginalise’ the drug user. Whilst ‘name calling’ should never be condoned, conduct that is illegal and destructive needs to be called for what it is and measures taken to change it. Whether the terms are legal or medical, they can never be ‘neutral’, or worse complimentary and condoning.

What is of greater concern is the tacit message oozing through the permissive interpretation of Harm Minimisation policy by the Harm Reduction Only Lobby, which is that the State sanctions and promotes – not challenges or changes – a drug user’s ‘habit’. (Yet it is the ‘habit’ that needs to change – more on that later.)

For example, they seem to be saying :

 

a) Please come to a special place with your illegal substance and we will assist you to take the drug of your choice (Medically Supervised Injecting Centre – MSIC). At no point will anyone ‘judge’ you for your ‘lifestyle choice’. Instead we will ensure you are comfortable and enabled in your drug taking activity whilst funding this process with tax-payer’s money. (No matter that this process breaks international laws on illicit drug use)

 

b) We will give you as many clean ‘needles’ as you like and will not hold you accountable for the return of used ones. In fact we will pay someone to go around and pick up your discarded syringes so you can continue to be free (not irresponsible, that would be pejorative)to continue, unhindered in your substance use, wherever and whenever you choose.

 

c) If the substance user opts to seek a change in conduct, only then may we humbly recommend a referral to a treatment facility. However, after we have just enabled you to continue your substance abuse (in our MSIC) and you are ‘feeling’ better (yet getting worse) after your State assisted ‘fix’, then it is unlikely that you’ll ‘feel’ the need for detox, let alone rehabilitate. So, the passive referral is ignored or forgotten.

 

d) If you are one of the single digit percentage of substance users that actually ‘follows through’ on referral, then no requirement will be placed on you to become drug free. No, we are only interested in trying to minimise your potential to kill yourself and make you as comfortable as possible. We will introduce you to other substances that may, or may not lead you to drug free recovery, but again, that is NOT our aim. This, after all, is only for the ‘problematic’ drug user and we must not have anyone feeling discomfort or distress from the withdrawal from drug use, even if is for a week – That would be ‘unkind’. So rather than treat you like a precious, intelligent, whole human being, we’ll simply treat you like a wounded pet and only treat the symptoms and not address the real problem.

 

e)  The recent aggressive upsurge of promotion and use of, so called, ‘legal highs’ has produced an even clearer manifestation of this policy D.I.D/hypocrisy/inconsistencies. As these synthesized ‘designer’ concoctions started getting a more public profile, several States in Australia were quick to react by imposing age restrictions and then applying significant financial penalties (six figure fines) for those involved in distributing/using these products. Yet in some of these same States the use of current illicit drugs such as cannabis (and other currently illicit drugs that have clearly documented health damaging properties) attracts no more than a slap on the wrist for use and little more for trafficking!

It would seem no effort is spared, to ensure the drug user is rarely, if ever, is called to make changes. More than that, and at any point, an act of horrendous nature can be perpetrated against another citizen as we saw recently in the senseless murder of a deaf octogenarian pensioner, murdered by yet another (it would appear by the new label) ‘problematic drug user’. Diminished responsibility, mitigation, equivocation, even obfuscation, are employed to avoid ownership of the issue by the substance user. What’s more disturbing is that at no point is the abysmally interpreted Harm Minimisation Policy used to bring about change, let alone drug free wellness of these dysfunctional people.

The following (conveniently) long forgotten words of the remarkable Statesmen, Edmund Burke, are even more appropriate today than at any other time in recent history…

 

“Men are qualified for liberty in exact proportion to their disposition to put moral chains upon their own appetites… Society cannot exist, unless a controlling power upon will and appetite be placed somewhere; and the less of it there is within, the more there must be without. It is ordained in the eternal constitution of things, that men of intemperate minds cannot be free. Their passions forge their fetters.” Sir Edmund Burke

 

The very thing that is needed as outlined by Burke is the very thing the pro-drug lobby works tirelessly to negate. Morality is ‘off the table’ in this arena (The only time morality is invoked these days is when it comes to climate change; nowhere else is this allowed in the public discourse) In this ‘amoral’ space all attempts to impugn drug taking are perceivably removed. Terms like ‘wrong’, ‘bad’ ‘irresponsible’ are no longer permitted. So, if it is no longer referred to as ‘wrong’ then comes the next manipulative question: on what grounds should substance use still be illegal? The next step is to turn the debate into a purely ‘health’ issue. It is true, it is also a health issue, but, it is still a social, psychological and moral issue as well. But even just at the level of health policy, would think that all measures should be taken to rectify the dysfunction /disorder/ailment in order to remove the health damaging substances at least from the patient, even if not the community. Ah, but no, that’s not the agenda of this lobby faction is it!

 

The health issue is invoked only to manage some of the damage of substance taking and other second tier outcomes of these bad health choices, such as blood borne infections and or death. The call now in this decriminalised, so called amoral and consequence avoiding space, is that all health measures be taken to keep the patient alive and as healthy as possible to continue their ‘lifestyle choice’ of drug consumption.

 

This is not Australian – Time to Stand up!

At the moment the vast majority of Australians are still smart enough to know (perhaps drug free enough to know) that ultimately there I absolutely no gain/benefit in illicit drug use for individuals or society;

Ø The current National Household survey (2007) has the vast majority of Australians declaring their disapproval of illicit drugs and their use.

 

99% don’t want use of hard drugs accepted 

95% don’t want hard drugs legalized 

94% don’t want use of cannabis accepted 

79% don’t want cannabis legalized 

Most Australians want tougher penalties for drug dealers.15 

 

Ø The largest youth survey done in our nation with a sample of around 50,000 young people saw alcohol and others drugs as the second highest on ‘what is an important issue for Australia’. This issue is the most worrying to the youngest in this most susceptible to damage of Australia’s demographic – the ones we need most protect – our children 16

 

When the overwhelming majority of people disapprove of illicit drugs, it might just be a cue to do something more significant than concede ground to it. You’d think that even the process (let alone value) of democracy, had any weight then the above mentioned majority opinion would mandate all and every action be taken to eradicate illicit drug use from society. According to collected data, around 6% of the world’s population aged between 15 and 64 currently use illicit drugs. 17 Australia’s stats are only a little higher than that. So here we have a user group that is arguably (at most) between a half or a third of current tobacco users, who are involved in a wilful breaking of the law to their own and the wider community’s detriment generating an exorbitant cost to our community.

So what has the response been to this? Well, it depends on where you look, who you talk to and who is playing the strings of the propaganda harp.

 

In recent years there has been a rising noise, about the need for illicit drug policy change. The standard mantra has been ‘the war on drugs has failed!’ Consequently we need to stop and rethink our processes and priorities.

 

What ‘war on drugs’? Where did this notion come from?

Well, let’s pretend for a moment there actually was a ‘war on drugs’. How could it possibly be won? Well, again it depends on how this ‘war’ was fought and what priorities were set. If the war on drugs simply attempted supply removal and arrest, then it will have limited success. However, as with most ‘battle strategies’, if they only have one tactic, then success will always be limited or the potential for failure increased. If a ‘war on drugs’ isn’t really waged as it should be then it is locked into only limited success and more likely subject to criticism of its limitation. However, as in all wars the first casualty is always truth and that is no different in this theatre of combat, as the following reveals…

The term “war on drugs” was not used in 1971 and is not used today by anyone except those who mischaracterize history and current drug policy in the US. However, if one were going to connect the term to President Nixon, then it would be more accurate to say that Nixon ended, rather than launched, the “war on drugs.”

The Nixon Administration repealed federal mandatory minimum sentences for marijuana, and on June 17, 1971, for the first time in US history, the long-dominant law enforcement approach to

drug policy, known as “supply reduction”, was augmented by an entirely new and massive commitment to prevention, intervention and treatment, known as “demand reduction”. President Nixon announced this new, balanced approach to drug policy and it received full bipartisan support. Since that time, the idea of taking a balanced approach has enjoyed strong and sustained support through the terms of the seven US Presidents that followed. The US drug prevention policy, fully described in the annual National Drug Control Strategy published by ONDCP, maintains this twin-commitment to supply reduction and demand reduction, with the aim of reducing illegal drug use and the corresponding medical and social burdens that drug abuse imposes upon our nation.18

Supply reduction remains a key tactical component and criminalisation will always lend weight to that vital strategy component. Time and space here will not permit us to go into all the local and national impact on drug use that supply reduction has facilitated, but just two examples will give us a clear indication

a) ABS 2000 death stats collection: Heroin: 417; methadone: 118;Benzos: 403; anti-depressants: 268; Cannabis: 49 Note the reduction in Heroin deaths the following year when the heroin drought (for whatever reason) caused availability to dry up, the ABS 2001 death stats collection showed: Heroin: 113; methadone: 107;Benzos: 252; anti-depressants: 194; cannabis: 28!

b) According to the Australian Institute of Criminology, the four top reasons why detained illicit drug users had not used in the previous month 19 was in order of main reason to least.

1) Dealer didn’t have drug of choice (highest reason by far)

2) No Dealers available

3) Poor quality product

4) Police presence

 

 

“When you reduce permissibility, accessibility and availability you reduce consumption.”  

I want you to notice that supply reduction elements are the key factor in reducing illicit drug consumption. Again, when you reduce permissibility, accessibility and availability you reduce consumption. This is why complementary Supply Reduction strategies are imperative in conjunction with Demand Reduction strategies and compulsory detox and rehabilitation strategies.

When Ethan Nadelmann and Dr. Alex Wodak, the well-known supporters/ purveyors of the George Soros brand of cultural chaos, were on the media stage peddling their brand of harm ‘reduction’( (including the decriminalisation of illicit drugs), the voices of dissent from any other quarter were hard to hear, but not because they don’t exist considering over 90% of Australians disapprove of illicit drugs. It was the classic situation where the sane majority simply expect the government to do all that is necessary to eliminate drug use without bothering to mobilise against that small, but very ‘squeaky wheel ‘of pro-drug propaganda at legislators doors. Consequently, the long standing anti-drug movements were given no space at all.

The Nadelmann/Wodak ‘spin’ had people believing prohibition drug policy had failed and therefore the only option left was to decriminalise or legalise. They even used cleverly spun unrelated science and misrepresented data from other nations and calling that ‘enlightened’ (Such as the so called Portugal decriminalisation ‘success’). Or they hijacked the debate away from drug use and placed it in the framework of management of damage caused by drug use, which actually increases dysfunction.

 

It is remarkable that few clinicians or policy makers care to see or even acknowledge that the current illicit drug policy in Australia (among other western nations) has be completely hijacked by the single dimensional ‘harm reduction’ element and that has distanced them even further from the problems of drug use.

This one dimensional focus has barely anything to do with drug use and absolutely nothing to do with reducing drug use. ‘Harm Reduction’ as it currently stands, when it is all distilled down to its core (a one step process) is only focused on the attempted prevention of death and blood borne infections. Whilst this may be a noble aim, we need to move drug policy back to the forgotten reduction or prevention of drug use in our society. We are all for having a policy for reducing the spread of blood borne infections and death, but let’s call it that and move drug policy back to what drug policy is supposed to be about – the prevention and reduction of drug use in our society. Of course, even a ‘blind man’ could see, that if you prevent and/or reduce drug use, you reduce the incidence of the other damage so focused on – but that is the very thing the pro-drug lobby doesn’t want to happen, the reduction of drug use! They advocate continuation of drug use, funded by tax-payer’s who keep them alive and pay for their treatment.

 

So in our mind, an unavoidable question is – Where was Federal Minister for Health, Roxon on these issues? Where was the same zeal that was focused on cigarettes? At the time where this ‘drug reform’ lobby has used special arguments to remove the protection, where was the declaration, ‘making laws that protect Australians’ from substances that have long been banned because of the undeniable damage they do?

 

Is it utter ignorance that generates this silence? Or is it as one prominent AOD Clinician once said ‘Harm minimisation is just a euphemism for ‘we don’t know what the hell to do, so we’ve just given up!’. Or is it, reason spare us, a tacit yet wilful pursuit of cultural sabotage foisted on society because a minority of drug users who believe they can control their ‘habit’ have ‘friends’ in high places?

 

Prohibition is a word that has been marginalised and disparaged, again by hijacking the meaning and reinterpreting it in a different context – the context of purely a moral control of a majority. However, prohibition is, in this context, a matter of law and not a simple moral based endeavour. We prohibit by law things that are injurious to individuals and the community. With Tobacco law, cigarette smoking is prohibited in restaurants, government buildings, some public spaces, inside cars and so on. Illicit drugs are prohibited at a higher level because of the health, family and social damage and the impediment of function and increased danger they that create. The prohibiting is based on minimising the harms done by these toxins to the community and individuals. Decriminalisation will only lead to greater substance use and experimentation and simply bolsters well the ranks of the damaged and dysfunctional. It will perpetuate this damage in an emerging generation that has little capacity to handle it. This is a crime!

Will the real drug policy emphasis, please stand up and will it stand for health, justice, responsibility and protection of the young?

Shane Varcoe – Executive Director, Dalgarno Institute.

*“Alcohol and Cancer in the spotlight: Studies in Europe and Australia confirm alcohol as a cause of cancer, but role of moderate drinking controversial”, The Globe, Issue 2, 2011

 

 

Endnotes

1 http://www.cancercouncil.com.au/editorial.asp?pageid=371

2 CHANGES ASSOCIATED WITH THE NATIONAL TOBACCO CAMPAIGN PRE AND POST CAMPAIGNSURVEYS COMPARED by Melanie Wakefield http://www.health.gov.au/internet/main/publishing.nsf/Content/health-pubhlth-publicat-document-metadata-tobccamp.htm/$FILE/tobccamp_c.pdf

3 Stark , Jill The Age, 22.5. 2011 http://www.theage.com.au/victoria/now-butt-out-new-push-seeks-to-outlaw-cigarettes-20110521-1ey2s.html#ixzz1OBTg5SRQ

4 http://www.smokernewsworld.com/market-cheap-cigarettes/

5 Nicola Roxon solid on cigarette packaging Sallie Don and Sue Dunlevy From: The Australian May 27, 2011 http://www.theaustralian.com.au/national-affairs/nicola-roxon-solid-on-cigarette-packaging/story-fn59niix-1226063781056

6 James Campbell – wowsers enough to drive you to drink, page 78, Sunday Herald-Sun May 28, 2011,

7 http://www.theage.com.au/lifestyle/wellbeing/quit-drinking-to-cut-cancer-risk-20110501-1e38g.html

8 Global Status Report on Alcohol and Health. Taken from Introduction page x, ISBN 978 92 4 156415 1 (NLM classification: WM 274) © World Health Organization 2011

9 Alcohol Education and Rehabilitation Foundation – Range and Magnitude of Alcohol’s Harm to Others August 2010

10 Wine link to rise in alcohol intake, Sikora, Kate; Page 16, Herald-Sun Edition 1 – 2/11/2010

11 Medical Journal of Australia (published May 2011)

12 Alcohol Education and Rehabilitation Foundation – Range and Magnitude of Alcohol’s Harm to Others August 2010

13 http://www.heraldsun.com.au/news/more-news/mateship-abandoned-drunks-left-behind/story-fn7x8me2-1226063706968

14 “Punch Drunk Campaign”, QLD Courier Mail – July 2009

15 The 2007 Illicit Drug Strategy Household Survey of Australian attitudes to illicit drug usage and “Drugs and suicide main worries for the young, says survey, The West Australian, 26/11/2009

16 National Survey of Young Australians 2010 – key and emerging issues; Mission Australia. 2011

17 ‘Should drugs be legalised” by Dr Ian OLIVER is a former Chief Constable of Grampian Police, 2009

18 Global Commission on Drug Policy Offers Reckless, Vague Drug Legalization Proposal; Current Drug Policy Should be improved through innovative linkage of Prevention, Treatment and the Criminal Justice System

(Commentary – IBH (Institute for Behaviour & Health) July 2011

19 Crime Fact Sheet No 152 ‘Reasons for not buying drugs’ ( July 2007)

 

 

 

 

Filed under: Australia,Law (Papers) :

Berlin, like many big cities has a heroin problem. People presenting for help are being prescribed opioid replacement therapy (ORT) in greater numbers. That’s a good thing isn’t it? Well it depends on what you think is the end goal of treatment. At the start of this interesting recent German paper “Why do patients stay in opiod maintenance treatment?”, Dr Stefan Gutwinski and colleagues say that the scientific literature indicates the point of ORT is: “to increase survival and bring stabilization to patients, in order to enable them to reach abstinence of opioids.” The Scottish Government’s drugs policy and the UK policy agree.

We can simplify this into two aims:

1. To make things better, then

2. To move on to abstinence

The problem is that while the evidence is pretty solid that number one is generally achieved, there is less to convince us that the next bit is happening. The paper outlines that retention in ORT is not great, with just over half of patients sticking with methadone and fewer with Suboxone. Despite this, in Berlin, as we have said, there are growing numbers of people on ORT. These are people who are not moving on; I suppose the ones the press call ‘parked’ on methadone. So the authors ask: “Why is this?”

The researchers speculated that it could be because:

* fewer people are dying;

* that people don’t want to move on because of the benefits they are getting;

* that detox is generally unsuccessful, or

* that what staff think patients want is not what patients actually want.

To test this out they sent out an anonymous questionnaire to treatment settings in Berlin. Forty-six staff (more than half doctors and the rest nurses and admin) and 986 patients completed it. They focussed on whether ORT was of benefit, whether it was perceived as harder to detox from than heroin and how strongly patients wished to come off of ORT compared to how strongly staff thought their patients wanted to come off.

What did they find?

1. Both patients and staff thought ORT helped physical and mental health. Beneficial effects of ORT on the ability to work and on crime were rated significantly higher by patients compared to staff.

2. Staff and patients agreed that coming off ORT was hard. Patients thought it harder than coming off heroin.

3. Patients wanted to eventually come off ORT at a significantly higher rate than staff estimated.

About half of the patients in the sample were over 40 years old and more than one in ten were over 50 with almost three quarters of patients struggling with opiate dependency for more than ten years. Only ten percent had never tried to detox, suggesting high failure rates which may have reinforced the belief that ORT was hard to more on from. There was no differentiation made between methadone and Suboxone. Perhaps methadone is seen as more ’sticky’ to move on from. The study didn’t look at whether evidence based support and treatment was given at the time of the detox.

The thing that intrigues me the most is the “striking discrepancy between the patients’ and staff members’ assessment of the patients’ desire to end OMT on the long term. The large majority of patients report the desire to end OMT on the long term, whereas only a minority of staff members believe that their patients might really have such a desire.”

David Best found much the same thing (in aspirational terms) in a sample of drugs workers in the UK. They believed only 7% of their clients would eventually recover. The DORIS study in Scotland angered some professionals when it reported that many patients entering treatment wanted only to become drug-free; something treatment was not delivering. A recent study in Leeds found that service users, their families and friends placed “considerable weight” on abstinence and “ways of maintaining abstinence”. It’s clear to me that where there is such a mismatch, when the bar is set so low and when there is little hope pervading treatment settings, then it’s no wonder that so few actually do move on.

By the conclusion the authors find themselves at odds with the assertion at the start of the paper (that ORT has an aim of ‘abstinence from opioids’.) Here’s what they say (my emphasis):

 

“Finally, detoxification of OMT is not the prime objective of treatment. The prime objective of treatment is continued physiological and social stabilization. As yet, there is no validated medical cure for opioid addiction. Until a curative medication or a safe curative procedure is developed, many of the patients may have to remain in treatment for the duration of their lives to avoid relapses, increased criminality, subsequent overdoses, and death during the post treatment period.”

So the solution to the mismatch between the low expectation of staff and the higher expectation of patients is to lower the expectation of patients to that of staff? Well that’s one way of looking at it. We still have the problem that lifelong ORT, whatever its evidenced benefits, is not what people want and that, in fact, many do move out of opiate dependence into long term abstinent recovery. These people would no doubt agree that methadone did make things better, but for them it was not the final destination.

What would it be like if the dearth of recovery-oriented research in the UK was addressed, if we focussed on what works rather than what doesn’t? If all we do is compare ORT with stand-alone detox, then we are always going to see poor outcomes. Another more enlightened and rewarding approach might be to move away from thinking about a drug or a medical ‘cure’ as being the solution to addiction and looking to introduce recovery-oriented systems of care using strongly evidence-based psychosocial interventions and treatment where those interventions are of adequate intensity and duration. Linking people to recovery communities is protective with regards to relapse, but there is little evidence that it is happening.

In the UK we have recovery-oriented drugs policies which aim for rapid access to treatment with a variety of approaches on offer. The answer is not to lay out the choice as ‘methadone or abstinence’ but to see how we use ORT as a tool and to find ways of bridging people out of treatment and reliance on services into recovery. Some may have to remain in treatment in the long term, but we need to set the bar high and be positive about patients’ ability to move on. Professionals should spend time with people in recovery to engender hope in themselves. The ethos and structure of systems of care need to change so that recovery becomes the norm instead of a wild aspirational status that we actually believe most people will never achieve.

Now how do we make that happen?   D. J. Mac

Thanks to Stefan Gutwinski for a copy of the paper to review. For information: I wrote a shorter piece on this based on the abstract a few weeks ago.

Source: Substance Use and Misuse, 49:694-699, 2014

To understand how Minnesota’s Drug Court system is working, you need only to consider this before-and-after scenario.

Before: In March of 2012, Steve B. of Hastings was facing a prison sentence of seven to 10 years on felony charges of possession and sale (to an undercover cop) of methamphetamines. There were restraining orders against him. He had lost his wife, his house, his job in the construction industry, parental rights, and access to his then 5-year-old daughter. He’d been using for five years, was “caught up in the lifestyle,” and keeping company with others on the same hellish trajectory. “I was willing to give up everything for the drug,” he says in retrospect. “I had a good life, and I lost it all.”

After: Last Monday, in Dakota County Adult Drug Court, Steve B. was accepting a round of courtroom applause and personal congratulations from Judge Kathryn Messerich, who told him that he’d be “graduating” March 10 after successfully completing 18 months in the rigorous program. He had done a few months of jail time, finished treatment, remained sober, followed the rules, returned to the work force and recovered his relationship with his daughter. They were going to Disney World, he proudly told the court. “You have really earned this trip,” Messerich told him. “I have to commend you for how hard you have worked to be a good dad. There is one young lady who is going to have a good life because [you] are her dad.”

He was one of four people in the courtroom that day who were told they’d be graduating. “I’m losing all my people,” Messerich said earlier Monday during a team meeting to review the day’s cases. And that was a good thing.

Cost-effective outcomes

The state’s first drug court was established in Hennepin County in 1996 and has grown to more than 37 specialty courts (including drug, DWI, veterans, family dependency, juvenile and some hybrids) serving more than 30 counties.  The goal is to stop felony drug offenders’ revolving-door interactions with law enforcement and to give them a foothold in a productive, drug-free life. Other goals include improving public safety and reducing the overall costs of illegal drug activity and incarceration. A 2012 statewide study confirmed that the labor-intensive but cost-effective effort was paying off: The study of 535 participants in 16 different courts who entered drug court between July 2007 and December 2008 found a 37 percent reduction in recidivism rates (compared with nonparticipants); a 47 percent reduction in reconviction rates; a 54 percent graduation rate (62 percent if you exclude Hennepin County); higher rates of completing drug treatment programs and maintaining sobriety; higher rates of employment and educational achievement; and greater command of such life skills and responsibilities as obtaining a driver’s license, locating housing and making child-support payments. Most were diagnosed with drug-use disorders, and slightly less than half also had mental-health diagnoses.

The study also found that incarceration costs (both prison and jail) were about $3,000 less for drug court participants (who oftentimes must also do some time) than nonparticipants.

“Before specialty courts, there was no focus at all on rehabilitating the offenders,” said Dakota County Attorney James Backstrom in an interview last week. “We just did our job, which was to prosecute them, convict them, and put them in jail or prison. And then you didn’t worry about what was going to happen next. But … if we want to keep our communities safe, the most important thing we can do is ensure that these offenders get the help they need for the chemical addictions they have so they don’t break the law again.”

A team approach

If it takes a village to raise a child, it also takes one to help a repeat felony drug offender break the cycle. Each drug court takes a team approach, with all players at the table – a judge, a prosecutor, a public defender, a law-enforcement official, probation officers, chemical dependency experts, and community volunteers. Traditional adversaries in the courtroom now become advocates – all pulling in the same direction.

The Dakota County team provides a good example of how it works.

The day’s caseload (last Monday) includes 14 drug-court participants in various stages of program completion. Some are in Phase I, which requires a courtroom appearance every other week before the judge, twice-weekly random urine tests and meetings with probation officers, compliance with all chemical dependency assessments and treatment recommendations, attendance at the pre-court hearing AA meetings, and participation in cognition skills courses – just to name a few of the stringent requirements. Some are in stepped-down phases II and III, and some are ready to graduate. Still others are applying to enter the program, and team members try to gauge each person’s level of motivation and possibility of success. Criminal charges in other jurisdictions are considered, and past crimes are weighed.

To opt in, you must agree to plead guilty. And not everyone is eligible: Those who committed violent crimes, have gang affiliations, sold drugs to children, or caused vehicular homicide need not apply.

It gets personal

It’s clear that the relationships have become quite personal.

The team members take note of any program participant’s life stressors – a child-custody battle, a new job to learn, an illness, a bout of depression. They discuss victories – graduation from school or treatment, reconciliation with a family member, landing a job. They discuss any violations of the program rules. One man whose urine test was positive for cocaine, and who then attributed it to medication that had been prescribed by a doctor, will get seven days in jail – not just for using but for lying about it. (Other possible sanctions include repeating a phase, community service, electronic home monitoring, or termination from the program.) A woman spotted in a liquor store by a county employee will get a stern reminder about the company she keeps and the choices she is making.

Sure, it gets personal, said Barbara Bauer, drug court coordinator and probation officer. “Sometimes they tell me I’m nosy. We go to their homes. We go to their jobs, if that’s possible. We go to their treatment programs and coordinate with their case managers and therapists. We go to their graduations.” And sometimes there’s a “knock-and-talk” surprise visit from a community police officer. To know them [the program participants] is to “help them figure it out,” she said.

Backstrom agreed, saying that it’s one of the features of drug court that he likes best. “It’s the relationships that you develop with these offenders – letting them know that you believe in them, and that you’re proud of what they’ve accomplished. I think that really helps these individuals get some hope back in their lives. That’s one of the things you lose when you become addicted: hope for your future. You become despondent, depressed. And it’s a cycle that can lead to your death – at a premature age in many cases – or continuing criminal involvement, which we can stop.”

To the courtroom

After discussing and deciding on a course of action for each case, the team then heads for the weekly courtroom session (every Monday in Dakota County), where all the program participants and hopefuls sit waiting in the jury box. Some are in handcuffs. A scattering of family members – some in agony, and some filled with pride – also are present.

The mood is mostly upbeat, as Messerich praises the four who will graduate. Her words are authentic and believable and land with impact.

“It’s hard to lose participants who are such good role models,” she tells Steve B. There are affirmations for others as well: “You look like you have a sense of calmness about you.” “I can’t tell you how happy I am to see that smile on your face.” “You have always impressed me with your energy and focus.”

The county attorney, defense attorney and probation officers also add their words of encouragement. In turn, the participants are given a chance to convey their gratitude and answer the questions, “How did you do it? What advice do you have for others?”

One woman tells Messerich with pride that she has been hired after completing a job-training program and is giving back by volunteering at a halfway house for teens – the very same place where she sought refuge as a teen.

For those who are in violation of the rules, Messerich is firm but not retributive. And even here, she manages to inspire rather than discourage. “This is not just an issue of your health but your freedom,” she tells a man who has been caught using and who will spend the next seven days in jail. “I hope we can get you back on track.”

No one’s immune

Backstrom, who participated in the formation of the state’s drug court system and the establishment of its standards, takes a personal interest in its long-term success. His own family has not been immune from the disease of addiction, he said. An uncle died of alcoholism in his 50s, and a beloved nephew died recently of complications from alcoholism. Though his nephew had been through treatment and was attending AA meetings, he had relapsed. Fearful of being found out, he put off getting treated for a bacterial infection until it was too late to save him. “It’s been terrible,” Backstrom said. “My sister and her family have really struggled – as we all have.”

An even earlier tragedy left its mark, when a young man who had been drinking crashed head-on into Backstrom’s parents’ car. Backstrom was just 19 years old, a college freshman. His father recovered from his injuries, but his mother, who died in 2004, suffered permanent brain damage. “It destroyed my family in many ways,” Backstrom said. “The mother I grew up knowing really wasn’t with me anymore. She was a different mother. I loved her just as much. But she could never say a sentence for the rest of her life. She could never walk normally. She could never move her right hand again. She suffered every day for the final 31 years of her life because of a poor decision a young man made.”

Backstrom says he sometimes wonders what became of the young man who caused the accident: “I’ve always wondered if he really, fully understood the extent of the damage he caused to my mother and my family. I hope he didn’t have any further violations, and I hope he lived a good life.”

As he wonders, perhaps he can take some comfort from Steve B., who said of the Dakota County Drug Court team: “They gave me the strength. They cared for me when I couldn’t care for myself.”

Source: www.minnpost.com  5th March 2014

Filed under: Law (Papers),USA :

New evidence shows that ‘God consciousness’ can keep young people off drugs.

Young people who regularly attend religious services and describe themselves as religious are less likely to experiment with alcohol and drugs, a growing body of research shows. Why? It could be religious instruction, support from congregations, or conviction that using alcohol and drugs violates one’s religious beliefs.

Moreover, frequent involvement in spiritual activities seems to help in the treatment of those who do abuse alcohol and drugs. That’s the conclusion of many reports, including our longitudinal study of 195 juvenile offenders that will be released in May in Alcohol Treatment Quarterly.

Fewer and fewer adolescents today are connected to a religious organization. Young people are less affiliated than previous generations, with 25% of the millennial generation unattached to any particular faith, according to a 2010 Pew Research report. The problem is more fundamental than missing church on Sunday. Young people in our study of juvenile offenders seem to lack purpose and are overwhelmed by feelings of not fitting in. Meantime, the legalization of marijuana in several states, the flood of prescription medications, and the availability of harder street drugs gives youth wide access to mind-altering substances.

How do we help them? As one troubled young woman in our study, whom we will call Katie to protect her identity, said: “I started to get better when I started to help out in Alcoholics Anonymous. When we help others, we get connected to a power greater than ourselves that can do for us what alcohol and drugs used to do.”  Katie’s idea, to connect those who are struggling to a “higher power,” may seem too simple. Clinicians remain divided about whether AA’s goal of helping alcoholics find a higher power to solve their problems is appropriate in treatment planning. But new research, including our own study, is beginning to lend support to Katie’s conclusion.

There are two key elements of the 12-step program AA uses: helping others and God-consciousness. Those who help people during treatment—taking time to talk to another addict who is struggling, volunteering, cleaning up, setting up for meetings, or other service projects—are, according to our research, statistically more likely to stay sober and out of jail in the six months after discharge, a high-risk period in which 70% relapse.

Increasing God-consciousness also appears to produce results. Our study showed daily spiritual experiences predicted abstinence, increased social behavior and reduced narcissistic behavior. Even those who enter addiction treatment without a religious background can benefit from an environment where they are encouraged to seek a higher power and serve others.  Nearly half of youth who self-identified as agnostic, atheist or nonreligious at treatment admission claimed a spiritual affiliation two months later. This change correlated with a decreased likelihood of testing positive for alcohol and drugs during treatment.

A connection with the divine and service to others both seem to enhance sobriety. That’s because they provide what young people like Katie have been missing: a deep sense of purpose, opportunities to provide help to other people, connections with others, and the chance to make a difference in the world. This reduces self-absorbed thinking, something AA cites as a root cause of addiction.

Though AA was designed with Christian principles, its founders ultimately developed an approach that did not require participants to hold any particular religious beliefs. But the founders were on to something when they rooted AA core tenets in a connection with a higher power and service to others.   Why might this combination work? Neuroscientists, including Andrew Newberg in his 2010 book “How God Changes Your Brain,” are beginning to uncover what happens to the mind when the unconscious neurological foundations of addiction are short-circuited by spiritual awakening and a new focus on helping others. Neuronal pathways in the brain appear to be instantaneously realigned.

Research suggests that addicts may be prisoners of the left hemisphere of their brain, which tends to ruminate on problems such as social anxiety. But when their right brains are triggered by an intense emotional experience, unexpected solutions appear. Spiritual experience can be an important catalyst to this kind of brain rewiring.

As a teen we will call Ben told us, “I am aware today in sobriety that my thinking has drastically changed. You take a telescope and move it a centimeter, and your whole world changes. Now I ask myself: What can I bring to the table? How can I help?” How does a person rewire their own brain? There are many paths, but some adolescents agree with “Allen,” who told us, “I need a power greater than myself to enter my life.”

Source:  WALL STREET JOURNAL    March 27, 2014 

The NDPA have been concerned for some time about the easy availability of drugs online.   There are sites actively promoting the legalization of drugs, misinformation about drugs, and even sites showing young children smoking cigarettes and encouraging others to do so.   Shocking research showed recently that 8 out of 10 of  UK youngsters watch porn online.   The world wide web has been a tremendous force for good in many ways – but there is a very dark side to the internet.  The following items show the extent of  big business involved in making money out of selling illegal drugs online.   (is Google the Tesco of  the internet ?)

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The article below from today’s Wall Street Journal shows the effectiveness of going after companies that aid and facilitate the illicit drug trade. Several years ago, I queried Amazon.com for a book on a particular drug that I was interested in learning more about and along with the responses from the Amazon.com search engine came a pop-up offering to sell me the very drug I was asking about — a Schedule II controlled substance – without a prescription! I wrote a letter to Amazon.com indicating that this could be interpreted as a “facilitation” violation of the Controlled Substances Act and needed to be stopped immediately.

Back came a nice letter (by FedEx) from Amazon.com’s chief counsel  advising me that the company was just as upset and concerned as I but was powerless to stop these “pop-ups.” The chief counsel said that the ad likely was inserted by one of the anonymous servers used to transmit my Internet request to Amazon.com. It seems that data mining software used by the servers detect key words used in emails and unencrypted messages that pass through them and automatically generate unsolicited return messages to the sender offering, as in my case, something for sale. On the basis of what little I knew about all this, I concluded nothing further could be done.

I was wrong! Fortunately, in the interim, brighter minds at my alma mater (DOJ) and elsewhere figured this out and concluded that Google was one of several companies at fault.

A fine of $500  million is a drop in the proverbial bucket for Google. Of potentially greater interest here may be what happens after Google settles the current criminal case. Unlike a civil case in which a defendant may settle without having to admit wrongdoing, a settlement in a criminal case usually requires admissions of guilt to specific law violations. If this is the case, will there be subsequent state actions filed against Google on behalf of harmed residents? Will we begin seeing TV ads asking “If you or a loved one ever ordered drugs via the Internet, call the law offices of so-and-so; you may be eligible for a cash settlement, etc.”?

Given the fact that unregistered Internet “rogue” pharmacies more often than not sell counterfeit drugs or outdated, toxic, and/or ineffective drugs and, in doing so, accept only credit cards or international money orders in payment, I’m sure there are retrievable records of such purchases and possibly aggrieved patients who may have been harmed by products illegally advertised and sold via the Internet and facilitated by the advertising services provided by Google. When all is said and done, the total payout for these potential claims, if indeed they are viable, could be several times the amount of the proposed settlement in the current criminal case against Google. Better yet, it should be enough to end or severely curtail this aspect of modern-day drug dealing.

John J. Coleman, PhD  President, Drug Watch International  2011

Google Near Deal in Drug Ad Crackdown

Read more: http://online.wsj.com/article/SB10001424052748703730804576319572448399628.html#ixzz1MGNqwAfe

Google Inc. is close to settling a U.S. criminal investigation into allegations it made hundreds of millions of dollars by accepting ads from online pharmacies that break U.S. laws, according to people familiar with the matter.

The Internet company disclosed in a cryptic regulatory filing earlier this week that it was setting aside $500 million to potentially resolve a case with the Justice Department. A payment of that size would be among the highest penalties paid by companies in disputes with the U.S. government.   Google gave few details in its filing about the probe, saying only that it involved “the use of Google advertising by certain advertisers.”   The federal investigation has examined whether Google knowingly accepted ads from online pharmacies, based in Canada and elsewhere, that violated U.S. laws, according to the people familiar with the matter.

A Google spokesman declined to comment, as did a Justice Department spokeswoman.     WSJ’s Thomas Catan reports that Google is close to settling with the government over allegations that the company made millions from illegal ad companies.

Search engines can be liable if they are found to be profiting from illegal activity. In December 2007, the three largest Internet companies, Google, Microsoft Corp. and Yahoo Inc. agreed to pay a combined $31.5 million fine to settle civil allegations brought by the Justice Department that they had accepted ads from illegal gambling sites.

Prosecutors can charge such acts under a number of different statutes. From a legal standpoint, a key distinction for Google would be that the illegal activity allegedly took place through its paid advertising service, not just the results that its search engine produces.

There are scores of websites that offer to sell prescription drugs. Some violate U.S. laws by selling counterfeit or expired medicines or dispensing without a valid doctor’s prescription.  One question under investigation is the extent to which Google knowingly turned a blind eye to the alleged illicit activities of some of its advertisers—and how much executives knew, the people familiar with the matter said.   The probe has been conducted by the U.S. Attorney’s Office in Rhode Island and the Food and Drug Administration, among other agencies, according to these people. A spokesman for Rhode Island U.S. Attorney Peter Neronha declined to comment. A spokeswoman for the FDA said the investigation was ongoing and declined to comment further.

Google generated nearly $30 billion in total ad revenue in 2010, largely from its AdWords system. AdWords helped revolutionize online advertising, offering marketers the chance to bid to display their ads when people searched for certain keywords on the Google search engine. An advertiser only pays when a user clicks on the ad.

Google, like other Internet companies, has struggled for years to deal with what it calls “rogue online pharmacies.” In 2003, for instance, Google said it banned ads from U.S. companies that offer drugs like Vicodin and Viagra without a prescription.   Google acted after rivals, including Yahoo and Microsoft, made similar moves as the FDA began publicly pressuring sites to accept only drug ads from licensed Internet pharmacies.

But Google said in 2004 it would continue carrying ads for Canadian pharmacies that send medicines to U.S. customers. The decision riled some U.S. druggists and drew criticism from regulators.  After the FDA began its latest investigation, Google made changes last year to its policies for drug ads, according to a person familiar with the matter.

Google said in February 2010 it would begin allowing ads only from U.S. pharmacies accredited by the National Association of Boards of Pharmacy and from online pharmacies in Canada that are accredited by the Canadian International Pharmacy Association.   In September Google filed a federal lawsuit in San Jose, Calif., seeking to block individuals running illegitimate pharmacies from advertising on its search engine and to recover damages.

“Rogue pharmacies are bad for our users, for legitimate online pharmacies and for the entire e-commerce industry—so we are going to keep investing time and money to stop these kinds of harmful practices,” Google lawyer Michael Zwibelman wrote on the company blog at the time.

Sergey Brin, Google’s co-founder and a current high-ranking executive and board member, sidestepped questions about the investigation at a conference Wednesday and alluded to the fact that Larry Page is now running the company.

“Luckily, since we changed roles a few months ago, I don’t have to deal with filings, and the DOJ, the SEC or other acronyms,” Mr. Brin said, using the initials for the Justice Department and Securities and Exchange Commission.

The current investigation is Google’s latest brush with law enforcement and regulatory agencies in both the U.S. and abroad. The company is facing multiple investigations into possible antitrust and privacy violations in several nations. Google maintains that its breakneck growth will inevitably attract greater regulatory scrutiny, and that it’s done nothing wrong in connection with other probes.    There are other signs the government is serious about cracking down on illegal online pharmacies. On Thursday, entering the words “no prescription required” into Google’s search engine produced an ad that led to a Justice Department alert reading: “Prescription Drugs. Buying online could mean doing time.”

Source:  Wall Street Journal     MAY 13, 2011

 

 

 

The only thing green about that bud is its chlorophyll.

You thought your pot came from environmentally conscious hippies? Think again. The way marijuana is grown in America, it turns out, is anything but sustainable and organic. Check out these mind-blowing stats, and while you’re at it, read Josh Harkinson’s feature story, “The Landscape-Scarring, Energy-Sucking, Wildlife-Killing Reality of Pot Farming.”

 

 

 

 

 

 

 

 

 

 

 

 

Sources: Jon Gettman (2006), US Forest Service (California outdoor grow stats include small portions of Oregon and Nevada), Office of National Drug Control Policy, SF Public Utilities Commission, Evan Mills (2012).

 

Facts and Talking Points

Components of marijuana have medical value, but that does not mean we should smoke or vaporize non standardized products to get that value.

Recently, due to CNN and other media outlets, there has been a flood of interest in CBD a component contained in marijuana.  CBD does not get you high, and as such, it has been generally bred out of modern, smoked marijuana. But it can be grown under special conditions.

There is some limited anecdotal and other evidence showing CBD effectiveness for epilepsy, especially in children.

We should find a way to get CBD to patients who need it, but we owe those who suffer a product with safety assurances. Many products on the current “medical” marijuana market have no such assurances, are never tested in FDA-registered labs, and have no guarantees of quality and content or information on dosing or side effects.

For those who might benefit from CBD, a company in Britain has developed a standardized CBD product which will soon be in clinical trials in the U.S. and which may also be available from physicians through special FDA-approved channels.

What is CBD?

 CBD and THC are the two primary cannabinoids produced by the cannabis (marijuana) plant. CBD does not have THC like psychoactivity. CBD was essentially bred out of high potency modern recreational cannabis, but there has been recent interest in its therapeutic potential. As a result, a number of breeders claim to have “high CBD” strains and numerous purveyors are selling products that they claim are high in CBD. However, many of these products also contain significant levels of THC.

How does CBD work?

CBD works through a number of complex mechanisms. Preclinical studies indicate that

CBD has analgesic (pain relieving), anti-convulsant, anti-psychotic and neuroprotective effects. Unlike THC, it does not bind to the CB1 or CB2 cannabinoids receptors, which is why it does not produce THC-like psychoactivity.

Many groups are trying to sell or give away CBD in different states without going through any FDA or NIH process. However these products have no such safety assurances.

SAM is working on a long-term solution to expand and accelerate the current research so that every patient who might benefit from CBD can obtain it.

Are these CBD products safe? 

“High CBD” plant material usually also contains varying levels of THC, sometimes significant amounts. Most simple extraction processes cannot reliably extract CBD solely or primarily. Indeed, extremely complex and expensive equipment is required to remove the THC from a “high CBD” extract.  The situation is made more hazardous by the fact that existing research demonstrates that, in many cases, large doses of CBD are needed to achieve a specific therapeutic effect. Accordingly, a child taking a therapeutic dose of CBD (100-1000 milligrams per day) would potentially also be exposed to a large amount of THC. For example, using a 10:1 preparation, a child who ingested 300 mg of CBD per day would also be ingesting 30mg of THC. That is the equivalent of three of the highest dose (10mg) Marinol capsules, which would make most adult patients intoxicated.  A 2:1 or 1:1 plant ratio product would contain even higher levels of THC.

What is the legal status of CBD?

Because CBD is a component of the cannabis/marijuana plant, it is a Schedule

I substance under the federal Controlled Substances Act (CSA). The FDA has recently confirmed that CBD is, indeed, a Schedule I substance. Lisa Kubaska, PharmD, who works for the FDA’s Center for Drug Evaluation and Research stated in an email to an inquiry from a journalist:“CBD meets the definition of Schedule 1 under the Controlled Substance Act.”  For example, some companies advertise the following as “high CBD” strains:

Harlequin at 11.6%/6.9% CBD: THC;

Canna Tonic at 8.11%/6.9% CBD: THC;

Sour Tsunami at 7.24%/4.32% CBD: THC (see http://www.synergymmj.com/products.html).

It is also unclear whether their advertised ratios are accurate, i.e., whether the testing results are valid. Recent internet comments by parents complain that batches of “artisanal” CBD products do not have a consistent or anticipated effect and/or they are horrified that their children become “high”. This is a problem because medicines should be standardized and consistent among batches.  Finally, in many cases, the “high CBD” products may be contaminated by pesticides, synthetic fertilizers, and dangerous microbes.  Pesticides are neurotoxic, which could be quite dangerous to children with epilepsy. A number of physicians are reporting instances of bacterial infections, allegedly resulting from the use of these products.

Don’t you need some THC to synergize with CBD?

There is absolutely no reliable scientific evidence that THC is necessary to synergize the effects of CBD. Instead, there is evidence from preclinical research that THC may be pro-convulsant in sensitive brains; other research indicates that chronic use of THC can impair IQ in adolescents. Physicians are beginning to report instances of THC toxicity in children taking “high CBD” preparations, e.g., high anxiety, increased seizures, insomnia, etc. Until more is known, the most conservative course of action would be to remove THC entirely from a CBD product.

Why is there so much interest in CBD now?

 A number  of years ago, Project CBD in California, inspired by research being conducted by GW Pharmaceuticals in the U.K. (see below), began to educate interested patients and others about the therapeutic potential of CBD, which was virtually absent in high-THC marijuana in the U.S. Indeed, before GW embarked on its cannabinoid research and development program, many individuals in the U.S. believed that CBD was an inert compound. There were also anecdotal reports of some adults with epilepsy who discovered that inhaled marijuana seemed to prevent or reduce their seizures. As more and more scientific research demonstrated that CBD had a variety of therapeutic effects, interest in the use of CBD in epilepsy grew.

The CNN program hosted by Dr. Sanjay Gupta in August 2013 portrayed the case of a little girl with horrible, life-threatening intractable epilepsy. According to Dr. Gupta, her condition was greatly improved by a CBD-rich preparation produced by a company in Colorado. Understandably, this program resulted in enormous interest in CBD from families of children with epilepsy. As desperate parents sought “high CBD” products wherever they could purchase them, a number of dispensaries and other opportunistic vendors began to sell these products. However, the labelled potency and composition are often inaccurate and uneven, depending on the marijuana strain from which they come, the methods of manufacture used to prepare them, and the quality of the testing facility/procedures. At many places in the cultivation and manufacturing process, lack of standardization can result in higher levels of THC and lower levels of CBD –as well as the varying levels of dangerous microbes or pesticides -in the final preparation, e.g. growing from seed rather than clones; differences in the cultivation, harvesting, and drying conditions; uneven decarboxylation; and use of toxic extraction chemicals, such as butane or non-pharmaceutical ethanol.

Should the law be changed to allow high CBD, low THC products? 

 A state considering such a change in law should look to the example of other states where “high-CBD” products are legal for medical use, such as California.

In California, various preparations are available, and children can readily be given these products with 1) parental consent and 2) a physician’s recommendation.

Nevertheless, for the reasons stated above, the “legality” of these products has not made properly tested and standardized CBD products available to parents.

Products vary in consistency; testing laboratories do not provide reproducible and reliable results; testing each batch is expensive; most testing CBD laboratories do not test for pesticides or microbes; parents do not know how to prepare extracts from plant materials; the products themselves can be expensive; no dosing information is available; and more. Legislation is a blunt instrument, and any change in state law will, necessarily, be quite broad (e.g. “high CBD, low THC”) to permit various opportunistic growers and vendors to enter the state and prey upon vulnerable parents. Unless an elaborate testing system is established and enforced by the state, this will not ensure the safe, tested, and standardized products that parents seek for their children. Even certain more popular products are of uncertain composition, quality and efficacy. Companies selling these products have not made public the composition/ratio of an adequate number of batches, nor have they provided full battery anonymized case studies showing how many patients benefit and to what extent, how many patients get little or no benefit, what side effects they experience, and what they charge for the product. At most, 11 “selected” case studies have been presented, all of which show

However, these are anecdotal cases reported by parents, and it is unlikely that current CBD preparations work for all seizure conditions.

Source:  www.learnaboutsam.org  2013

Filed under: Medicine and Marijuana :

Why are we doing this? It would be a lot easier not to have the headaches and hate-mail that come with fighting legalisation. But we want to safeguard the next generation, to protect our children. We want to stop the creation of the next Big Tobacco.

We don’t have the $100million megaphone of the pro-legalisation lobby figure-headed by Nathan Edelman and George Soros. So not enough people know the truth. Just as the tobacco industry put out false science when it started, so does the marijuana industry. We must bridge the gap between the public misunderstanding of the drug and the scientific understanding. We must give information to decision-makers so that they have the courage to go forward.

We don’t want to replace one public-health tragedy with another one.

Having said that, people are beginning to recognise that Big Marijuana, like Big Tobacco, is an industry that relies on addiction for profits. It is sending people to hospital emergency rooms as you read this. They will profit over people who have no voice, or the budget for a voice.

Our two choices are not “lock ‘em up or legalise”. That is a false dichotomy. We need a real conversation about pot instead. Families deserve that. “Incarceration or legalisation?” “Lock ‘em up, or let ‘em loose?” … These phrases have dominated the discussion about marijuana over the past decade. As a result, marijuana-legalisation advocates — not scientists, doctors, people in recovery, disadvantaged communities or young people affected by marijuana use and its policies — have been at the forefront of changing marijuana laws.

So we founded Project SAM to consist of experts and knowledgeable professionals advocating for a fresh approach that neither legalises, nor demonises, marijuana. We are a nonpartisan alliance of lawmakers, scientists and other concerned citizens who want to move beyond simplistic discussions of “incarceration versus legalisation” when discussing marijuana use, and instead focus on practical changes in marijuana policy. We support a treatment, health-first marijuana policy. CONFRONTING PRESIDENT OBAMA…

In January, the US president commented that marijuana was less dangerous than alcohol, which led to an international media frenzy in support of global legalisation of the drug. On 22 January, we took the decision to release a statement about this, as follows.

“We at Smart Approaches to Marijuana, joined by leaders of major medical associations, recognise that marijuana legalisation goes against the President’s own goals of effective education and health care reform. We have identified many of the same problems with marijuana legalisation that he acknowledged when quizzed about his views of the drug by a reporter for The New Yorker. Chief among them: the legalisation of marijuana leads quickly to a slippery slope that could open the gates to legalisation – and commercialisation – of other addictive substances for recreational use. Clearly, the President knows that, for decades, several of today’s largest pro-marijuana-legalisation groups have been advocating for the full-scale legalisation of all recreational drugs, including psychedelics and cocaine.  As the President noted, the case for marijuana legalisation is overstated. As parts of the US plunge headlong into ill-informed drug policies rooted in opinions, political agendas and corporate greed, the President astutely notes that it is a matter of time before we’re also asked to consider the legalisation of a “negotiated dose of cocaine” or “a finely calibrated dose of meth”. That is the nature of addiction and substance abuse. It leads to the next problem, and the next problem and the next – and many times, the damage is irreversible and irreparable.

“However, we take issue with the President’s comparisons between marijuana and alcohol, and we strongly encourage him – a president who has, on many occasions, championed rigorous science – to work closely with his senior drug policy advisors and scientists, who fully acknowledge the growing world body of science showing the harms of marijuana use to individuals and communities. Today’s marijuana is far more potent than the marijuana the President acknowledged using during his teens and early adulthood. The President must also stop to consider the highly concentrated – and increasingly popular – form of marijuana called “hash oil.” Doses of that oil often exceed 80% THC – which is essentially a different drug than the weed of Woodstock, which ranged around 1-3% THC. “We should know better than to follow the same path by legalising a third, addictive substance that will inevitably be commercialised and marketed to children. Two wrongs don’t make a right: just because our already legal drugs may have very dangerous impacts on society it does not mean that other drugs should follow the same path.”

On 31 January, Obama stated on CNN that “If we start having a situation where big corporations with lots of resources and distribution and marketing arms are suddenly going out there, peddling marijuana, then the levels of abuse that may take place are going to rise further”.

Despite the hate mail we receive, we are doing something right. Perhaps the hate mail is because we are doing something right.

ALCOHOL vs MARIJUANA?

Coming back to the alcohol argument: what is the No 1 most dangerous drug? Alcohol. Why would we want to create another alcohol? This big, legal, ‘regulated’ business knows that 80% of its revenue comes from the 20% of people who abuse substances, the people who are most vulnerable, from people who shouldn’t be drinking any more. That is how they have marketed for decades. The people who will suffer most will be the most vulnerable, those who cause trouble to their communities – and cannot afford rehab when problems worsen. They are the target market for Big Pot.

People raise the issue of alcohol harms ‘versus’ marijuana harms. Yes, alcohol is worse when it comes to violence or liver damage. But marijuana is worse when it comes to IQ and loss of competitiveness and motivation, lung issues, mental health. Both cause traffic fatalities when drivers drug/drink drive. Two wrongs don’t make a right.

Once we have an industry whose business it is to increase addiction, then we will have a public-health problem on our hands.

Legalisers constantly refer to people in prison for marijuana. But there are three times as many alcohol arrests as there are for marijuana; do we want marijuana arrests to soar to that level by legalising it? In the UK, only 0.2% of people in prison are there for marijuana offences alone; in the US it is also less than 1%.  What do we have to say about our legal drugs: alcohol, tobacco and prescription drugs?  “600,000 deaths a year. A trillion dollars in the cost to society. And some of the most effective lobbies accessing governments.”

4TH WAVE OF LEGAL PHARMACEUTICALS

People have not woken up to what legalisation is all about. It would be the fourth wave of legal pharmaceuticals, following alcohol, tobacco, prescription drugs. After the debate about marijuana legalisation, there will be debates about heroin legalisation, cocaine legalisation: in a TV interview, Edelman has publicly expressed his ambition to legalise all drugs.

People are beginning to wake up to the fact that legalising marijuana is not about ‘responsible’ adults using pot in the privacy of their own homes. It is about the pot shop in your neighbourhood, about the advertising being viewed by children – and this is an industry which cannot be tamed once it is unleashed. There is smuggling of drugs across state lines in Washington and Colorado; the black market is alive and well, undiminished by legalisation.

On 17 February, we announced that Conspire, a company that provides drug testing to businesses and schools via Alere Toxicology and others, found that the number of their clientele testing positive for THC, the active ingredient in marijuana, rose 44% since December 2013. The announcement was made as we launched www.legalizationviolations.org to track legalisation’s effect in Colorado and Washington. With new data coming in every week to confirm that negative impact and the fuelling of drug use, it is important to have a central repository for tracking and collecting information.

We hope that other states and countries will pause and take note before they consider change so that we don’t have to relearn damaging lessons over and over again. While it is good to learn from experience, it is better to learn from other people’s experience!

Sadly, the marijuana conversation is mired with myths. Recent surveys show that many people do not think that marijuana can be addictive, despite scientific evidence to the contrary. Many would be surprised to learn that the American Medical Association has come out strongly against the legal sales of marijuana, citing public health concerns. Its opinion is consistent with most major medical associations, including the American Academy of Paediatrics and American Society of Addiction Medicine.

Because today’s marijuana is at least 5-6 times stronger than the marijuana smoked by most of today’s parents, we are often shocked to hear that, according to the National Institutes of Health, one in six 16-year-olds who try marijuana will become addicted to it; marijuana intoxication doubles the risk of a car crash; heavy marijuana use has been significantly linked to an 8-point reduction in IQ; and marijuana use is strongly connected to mental illness.

Constantly downplaying the risks of marijuana, its advocates have promised reductions in crime, flowing tax revenue and little in the way of negative effects on youth. We shouldn’t hold our breath, though.  We can expect criminal organisations to adapt to legal prices, sell to people outside the legal market – children – and continue to profit from larger revenue sources, such as human trafficking and other drugs. If drugs become legal, criminals will not become saintly citizens overnight but merely change commodities, such as profiteering from human trafficking instead of drugs.

We can expect the social costs ensuing from increased marijuana use to greatly outweigh any tax revenue — witness the fact that tobacco and alcohol cost society $£10 for every $£1 gained in taxes. Probably worst of all, we can expect our teens to be bombarded with promotional messages from a new marijuana industry seeking lifelong customers.

In light of the currently skewed discourse on marijuana, these are difficult facts to digest. People have been promised great things with the legalisation experiment. They can expect to be let down.

What makes a person great is the power and ingenuity and imagination of their brain. Their brain is the single most important organ in the body. It is everything to who we are as human beings. Our countries should be doing better to protect our most vital natural resource: our brains. We should not consign the next generation to substandard opportunities, simply because we have not been grown-up enough to know that there are consequences to public policies which we did not consider. Every life is so important that it must be given the best chance.

Legalisation is not inevitable. We must remind people who struggle with addiction that they are not alone: we are with them. The APA, ASAM are with us. On the other side is an alliance of people who want to line their pockets with money from those are addicted. We cannot give up. We are in this for the long haul.

Source:   addictiontoday.org  March 07 2014

This excerpt from the book Keep Off The Grass gives an interesting background to current situation of the push to legalize cannabis – early last century the majority of delegates to the conventions were aware of both mental and physical harm produced by the drug; and in the international community, at least, there was no doubt of the dangers to health inherent in marijuana.

KEEP OFF THE GRASS   by Gabriel G. Nahas, M.D., Ph.D., D.Sc.

Foreword by Jacques Yves Cousteau

PAUL S. ERIKSSON, PUBliSHER Middlebury, Vermont 05753

IV.              An International Problem (Pages 33-37)

Americans think that anti-marijuana laws were created in recent years just to thwart use of the drug by younger people.  Not true! They are actually the result of international agreements signed by the United States a half century ago in order to halt traffic in what was then considered to be a dangerous substance.

Aware of this fact, on my return to the United States in the autumn of 1970, I decided that the logical place for my own detailed research into that aspect of marijuana would be the Dag Hammarskjold Library for International Scholars at the United Nations in New York. If the nations of the world had seen fit to meet on several occasions in order to control the Distribution of cannabis derivatives, then they must have suspected or known of specific health hazards. The examination of these international documents might lead to some clues that would aid me in the direction of my own laboratory work.

My study soon revealed that at the turn of the century, with the development of intercontinental communications, it became apparent to the nations of the world that the control of substances dangerous to man’s health and to society-mainly opium at that time-had to be controlled on a global basis.  Representatives of sovereign nations held conferences to formulate regulations for the international control of opium and other dangerous drugs. The first such gathering was held in Shanghai in 1904 at the instigation of President Theodore Roosevelt. This preliminary meeting set the stage First Opium Conference at The Hague in 1912. The preamble to the text of this conference spells out its general goals:

“The Emperor of all Russias, the King of England’/ Emperor of India, the Kaiser of Germany , the President of the  French Republic, the President of the United States of America. . . desirous of advancing a step further on the road opened by the International Commission of Shanghai of 1909; determined to bring about the gradual suppression’ the abuse of opium, morphine and cocaine and also of the drugs prepared or derived from these substances which might give rise to similar abuses; taking into consideration the necessity and the mutual advantage of an international agreement on this point; convinced that in this humanitarian endeavor they will meet with the unanimous adherence of all States concerned: have decided to conclude a convention with this object.”

Almost as an afterthought, an “Indian Hemp Re801 was tacked on, calling for the “study [of] the question of Indian Hemp from the statistical and scientific point of with the object of regulating its abuses, should the necessity  be felt, by internal regulation or by international agreement.”

By the time of the Second Opium Conference, her Geneva in 1924, some scientists had agreed that the time for cannabis control was at hand. While opium was still major consideration, Egypt’s delegate, Dr. El Guindy, said, “There is, however, another product, which is at least as harmful as opium, if not more so, and which my government would be glad to see in the same category as the other narcotics already mentioned. I refer to hashish, the product of Cannabis sativa. This substance and its derivatives work such havoc that the Egyptian government has for a long time past prohibited their introduction into the country. I cannot emphasize sufficiently the importance of including this product in the list of narcotics, the use of which is to be regulated by this Conference.”

In answer to questions from other delegates, Dr. EI Guindy claimed that although the Egyptian government had banned the growing of cannabis, large amounts were still smuggled in from neighboring countries. “This illicit use of hashish,” he told the Conference, “is the principal cause of insanity in Egypt, varying from thirty to sixty percent of the total number of cases reported. Taken occasionally and in small doses, hashish perhaps does not offer much danger, but there is always the risk that once a person begins to take it, he will continue. He acquires the habit and becomes addicted to the drug and once this happens it is very difficult to escape.”

The greatest hazards of cannabis intoxication mentioned by Dr. EI Guindy were “acute hashishism,” marked by crises of delirium and insanity, and “chronic hashishism;” marked by visible mental and physical deterioration. Because of pressure from the Egyptian and Turkish delegates, who would not sign a ban on opium unless cannabis was also included, after some debate all the delegates voted in favor of controlling “Indian Hemp” as defined by the “dried flowering or fruiting tops of the pistillate plant Cannabis sativa from which the resin has not been extracted, under whatever name they may be designated in commerce.”  Thus, cannabis was put on the forbidden list, not because of medical reasons, but for social ones.

After World War II, the United Nations inherited the duty of enforcing the highly complex international agreements on control of dangerous drugs, including the above cannabis control resolution. When the World Health Organization came into being in 1948, this responsibility was shifted to them in the form of an: expert Committee on Drug Depen-dence that served as an advisory group to the United Nations Commission on Narcotics. The committee, made up of physicians and scientists, reviewed the cannabis situation and quickly came to the conclusion “that use of the drug was dangerous from every point of view, whether physical, mental or social. The ultimate result of this review was the 1961 Single Convention on Narcotic Drugs in which 500 delegates from seventy-four nations, including some of the best toxicologists and pharmacologists in the world, recommended that cannabis, in all its forms, be limited exclusively to medical and scientific purposes.” The primary reason for this strict regulation was that all the available expert advice from the World Health Organization indicated that cannabis did constitute a danger to health and a hazard to society although, admittedly, not well-documented.

While the United States was a signatory member of both the Second Opium Conference and the United Nations agreements, the signing was done with the attitude that the inclusion of cannabis in an international drug ban was “more important to them than to us.”  Marijuana was not’ problem in America, and there were only a farsighted few like the head of the American delegation, career diplomat, Harry Anslinger, who recognized its dangers.

The Single Convention was hailed by most countries as a landmark for the control of dangerous drugs throughout the world. It was also hailed as a model of the kind of international cooperation the United Nations can achieve.  The agreements reached by the Convention were unanimously ratified by the participating nations.

Ten years later, however, in the United States the climate of opinion had changed as the use of marijuana had become widespread. Now there were dissenters who objected to the inclusion of cannabis in the Single Convention. Thus, Harry Anslinger became the focal point of the attack of the new proponents of pot. One critic said, “The inclusion of cannabis into an international agreement mainly concerned with opiates and cocaine was due to the efforts of one determined man, Harry Anslinger.” But anyone who has read the documents would realize that the agreement was the result of a historical movement to control or eliminate dangerous psychotropic drugs, including cannabis-as are virtually all the United States federal and state anti marijuana laws.

In any event, the United Nations Single convention of 1961 was not the last one to be held on this subject.  A new conference in Vienna in 1971 produced an international agreement to control many of the newer psychotropic drugs such as hallucinogens, barbiturates, and stimulants.

‘While my research at the Dag Hammarskjold Library did not produce any major revelations, it did clarify certain points that I considered to be important to the evolution of my own work. Essentially, I became convinced that the present legal strictures against marijuana in the United States were not based on one man’s perversity but were the result of international agreements that went back to the beginning of this century; cannabis was included in these international agreements because the majority of delegates to the conventions were aware of both mental and physical harm produced by the drug; and in the international community, at least, there was no doubt of the dangers to health inherent in marijuana.

Source:  Book,  Keep Off The Grass by Gabriel Nahas

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