2023 November

A NEW cannabis compound has been discovered and it may be 30 times more potent than THC.

Scientists aren’t yet sure whether the compound causes a high or has medical benefits so they’ve been conducting tests to try and figure this out.

Little is known about the potential effects of the new strong compound Credit: Getty – Contributor

The compound is one of two newfound cannabinoids that have been discovered in the Cannabis plant glands of the sativa L species.

Cannabinoids is the collective term for the group of diverse chemical compounds that act on the cannabinoid receptors of the brain.

THC is just one of these cannabinoids and it’s currently considered to be the principal psychoactive component of cannabis.

THC, or tetrahydrocannabinol, plugs into brain receptors and can alter our ability to co-ordinate movements, reason, record memories and perceive things like time and pleasure.

THC in cannabis is what can give smokers a high feeling Credit: Getty – Contributor

It’s thought that cannabis contains over 140 similar chemicals that can interact with receptors all over the body.

However, THC is currently the only one we know can result in a high spaced out feeling.

Of the two new cannabinoids discovered, one looks similar to the compound CBD, which isn’t psychoactive.

The other appears similar to THC but may even produce stronger mind-bending effects.

This THC lookalike is called tetrahydrocannabiphorol (THCP).

Recent research suggests that it interacts with the same brain receptor as THC but has slight differences in its chain of atoms.

The slight difference in shape of THCP means it can technically fit more snugly into its preferred brain receptor than THC.

A test showed that the compound can actually bind 30 times more reliably than THC.

When given to lab mice, the THCP made them behave as if they were on THC with slower movements and decreased reactions to pain.

The mice reached this state with a much lower dose than would have been required with THC meaning the new compound is stronger.

However, this lab experiment still doesn’t mean that the same effect would happen in humans.

THCP doesn’t appear to be present in large amounts in cannabis plants but even if it was, increased psychoactive properties would still not be guaranteed.

Being caught with cannabis comes with a maximum of five years in prison, an unlimited fine, or both.

  • While being convicted of producing and supplying the Class B drug carries up to 14 years behind bars, an unlimited fine, or both.
  • Police can issue a warning or on-the-spot fine if you’re caught with a small amount – generally less than one ounce – if it is deemed for personal use.

Source:  The Sun  14th Jan. 2020

Source: Preventing Marijuana Use Among Youth & Young Adults (getsmartaboutdrugs.gov) March 2017

Researchers have found that even occasional cigarette use is enough to affect the volume and connectivity of developing brains

After decades of educational programming and advertising, regular cigarette smoking and sales in the United States have declined to their lowest levels in 50 years. But doctors and parents are now racing to deal with another health crisis that has popped up in its place: the meteoric rise of electronic cigarettes (or e-cigarettes) among adolescents.

This nicotine electronic delivery device was originally introduced to the market as a promising tool to aid smoking cessation among already current smokers. Yet, the lack of federal regulations, the appealing flavors available, and perceptions that these devices were less harmful than regular cigarettes have led to a worrying spike in use among U.S. adolescents. One in five U.S. high school students and one in 20 middle school students currently use e-cigarettes.

E-cigarette use among youth has skyrocketed in the past few years

U.S. Surgeon General Jerome Adams has declared e-cigarettes an epidemic among youth, stressing that e-cigarette aerosols containing nicotine increase the risk of addiction to nicotine and other drugs, and impact brain development which can induce mood disorders and lower impulse control. Now, new research led by Dr. Bader Chaarani of the University of Vermont and published in the journal Biological Psychiatry: Cognitive Neuroscience and Neuroimaging has found adolescents that smoked only a few cigarettes had smaller and less connected brain areas than their peers who never smoked. This could mean that adolescent smokers’ brains will develop and function differently, which may affect decision-making and self-control in adulthood. 

Just like regular cigarettes, e-cigarettes contain nicotine, a neuroactive chemical and an addictive component whose main target is the brain. Nicotine acts upon receptors in our brains -through nicotinic acetylcholine receptors (nAChRs)- to promote the release of a neurotransmitter called dopamine. Dopamine is a feel-good chemical, triggering a pleasurable response in our brains. When linked with the action of smoking, it plays a fundamental role in nicotine addiction.

Adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired

Nicotine exposure among adults presents lower risks compared to adolescents. This is because our brains develop throughout our first three decades of life. During this maturation period, the brain circuits are being remodeled, especially those involved in reward function (dopamine) and cognitive function (acetylcholine). Therefore, adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired, making young people even more vulnerable to future addiction. 

Previous studies have shown that adolescent smokers have reduced neural activity and show symptoms of nicotine dependency at lower nicotine levels than adults, and that individuals that begin smoking during adolescence are more likely to develop nicotine dependence than individuals that start in their late 20′s.

Studies of smoking’s effects on the brain have largely focused on adults, not youth – until now

One big gap in research observing the effects of cigarette smoking on brain volume, connectivity, and function to date is that such studies have been mostly performed on adult smokers rather than adolescent smokers. The majority have also focused on daily and heavy smokers, yet have overlooked occasional smokers, which is relevant due to common experimentation behaviors during adolescence

The new research by Dr. Chaarani and their team finally addresses these gaps by looking at the brains of adolescent light smokers. They found that just a couple of cigarette puffs can potentially alter the development of adolescent brain. 

The research team recruited over 600 14-year-old adolescents and calculated a cigarette-smoking score for each participant based on how many times, during their lifetime, they had smoked cigarettes. Participants ranged from young people who had never smoked to those who have smoked more than 40 times.

Smoking even a few times is significantly linked to a decreased volume of the gray matter and neuronal connectivity

The researchers also looked at the brain of each of the participants using functional magnetic resonance imaging (fMRI). These images were used to estimate the brain gray matter volume corresponding to the neuron bodies where synapses occur, and white matter connectivity, meaning the “telephone wires” that connect neurons and brain areas by carrying electrical signals. 

Interestingly, Dr. Chaarani and their team found that smoking even a few times was significantly linked to a decreased volume of the gray matter and neuronal connectivity. And the more teens smoked, the more the gray matter volume at the ventromedial prefrontal cortex (vmPFC), and the connectivity at the corpus callosum of their brains was reduced. Scientists have previously linked alterations in the vmPFC volume with a reduction in reward and with an increased risk of anxiety disorders. 

Moreover, reduction in the connectivity could indicate that nicotine induces axonal damage, meaning it may be altering the communication between brain areas. These alterations in brain connection have also been reported in individuals with substance addiction and alcohol dependence. While the research only showed a link between low doses of cigarette smoking and brain alterations, rather than a causal effect, these type of consequences have been consistently reported in many studies on brains of adult smokers.

E-cigarettes may look harmless, but they have lasting effects on developing brains

Although this study focused on adolescents who smoked traditional cigarettes, scientists have demonstrated that such risks are applicable to teenagers who vape using the popular JUUL brand of e-cigarettes since the two methods deliver similar amounts of nicotine.

Researchers are still working to understand the impact of nicotine in the brain of young smokers, particularly now that e-cigarette use among youth has increased rapidly. This new study could play a critical role in educational campaigns, and spur regulatory agencies, parents, and teachers to take an active role in preventing this newest addiction. 

Source:  https://massivesci.com/articles/smoking-vaping-risks-adolescent-brain-function-development-addiction-nicotine/   June 2019

Cannabis Use in Pregnancy –  A Tale of 2 Concerns

In an article in JAMA, Corsi and colleagues present the results of a retrospective cohort study of 661 617 women designed to assess associations between maternal cannabis use during pregnancy and adverse obstetrical and birth outcomes.

In a matched analysis designed to control for confounding, the investigators compared 5639 self-reported cannabis users with 92 873 nonusers and found elevated rates of preterm birth (defined as gestational age <37weeks) among those who reported cannabis use. Specifically, the rates of pre term birth in the matched cohort were 10.2% vs 7.2% (risk difference, 2.98% [95% CI, 63%-3.34%]; relative risk, 1.41 [95%CI, 1.36-1.47]). While similar risks were observed for small-for-gestational-age birth and placental abruption, there appeared to be a small protective association between cannabis use and preeclampsia and gestational diabetes.

In another article in JAMA, Volkow and colleagues report findings on cannabis use among 4400 pregnant women and 133,900 nonpregnant women aged 12 to 44 years who participated in the National Survey on Drug Use and Health from 2002 to 2017. The authors documented an increase in the adjusted prevalence of cannabis use during pregnancy from 3.4%in 2002 to 7.0%in 2017—almost of all which appeared to be explained by nonmedical use.

These studies send a straightforward message: cannabis use in pregnancy is likely unsafe; with an increasing prevalence of use (presumably related to growing social acceptability and legalization in many states), its potential for harm may represent a public health problem.

This message is based on the sound, if imperfect, epidemiology of these  studies and is heightened by a misperception that marijuana is safe, as evidenced by its direct marketing to pregnant women for morning sickness despite accumulating evidence of harm.

However, there is an additional series of equally legitimate concerns, rooted more in history than epidemiology. These historical concerns relate to past and ongoing discourses on alcohol use in pregnancy and to the cocaine “epidemic that wasn’t” of the 1980s.

Both of these histories, although imperfect comparators with the emerging data on cannabis, illustrate points that provide important context to the present studies published in JAMA

First, there are issues involving the epidemiology. Randomized designs are impractical for studying risks and harms, and observational studies are prone to unmeasured confounding.

In this respect, the study by Corsi and colleagues is no different

From any other cohort study; it is, however, further limited by use of registry data, derived primarily from clinical encounters, to assess cannabis exposure.  Although the investigators performed some internal validity checks on their measurement of exposure, clinical data in the field of substance use tend to lack validation (and thus are prone to mis- classification error), particularly when unaccompanied by biological markers .  Compounding this limitation is the inability to glean from the data the timing of cannabis exposure or a dose-response relationship between exposure and out comes, both of which represent fundamental epidemiologic principles to support causality.

There was also no assessment of birth weight, which tends to be measured more accurately than gestational age.  Despite these limitations, the study is consistent with previous studies that have assessed the association between cannabis use in pregnancy and birth outcomes and provides important, population-based data.

Second, the historical context requires consideration. What has been learned from the debates about alcohol and cocaine use in pregnancy? Although it is accepted that heavy alcohol drinking during pregnancy poses an unacceptable risk to the developing foetus, the effect of moderate alcohol consumption continues to be controversial. 

On one side of this argument, those who interpret the data using a strict, by-the-numbers approach conclude that there is only minimal evidence that moderate alcohol consumption poses a demonstrable risk.

On the other side of the argument are those who interpret the data more broadly to conclude that without an empirically proven safe level of exposure, abstinence is the only reasonable advice the medical community can give to pregnant women.

One lesson of the current alcohol debate—which is often couched in terms of women’s ability to enjoy wine with dinner and thus assumes the perception of an issue that predominantly affects the privileged—is that two reasonable perspectives can be applied to the same body of opposing, non literature and reach stigmatizing conclusions.

In other words, the issue is not the data but the values that individuals bring to the data and to whom the data are thought to be most relevant.

Extrapolating this logic to the data Corsi et al present on cannabis, some might choose to focus on the reported 41% increased relative risk of pre -term birth as unacceptably high; others might choose to focus on the 2.98% absolute risk difference to be such that cannabis-related relaxation or improvement in morning sickness may not be worth abstaining from this drug.

The study by Corsi and colleagues could also be interpreted through a slightly different lens. Perhaps it represents part of an emerging story of an in utero substance exposure that is neither highly prevalent nor extremely rare, an outcome that is consequential more on a population than individual level, and an association between exposure and outcome that is moderate in both its magnitude and degree of certainty.

Unlike the “wine with dinner” debate, the dialogue on cannabis use is likely to be relevant to many sectors of society and may end up focusing on young people, especially those of colour, among whom use is markedly increasing. In these respects, a comparison with certain aspects of the history of cocaine use in pregnancy may be instructive. In 1985, the first “scientific” observation of the relationship between in utero cocaine exposure and neonatal outcomes was published. Even by the standards of its day, this study (and many that followed) were fundamentally flawed.  Yet they provided “evidence” for those in the medical community and lay press to publicly exaggerate risks of cocaine in pregnancy and to attribute (both implicitly and explicitly) lifelong disability to a large cohort of primarily minority children, for whom subsequent research demonstrated similar outcomes to unexposed children raised in similar environments.

Perhaps worse, this exaggerated risk amplified judgment and stereotype, leading to the enduring racist social constructs of the “cocaine mother” and “crackbaby” and to criminalization of substance use among pregnant women. Regrettably, the exaggerated dialogue on cocaine did little to shed light on the sequelae of urban poverty and legacy of racism in the United States. It is possible to argue that the comparisons of cannabis vs alcohol and cocaine are not entirely fair. Cocaine in particular is biologically more destructive than cannabis, universally illegal in the United States, and without health benefit.

Furthermore, the dialogue on cocaine was defined by exaggeration; so far, the dialogue on cannabis has largely been defined by a false perception of safety. While these are fair criticisms, some historic lessons of both alcohol and cocaine apply: it is impossible to separate data from the values that individuals bring to those data, no group is immune to the judgment of others, and women and minority groups (particularly pregnant women of colour) tend to bear the greatest burden of many of these judgments.

While an obvious reaction to these new data on in utero cannabis exposure is that more research is necessary, more epidemiology is unlikely to completely resolve the complex issue of potentially safe moderate use or to completely remove the tendency to imbue data interpretation with implicit biases about groups of people.

Perhaps the best reflection that can be offered is a reprise of that offered by Mayes et al in 1992. This commentary acknowledged the potential harms of prenatal cocaine exposure, dispassionately delineated the methodologic problems with the state of the literature at the time, and expressed concern that premature conclusions attributing irremediable damage in children to exposure to a single substance (isolated from the broader social milieu) were, in and of themselves, harmful. This harm, the commentary argued, accrued by way of permanently lowered expectations and by a discourse that focused on judgment and attribution as opposed to prevention and positive intervention.

The current data reported by Corsi et al and Volkow et al should spark genuine concern about the association of cannabis use in pregnancy with pre term birth. However, there should be additional concern about whether such findings may ripple through society and re-create some of the mistakes of the past.

Source:  Cannabis Use in Pregnancy: A Tale of 2 Concerns – PubMed (nih.gov) June 2019

Limited information exists on marijuana use and male reproductive health. A recent study from Duke University evaluated differences in sperm quality resulting from tetrahydrocannabinol (THC) exposure in both rats and humans. Findings suggest that paternal marijuana use, prior to conception, may present epigenetic risks to potential offspring.

Public perceptions pertaining to marijuana have evolved radically over the past 2 decades. While marijuana remains criminalized at the federal level, 33 states and the District of Columbia have legalized marijuana, in some capacity, for either medical or recreational use. According to the most recent National Survey on Drug Use and Health, nearly 26 million Americans, over the age of 12, currently use marijuana. While the gender gap is narrowing, men remain significantly more likely to use marijuana than women (11.7% vs. 7.3%, respectively).

In 2017, approximately 1.9 million men, between the ages of 26 and 29, reported using marijuana in the past month. Given that the average age of first-time fathers in the U.S. is around 30, these findings suggest that a substantial number of “fathers-to-be” are using marijuana at the time of conception. Little is known, however, about the impact of paternal marijuana use on reproductive outcomes.

Epigenetics, which literally translates to “above” or “on top of” genetics, refers to the biological mechanism through which genes are activated and expressed. This process acts like a light switch, turning on or off how cells read certain heritable traits written within an individual’s unique genetic code. Sperm matures continually throughout adulthood, making it particularly vulnerable to potential epigenetic modifications, such as DNA methylation, that may result from marijuana use. This study explores differences in sperm profiles, based on cannabis exposure in both humans and rats, to better understand potential heritable effects.

Key Findings

  • Individuals who used marijuana can have higher and also can have significantly lower sperm concentrations, compared to those who did not, posing potential complications for fertility.

  • THC-exposed sperm was associated with significantly altered DNA, in both rat and human samples.

*Associations were even stronger among individuals with higher levels of THC in their urine, implying a “dose-response relationship” such that chronic marijuana users may be impacted more severely.

  • Authors identified three unique potential genetic pathways modified by THC exposure.

Looking to the Future

Past research suggests that offspring born to rats exposed to THC during adolescence demonstrate significant DNA alterations in their brains, display heightened drug-seeking behavior, and are at increased risk of developing opioid dependency over time, compared to controls. The present study is the first to extend this line of research to men of childbearing age, lending additional evidence for potential intergenerational, heritable consequences, resulting from paternal marijuana use. Just as other environmental triggers, such as air pollution, cigarette smoking, certain pesticides (i.e. DDT), and exposure to radiation are known to affect sperm health, THC may also increase the potential for genetic mutations.

For Clinicians

  • Primary care physicians and healthcare professionals, both inside and outside of substance use disorder treatment landscapes, should take time to educate patients about the impact of THC on sperm so individuals may consider potential implications for fertility and children conceived during periods of active use.

For Researchers

  • This article adds to a growing literature on the potential epigenetic impact of paternal marijuana use prior to conception. Findings must first be replicated in larger samples. Additionally, future longitudinal studies are necessary to explore the extent to which THC induced DNA alterations in sperm are passed down to offspring, as well as their long-term consequences.

For Policymakers

  • Marijuana potency continues to increase rapidly, with THC level increasing 300% over the past 20 years. Within the current political landscape and shift towards increased access to medical and recreational marijuana, policymakers should work closely with scientists to stay informed on the extent to which increased THC levels and evolving public attitudes impact men’s reproductive health.

For General Public

  • The full impact of passing THC-related DNA modifications onto offspring, and whether or not these changes are reversible is still unknown. Evidence of DNA alterations to existing Hippo signaling and Cancer genetic pathways may disrupt growth, enhance the potential for miscarriage, or impede healthy embryo development.

Methods

The authors employed a quantitative genome-scale approach, referred to as reduced representation bisulfite sequencing, to compare DNA methylation alterations in sperm across human and rat samples. A number of factors including, time since last ejaculation, semen volume, pH, morphology, and motility were controlled for across participants. Pyrosequencing, a DNA synthesizing method that relies on light detection, was implemented to identify genes with significant methylation differences. Data were then analyzed to uncover specific genetic pathways potentially impacted by paternal, preconception cannabis use.

Study Limitations

  • A relatively small sample size of human subjects, limiting the generalizability of study findings.

*24 males, age 18-40 years: (12 marijuana users & 12 non-users)

  • The methodological approach may fail to identify epigenetic modifications that affect multiple genes simultaneously.

Source: What you should know about Marijuana and Sperm (addictionpolicy.org) March 2019, updated October 2022

Alexandria, VA) – A new study released yesterday in the Annals of Internal Medicine found that the rise in marijuana use in Colorado since the state legalized the drug has led to increased emergency room visits. The study found that 9,973 marijuana-related emergency room visits occurred from 2012-2016, more than triple the number that occurred prior to legalization. Additionally, the study found that 10.7% of visits at UCHealth were due to the ingestion of high potency marijuana edibles. 

“Evidence continues to build the case that marijuana legalization results in harmful impacts on public health and safety,” said Dr. Kevin Sabet, founder of Smart Approaches to Marijuana and a former senior drug policy advisor to the Obama Administration. “Marijuana is no longer the weed of Woodstock. The industry is churning out new, highly potent candies, gummies, sodas, and ice creams as well as concentrates and vape pens that contain up to 99% THC. These kid-friendly products are regularly getting into the hands of children, whose developing brains are incredibly susceptible to permanent damage from this highly potent pot.”

The study found that 17% of emergency room visits were due to uncontrolled vomiting that was associated with the smoked form of the drug. Previous research has labeled this phenomenon as “scromiting,” or Cannabinoid Hyperemesis Syndrome. 12% of the visits were for acute psychosis and this was associated with high potency edibles. 8% of visits were associated with cardiovascular issues such as irregular heartbeat or even heart attacks after ingestion of edibles.

Another recent study found that the use of high potency edibles was directly linked with increases in severe mental illness, such as psychosis, and stated that if higher potency concentrates and edibles were removed from the market, instances of psychosis would be reduced by a third. 

“Lawmakers rushing to legalize marijuana need to slow down and consider the implications it could bring upon their state,” continued Dr. Sabet. “They are certainly not receiving information such as this from the pot industry’s army of lobbyists. This is why organizations such as SAM are so important. We work tirelessly to combat the industry narrative that marijuana is harmless.

Email from SAM https://www.learnaboutsam.org March 2019

Summary

Background

Cannabis use is associated with increased risk of later psychotic disorder but whether it affects incidence of the disorder remains unclear. We aimed to identify patterns of cannabis use with the strongest effect on odds of psychotic disorder across Europe and explore whether differences in such patterns contribute to variations in the incidence rates of psychotic disorder.

Methods

We included patients aged 18–64 years who presented to psychiatric services in 11 sites across Europe and Brazil with first-episode psychosis and recruited controls representative of the local populations. We applied adjusted logistic regression models to the data to estimate which patterns of cannabis use carried the highest odds for psychotic disorder. Using Europe-wide and national data on the expected concentration of Δ9-tetrahydrocannabinol (THC) in the different types of cannabis available across the sites, we divided the types of cannabis used by participants into two categories: low potency (THC <10%) and high potency (THC ≥10%). Assuming causality, we calculated the population attributable fractions (PAFs) for the patterns of cannabis use associated with the highest odds of psychosis and the correlation between such patterns and the incidence rates for psychotic disorder across the study sites.

Findings

Between May 1, 2010, and April 1, 2015, we obtained data from 901 patients with first-episode psychosis across 11 sites and 1237 population controls from those same sites. Daily cannabis use was associated with increased odds of psychotic disorder compared with never users (adjusted odds ratio [OR] 3·2, 95% CI 2·2–4·1), increasing to nearly five-times increased odds for daily use of high-potency types of cannabis (4·8, 2·5–6·3). The PAFs calculated indicated that if high-potency cannabis were no longer available, 12·2% (95% CI 3·0–16·1) of cases of first-episode psychosis could be prevented across the 11 sites, rising to 30·3% (15·2–40·0) in London and 50·3% (27·4–66·0) in Amsterdam. The adjusted incident rates for psychotic disorder were positively correlated with the prevalence in controls across the 11 sites of use of high-potency cannabis (r = 0·7; p=0·0286) and daily use (r = 0·8; p=0·0109).

Interpretation

Differences in frequency of daily cannabis use and in use of high-potency cannabis contributed to the striking variation in the incidence of psychotic disorder across the 11 studied sites. Given the increasing availability of high-potency cannabis, this has important implications for public health.

Funding source

Medical Research Council, the European Community’s Seventh Framework Program grant, São Paulo Research Foundation, National Institute for Health Research (NIHR) Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London and the NIHR BRC at University College London, Wellcome Trust.

Source: The contribution of cannabis use to variation in the incidence of psychotic disorder across Europe (EU-GEI): a multicentre case-control study – The Lancet Psychiatry March 2019

The study by Sadananda et al published in the current issue of the IJMR highlights the neurophysiological basis of altered cognition in subjects with opioid addiction. The study demonstrated aberrant network activity between the default mode network (DMN) and fronto-parietal attentional network (FAN) as a major cause for working memory deficits in drug addiction. Working memory is an important to retain the cognitive information essential for goal directed behaviours. Human beings are endowed with an efficient cognitive faculty of working memory, essential for efficient functioning of the executive network system of the brain. As working memory is the key to carry out any cognitive process involving attention, volition, planning, goal directed behaviour, etc., consciousness is linked largely to working memory processing. The importance of integrating neuroscience knowledge especially the executive functions of human brain in leadership has been taught in neuro-leadership programs as a mean to maximize the human capabilities, productivity, creativity, leadership, wellness, positive attitude.

Aberrant network activities and structural deficits in brain areas of executive functioning impede most of our intellect including mental flexibility, novel problem solving, behavioural inhibition, memory, learning, planning, judgement, emotion regulation, self-control and other social functioning. Deficits in working memory and attention owing to reduced fronto-parietal network (FPN) activity is reported in schizophrenia, autism, attention deficit hyperactive disorder (ADHD) and anxiety disorders. Opioid addiction is reported to impede such dynamicity of the executive system leading to a wide range of deficits in cognition. Opioid addiction alters the network integrity between DMN and FPN networks and weakens the cognitive information processing in cognitively challenging paradigms. Dysfunctional dynamics of DMN activity is believed to contribute to impaired self-awareness, negative emotions and addiction related ruminations. Aberrant DMN activity and reduced medial prefrontal cortical functions are common neural phenotypes of cognitive deficits in conditions like mental illness, drug addiction, sleep deprivation and neurodegenerative disorders. People with substance use disorders develop mental illnesses as a serious comorbidity that in turn, leads to severe behavioural impairments at the social, emotional and cognitive domains. Chronic sleep deprivation associated with drug addiction and substance abuse is another predisposing factor that worsen the behavioural impairments. Over all, drug addiction, substance abuse and the subsequent maladaptive behaviours including mental illness and sleep deprivation trigger a complex set of network instability in the domains of cognition and affect. The euphoria and hallucinating experience of drugs of abuse would soon lead to psychological distress and to cognitive and emotional behavioural impairments due to the disruption of various top down and bottom-up network dynamics.

Substance use disorders are an imminent socio-economic burden and have become a major public health concern worldwide. Despite knowing the harmful effects and consequences of drug use, reports say that the youth especially the adolescents have a tendency to continue the habit. There is a need to have effective measures in place such as educational programmes to improve the self-efficacy of parents and family members to help their children to develop the right behavioural attitude, enhance the capacity building in teachers to strengthen the self-esteem and wellness of students to organize substance use control awareness programmes in coordination with NGOs at educational institutions, involvement of television and other visual and social media platforms to organise substance abuse control programmes and for interactive opportunity for children/youth with educators, researchers and professionals, organization of knowledge dissemination programmes to the public/schools/colleges to highlight the adverse effects of drug abuse on mental health and cognition. Introduction to such knowledge sharing platforms such as the Virtual Knowledge Network (VKN) at NIMHANS, Bengaluru, provide interactive skill building opportunities to safeguard them from substance abuse and addiction. People should have easy access to such services and rehabilitation centers. Various behavioural intervention strategies such as cognitive retraining, psychotherapy, yoga therapy, mindfulness-based intervention programmes etc. are reported to improve cognitive abilities, regulation of negative emotions and restoration of motivational behaviours. A study on single night exposure to olfactory aversive conditioning during sleep helped to quit addiction to cigarette smoking temporarily. Such studies highlight the possibility of learning new behaviours during sleep and its positive impact on wake associated behaviours. Such approaches are quite useful, easily testable and cost-effective. Thanks to the incredible phenomenon of adult brain plasticity, it is possible to re-establish social intelligence, prosocial motivation among people with substance abuse.

Source: Drug addiction – How it hijacks our cognition & consciousness – PMC (nih.gov) October 2021

Abstract

Rates of cannabis use among adolescents are high, and are increasing concurrent with changes in the legal status of marijuana and societal attitudes regarding its use. Recreational cannabis use is understudied, especially in the adolescent period when neural maturation may make users particularly vulnerable to the effects of Δ-9-tetrahydrocannabinol (THC) on brain structure. In the current study, we used voxel-based morphometry to compare gray matter volume (GMV) in forty-six 14-year-old human adolescents (males and females) with just one or two instances of cannabis use and carefully matched THC-naive controls. We identified extensive regions in the bilateral medial temporal lobes as well as the bilateral posterior cingulate, lingual gyri, and cerebellum that showed greater GMV in the cannabis users. Analysis of longitudinal data confirmed that GMV differences were unlikely to precede cannabis use. GMV in the temporal regions was associated with contemporaneous performance on the Perceptual Reasoning Index and with future generalized anxiety symptoms in the cannabis users. The distribution of GMV effects mapped onto biomarkers of the endogenous cannabinoid system providing insight into possible mechanisms for these effects.

SIGNIFICANCE STATEMENT Almost 35% of American 10th graders have reported using cannabis and existing research suggests that initiation of cannabis use in adolescence is associated with long-term neurocognitive effects. We understand very little about the earliest effects of cannabis use, however, because most research is conducted in adults with a heavy pattern of lifetime use. This study presents evidence suggesting structural brain and cognitive effects of just one or two instances of cannabis use in adolescence. Converging evidence suggests a role for the endocannabinoid system in these effects. This research is particularly timely as the legal status of cannabis is changing in many jurisdictions and the perceived risk by youth associated with smoking cannabis has declined in recent years.

Discussion

We present evidence of GMV differences in adolescents associated with only one or two instances of cannabis use. Although novel, this work is consistent with reports of a dose–response effect of cannabis on behavioral and brain measures following heavier use (Lorenzetti et al., 2010Silins et al., 2014). We identified significantly greater GMV in adolescents who reported only one or two instances of cannabis use relative to cannabis naive controls in large medial temporal clusters incorporating the amygdala, hippocampus, and striatum, extending into the left prefrontal cortex. Significantly greater GMV was also observed in the lingual gyri, posterior cingulate, and cerebellum. The regions identified in this whole-brain, VBM approach replicated previous findings of differences in volume (Yücel et al., 2008Ashtari et al., 2011Schacht et al., 2012) and shape (Gilman et al., 2014Smith et al., 20142015) associated with cannabis use in ROI studies and with the spatial distribution of the eCB system (Burns et al., 2007). Although cannabis use has been associated with reduced brain volumes, studies typically report on adults with heavy substance use histories (cf. Ashtari et al., 2011). Gilman et al. (2014), however, have reported gray-matter density increases in the amygdala and nucleus accumbens of young adult recreational users and Medina et al. (2007) observed hippocampal enlargement in cannabis using adolescents. Our results are also consistent with the Avon Longitudinal Study of Parents and Children (French et al., 2015), which showed a trend for greater cortical thickness in male adolescents with <5 instances of cannabis use relative to THC-naive controls.

Converging evidence suggests that these effects may be a consequence of cannabis exposure. GMV differences could not be explained by group differences in demographic, personality, psychopathology, or other substance use factors. Examination of THC-naive 14-year-olds who later used cannabis showed no GMV differences, even using a more liberal ROI test, suggesting that the differences do not precede cannabis use and are not because of unidentified factors in those predisposed to use. Finally, the spatial distribution of GMV effects was associated with the eCB system, suggesting cannabis exposure may cause these findings.

The preclinical literature presents a number of possible mechanisms by which low levels of cannabis exposure could result in greater GMV relative to THC-naive controls. Adolescent rats treated with cannabinoid agonist showed altered gliogenesis in regions including the striatum and greater preservation of oligodendroglia relative to control animals (Bortolato et al., 2014). Zebra finches treated with cannabinoid agonist showed greater dendritic spine densities (Gilbert and Soderstrom, 2011); critically, these effects were observed in late-prenatal but not adult animals. Of particular relevance to this study, a single dose of Δ9THC transiently abolished eCB-mediated long-term depression (LTD) in the nucleus accumbens and hippocampus of adolescent mice (Mato et al., 2004). Suspension of LTD may interrupt maturation-related neural pruning and preserve gray matter. Future studies should assess whether these processes operate in human adolescents and whether they produce persisting alterations in GMV.

These findings should be interpreted in light of the study’s limitations. The IMAGEN sample is racially and ethnically homogenous so it remains to be determined whether the findings generalize to youth from more diverse backgrounds. Substance use was assessed using self-report and we do not have standard dose units of cannabis nor information on mode of use or a measure of drug metabolites. Combining images from different sites and imaging platforms remains controversial and is not completely controlled by including site as a covariate. Future studies should replicate the present results using images acquired at the same site on the same scanner or with equal numbers of cases and controls per scanner. We also note that the CNR1 gene expression (Hawrylycz et al., 2012) and CB1 receptor density (D’Souza et al., 2016) maps were generated in independent samples of adults and may not accurately represent the eCB system in our sample of adolescents. Although we report significant spatial associations between GMV effects and both CNR1 gene expression and CB1 receptor density, the effect sizes were small and any suggestion that these associations represent mechanisms for the effects we observe is speculative and requires further investigation.

We adopted a whole-brain, VBM approach to detect effects that were not limited by anatomical boundaries and to allow exploration of spatial relationships between GMV effects and the eCB system. There is evidence, however, that brain perfusion can influence VBM measures of local volume (Franklin et al., 20132015Ge et al., 2017; cf. Hawkins et al., 2018) so future studies should combine VBM with other measures of brain structure to provide confirmatory evidence. In particular, shape analysis has been shown to be sensitive to brain structural differences associated with cannabis use (Gilman et al., 2014Smith et al., 20142015Weiland et al., 2015). Moreover, combining morphometry metrics allows for testing of associations between them, which can identify different relationships between shape deformations and local volume (Gilman et al., 2014) providing evidence of further differences between cannabis users and controls.

One source of variability in the human findings on brain structural correlates of cannabis use may be comorbid substance use (Weiland et al., 2015Gillespie et al., 2018). Given recent evidence of different patterns of functional connectivity in groups using alcohol, nicotine, and cannabis alone and in combination (Vergara et al., 2018), it will be important to account for any possible interaction effects of cannabis with other psychoactive substances. This issue is particularly important considering the ways in which comorbid substance use has been addressed in two recent, widely cited studies. Gilman et al. (2014) covaried for alcohol and nicotine use and found gray-matter density increases and shape deformations associated with cannabis use. Weiland et al. (2015) matched groups on alcohol and nicotine use and reported no morphometric differences associated with cannabis use, concluding that previously reported differences associated with cannabis may instead be attributable to alcohol use. The participants in Weiland et al.’s (2015) study, however, were using alcohol and nicotine at higher levels than those in Gilman et al.’s (2014) study. It is possible that cannabis, alcohol, and nicotine have differential effects on brain morphometry; specifically, recreational cannabis use has been associated with volume increases, whereas alcohol has been associated with volume reductions. In the current study, we matched the groups on alcohol and nicotine use and, within the cannabis using group, neither alcohol nor nicotine use was associated with individual differences in GMV, suggesting that the GMV differences we report are associated with cannabis use.

We note individual differences in GMV effects: although regional GMV was greater at the group level for adolescents with low levels of cannabis exposure, the distributions showed a high degree of overlap such that many cannabis users had GMV equivalent to that of controls. None of the tested demographic, personality, or substance use factors stratified GMV in the cannabis users. We note evidence that an association between cannabis use and cortical thickness was stratified by genetic risk for schizophrenia (French et al., 2015) and that an association between cannabis use and hippocampal shape was stratified by dopamine-relevant genes (Batalla et al., 2018). Some adolescents may be vulnerable to GMV effects at extremely low levels of cannabis use and it will be critical to identify those at risk as these structural brain changes may be associated with individual risk for psychopathology and deleterious effects on mood and cognition.

Of the behavioral variables tested, only sensation seeking and agoraphobia differed between the cannabis users and controls and these factors were not related to GMV differences. In the cannabis using participants, GMV in the medial temporal clusters was associated with PRIQ and psychomotor speed such that greater GMV in these regions was associated with reduced performance. The finding that right medial temporal GMV predicted generalized anxiety symptoms at follow-up for those participants who had used cannabis should be interpreted with caution given the small sample size and that we were not able to identify factors that drove the individual differences in cannabis effects on GMV at baseline. These findings are notable, however, as panic and anxiety symptoms are frequently reported side effects by naive and occasional cannabis users (Hall and Solowij, 1998). We also note fMRI evidence of hypersensitivity of the amygdala to signals of threat in a partly overlapping sample of cannabis using adolescents (Spechler et al., 2015) and a relationship between adolescent cannabis use and future mood complaints (Wittchen et al., 2007), even with comparatively low levels of use (Cheung et al., 2010).

We have revealed greater GMV in adolescents with only one or two instances of cannabis use in regions rich in CB1 receptors and CNR1 gene expression. Critically, we were able to control for a range of demographic and substance use effects, to confirm that these structural brain effects were not associated with comorbid psychopathology, and to demonstrate that these effects were unlikely to precede cannabis use. The pattern of results is characterized by individual differences in GMV effects in the cannabis users; these individual differences were associated with PRIQ and with vulnerability to future symptoms of generalized anxiety. Given the increasing levels of cannabis use among adolescents today, we suggest that studying the effects of recreational use early in life is an area of particular importance that should be addressed in the future by large scale, prospective studies.

Source: Grey Matter Volume Differences Associated with Extremely Low Levels of Cannabis Use in Adolescence | Journal of Neuroscience (jneurosci.org) March 2019

Opioids have become a full-blown national crisis of epidemic proportions, killing 130 people each day. Drug overdose is now the number-one cause of death for Americans under 50. One doctor at the top of her game—who knew the risks better than anyone—almost became another statistic.

Alison ran around her palatial six-bedroom house in Georgia on a crisp January night in 2016, preparing to depart the next day for a family ski trip in Colorado. She washed dishes, tidied counters, put in several loads of laundry, and crossed items off her packing list. Whenever she found a moment alone—every 45 minutes or so—she retrieved the syringe containing sufentanil she’d tucked inside the Ugg boots she wore around her house, pulled a makeshift tourniquet out of her hooded sweatshirt, found a usable vein, and plunged the needle into her arm, delivering one tenth of a milliliter of the most powerful opioid available for use in humans.

That night, as Alison hustled her house into order, she shot up in her 13-year-old daughter’s closet (she once used her ballet-shoe laces as a tourniquet), her oldest son’s bathroom (he was away at college), the kitchen pantry (she sometimes kept vials inside boxes of dry pasta), the laundry room (her favorite place to use), the bathroom (her least favorite), and the stairway leading up to the second floor, where she could gauge if family members were getting close.

By the end of the night, she had polished off two milliliters, an amount that could kill an average-size adult if given in a single dose. Sufentanil is an opioid painkiller five to seven times more potent than fentanyl—another powerful opioid—at the time of peak effect and 4,521 times more powerful than morphine, but Alison wasn’t intimidated. As an anesthesiologist, she’d spent her entire professional life delivering such substances to patients during surgery.

What Alison didn’t know then was that in just over two months, her whole world would come crashing down. She had no idea that three nurses would grow wise to the ways she was stealing drugs from the hospital. Or that she’d spend 90 days at an in-treatment center, followed by a five-year monitoring program for physicians. All she was thinking about that night was that her drugs of choice, sufentanil and fentanyl, made her happy at a time when her work demands were overwhelming and her second marriage was falling apart. “It was immediate; everything just chilled out. For me, it felt like when you have a really good glass of wine and you’re like, ‘Ahhh,’ ” says Alison, now 46. “During that time, that was the only thing I looked forward to. That was really the only thing that was good in a day of life for me.”

Before she started abusing opioids six months earlier, Alison had never used a drug recreationally other than a puff of marijuana during high school. (She didn’t like it.) She enjoyed a glass of red wine with dinner once or twice a month but hadn’t ever thought of using the substances she injected into patients all day, every day. “I’d been in anesthesia for 18 years, and it never even tempted me,” she says. “I never wondered what it felt like. It did not enter my mind.”

Alison was raised in a small town in Tennessee, the third youngest of seven children born to strict, conservative Christian parents. Her father is a physicist who liked to pose math questions at the dinner table (“In a group of 27 kids, there are 13 more girls than boys. How many girls and boys are there? Go!”), and her mother is a stay-at-home mom. For vacation, “we didn’t go to the beach or Disney World; we went to a place with a telescope or a planetarium,” says Alison, recalling one trip in which they piled in a station wagon and drove to South Dakota to watch an eclipse.

Today, three siblings are physicians, one worked for the CIA, and another chaired a university department. Alison likes to joke that she’s the underachiever in the family, and though she deserves no such title, the lifelong pressure she felt to outperform her siblings took a toll. “I was raised in a family where the lowest thing that was allowed was perfection,” she says. “I felt like I needed to do more, always. That was a big thing that came up in treatment—that my ‘good enough’ wasn’t good enough.” She had an eating disorder as a young teen and remembers dropping 30 pounds from her petite frame one summer by consuming only iceberg lettuce and fat-free French dressing. She says she felt like a failure because a younger sister weighed 15 pounds less.

One of Alison’s older brothers taught her square roots when she was two years old. (“It was like his little dog and pony trick to show me off to his friends,” says Alison, laughing.) She took up the violin at age four and started piano lessons when she was six. She skipped first and seventh grades and completed high school in three years, graduating days after she turned 16. She finished college in three years too and enrolled in medical school in California at 19. A wunderkind, yes, but she wonders now about the damage racing through her youth caused. “Perfectionism is horrible,” Alison says. “I know that I didn’t develop good coping mechanisms. Some of my treatment team thinks I got stunted.”

Medical school was the first time Alison had to study in her life. She chose to specialize in anesthesia because of how tangible it was. “I liked how when someone’s blood pressure is high, you give them medicine and it goes down,” she says. “That immediate gratification.” She married a man she met while she was in medical school when she was 22 and had her first son one month before graduation. (Her second son was born during her residency.)

Three years of her medical schooling were paid for by the Navy (“With my dad being a teacher and me being one of seven kids, there was no money,” she explains), so after finishing her residency, she paid the military back with three years of service, during which she was stationed at Walter Reed National Military Medical Center in Bethesda, Maryland. True to form, Alison was not just any anesthesiologist in the Navy, she was the one asked to do the anesthesia for a president (“A huge honor,” she says) and a high-ranking senator. (She was called in from maternity leave after giving birth to her daughter at the surgeon’s request.)

Alison left the Navy in 2003 and moved to Georgia, about an hour from where she grew up. She and her husband wanted to raise their kids in the South, and she was eager for a slower pace. The years of schooling and success with three young children had been hard on her marriage. “I fell in love with my kids immediately, and I let the marriage slip,” Alison explains. “I put my kids before my husband.”

Source: An Opioid Addict Who Was Also a Top Doctor Shares Her Story of Recovery | Marie Claire February 2019

This article is distilled from a paper given at the Recovery Plus conference in London on 26th June 2018 by Peter Stoker, Director of the National Drug Prevention Alliance.

References available on request.

Prevention, the word and meaning, comes from the Latin “praevenire” which means “to come before”. In other words, to act pre-the event – not during it or after it. Any action later than pre-the event is not prevention, it is repair. And both are required.

 

When it comes to funding, Prevention is the Cinderella service, and reasons why could include that Treatment has more workers with a resulting vigour; Treatment is easier to count, pleasing accountant-oriented funders; Prevention is (falsely) depicted as inhibiting Human Rights, and libertarian campaigners have always had deeper pockets that Prevention ever had.

INTERNATIONAL HISTORY

Early responses to the drug problem were characterised by being reactive rather than proactive, often with a legal or enforcement flavour.

There was also a tendency to focus on transmission of knowledge, sometimes coupled with a challenging of the users’ attitudes – unintended consequences could follow, for example:

  • if you give knowledge to a user you may produce a knowledgeable user, and
  • if you challenge a user’s attitude you may produce a knowledgeable user with an attitude.

In due course a more complete model was developed using the simple synonym – KAB, meaning you should address a mixture of Knowledge, Attitudes and Behaviour. (And focus on encouraging positive behaviour, rather than punishment).

Libertarians spotted the educational arena as fertile ground for their campaigns; their speculative allegation that the so-called ‘war on drugs’ was failing was the launchpad for harm reduction (HR1) – this was later augmented by inclusion of human rights (HR2). I witnessed all this being promoted vigorously at the 2009 UNGASS/CND conference in Vienna – we were emphasising ‘Whole Health’ as a goal, but throughout the proceedings there was an apparently innocuous and almost irresistible request from ACLU delegates that human rights should be included in all clauses. It wasn’t evident at this moment that they would later insist that using drugs was itself a “human right”, which therefore meant that prevention was, in effect, a breach of human rights. This activism was bankrolled by George Soros’ Open Society.

You can explore people’s thinking on this every day, in the Google Alerts, but remember what H.L.Mencken had to say: “For every complex problem there is a simple solution … and it doesn’t work”.

Exemplary practice can be observed in several initiatives. There are too many to cover them all, but here are some indicative examples and source materials:

DFAF – Drug Free America Foundation – www.dfaf.org – internationally active, establishing conferences in Europe and the Americas. Publishes a learned journal, and holds an enormous library.

NFIA – National Families In Action – Atlanta USA – www.nationalfamilies.org – countless years of detailed research and practice. Many learned papers. They have just published a very useful technical paper called ‘The MJ File’ – requires reading.

CADCA  – www.cadca.org – Community Anti-Drug Coalitions of America – until recently under direction of Major General Arthur Dean, US Army retired. CADCA is well-resourced; in 2016 alone it trained over 8,000 youth.

A very useful publication by NIDA/CSAP www.drugabuse.gov (Center for Substance Abuse Prevention) is ‘Preventing Drug Abuse’ – a slim volume, its first edition in 1997, revised in 2003 … about due for an update, one might say!

DARE – www.dare.org –  has suffered attacks in recent years but has survived, to the extent that it is signing new client organisations at the rate of about 200 a year even now.

DWI – Drug Watch International –  www.drugwatch.org a long-standing forum of experts in America and abroad. Membership by invitation only.

Straight – peer-led youth rehab service, now closed. Featured in the movie ‘Not My Kid’ starring George Segal and Stockard Channing.  Straight came in for criticism from the liberal left, and eventually closed, but not for this reason. I asked Bill Oliver, Chief Executive for many years, what caused the collapse of Straight. He told me “We were very good drug workers but lousy accountants”. A salutory comment!

SAM – Smart Approaches to Marijuana – www.sam.org . One of the most potent bodies in recent years, in the legalisation battle zone. Under the direction of Kevin  Sabet, a former policy adviser in the  US drug czar’s office. Senior staffers include former Congressman Patrick Kennedy. Their approach is soundly based on scientific evidence.

 And NDPA – National Drug Prevention Alliance – based in Slough, near Heathrow, and almost 30 years old. NDPA has provided support and training for parents, young people, drugs professionals and teachers. It has provided counselling and referral for users, and has done a large amount of work in the broadcast and print media,. It runs two websites – one for drugs professionals www.drugprevent.org.uk and one – more accessible in its presentation –  for parents – www.pinpoints.org.uk The websites include thousands of technical papers as well as other advisory publications. The websites are regularly visited internationally, several hundred thousand visits per year, and readers include our own Home Office.

EXAMPLES OF SUCCESS

Perhaps the earliest example was almost 40 years ago, in the late 1980s. Increased drug use sparked large numbers of parents to press academics into action, with the most memorable campaign being ‘Just Say No’ – under Ronald Regan’s wife Nancy. It was ridiculed by the left, but the campaign was very much more than a slogan, included detailed trainings for parents and youth, plus media activism, and the hard evidence is that it reduced prevalence by more than 60% – 11 million fewer users. Any other health-related campaign today would kill for such a result.

Perhaps the best example of this in recent years has been around the use of tobacco. Historically tobacco was used freely everywhere. Even doctors said it was good for you – it would soothe your throat, for example. Advertising sold it vigorously. Such protests as were made, were largely ignored. And if any people suggested that smoking had made them ill, the rest of us felt that that was their own fault and nothing to do with the us – they were getting what they deserved

Then, one day, the US Surgeon General announced that tobacco smoking by one person could give other persons cancer (through passive smoking). This was a game-changing announcement; we could no longer ignore what these drug users were doing – now it was affecting all of us. Anti-smoking articles and adverts appeared in the media; doctors advised strongly against it, schools told their pupils to avoid it, offices prohibited smoking in the premises, causing those who still were dependent on cigarettes to huddle in unpleasant external doorways, and the newly emerging Health and Safety brigade put in their six-pennorth. In due course the government reacted, producing new and influential legislation, banning smoking in many places. Before long the culture changed markedly, and in consequence so did the prevalence.

But if you want a bang up-to-date success, story you need look no further than Iceland. Comparing latest European figures with a couple of decades ago, teen drinkers have dropped from 42% to 5%, cannabis use has dropped from 17% to 7%, and tobacco smoking from 23% to 3%. The emphasis is on providing stimulating activities for youth, and on schooling parents in now to be more engaged with their families. Countries are following the Icelandic model, and research shows Risk factors and Protective Factors are pretty much the same everywhere.

There are localised examples of how to get ahead of the game – for example, one effective program was run in New York – called ‘Fixing Broken Windows’ the approach was to keep the streets and buildings clean and tidy – it reduced drug abuse and other social aspects.

In society as a whole, what promises the best results? In essence, the most effective  strategy will come from changing the culture.

Balanced prevention policy and strategy

I have yet to find a better definition what we should do than that written by a leading expert in the prevention field, based in Arizona – William Lofquist:

“We need to get beyond the notion that prevention is stopping something happening, to a more positive approach which creates conditions which promote the well-being of people”.

Lofquist found the importance of treating youth as resources, rather than objects or recipients of project work. He also emphasised that it should engage the whole of society, not in some rigid formulaic way but in a fluid, proactive approach which is alive to changes in society and always works to stay ahead of the game.

An assembly of this co-ordinated strategy and policy might include the following:

Government

Health

Education

Higher ed

Youth peers

Parents

Religions

Pharmacists

Businesses

Media

Volunteers

Sport

Leisure

Drugs services

–  specify, resource, oversee, evaluate and improve

–  address all health elements

–  focus on health promoting approaches

–  train teachers and youth workers in prevention

–  develop and utilise their potential

–  de-marginalise, train, resource, support

–  spiritual lead, network, interface working

–  more proactive, preventing, reducing harm

–  health promoting environments. EAPs, RDTs

–  educate and support editorial staff, no mixed messages

–  realise their potential, utilise more widely

–  health promoting environments, health image

–  widen education and training. Explore expansion

–  encourage plurality, with more emphasis on recovery

We can also learn much from the science of ‘Behaviour Modification’  – as practised by, inter all, Professor Brian Sheldon of the Royal Holloway University.

Constructive selfishness …

The tobacco example above describes what I mean by this expression. We should not shrink from recognising that selfishness is a powerful driving force across society. And since it is a powerful driving force, we should seek to drive it to our advantage.

We have yet to wake up to the potential of defining and communicating to society at large the various ways in which one person’s drug misuse adversely affects the rest of us.

Establishing readiness for prevention – CULTURAL CHANGE

What influences culture?

  • Peer group influence
  • Personal perceptions
  • Income versus cost of any action
  • Health issues
  • Moral structure
  • Spiritual structure
  • Family values
  • Attraction of risk-taking
  • Media
  • Mental state
  • Legislation
  • Economy – the well-off or the poor
  • Employment – job or no job

CSAP found in their comparison of practices that the best prevention results come through co-ordinated prevention efforts, offering multiple strategies, and providing multiple points of access.

*                 *                   *                 *                  *

This is but a quick canter through the jungle of Prevention. There is much more to it, but I hope I have whetted your appetite – and you may even see the sense in building prevention into your work spectrum. (As co-operators rather than competitors with other agencies).

Don’t fear that prevention will reduce your treatment client base – as treatment workers, you are going to be in demand for a long time yet! Whilst some will be prevented from drug and alcohol abuse, and some will manage to cure themselves, most people need expert help.

We are, after all, working towards the same objective.  I once saw a cartoon in which a drug worker was asking a guru how to solve the drug problem. ‘Why do people use drugs?’ asked the guru. ‘To escape reality’ said the worker. ‘Then the solution is obvious’. Said the guru. ‘Improve reality’

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