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Report by prominent marijuana policy group finds costs would outweigh any tax revenue under legalization; Healthy and Productive Illinois coalition urges rejection of legalization

Today, the day before the unofficial “marijuana holiday,” Healthy and Productive Illinois (HPIL) – a project of Smart Approaches to Marijuana Action (SAM Action) – released a comprehensive working paper on the projected costs of legalization in Illinois, finding that legalization would cost the state $670.5 million, far outweighing estimated tax revenue projections of approximately $566 million. The report will be released today at 9:30 am in Room N505 of the Thompson State Building in Chicago, during a press conference by HPIL to announce opposition to legalization.

This report uses data from states like Colorado that have legalized marijuana to debunk the myth that taxed marijuana sales will be a boon to the state’s well-reported fiscal crisis. A conservative approximation of quantifiable data such as administrative and regulatory enforcement, increased drugged driving fatalities and other vehicle related property damages, short term health costs, and increased workplace absenteeism and accidents would cost the state $670.5 million in 2020.

“This study clearly demonstrates that the only people who will make money from marijuana commercialization are those in the industry that grow and sell it, at the direct expense of public health and safety,” said Dr. Aaron Weiner Director of Addiction Services at Linden Oaks Behavioral Health. “This industry is actively lobbying in Springfield to move their agenda forward, misleading our leaders and the general public. We have to speak up about the truth to protect the health of our State,” continued Dr. Weiner.

Healthy and Productive Illinois is a coalition formed to spread science-based awareness on marijuana harms and push back against the movement to legalize marijuana. The group believes the marijuana industry is mimicking the tactics of the Big Tobacco industry.

“We know that when citizens of Illinois are informed that marijuana is already decriminalized, only 23% want to fully legalize it,” said Andy Duran, Executive Director of Linking Efforts Against Drugs (LEAD). “Lack of knowledge and confusion is the fuel that drives the commercial marijuana market forward, just like tobacco before it. Imagine what would happen if everyone was aware that the State will lose money, too,” continued Duran.

There is sufficient information available to suggest that marijuana legalization could incur additional costly side effects, but at this time data is not robust enough to quantify their long-term impact. One of these additional costs would be controlling an expanded black market.

“In Oregon and Colorado, we are seeing thriving black markets and illegal grow operations hiding amongst legal growers,” said Chief James Black, Vice President of the Illinois Association of Chiefs of Police. “This expanded black market creates a real problem for law enforcement who now have to work even harder and allocate more precious resources to weed out illegal grow ops,” continued Chief Black.

Additional costs include:

* Additional workplace injuries among part-time employees

* Increases in alcohol use and abuse

* Increases in tobacco use

* More opioid abuse

* Increases in short-term/long-term recovery for marijuana use disorders

* Greater marijuana use among underage students

* Property and other economic damage from marijuana extraction lab explosions

* Controlling an expanded black market, sales to minors, and public intoxication

* Other administrative burdens of most state legalization programs, such as:

– money for drugged driving awareness campaigns;

– drug prevention programs; and

– pesticide control and other agricultural oversight mechanisms

* Long-term health impacts of marijuana use

“Cost reports such as this are the dirty truth that the pot industry doesn’t want law makers and the general public to see,” said Dr. Kevin Sabet, Founder and President of SAMA and former senior drug policy advisor to President Obama. “The pot industry is dead set on becoming the next Big Tobacco. The men in suits behind Big Pot will become rich while communities of color continue to suffer with addiction, black markets thrive, and states are left to foot the bill,” continued Dr. Sabet.

Source: Email from SAM (Smart Approaches to Marijuana) <info@learnaboutsam.org>

April 2018

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

There was big news in Congress today that I wanted you to know about. A proposed government spending bill released today eliminated a provision that has protected the marijuana industry from federal prosecution for violating the Controlled Substances Act.

The Rohrabacher-Farr language was eliminated from the Commerce, Justice, Science bill that funds the Department of Justice, even though the language had previously been included in the 2017 base text. In addition, the Financial Services bill retained language preventing Washington, DC from implementing full retail sales and commercialization of recreational marijuana.

Smart Approaches to Marijuana (SAM) submitted testimony to the Appropriations Committee to push back against this provision, which has allowed unsafe and untested products to masquerade as medicine. Rather than submit their products to the FDA for approval as safe and effective medicines, the marijuana industry has instead been using medical marijuana laws as a guise to increase demand for marijuana consumption and service the black market with large amounts of high-potency marijuana.

“If I were an investor, I would sell my marijuana stocks short,” said Kevin Sabet, President of SAM. “The marijuana industry has lost in every state in which they were pushing legislation in 2017, the industry’s largest lobbying group is losing its bank account , and now they are losing protection that has helped them thrive despite marijuana’s illegal status. Although the debate over Rohrbacher-Farr is far from over, the bad news just keeps coming for the pot industry. But it’s great news for parents, prevention groups, law enforcement, medical professionals, victims’ rights advocates and everyone who cares about putting public health before profits.”

Evidence demonstrates that marijuana – which has skyrocketed in average potency over the past decade – is addictive and harmful to the human brain, especially when used by adolescents. Moreover, in states that have already legalized the drug, there has been an increase in drugged driving crashes and youth marijuana use. States that have legalized marijuana have also failed to shore up state budget shortfalls with marijuana taxes, continue to see a thriving black market, and are experiencing a continued rise in alcohol sales.

Thank you for the work that you are doing to help with these big wins for public health and safety!  

Source: Email from Smart Approaches to Marijuana (SAM) June 2017

There was big news in Congress yesterday that I wanted you to know about. We are pleased to report that the House has not included any pro-pot riders in its spending bills this year! Thank you for all of your efforts, including calls and emails. Congress has heard your voice and acted to preserve the public health and safety of our kids and communities.

Pro-pot advocates filed more than ten amendments to protect the marijuana industry and increase marijuana investment opportunities, but none of the amendments were allowed to proceed. The lessons of legalization are getting out, and it’s clear the experiment has failed, as our recent Cole Memo Report has shown. The black market is thriving, kids are ending up in emergency rooms, and drugged driving fatalities are soaring .

The fight isn’t over, though. Even though the House bill is clear, the Senate version of the spending bill still contains key marijuana industry protections. Those differences will be resolved in the coming months. We will continue to send out alerts to let you know when it’s time to come together and act.

Thank you again for all your work over the past years. You’ve made a difference, and we are grateful for your partnership. Please consider a donation to help with our efforts as we continue this battle in the coming months.

Source: Email SAM Action <info@samaction.net> from Kevin Sabet September 2017

The opioid crisis is unlike any drug epidemic America has ever known. It’s claiming lives at an almost unimaginable rate.

But to get an idea of why these drugs are taking such a toll, you have to look at the people who are dying.

This is not just the curse of the stereotypical addict.

Many of those admitted to the country’s fast swelling mortuaries were middle class professionals whose first fix was dealt to them by a doctor.

Back in the 90s and early 2000s, pharmaceutical firms began a major lobbying exercise, persuading doctors to prescribe their synthetic forms of heroin for pain relief.

Soon GPs across the country were handing out powerful prescriptions for relatively minor ailments.

The drugs worked, but they proved highly addictive and when patients’ prescriptions ran out, many took to the streets to feed what had fast become a habit.

That’s where the problem really starts. In pill form, this medication could be controlled, but by going to “street chemists” for their fix, people were taking a huge risk.

They’d buy the drugs, illegally imported from China, ready mixed with harmless powders. Just a few grains of opioid in each capsule, which they’d either snort, smoke or inject.

Most of the powders are phenomenally potent. One, Carfentanil, is said to be 10,000 times stronger than heroin.

Originally created as an elephant tranquiliser, a couple of grains could be enough to kill.

Others are less powerful but still deadly, and here’s the real issue – most addicts have no idea which kind of opioid they’re taking.

Yet across America people are seeking out dealers and buying this stuff for as little as two dollars per fix.

Some have reached a truly hopeless stage.

Ian Blackburn, a long-time addict, told me he’s never known anything like it. He’s felt in control of his drug habit in the past. Not any more.

“Three hits, that’s all it takes”, he told me: “You take this stuff three times and it’s forever”.

He explained how he doesn’t get a buzz from the drug any more, he simply takes it to feel normal, to take the pain of withdrawal away. Without it, his legs start to cramp, his stomach wrenches and he loses control of his functions.

“Every couple of hours you need a hit”, he says “no ifs ands or buts, you’re going to find it and you’re going to get money to get it, no matter what”.

Source: http://www.itv.com/news/2017-06-27/opioid-crisis-claiming-record-number-of-addicts-lives-in-the-us/

September 2017

I was just learning this morning that CBD is well documented to trigger and act via PPAR gamma receptors which are well known to physicians as used in a class of diabetes drugs called the thiazolidinediones (pioglitazone and its congeners).

So I thought I should just check if this was involved in pregnancy and gestation.

Sure enough – BINGO!!!

Another strike of GOLD!!!

So I wrote this to add in the references…

Cannabidiol is known to interact with the (Peroxisome Proliferation Activated Receptor) PPARγ pathway 1-8.

PPARγ is known to be a very important transcription factor in metabolic regulation and is also the master regulator of the adipogenic differentiation pathway.

It also plays a key role in the reproductive tract with actions on the corpus luteum and developing gametes.

It has been documented in a rich literature to have a major effect on developing embryos and the reproductive tract 9-32.

References

1 De Filippis, D. et al. Cannabidiol reduces intestinal inflammation through the control of neuroimmune axis. PLoS One 6, e28159, doi:10.1371/journal.pone.0028159 (2011).
2 Esposito, G. et al. Cannabidiol reduces Abeta-induced neuroinflammation and promotes hippocampal neurogenesis through PPARgamma involvement. PLoS One 6, e28668, doi:10.1371/journal.pone.0028668 (2011).
3 Hegde, V. L., Singh, U. P., Nagarkatti, P. S. & Nagarkatti, M. Critical Role of Mast Cells and Peroxisome Proliferator-Activated Receptor gamma in the Induction of Myeloid-Derived Suppressor Cells by Marijuana Cannabidiol In Vivo. J Immunol 194, 5211-5222, doi:10.4049/jimmunol.1401844 (2015).
4 Hind, W. H., England, T. J. & O’Sullivan, S. E. Cannabidiol protects an in vitro model of the blood-brain barrier from oxygen-glucose deprivation via PPARgamma and 5-HT1A receptors. Br J Pharmacol 173, 815-825, doi:10.1111/bph.13368 (2016).
5 O’Sullivan, S. E. & Kendall, D. A. Cannabinoid activation of peroxisome proliferator-activated receptors: potential for modulation of inflammatory disease. Immunobiology 215, 611-616, doi:10.1016/j.imbio.2009.09.007 (2010).
6 O’Sullivan, S. E., Sun, Y., Bennett, A. J., Randall, M. D. & Kendall, D. A. Time-dependent vascular actions of cannabidiol in the rat aorta. European journal of pharmacology 612, 61-68, doi:10.1016/j.ejphar.2009.03.010 (2009).
7 Ramer, R. et al. COX-2 and PPAR-gamma confer cannabidiol-induced apoptosis of human lung cancer cells. Mol Cancer Ther 12, 69-82, doi:10.1158/1535-7163.MCT-12-0335 (2013).
8 Scuderi, C., Steardo, L. & Esposito, G. Cannabidiol promotes amyloid precursor protein ubiquitination and reduction of beta amyloid expression in SHSY5YAPP+ cells through PPARgamma involvement. Phytother Res 28, 1007-1013, doi:10.1002/ptr.5095 (2014).
9 Adaikalakoteswari, A. et al. Low Vitamin B12 in Pregnancy Is Associated With Adipose-Derived Circulating miRs Targeting PPARgamma and Insulin Resistance. The Journal of clinical endocrinology and metabolism 102, 4200-4209, doi:10.1210/jc.2017-01155 (2017).
10 Anghebem-Oliveira, M. I. et al. Type 2 diabetes-associated genetic variants of FTO, LEPR, PPARg, and TCF7L2 in gestational diabetes in a Brazilian population. Arch Endocrinol Metab 61, 238-248, doi:10.1590/2359-3997000000258 (2017).
11 Casamadrid, V., Amaya, C. A. & Mendieta, Z. H. Body Mass Index in Pregnancy Does Not Affect Peroxisome Proliferator-activated Receptor Gamma Promoter Region (-359 to -260) Methylation in the Neonate. Ann Med Health Sci Res 6, 38-43, doi:10.4103/2141-9248.180272 (2016).
12 Cawyer, C. et al. Attenuation of hyperglycemia-induced apoptotic signaling and anti-angiogenic milieu in cultured cytotrophoblast cells. Hypertens Pregnancy 35, 159-169, doi:10.3109/10641955.2015.1122035 (2016).
13 Drew, P. D. & Kane, C. J. Peroxisome Proliferator-Activated Receptor-gamma Agonists: Potential Therapeutics for Neuropathology Associated with Fetal Alcohol Spectrum Disorders. J Clin Cell Immunol 7, doi:10.4172/2155-9899.1000469 (2016).
14 Gao, F., Hu, W., Li, Y., Shen, H. & Hu, J. Mono-2-ethylhexyl phthalate inhibits human extravillous trophoblast invasion via the PPARgamma pathway. Toxicology and applied pharmacology 327, 23-29, doi:10.1016/j.taap.2017.04.014 (2017).
15 Hasby Saad, M., El-Anwar, N., Lotfy, S., Fouda, M. & Hasby, E. Human placental PPAR-gamma & SOX2 expression in serologically proved toxoplasmosis. Parasite Immunol, e12529, doi:10.1111/pim.12529 (2018).
16 Hu, W. et al. Activation of Peroxisome Proliferator-Activated Receptor Gamma and Disruption of Progesterone Synthesis of 2-Ethylhexyl Diphenyl Phosphate in Human Placental Choriocarcinoma Cells: Comparison with Triphenyl Phosphate. Environ Sci Technol 51, 4061-4068, doi:10.1021/acs.est.7b00872 (2017).
17 Kurzynska, A., Chojnowska, K., Bogacki, M. & Bogacka, I. PPAR ligand association with prostaglandin F2alpha and E2 synthesis in the pig corpus luteum-An in vitro study. Anim Reprod Sci 172, 157-163, doi:10.1016/j.anireprosci.2016.07.014 (2016).
18 Lecoutre, S. et al. Depot- and sex-specific effects of maternal obesity in offspring’s adipose tissue. The Journal of endocrinology 230, 39-53, doi:10.1530/JOE-16-0037 (2016).
19 Lendvai, A., Deutsch, M. J., Plosch, T. & Ensenauer, R. The peroxisome proliferator-activated receptors under epigenetic control in placental metabolism and fetal development. Am J Physiol Endocrinol Metab 310, E797-810, doi:10.1152/ajpendo.00372.2015 (2016).
20 Lin, Y., Bircsak, K. M., Gorczyca, L., Wen, X. & Aleksunes, L. M. Regulation of the placental BCRP transporter by PPAR gamma. J Biochem Mol Toxicol 31, doi:10.1002/jbt.21880 (2017).
21 Maekawa, M. et al. Polyunsaturated fatty acid deficiency during neurodevelopment in mice models the prodromal state of schizophrenia through epigenetic changes in nuclear receptor genes. Transl Psychiatry 7, e1229, doi:10.1038/tp.2017.182 (2017).
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23 Marginean, C. et al. The role of TGF-beta1 869 T > C and PPAR gamma2 34 C > G polymorphisms, fat mass, and anthropometric characteristics in predicting childhood obesity at birth: A cross-sectional study according the parental characteristics and newborn’s risk for child obesity (the newborns obesity’s risk) NOR study. Medicine (Baltimore) 95, e4265, doi:10.1097/MD.0000000000004265 (2016).
24 Meher, A. P. et al. Placental DHA and mRNA levels of PPARgamma and LXRalpha and their relationship to birth weight. J Clin Lipidol 10, 767-774, doi:10.1016/j.jacl.2016.02.004 (2016).
25 Papamitsou, T., Toskas, A., Papadopoulou, K., Economou, Z. & Sioga, A. Expression of peroxisome proliferator activation receptors (PPARs) and TNFalpha in placenta tissues in unexplained recurrent pregnancy loss: an immunohistochemical study. Histology and histopathology 31, 1029-1036, doi:10.14670/HH-11-734 (2016).
26 Roberti, S. L. et al. Critical role of mTOR, PPARgamma and PPARdelta signaling in regulating early pregnancy decidual function, embryo viability and feto-placental growth. Molecular human reproduction, doi:10.1093/molehr/gay013 (2018).
27 Shapiro, A. L. et al. Nicotinamide Promotes Adipogenesis in Umbilical Cord-Derived Mesenchymal Stem Cells and Is Associated with Neonatal Adiposity: The Healthy Start BabyBUMP Project. PLoS One 11, e0159575, doi:10.1371/journal.pone.0159575 (2016).
28 Singh, S. P. et al. Gestational Exposure to Sidestream (Secondhand) Cigarette Smoke Promotes Transgenerational Epigenetic Transmission of Exacerbated Allergic Asthma and Bronchopulmonary Dysplasia. J Immunol 198, 3815-3822, doi:10.4049/jimmunol.1700014 (2017).
29 Sonanez-Organis, J. G. et al. HIF-1alpha and PPARgamma during physiological cardiac hypertrophy induced by pregnancy: Transcriptional activities and effects on target genes. Gene 591, 376-381, doi:10.1016/j.gene.2016.06.025 (2016).
30 Wang, L. L., Yu, Y., Guan, H. B. & Qiao, C. Effect of Human Umbilical Cord Mesenchymal Stem Cell Transplantation in a Rat Model of Preeclampsia. Reprod Sci 23, 1058-1070, doi:10.1177/1933719116630417 (2016).
31 Wu, Y., Ruan, Y., Shen, L. & Gong, Q. Protective effects of PPAR-gamma against pregnancy-induced hypertension by differential ETR expression in rat models. J Cell Biochem 119, 3118-3128, doi:10.1002/jcb.26454 (2018).
32 Xu, Y. et al. An M1-like Macrophage Polarization in Decidual Tissue during Spontaneous Preterm Labor That Is Attenuated by Rosiglitazone Treatment. J Immunol 196, 2476-2491, doi:10.4049/jimmunol.1502055 (2016).

Source: Email to www.drugwatch.org from Stuart Reece April 2018

The Oregon Health Authority also issued this month a baseline report titled Marijuana Report: Use, Attitudes, and Health Effects in Oregon. This comprehensive report includes several key findings.
 
Pictured above, for example, is a state map showing the 40 cities and 11 counties that have banned marijuana businesses within their boundaries. However, the Oregon Medical Marijuana Dispensary Program shows those numbers to be higher. Some 80 of the state’s 242 cities and 17 of its 36 counties have banned marijuana processing businesses and marijuana dispensaries from conducting business within their boundaries.
 
Oregon legalized marijuana for medical use in 1998 and for recreational use in 2014. Possession of up to eight ounces became legal for those age 21 or older July 1, 2015. Because recreational dispensaries will not open until late this year, the state allowed dispensaries selling pot for medical use to begin selling pot for recreational use as well October 1, 2015.
 
In just three months, however, some changes are already being seen. Marijuana-related calls to the state’s Poison Control Center increased in the last half of 2015, for example, from 105 in 2014 to 158 in 2015.
 
Other data include:

  • One in ten 8th-graders and one in five 11th-graders used marijuana in the past month, about the same as national levels.
  • Approximately 90% of marijuana users smoke the drug.
  • Some 62% of 11th-graders report marijuana is easy to get, some say easier than cigarettes.
  • Nearly half of current marijuana using 11th-graders who drive say they drove within three hours of using the drug.
  • Half (51%) of Oregon adults have seen marijuana store or product advertising, but less than one-third (29%) have seen information about marijuana health effects.
  • Nearly two-thirds (63%) of Oregon adults say they don’t know when it is legal to drive after using marijuana.

Read this report here.

The Oregon Health Authority has issued two new reports on marijuana. Oregon’s Medical Marijuana Program: Statistical Snapshot, January 2016 finds that 22 physicians have recommended marijuana for medical use to 85% of the state’s registered patients.
 
Some 1,700 physicians serve between 1 and 449 patients and account for a total of 19,087 patients, while 22 physicians account for a total of 60,908 patients, an average of 2,769 patients each.
 
Oregon now has registered:

  • 77,155 patients
  • 35,736 caregivers
  • 46,812 growers
  • 32,171 grow sites

Patients are 59% male, 41% female. Conditions they registered for (they may register for more than one condition) include:

  • Severe pain, 71,533 (92%)
  • Spasms, 22,501 (28.9%)
  • Nausea, 10,680 (13.7%)
  • PTSD, 5,527 (7.1%)
  • Cancer, 4,460 (5.7%)
  • Seizures, 2,122 (2.7%)

Those listing cachexia, HIV/AIDS, glaucoma, and Alzheimer’s disease are less than 1.5% each.
 
Read this report here.

Source:

https://www.oregon.gov/oha/ph/DiseasesConditions/ChronicDisease/MedicalMarijuanaProgram/Documents/OMMP%20Statistic%20Snapshot%20-%2001-2016.pdf

Cannabis oil has come under scrutiny

RUNGROJ YONGRIT/EPA-EFE/REX/Shutterstock

By Alison George

Cannabis is in the headlines for its potential medical benefits after the recent confiscation of cannabis oil medication from the mother of a 12-year-old British boy with severe epilepsy. The furore that ensued is shining a light on campaigns for cannabis oils to be made legal for medical reasons, and the UK government has now announced a review into the use of medicinal cannabis. Here’s what you need to know.

What is cannabis oil?

Cannabis oil is extracted from the cannabis plant Cannabis sativa. The plants medicinal properties have been touted for more than 3,000 years. It was described in the ancient Eygyptian Ebers papyrus around 1550BC, and it was likely used as a medicine in China before that. Some varieties of the plant contain high levels of the psychoactive substance tetrahydrocannabinol (THC), which is responsible for the “high” that comes from smoking or eating cannabis leaves or resin. The plant’s other major chemical component is cannabidiol, which has no psychoactive effect. Both act on the body’s natural cannabinoid receptors which are involved in many processes such as memory, pain and appetite. The cannabis plant also contains more than 100 other different cannabinoid compounds at lower concentrations.

So can cannabis oil make you high?

It depends on the THC content. Some types of Cannabis sativa plant, known as hemp, contain very little THC. The extracts from these plants contain mainly cannabidiol, so will not get anyone stoned.

Is it legal?

That’s a complicated question. In the UK cannabidiol is legal. Cannabis plant extracts (known as hemp or CBD oils) are available in high-street stores but the THC content must be below 0.2 per cent. “THC is not psychoactive at this level,” says David Nutt, a neuropsychopharmacologist at Imperial College London. But cannabidiol is illegal in many other countries.

In the USA for example, cannabidiol is classed as a schedule 1 controlled substance, and can only be sold in states where cannabis use is legal.

However, the tide may turn in favour of cannabidiol after a recent World Health Organisation review. This concluded that cannabidiol “exhibits no effects indicative of any abuse or dependence potential” but “has been demonstrated as an effective treatment of epilepsy … and may be a useful treatment for a number of other medical conditions.”

What is the evidence that cannabis oils can help treat epilepsy?

Although there is some scientific evidence that THC has potential to control convulsions, its mind-altering effects mean that much of the focus has turned to cannabidiol – particularly for childhood epilepsies that conventional drugs fail to control.

Two recent high quality randomised and placebo controlled trials showed that cannabidiol is an effective treatment for Lennox-Gastaut syndrome and Dravet syndrome, severe forms of epilepsy. The mechanism of action is unknown, but it may be due to a combination of effects, such as inhibiting the activity of neurons and dampening inflammation in the brain.

The situation is less clear when it comes to the use of commercial cannabis oils to control seizures, where the evidence is mainly anecdotal, and the oils can contain differing concentrations of cannabidiol and THC.

The UK government announced on 19 June that it would review the use of medical cannabis.

Are there any cannabis-based epilepsy drugs on the market?

Not yet. In April the US Food and Drug Administration recommended the approval of a drug called Epidiolex for Lennox-Gastaut syndrome and Dravet syndrome. Its active ingredient is cannabidiol, and final approval is due at the end of this month.

However, it is possible the drug is not as effective as cannabis oil containing THC, says Nutt. For example, the cannabis oil used to treat Billy Caldwell, the boy at the centre of the recent cannabis oil confiscation furore, contained cannabidiol and a low dose of THC, because cannabidiol alone did not stop all his seizures.

This is one of the big unknowns. “It is important to remember that there is currently very little scientific evidence to support cannabis oil containing both THC and cannabidiol as a treatment for epilepsy,” said the charity Epilepsy Action, in a statement issued this month.

Are cannabis-based medications available for other conditions?

Yes. A synthetic version of THC called Nabilone has been used since the 1980s to treat nausea after chemotherapy and to help people put on weight. A drug called Sativex is also approved for the treatment of pain and spasms associated with multiple sclerosis. It contains an equal mix of THC and cannabidiol, but would not be suitable for the treatment of children with epilepsy such as Billy. “If you used that to treat epilepsy, the kids would be stoned off their heads,” says Nutt.

What is the aim of the UK government’s review of medical cannabis? 

The first part of the review will look at the evidence for the therapeutic value of cannabis-based products. It can recommend any promising ones for the second part of the review. This will be carried out by the government’s Advisory Council for the Misuse of Drugs, which can recommend a change to the legal medical status of cannabis and cannabinoids.

This will hopefully lead to a relaxation of the rules surrounding research into cannabis-based medicines says Tom Freeman, a clinical psychopharmacologist at King’s College London.

In the UK cannabis currently has Schedule 1 status, the most restrictive category, which is for drugs which are not used medicinally such as LSD. “This creates a Catch 22 situation,” says Freeman. “You can’t show that cannabis and cannabis-based products have medicinal value because of restrictions on medical research.”  If cannabis is moved to the Schedule 2 category, it will join substances such as morphine and diamorphine (heroin) which can be prescribed by doctors if there is a clinical need. 

Source: https://www.newscientist.com/article/2172415-cannabis-oil-what-is-it-and-does-it-really-work-as-medicine/  June 2018

Watch Here and Share!

As the legal status of marijuana changes its perceived dangers are lessening while the potency of the drug is increasing.

This video covers marijuana as a psychoactive substance that induces its effects by manipulation of natural brain chemicals known as  the endocannabinoids.The toxic and addictive impact that results from the drug’s disruption of natural endocannibinoids is characterized in this video by the testimony of those impacted by the drug and by the scientists who are studying its effects.

This video is 26 minutes and will help to clarify the many myths and misconceptions regarding the effects of marijuana.

Source: Email from SAM (Smart Approaches to Marijuana) <info@learnaboutsam.org>

March 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

There will never be fundamental change in west Belfast’s drug problem without addressing the poverty and conflict legacies affecting it, a new report has found.

Launched on Monday, the West Belfast Community Drugs Panel’s report examined all aspects of drugs misuse in the area and provided a series of recommendations.

The panel was set up in October last year in reaction to a spate of drug-related deaths in the west of the city and is made up of representatives from several government departments, including the Belfast Trust and the Public Health Agency.

Families in the area affected by drugs, including bereaved parents, were also invited to give their views through community representatives on the panel, which was chaired by Noel Rooney, former head of the Probation Board for NI.

Funding for the report was provided by the Belfast Policing and Community Safety Partnership, which is made up of councillors and representatives from statutory agencies.

The report found significant issues relating to drugs misuse in west Belfast, many related to chronic under-funding by successive governments and the lack of a coherent, multi-agency strategy to deal with the problem.

It also identified significant contributing factors relating to the area’s social housing provision.

Several of the root causes detailed in the report, however, are generational and systemic.

“The West Belfast drugs issue is directly related to the area being affected by systemic poverty and the legacy of the NI Conflict and, unfortunately, this looks set to worsen over time,” the report reads.

“There will never be a fundamental change for west Belfast without addressing the poverty and conflict legacies.”

Elsewhere, the panel found addiction to prescription medications to be disproportionately high in the area.

“Evidence shows the level of prescribing medication in west Belfast is higher than in most other parts of Belfast, the north of Ireland and Great Britain,” the document states.

The report recommends several measures that public agencies could take to try and tackle the problem, including:

– An anti-poverty plan aligned with appropriate, long-term funding (10-15 year minimum)

– A multi-layered education strategy with a focus on early intervention

– A co-designed pilot social housing model, specifically for the area

– A zero-tolerance drugs policy from the PSNI, with a stronger focus on small level dealing

In addition, the report includes a ‘What We Heard’ section summarising key information providing to the panel by members of the public, community representatives and others.

“Criminal gangs, some claiming to have paramilitary connections, are controlling the supply of cocaine and heroin in some streets to children as young as 12-years-old,” the report reads.

“They decide what to provide and how much it will cost local people.”

Prescription medications being reported as being currently misused in west Belfast include: Tramadol, an opiate-based painkiller, and Fentanyl, a tranquiliser 100 times stronger than heroin.

It is now in the hands of government agencies to decide which, if any, of the report’s recommendations they might adopt.

Source:  https://www.belfasttelegraph.co.uk/news/northern-ireland/children-as-young-as-12-taking-drugs   11th June 2018

 

Submitted by Livia Edegger

Strengthening Families Programme, a family-focused prevention programme used in 26 countries around the world, was found to be nine times more effective than individually-targeted programmes and yielded a $10 return for every dollar spent on it. The programme, designed for youth and their families, aims to improve parent-child interactions, parenting skills and strengthen young people’s social and problem-solving skills.

Submitted by Livia Edegger 

As support for decriminalising and legalising marijuana is growing, several new studies highlight the potentially harmful effects of the drug on its user’s brain and heart. The findings are particularly revealing in the field of recreational cannabis use. While studying the brains of a group of twenty occasional cannabis smokers, researchers from Harvard University found that as few as one or two uses a week can change the brain. Smoking marijuana was found to primarily affect the areas involved in decision making, emotions and motivations. Along the same lines, a group of French researchers found that marijuana use ups the risk of developing heart problems (i.e. strokes, heart attacks and circulation problems). More research is needed to better understand the health risks associated with marijuana.

Links:

Source:

http://preventionhub.org/en/prevention-update/even-casual-cannabis-use-can-affect-health

Submitted by Andy Travis 

Those who first used alcohol at or before the age of 14 were nearly four times more likely to meet the criteria for past year alcohol abuse or dependence than those who started using alcohol between the ages of 18 and 20 (16.5% vs. 4.4%) and more than six times more likely than those who started using alcohol at or after age 21 (16.5% vs. 2.5%).

These findings illustrate the need for alcohol education and prevention efforts as early as middle school.

Percentage of Adults (Ages 21 or Older) Who Abused or Were Dependent on Alcohol in the Past Year, by Age of First Alcohol Use, 2009.

 

Similarly, adults who first started using marijuana at or before the age of 14 are most likely to have abused or been dependent on illicit drugs in the past year. Adults who first used marijuana at age 14 or younger were six times more likely to meet the criteria for past year illicit drug abuse or dependence than those who first used marijuana when they were 18 or older (12.6% vs. 2.1%) and almost twice as likely as those who started between the ages of 15 and 17 (12.6% vs. 6.6%).

Percentage of Adults (Ages 21 or Older) Who Abused or Were Dependent on Illicit Drugs in the Past Year, by Age of First Marijuana Use, 2009.

 

Links:
• Adults Who Initiate Alcohol Use Before Age 21 More Likely to Abuse or Become Dependent on Alcohol(link is external) – CESAR FAX, University of Maryland, USA.
• Early Marijuana Use Related to Later Illicit Drug Abuse and Dependence(link is external) – CESAR FAX, University of Maryland, USA.

Source:

http://preventionhub.org/en/prevention-update/adults-who-initiate-alcohol-and-marijuana-use-age-21-are-much-more-likely-abuse-or-become-d

Submitted by Andy Travis

This forthright editorial in the journal ‘Addiction’ joins over 500 public health leaders and 27 organisations in questioning the role of the global alcohol industry in making alcohol policy. Conflict with the tobacco industry is well documented, where vested interests have fought an aggressive rearguard action against efforts to reduce tobacco harm. Alcohol interests are now seen to be moving intensively into areas of policy making. Addiction’s editorial raises the strong suspicion that these moves are designed mainly to impede effective control and protect commercial interests. The WHO’s Global Strategy on the Harmful Use of Alcohol was endorsed unanimously in 2010, but in 2012 the alcohol producers issued their own strategy and claimed that the adoption of the WHO strategy, ‘…has legitimated industry’s ongoing efforts and has opened the door to the inclusion of producers as equal stakeholders’. Leading health professionals responded with dismay, arguing that the producer’s actions are weak, mostly lacking an appropriate evidence base and unlikely to reduce harm. Dr Chan, Director General of WHO, recently commented on the role of big business.

As the new publication makes clear, it is not just Big Tobacco anymore. Public health must also contend with Big Food, Big Soda, and Big Alcohol. All of these industries fear regulation, and protect themselves by using the same tactics. Research has documented these tactics well. They include front groups, lobbies, promises of self-regulation, lawsuits, and industry-funded research that confuses the evidence and keeps the public in doubt. Tactics also include gifts, grants, and contributions to worthy causes that cast these industries as respectable corporate citizens in the eyes of politicians and the public.

Concern has also been expressed over ‘aggressive marketing strategies’ in areas of the world with minimum alcohol and tobacco policies in place, such as many countries with emerging economies in Asia, Africa and Latin America (see Prevention Hub link below). The ‘Addiction’ editorial highlights the marketing of alcohol to young people and promotion of products such as alcopops.

Links:

Source:

http://preventionhub.org/en/prevention-update/international-outcry-grows-over-alcohol-industry-role-policy-making

Filed under: Alcohol,Economic,Latest News :

Submitted by Andy Travis

Much research on normative misconceptions among university students has been published in North America, but much less has surfaced in Europe. This cross-sectional study is based on 12 classes of second-year French college students in sociology, medicine, nursing or foreign language. Rather than focus on one substance the students were asked to estimate the proportion of tobacco, cannabis, alcohol use and heavy episodic drinking among their peers and to report their own use.

Researchers found that that substance use patterns and perceptions of the norms differ significantly across academic disciplines and that substance users are more likely to misjudge real peer use prevalence.

They conclude that social norms of substance use are an important factor among students personal use. Overestimating these norms is associated with increased levels of use. In addition to other strategies, the researchers recommend that prevention programs should consider changing use perception when it is overestimated.

“These results show that there are grounds for university level prevention campaigns based on local survey results.”

read more…

Source:

http://preventionhub.org/en/prevention-update/french-students-found-overestimate-their-peers-consumption-cannabis-tobacco-and-alcohol-pre

An effective drug-free workplace policy is one of the best ways for employers to protect their businesses. An effective program does not end with pre-employment screening, since any drug user can count up to three days before the test and then begin to use again after being hired.

Drug-free workplace policies reduce the amount of sick time, absenteeism, workman’s comp claims, insurance premiums, and protects against civil lawsuits because of an employee who inflicts damage on others because of impairment.

Communities that emphasize and encourage drug-free workplace practices can have an impact on overall drug use in the community. When combined with effective education and prevention, and by increasing the incentive of users to seek treatment, we can promote a drug-free culture and a thriving business environment that protects individuals, families and the community.

While some might think they don’t need a drug-free workplace policy, as we discussed last week, that’s really not true. Small businesses, not just large companies, need firm drug testing policies.

One new form of marijuana that’s growing in popularity nationwide underscores the need for workplace drug testing programs. This dangerous drug, wax marijuana, can easily be used in the workplace because it doesn’t look like regular marijuana — and frighteningly, it’s the most powerful form of the drug.

Here’s what employers need to know about wax marijuana, and why it shows the need to participate in Drug Free Work Week.

The 411 on Wax Marijuana – and What it Means for Drug Free Workplace Programs

With aliases like butter and honeycomb because of its waxy texture, wax is the most powerful form of marijuana.

According to wax marijuana users, a single hit can leave a high lasting all day. One dosage is equal to 20 marijuana cigarettes and can produce powerful hallucinations and psychotic effects. This potency is because wax marijuana is more than 80% pure THC.

Manufacturers produce wax by extracting the main psychoactive compound, Tetrahydrocannabinol (THC), from marijuana. They use flammable substances like butane in the process, which makes it quite dangerous, but renders the wax marijuana very strong.

While wax marijuana is legal in states like Colorado and Washington, it’s illegal under federal law and in most states.

Employers should take note – due to its appearance, wax marijuana can be passed off as lip balm.

This means that your employees could bring the most powerful form of marijuana into the workplace and use it right under your nose.

Remember, any on-the-clock substance abuse has lasting effects on your workplace, particularly when it comes to the safety of your employees. Just one hit of wax marijuana can result in an extremely powerful, daylong high — rendering your worker a serious danger to everyone around them.

Your workplace needs a drug testing policy to combat new trends in substance use, like wax marijuana.

Drug Free Work Week is a great opportunity for you to take stock of your existing drug testing policy or create a new workplace drug testing program. If you don’t take the time now to create or revise a policy, you may pay for it down the line as your employees try new drugs, such as wax marijuana, and end up causing injuries or financial damage to your workplace.

Partner With ARCpoint Labs for Workplace Drug Testing Policies.

Located nationwide, ARCpoint Labs provides workplace drug testing assistance. We can work with you to create and implement a drug testing policy that fits your unique needs, considering desired detection windows, new and emerging drugs, and your community’s particular substance abuse issues. Let us work with you to carry out a custom drug testing program.

Source: http://sober-work-place.com/drug-testing-2/with-wax-marijuana-use-on-the-rise-make-sure-you-celebrate-drug-free-work-week/  Introduction from Monte Stiles from DWI

This is a very powerful and heartbreaking story –  let us hope many young people will take notice and never ‘try’ drugs offered by ‘a friend’

Connor Reid Eckhardt added a new video.

“THIS IS SO IMPORTANT TO SHARE….THIS IS NOT A MOVIE!! OUR 19 YEAR OLD SON CONNOR IS NOT WAKING UP FROM THE SINGLE HIT OF “SPICE, K2,” HE TOOK. It has over 600 names. The credits are not going to roll. He is not going surfing this morning. He is GETTING “THAT HAIR CUT” we never wanted to give before he goes into surgery to donate 4 of his organs to SAVE FOUR OTHER LIVES. Connor died. Our son, our only son died from a legal high purchased at the corner market. No drugs or alcohol in his system. Most, not all legal highs are made in CHINA and sold to our youth. Millions are being affected by these legal highs. Please help us get the attention of presidential candidates. We must get this stopped. An entire generation of children and youth are at risk. Please get educated. The Connor Project Foundation is about Education, Awareness, and Prevention. Doit4connor. Do it for your kids and for your communities.

OUR 19 OLD SON CONNOR IS DEAD FROM ONE HIT OF A SYNTHETIC DRUG called spice. WHERE DOES MOST OF THIS POISON COME FROM??? CHINA!!! Who sells this poison to our kids? Go check out these shop owners. WE LET THESE CHEMICALS INTO THE USA?? Why?? Connor made a decision that night that changed our lives forever. He chose to try legal high offered to him “by a friend”. It is sold over the counter in gas stations, mini marts, smoke shops, etc. Targeted at our youth. Stop the madness and share with at least one person. We must take a stand for Connor and all the others who have died or are institutionalized because of these killer legal highs.”

Source:

https://www.facebook.com/270455916494386/videos/436695296537113/

Researchers at the Centre for Addiction and Mental Health (CAMH) have identified 428 distinct disease conditions that co-occur in people with Fetal Alcohol Spectrum Disorders (FASD), in the most comprehensive review of its kind.

The results were published today in The Lancet.

“We’ve systematically identified numerous disease conditions co-occurring with FASD, which underscores the fact that it isn’t safe to drink any amount or type of alcohol at any stage of pregnancy, despite the conflicting messages the public may hear,” says Dr. Lana Popova, Senior Scientist in Social and Epidemiological Research at CAMH, and lead author on the paper. “Alcohol can affect any organ or system in the developing fetus.”

FASD is a broad term describing the range of disabilities that can occur in individuals as a result of alcohol exposure before birth. The severity and symptoms vary, based on how much and when alcohol was consumed, as well as other factors in the mother’s life such as stress levels, nutrition and environmental influences. The effects are also influenced by genetic factors and the body’s ability to break down alcohol, in both the mother and fetus.

Different Canadian surveys suggest that between six and 14 per cent of women drink during pregnancy.

The 428 co-occurring conditions were identified from 127 studies included in The Lancet review. These disease conditions, coded in the International Classification of Disease (ICD-10), affected nearly every system of the body, including the central nervous system (brain), vision, hearing, cardiac, circulation, digestion, and musculoskeletal and respiratory systems, among others.

While some of these disorders are known to be caused by alcohol exposure – such as developmental and cognitive problems, and certain facial anomalies – for others, the association with FASD does not necessarily represent a cause-and-effect link.

Problems range from communications disorders to hearing loss

However, many disorders occurred more often among those with FASD than the general population. Based on 33 studies representing 1,728 individuals with Fetal Alcohol Syndrome (FAS), the most severe form of FASD, the researchers were able to conduct a series of meta-analyses to establish the frequency with which 183 disease conditions occurred.

More than 90 per cent of those with FAS had co-occurring problems with conduct. About eight in 10 had communications disorders, related to either understanding or expressing language. Seven in 10 had developmental/cognitive disorders, and more than half had problems with attention and hyperactivity.

Because most studies were from the U.S., the frequency of certain co-occurring conditions was compared with the general U.S. population. Among people with FAS, the frequency of hearing loss was estimated to be up to 129 times higher than the general U.S. population, and blindness and low vision were 31 and 71 times higher, respectively.

“Some of these other co-occurring problems may lead people to seek professional help,” says Dr. Popova. “The issue is that the underlying cause of the problem, alcohol exposure before birth, may be overlooked by the clinician and not addressed.”

The benefits of screening and diagnosis

Improving the screening and diagnosis of FASD has numerous benefits. Earlier access to programs or resources may prevent or reduce secondary outcomes that can occur among those with FASD, such as problems with relationships, schooling, employment, mental health and addictions, or with the law.

“We can prevent these issues at many stages,” says Dr. Popova. “Eliminating alcohol consumption during pregnancy or reducing it among alcohol-dependent women is extremely important. Newborns should be screened for prenatal alcohol exposure, especially among populations at high risk. And alerting clinicians to these co-occurring conditions should trigger questions about prenatal alcohol exposure.”

“It is important that the public receive a consistent and clear message – if you want to have a healthy child, stay away from alcohol when you’re planning a pregnancy and throughout your whole pregnancy,” she says.

It’s estimated that FASD costs $1.8 billion annually in Canada, due largely to productivity losses, corrections and health care costs, among others.

In addition to this review, Dr. Popova has been part of an expert group of leading FASD researchers and clinicians working with the Ontario Ministry of Children and Youth Services on its new FASD strategy. Her team is also undertaking a study to determine how common FASD is in Canada, as well as in other countries in Eastern and Central Europe and Africa.

Source:

https://m.medicalxpress.com/news/2016-01-conditions-co-occur-fetal-alcohol-spectrum.html

January 2016

Psychology of Addictive Behaviors journal makes corrections, SAM calls on media to correct stories

FOR IMMEDIATE RELEASE

January 19, 2015

Contact: Jeffrey Zinsmeister

jeff@learnaboutsam.org

+1 (415) 680-3993

[WASHINGTON, DC] – A prominent journal article about marijuana and health which resulted in media outlets reporting on marijuana’s harmlessness has now been corrected. A recheck of the statistics has now found that the incidence of psychotic disorders trended toward a 2.5-fold increase in marijuana users, a difference that went beyond a trend to reach significance in a one-tailed statistical test. This degree of impact matches very well the results of many prior studies involving marijuana use and psychosis though falls short of the five-fold increase in psychosis risk for marijuana users seen with the high strength strains that are more recently available.

Dr. Christine Miller, a former schizophrenia researcher from Johns Hopkins University and now Director of SAM Maryland, first alerted the journal, Psychology of Addictive Behaviors, last December. Some media outlets have already corrected their original story.

“We commend the Washington Post’s Ariana Cha for now updating her story, and hope many more will follow her lead,” remarked Dr. Miller. “The flaw in the original University of Pittsburgh report were certain correction factors applied to the raw data, factors which are strongly affected by psychosis rather than being causes of such a disorder. These inappropriate corrections overpowered the marijuana effect. We’re glad the corrections have been made.”

SAM urges other media outlets to correct their headlines and stories.

The new data comes on the heels of a major report released by the State of Vermont’s Health Department which found that marijuana worsened conditions ranging from mental illness to motor vehicle accidents to negative pregnancy effects – and almost all of them are found to be worsened by marijuana:

For more information about marijuana use and its effects, see http://www.learnaboutsam.org.

###

About SAM

Smart Approaches to Marijuana (SAM) is a nonpartisan, non-profit alliance of physicians, policy makers, prevention workers, treatment and recovery professionals, scientists, and other concerned citizens opposed to marijuana legalization who want health and scientific evidence to guide marijuana policies. SAM has affiliates in 31 states.

www.learnaboutsam.org

Source:

http://psycnet.apa.org/record/2015-58335-001

Submitted by Livia Edegger 

US researchers that analysed over a million lab samples found that prescription drug abuse is twice as likely to decrease in states with drug prevention programmes in place. The states of Florida, Georgia, Kentucky, New York and Tennessee have seen a decline of 10% in prescription drug abuse, a rate 2.5 higher than the average rate for the rest of the country. In addition to the nationwide drug monitoring programme, these states have implemented programmes such as awareness raising initiatives, training and guidance for physicians and additional regulations to curb prescription drug abuse. Overall, prescription drug abuse has fallen from 63% in 2011 to 55% in 2013 with the most significant decline in teen rates from 70% to 57%. Despite these improvements, prescription drug abuse continues to be widespread in the US with more than half the patients endangering their health by misusing prescription drugs.

Links:

Source:

http://preventionhub.org/en/prevention-update/prevention-measures-lower-prescription-drug-abuse-us

23rd July 2014

Submitted by Livia Edegger

Earlier this month Germany celebrated the results of the 2014 drug report which revealed a rapid decline in smoking, drinking and marijuana use among youth over the past ten years. Smoking among German teens aged 12 – 17 has halved in ten years (11.7%). Smoking rates have also dropped among 18 – 25 year olds, not as significantly though. Drinking rates have fallen from 17.9% in 2001 to 13.6% in 2012 among 12 – 17 year olds. In terms of gender differences, teenage boys are twice more likely to consume alcohol than their female counterparts. Little has changed among 18 – 25 year olds, the group that accounts for the highest alcohol consumption rate. Drinking in that age group was reported at 38.4% in 2012 which means it only dropped by a little over 1%. Cannabis ranks first among illicit drugs used with 5.6% of 12 – 17 year old teenagers using it compared to 9.2% in 2001. After years of steady consumption rates, cannabis use among 18 – 25 year olds is on the rise again and at 15.8% resembles figures of 2001.

Source:

http://preventionhub.org/en/prevention-update/germany-releases-drug-report

23rd July 2014

Submitted by Livia Edegger

A study conducted by the US Substance Abuse and Mental Health Services Administration (SAMHSA) found that individuals who had started taking drugs early on in life were more likely to develop mental disorders and become polydrug users. At the time of clinical admission, three quarters of drug users between 18 and 30 years of age had started taking drugs at age 17 or younger. A tenth of drug users had started at an even earlier age. 78.1% of drug users that had started taking drugs at age 11 or younger were taking more than one drug compared to 30.4% of individuals that had initiated drug use after the age of 25. 38.6% of drug users that had begun taking drugs at age 11 or under had developed some form of mental disorder. These results underline the importance of prevention programmes in childhood and early adolescence, phases that are critical for young people’s development.

Links:

Source:

http://preventionhub.org/en/prevention-update/early-onset-drug-use-linked-mental-disorders-and-multi-drug-use

Submitted by Livia Edegger

The findings of a report released by the Health and Social Care Information Centre (HSCIC) reveal a promising downward trend regarding drug use among secondary school students in England. Tobacco, alcohol and drug use among students have been cut in half in the past ten years. Smoking rates have dropped from 9% to 3% and alcohol rates have dropped from 25% to 9%. Illicit drug use has fallen by 50% between 2003 and 2013. The growing concern that e-cigarettes might fuel the uptake of smoking in teenagers was not supported by the report.

Links:

Source: 

http://preventionhub.org/en/prevention-update/drug-use-plunges-50-among-secondary-school-students-england

A teenage rugby player cut off his own penis and stabbed his mother while high on skunk, his father has revealed, as he called for the drug to be reclassified.

The father, named only as Nick because he wants to remain anonymous as his son is rebuilding his life, is backing Lord Nicholas Monson’s campaign to have skunk reclassified from a class B to a class A drug and for the traditional weaker form of cannabis to be decriminalised.

Lord Monson launched his call following the suicide of his 21-year-old son Rupert, who was addicted to skunk.

Nick, speaking for the first time in an interview with Radio Five Live, said his son, a county rugby player, started smoking “weed” when he was around sixteen and a half before switching to skunk because of “boredom”.

That was the beginning of what Nick said his son would describe as “two and a half years of hell” which culminated in a psychotic episode.

His son went from a “very bright, bubbly lad” to a “waste of space”. The teenager became delusional and paranoid, including sleeping “with a tennis racket in his bed because he thought people were living in the walls”.

Describing the horrific incident when his son attacked his mother and inflicted “incredibly deep self harm”, Nick said it had been a “perfectly normal day” before his son woke in the middle of the night ranting and raving.

“It was absolutely devastating, you can’t imagine anything of that nature happening…the whole episode was just surreal, I remember looking back its almost as if I’m peering in through a window and it’s happening to someone else.”

Nick’s son was in a mental institute for around 6 months, and in total spent almost two years in prison following the incident.

He has undergone surgery, and will have more operations to repair the damage, though Nick said he couldn’t say whether his son would be able to have children. He is clean of drink and drugs, but Nick cautioned that even being around other people smoking skunk could trigger another psychotic episode. His ex-wife has recovered, and has fully reconciled with her son who, Nick said, is “actually in really good form.”

“We recognise that this was an illness… he was totally oblivious, actually has no real memory of anything that happened, even now,” Nick said. “Maybe that’s for the best.”

Source:

https://www.telegraph.co.uk/news/2017/06/02/teenage-rugby-player-cut-penis-high-onskunk-says-father-wants/

A team of researchers from the UF Drug Policy Institute, Harvard University, and other institutions authored a lengthy response to a recent monograph written by the George Soros-funded ICSDP claiming that cannabis health claims have been overblown.

The team, led by former American Society of Addiction Medicine President Stu Gitlow, and other researchers with leadership ties to groups like the American Academy of Pediatrics, Boston Children’s Hospital, the University of Texas, the University of Pennsylvania, and other institutions found that the ICSDP report is an example of deceptive and biased research and that it contains abundant factual errors and logical flaws.

The report’s introduction reads: “The ICSDP conveniently cites evidence that supports its own predetermined narrative, concluding that only the pro-marijuana lobby has any substantive evidence in its favor-and ignores evidence to the contrary. Its main strategy is to attribute overblown “straw man” arguments to established marijuana researchers, misstating their positions and then claiming to “rebut” these positions with research.

“This response/critique reveals the lack of objectivity present in the report and, point-by-point, shows how the interests of the nascent Big Marijuana industry, private equity firms, and lobbyists lining up to capitalize on a new marijuana industry, are served.”

About the UF Drug Policy Institute

The UF Drug Policy Institute (DPI) serves the state of Florida, the Nation, and the global community in delivering evidence-based, policy-relevant, information to policymakers, practitioners, scholars, and the community to make educated decisions about issues of policy significance in the field of substance use, abuse, and addiction.

Read about our Distinguished Fellows Here

Just finished reading the cannabis section of the world drug report mentioned below and here were of the points that stuck out to me:

  • Cannabis herb (they make a distinction between herb and resin) seizures in North America account for 64% of worldwide seizures.
  • US outdoor eradication rates significantly dropped (6,470 in 2012 from 23, 622 in 2011) but it is unclear if the decrease was due to declining law enforcement activity in that area or to increasing legal grows due to new laws in CO and WA.
  • In 2012 , between 125 million and 227 million people who estimated to have used cannabis, that corresponds to 2.7 and 4.9% of the population aged 15-64 years.

We are changing laws to accommodate this small proportion of the population. These laws will have a deleterious knock on effect for the 95% majority of the population.

  • Over the past 5 years (in N. America, the largest cannabis herb market) prevalence rates in the US have increased but declined in Canada between 2008-2011 and increasing again between 2011-2012.

Cannabis use in the UK is down to the lowest levels since measurements began in 1996….. but the UK Government has not so far relaxed firm drug laws.

  • In the US, between 2006-2010 there was a 59% increase in cannabis-related ER visits and a 14% increase in cannabis-related treatment admissions.

•   Expert analyses predicts that legalization of cannabis will most likely reduce production costs which would in turn be expected decease prices overtime. Since cannabis consumption responds to prices, the lower prices will likely lead to high consumption. It is estimated that for each 10% drop in price there will be an approx. 3% increase in total users and a 3-5%

Source:

World Drug Report 2014

http://www.unodc.org/wdr2014/

 

Submitted by Livia Edegger

The most popular alcohol brands among US youth are the ones most often featured in advertisements in teenage magazines, according to a new study. Their ads are found to be five to nine times more likely to appear in those magazines. Leading researcher Craig Ross of Virtual Media Resources warns parents of the effects of alcohol ads on young adults, “Parents should take note that scientific evidence is growing that exposure to alcohol advertising promotes drinking initiation, and is likely to increase the frequency of consumption for kids already drinking”. Along with a group of researchers he called for developing standards that would limit alcohol advertising to magazines with less than 15% of young people among its readership.

Links:

Underage drinkers’ favourite alcohol brands are heavily advertised in magazines 

http://www.drugfree.org/join-together/underage-drinkers-favorite-alcohol…

Source:

http://preventionhub.org/en/prevention-update/us-teens-targeted-alcohol-advertising-magazines

16th July 2014

Filed under: Alcohol,Latest News,Youth :

Submitted by Livia Edegger on – 15:38

A group of researchers has developed a test to predict fourteen year old teenagers’ future drinking behaviour. The test takes a wide variety of factors that might influence young adults’ susceptibility to binge drinking into consideration such as family background, personality traits, availability of alcohol as well as brain-related variables. “There is no one really big thing. It’s a bunch of little things adding up to give you this prediction,” says Dr Robert Whelan from the University College Dublin. As of today, the test is far from practical as it lacks accuracy and relies on expensive brain scans. A more simplified and cost-effective version of the test could help identify at-risk adolescents for interventions in the future. Hugh Perry, chairman of the Medical Research Council Neurosciences and Mental Health Board, said further research could “lead to breakthroughs in this field and provide compelling evidence to inform public health policy and lay the groundwork for the design of interventions”.

Links:

Source:

http://preventionhub.org/en/prevention-update/researchers-create-tool-predict-teens%E2%80%99-drinking-behaviour

9th July 2014

Submitted by joanna

This month the Australian Drug Foundation published the latest issue of their Prevention Research journal which features alcohol and drug prevention programmes in communities across Australia. The issue provides guidelines for organisations, individuals, practitioners and others developing and running prevention programmes and activities in community settings. The issue highlights the importance of comprehensive community programmes involving families, schools and other community entities and offers guidelines to community-based organisations and groups working in the field of drug prevention.

Links:

Source:

http://preventionhub.org/en/prevention-update/guide-implementing-community-drug-prevention-programmes

3rd July 2014

Submitted by Livia Edegger 

A new study carried out by the European Institute of Studies on Prevention (IREFREA) explores the role of parenting styles on drug use among teenagers. A group of researchers interviewed almost 8,000 students between 11 and 19 years of age across six European countries. The study analysed four parenting styles – authoritarian, authoritative, indulgent and neglectful. The first two parenting styles were characterised by strict rules and control. Authoritative parenting was marked by good communication, affection and flexibility from the parents’ side while the authoritarian style lacked those characteristics. The more lenient parenting styles – ‘indulgent’ and ‘neglectful’ – differed to the extent that in the former parents were affectionate and understanding, qualities that were absent in the latter. The ‘authoritative’ and ‘indulgent’ parenting styles, in which parents were affectionate and understanding, were the most effective in keeping children from using drugs.

Links:

Source:

http://preventionhub.org/en/prevention-update/why-parenting-styles-matter-when-it-comes-drug-use-among-teens

17th June 2014

Submitted by Livia Edegger

As a country with a history of heavy smoking and drug use among youth, Ireland embraces the results of a new study indicating a substantial drop in teen smoking. Youth smoking rates fell from 21.1% in 1998 to 11.9% in 2010. Similarly, the percentage of teenagers that take their first puff at age 13 or younger has decreased significantly. While in 2002 more than 60% of Irish teenagers had their first cigarette at age 13 or younger, by 2010 that number had fallen to just under 50%. These positive developments were presented at the Irish Cancer Society’s X-Hale Film Festival in Dublin, which featured 43 short clips produced by youth groups that drew attention to the harms of smoking.

Links:

Source:

http://preventionhub.org/en/prevention-update/teenage-smoking-cut-half-ireland

23rd July 2014

Filed under: Latest News,Nicotine,Youth :

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

The Sun’s brief item describing a frightening new threat in Maryland’s drug addiction crisis (“Person who used synthetic marijuana suffers bleeding,” April 6) reveals the necessity of a renewed focus on substance abuse prevention and public education.

On April 4, the National Drug Early Warning System at the University of Maryland issued an alert about the detection of rat poison (brodifacoum) in synthetic marijuana in Illinois that resulted in two deaths and 81 emergencies. This drug, known on the street as spice or K2, causes severe bleeding, vomiting of blood, and other painful side effects. Two days later, as The Sun reports, this potentially-fatal fake weed arrived in Baltimore. The implication from this news calls for a renewed emphasis on prevention as part of Maryland’s overall response to the opioid crisis.

Specifically, while it’s essential that policymakers, health care and treatment providers, and related organizations stay steadfast in increasing the number of treatment beds, outpatient facilities, sober living houses, medication-assisted treatment and other evidence-based strategies, it also is vital to understand the treatment medications like Vivitrol, Suboxone, and Methadone are not effective in treating synthetic marijuana analogs like spice and K2.

This is another aspect of the tragedies and family horror stories caused by substance use disorder, the clinical term for drug addiction. Medications that are effective with one drug are ineffective with a different drug. This devastating dynamic requires that everyone in their respective communities work together to spread and reinforce prevention strategies and activities.

Source: http://www.baltimoresun.com/news/opinion/readersrespond/bs-ed-rr-addiction

Filed under: Latest News,Synthetics :

The following video is long – 52 minutes, but it is essential viewing to help people understand some of the consequences of legalisation for both medicinal and recreational use of cannabis in the USA. Make yourself a cup of coffee and watch this in its entirety.

Subject: Marijuana X https://m.facebook.com/story.php?story_fbid=10156320599628035&id=670743034&ref=content_filter

Public health officials say the nerve pain medication gabapentin is being found in an increasing number of overdose deaths, according to CBS News.

Gabapentin is a non-narcotic drug used to treat seizures and pain associated with shingles. Doctors have been prescribing it for a growing number of other conditions, as a way to offer pain relief without opioids. A study published last year found that for people who use heroin, the combination of opioids with gabapentin potentially increases the risk of overdose death.

“Unfortunately, we now need to worry about it because people are abusing it,” Dr. James Patrick Murphy, a pain and addiction specialist in Kentucky, told the Louisville Courier-Journal. “Alone, it’s not something that will stop your breathing or your heart,” he said. “But if you take it along with a drug like heroin or fentanyl, together it might be enough to make you stop breathing and put you over the edge.”

Source: https://drugfree.org/learn/drug-and-alcohol-news/nerve-pain-medication-gabapentin April 5th 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: Eur Neuropsychopharmacol. 2017 Dec;27(12):1223-1237. doi: 10.1016/j.euroneuro.2017.10.037. Epub 2017 Nov 10.

A growing number of drug overdose deaths are due to cocaine laced with fentanyl, NPR reports. Fentanyl is 50 to 100 times more potent than heroin. The image above shows two potentially fatal dosages of fentanyl and heroin

According to the Drug Enforcement Administration (DEA), 7 percent of cocaine seized in New England in 2017 included fentanyl, up from 4 percent the previous year. In Connecticut, the number of deaths involving fentanyl-laced cocaine has increased 420 percent in the last three years. Massachusetts officials say an increasing amount of fentanyl-laced cocaine is changing hands on the streets. The DEA, in its National Drug Threat Assessment, says people typically add fentanyl to cocaine for the purpose of “speedballing,” which combines the rush of cocaine with a drug that depresses the nervous system, such as heroin. Some experts told NPR fentanyl may be mixed with cocaine accidentally during packaging. Others say drug cartels are adding fentanyl to cocaine to expand the market of people who are addicted to opioids.

How Can I Protect My Child from Fentanyl? 5 Things Parents Need to Know

Deaths from fentanyl and other synthetic opioids (not including methadone), rose a staggering 72 percent in just one year, from 2014 to 2015. Government agencies and officials of all types are rightly concerned by what some are describing as the third wave of our ongoing opioid epidemic.

As a concerned parent, whose top priority is keeping your child safe — and alive — the following are the most important things to understand about fentanyl.

1. Fentanyl is 50 to 100 times more potent than heroin or morphine. It is a schedule II prescription drug typically used to treat patients with severe pain or to manage pain after surgery. It is also sometimes used to treat patients with chronic pain who are physically tolerant to other opioids. In its prescription form, fentanyl is known by such names as Actiq®, Duragesic® and Sublimaze®.

2. It is relatively cheap to produce, increasing its presence in illicit street drugs. Dealers use it to improve their bottom line. According to a report from the Office of National Drug Control Policy, evidence suggests that fentanyl is being pressed into pills that resemble OxyContin, Xanax, hydrocodone and other sought-after drugs, as well as being cut into heroin and other street drugs. A loved one buying illicit drugs may think they know what they’re getting, but there’s a real risk of it containing fentanyl, which can prove deadly.

3. Naloxone (Narcan) will work in case of overdose, but extra doses may be needed. Because fentanyl is far more powerful than other opioids, the standard 1-2 doses of naloxone may not be enough. Calling 911 is the first step in responding to any overdose, but in the case of a fentanyl-related overdose the help of emergency responders, who will have more naloxone, is critical. Learn more about naloxone and responding to opioid overdose >>

4. Even if someone could tell a product had been laced with fentanyl, it may not prevent their use. Some individuals claim they can tell the difference between product that has been laced with fentanyl and that which hasn’t, but overdose statistics would say otherwise. Some harm reduction programs are offering test strips to determine whether heroin has been cut with fentanyl, but that knowledge may not be much of a deterrent to a loved one who just spent their last dollar to get high.

5. Getting a loved one into treatment is more critical than ever. If you need help in determining a course of action, please reach out to one of our parent counselors on our free Parent Helpline. Learn more about all the ways you can connect with our free and confidential services and begin getting one-on-one help.

Source: https://drugfree.org/parent-blog April 2017

Abstract

Background

Marijuana is a widely used recreational substance. Few cases have been reported of acute myocardial infarction following marijuana use. To our knowledge, this is the first ever study analyzing the lifetime odds of acute myocardial infarction (AMI) with marijuana use and the outcomes in AMI patients with versus without marijuana use.

Methods

We queried the 2010-2014 National Inpatient Sample (NIS) database for 11-70-year-old AMI patients.

Pearson Chi-square test for categorical variables and Student T-test for continuous variables were used to compare the baseline demographic and hospital characteristics between two groups (without vs. with marijuana) of AMI patients. The univariate and multivariate analyses were used to assess and compare the clinical outcomes between two groups. We used Cochran–Armitage test to measure the trends. All statistical analyses were executed by IBM SPSS Statistics 22.0 (IBM Corp., Armonk, NY). We used
weighted data to produce national estimates in our study.

Results

Out of 2,451,933 weighted hospitalized AMI patients, 35,771 patients with a history of marijuana and 2,416,162 patients without a history of marijuana use were identified. The AMI-marijuana group consisted more of younger, male, African American patients. The length of stay and mortality rate were lower in the AMI-marijuana group with more patients being discharged against medical advice.

Multivariable analysis showed that marijuana use was a significant risk factor for AMI development when adjusted for age, sex, race (adjusted OR 1.079, 95% CI 1.065-1.093, p<0.001); adjusted for age, female, race, smoking, cocaine abuse (adjusted OR 1.041, 95% CI 1.027-1.054, p<0.001); and also when adjusted for age, female, race, payer status, smoking, cocaine abuse, amphetamine abuse and alcohol abuse (adjusted OR: 1.031, 95% CI: 1.018-1.045, p<0.001). Complications such as respiratory failure (OR 18.9, CI 15.6-23.0, p<0.001), cerebrovascular disease (OR 9.0, CI 7.0-11.7, p<0.001), cardiogenic shock (OR 6.0, CI 4.9-7.4, p<0.001), septicemia (OR 1.8, CI 1.5–2.2, p<0.001), and dysrhythmia (OR 1.8, CI 1.5-2.1, p<0.001) were independent predictors of mortality in AMI-marijuana group.

Conclusion

The lifetime AMI odds were increased in recreational marijuana users. Overall odds of mortality were not increased significantly in AMI-marijuana group. However, marijuana users showed higher trends of AMI prevalence and related mortality from 2010-2014. It is crucial to assess cardiovascular effects related to marijuana overuse and educate patients for the same.

Source: Desai R, Patel U, Sharma S, et al. (November 03, 2017) Recreational Marijuana Use and Acute Myocardial Infarction: Insights from Nationwide Inpatient Sample in the United States . Cureus 9(11): e1816. DOI 10.7759/cureus.1816

While writing, I wondered what kind of details I should publish about the previous lives of people in the marijuana industry. Virgil Grant, one of the article’s subjects, told me stories about how he would sell marijuana from his family grocery store in Compton in the 1980s and 1990s by putting the weed in empty boxes of Lucky Charms. He mentioned, without much elaboration, that would-be competitors in Compton regretted going up against him.

It’s an awkward and confusing transition period in the marijuana industry. What was illegal yesterday in California may be legal today, but that’s of course not the way the federal government sees it. Mr. Grant has spent time in both federal and state prisons.

Since legalization of recreational sales came into effect in California in January, there have been stories about cities and counties that banned marijuana. But I had never seen reporting on the bigger picture. So I reached out to a company called Weedmaps, a website that hosts online reviews of cannabis businesses. When they added it up, the data surprised me: Only 14 percent of California’s cities and towns authorize the sale of recreational marijuana. By contrast, Proposition 64, the ballot measure that allowed marijuana legalization, passed with 57 percent voter approval in 2016, a seemingly solid majority.

The low acceptance of marijuana businesses strikes me as part of the liberal, not-in-my-backyard paradox in California. Yes, Californians want shelters for the homeless, but just not across the street. Yes, Californians want more housing built, but not if it changes the character of the neighborhood. A marijuana dispensary? Sure, preferably in the next town.

A New York Times reporter wanted to find out why California cities are taking such different approaches to legal pot. Previously, he covered a story about why California growers are so reluctant to leave the black market and seek a state license to become legitimate. He found that only about 10 percent have done so. The other 90 percent remain in black market. California is the nation’s biggest producer and consumer of marijuana. One estimate projects the state produces seven times the amount of pot it consumes and exports the surplus to non-legal states. Pursuing this story took the reporter to Compton, in Los Angeles County, where residents voted in January to ban marijuana businesses by a 3-to-1 margin. He compared this to Oakland, near San Francisco, which has embraced the marijuana industry. It’s as if the two cities had been asked the same question and come up with completely different answers, he opined. To get a bigger picture, he consulted Weedmaps to find out how common industry bans are. He was surprised to find that only 14 percent of California’s cities and towns authorize marijuana sales, even though legalization passed in 2016 with 57 percent voter approval.

It’s still early days — it’s been less than three months since legal sales started — but for now the trend is that larger cities like Oakland, San Francisco, Los Angeles, Sacramento and San Diego are the hubs of the marijuana industry, while smaller cities and towns are ambivalent or outright hostile to the idea of opening marijuana dispensaries. Orange County, in Southern California, is a recreational marijuana desert, with only a handful of dispensaries allowed.

California has a reputation for very tolerant attitudes toward pot, and it’s the biggest consumer and producer of the drug in the United States by a wide margin. It is also the nation’s premier exporter to other states: By one estimate, the state produces seven times more than it consumes.

But the visit to Compton helped peel back another, more conservative set of attitudes toward marijuana.

At the Compton airport, Shawn Wildgoose, a former enlisted Marine who lives in Compton and works in the construction industry, told me he wanted to see the city focusing on its homeless problem and reducing crime, which is sharply down from previous decades.

Legal marijuana?

“Compton has other issues,” Mr. Wildgoose said. “We don’t need that distraction.”

Source: National Families in Action’s The Marijuana Report nfia@nationalfamilies.org 21st March 2018

Hamilton County Coroner Dr. Lakshmi Kode Sammarco released 2017 drug statistics Tuesday.

Last fall, the coroner said overdoses in Hamilton County had surpassed the total of last year, with 427 suspected deaths – and three months remaining in 2017, making the toll the worst since the heroin epidemic began. in the Tri-State.

Most overdose deaths have been due to fentanyl or chemically similar drugs, Sammarco said.

The county reported 403 overdose deaths in 2016 – up 30 percent, overdose deaths were totalled at 529 for 2017.

Sammarco described the increasing number of cases as “scary.” She said drug prevention efforts can only do so much without the help of the public.

“We can’t do this alone. Everybody here is busting their butt to try to get a handle on not just the supply, but to get help for the addicts and families. But we need the communities to step up, we need every neighborhood to keep an eye on their neighborhood. To try and help us get the dealers off the street, to try and get help to the addicts. You see something, say something.”

Sammarco noted the death toll was reduced by Narcan.

“The number of lives being saved is huge,” she said. “There’s no doubt they would’ve been double or triple what they were without Narcan.”

The coroner said 30,000 items were turned into the office’s drug section in 2017. Hfour drug analysts each processed well over 7,000 items, which 2.5 times higher than any other lab in Ohio.

Prevention First, a local non-profit aimed at reducing substance abuse released their findings from this year’s student drug-use survey.

They said of the more than 30,000 students grades 7 through 12 surveyed, nearly 14 percent have admitted to using alcohol in the past 30 days.

Tobacco use was only reported in five percent of students. Marijuana usage was slightly higher at more than eight percent.

Prescription drug abuse was reported in only 2.4 percent of students.

Commissioners said aside from marijuana use, the statistics have been trending downward since 2000.

“Hats off to Prevention First for leading the charge on that and for providing all of this really important information when it comes to prevention and what young people are doing in this community because this is the tip of the spear,” Commissioner Denise Driehaus said.

The survey, which is given every two years by Prevention First, was distributed to 80 public and private schools in six southwest Ohio counties.

To try to top overdoses before they happen, the Hamilton County Heroin Coalition is launching a Quick Response Teams early next month, on April 3.

The coalition is uniting with fire departments, law enforcement and social workers to create a team that follows up with overdose victims and offers them same-day addiction treatment. according to a prepared statement.

Modelled on an effort in Colerain Twp., the team will try to find overdose survivors using a database maintained by the Greater Cincinnati Fusion Center, a public safety data collecting agency.

Heroin Coalition commander and Norwood Police Lt. Tom Fallon told Hamilton County commissioners Monday the database would help locate overdose survivors who are otherwise hard to find.

The team will also use “predictive analysis” to track drug activity to target potential overdoses in with the help of University of Cincinnati’s Institute of Crime Science.

The effort is funded by a $400,000 grant from the U.S. Department of Justice funded through the Comprehensive Addiction and Recovery Act.

Source: http://www.fox19.com/story/37764381/hamilton-county-coroner

The mechanism by which dopamine cells in the brain signal the passage of time has received some new light via a recent study from researchers at University of Texas at San Antonio. To make decisions about the salience of a potential reward is mediated by small group of neurons in the midbrain that release dopamine.

The amount of dopamine released can influence our decisions by telling us how good a reward will be in the future. For example, more dopamine is released in response to the smell of turkey baking relative to the smell of leftovers.

But does the length of time between the anticipatory release of dopamine and the actual reward mediate the release and volume of dopamine? To answer this question, investigators used voltammetry to record dopamine release in rodents trained by Pavlovian conditioning.

This novel experiment utilized different audible tones that predicted the delivery of food. One tone was presented only after a short wait time— while the other tone was presented only after a long wait time.

The data showed that more dopamine was released during the short wait tone compared to the long wait tone. These results show that imminent reward is associated with dopamine release in the midbrain.

This is not unlike telling a 6-year-old child that her next birthday party is tomorrow versus telling her it won’t occur for two months. The time differentiation will predict the amount of excitement the child experiences.

Why Does This Matter?

We established many years ago the power of simply showing a recovering cocaine addict a piece of their drug paraphernalia. The release of dopamine is triggered by this visual cue and is also related to the amount of abstinence and how soon a drug reward could be attained. Monitoring via drug testing is one way that addicts are able to think through their behavioral choices when craving is induced.

For persons in early recovery from substance use disorder, anticipatory cues trigger the release of dopamine, cause craving and increase the risk of relapse. Continuing care planning for recovering addicts must address the power of anticipatory reward and help each recovery person set up obstacles that deter and delay access to a mood altering substance and avoid environmental drug cues.

Source: Fonzi KM, Lefner MJ, Phillips PEM, Wanat MJ. Dopamine Encodes Retrospective Temporal Information in a Context-Independent Manner. Cell Rep. 2017 Aug 22;20(8):1765-1774. doi: 10.1016/j.celrep.2017.07.076.

All creatures great and small are being poisoned by the pesticides and rodenticides in the water they drink, and in the food they eat. This polluted water from northern California marijuana grows eventually flows to much of the State. The lawless pot industry is nothing less than purveyors of poison. The recent scientific study “Cultivating Disaster: The Effect of Cannabis Cultivation on the Environment of Calaveras County,” points out that the cultivation of the drug was allowed by the State without adequate understanding of the impact on the environment and public health, welfare and safety. The chemicals that flow from the grow sites to the watershed had never been approved for these crops.

California does not regulate marijuana as a medicine because it is a Schedule 1 Controlled Substance under Federal Law, rather it is classified as an agricultural product. However, pot growers do not have to meet the same stringent requirements for chemicals and fertilizers as do all other farmers. Though there is limited testing being conducted by local water providers to determine if dangerous chemicals are leaching into water supplies or waste treatment systems, independent water experts testing water samples in Calaveras County found two thirds of the samples contained chemicals proven to be deadly poison to humans, fish and animals.

Of particular concern is carbofuron, an extremely toxic, water soluble granular pesticide banned in the U.S. but used among Mexican cartels. It is reported that an eighth of a teaspoon would kill a 300 lb black bear. In 2017, UC Davis researchers found harmful bacteria and deadly mold and Aspergillus fungi on marijuana in grows and dispensaries. This critical threat from marijuana grows to our environment and the human population is just beginning to surface.

The damaging effects of marijuana (cannabis), often considered a hallucinogenic drug, have long been known. High level THC, the mind-altering chemical in marijuana, is being grown and sold today as a “medicine.” It is long acting and addictive, causing brain damage, loss of intellect, psychotic breaks, suicides, mental illness, and birth defects and leads to other social costs from higher crime rates, highway deaths, excessive high school dropouts, and increased ER admissions, among others.

This lawless Big Marijuana Industry follows the playbook of Big Tobacco: GET KIDS HOOKED – ADDICTION OFTEN FOLLOWS. Their advertisements include images of Santa Claus, kids’ movies and cartoons, and they sell “edibles,” pot infused candy, lollipops and gummy bears with THC levels 50-70%. Many products are advertised as being 94-95% THC. Now there is crystalline THC that is 99.99% THC, known as “the strongest weed in the world.” Unfortunately, the public perception of marijuana is based on marijuana of the past – with 1- 5% THC.

The Calaveras Study estimates 1200 grows sites in that county; U.S. Forest Service estimates a tag of 2 billion to reclaim these sites. An estimated 50,000 grow sites in California would cost 50 – 80 billion to reclaim. The California Department of Fish and Wildlife says, “We are aware of the seriousness of the problem, but (we) do not know who is going to help clean it up.”

U.S. Attorney General Sessions has indicated his willingness to enforce our federal food and drug and environment laws when it comes to marijuana. Our California U.S. Attorneys must prosecute those who have broken federal, state, and county ordinances and explore funding to pay for cleanup of the land. This is not just a California issue, the U.S. Supreme Court

has ruled that federal marijuana laws preempt state laws and that marijuana control is a federal matter, not a states’ rights matter. There is no time to waste. Our future is at stake.

Source: Press Release Californians Against Legalisation of Marijuana Feb.6th 2018

BATON ROUGE — When a classmate died of a drug overdose, Symmes Culbertson bought a black suit for the funeral.

“It didn’t feel right to wear a blue sports jacket,” the 23-year-old political science major said.

What he didn’t count on was how many more funerals of classmates he would attend — six since he began attending Louisiana State University in 2013. “The number of people that I have known by name or in passing that have died from prescription drug overdoses, just in my college years, is well into the teens,” Culbertson said.

These kinds of events have become increasingly common at U.S. colleges, where many students view mixing pills and chasing them with alcohol as a rite of passage, rather than a dangerous and often deadly practice.

“It’s a dirty secret,” said April Rovero, whose son, Joey, a student at Arizona State University, overdosed in 2009 after taking prescription opioids, benzodiazepines and alcohol. (Dr. Lisa Tseng, who prescribed the drugs that led to the deaths of him and two other young men, is now serving a 30-years to life prison sentence for illegally prescribing the medication.)

In the year that followed, she said nine more students from there also died at the hands of drugs.

National addiction expert Dr. Drew Pinsky said one thing that is killing many students is mixing opioids with benzodiazepines, such as Xanax — something he says doctors should never prescribe together because it can be lethal.

Since 1999, drug overdose deaths of those 15 to 24 have quadrupled to 5,376 a year, far surpassing the number of those dying from alcohol-related accidents.

“These are perfectly healthy young people,” said Rovero, who founded the National Coalition Against Prescription Drug Abuse. “Every one of these deaths is avoidable.”

‘A Perfect Storm’

Ken Hale, associate director of the Higher Education Center for Alcohol and Drug Misuse Prevention and Recovery on the Ohio State University campus, said “a perfect storm” has hit college campuses and the nation, starting with “the drug-taking culture in which we live. We use more medication than any other country.”

In 2016, the nation filled more than 4.5 billion prescriptions, including antibiotics, cancer drugs and other drug treatment protocols — an average of more than 14 per person.

But Hale said many of those prescriptions are the powerful and often addictive opioids. Even though the U.S. makes up less than 5 percent of the world’s population, it consumes 80 percent of opioids.

As a result, these drugs are easily available to students through family members or friends, he said.

With these prescription drugs come misperceptions about safety and legality, he said. Of those addicted to heroin, 80 percent started on prescription drugs.

“If I go to a party and someone says, ‘Here’s some heroin,’ flags go up, but if someone hands me a Vicodin (an opioid painkiller), they don’t,” he said.

College campuses have become incubators for the bigger problem, where students “may not hit the wall in college, but they start behaviors that led to the problem we have,” he said.

Hale noted that the No. 1 cause of death of those under 50 is drug overdose and that fact has contributed to the U.S. seeing life expectancy decline for two years in a row for the first time since the 1950s.

Ohio State is one of more than 100 colleges that have recovery centers, where students can live, Hale said. “College dormitories are not a good environment for someone trying to get sober.”

Funeral for a friend

Culbertson grew up in Greenville, a fast-growing small town in South Carolina. “In high school, the most hardcore thing was weed,” he said.

By 2014, pills had begun to seep into college life, no longer just for the weekend parties.

Students took Adderall, the stimulant used to treat Attention Deficit Hyperactivity Disorder, if they needed to study or take a test.

And students who didn’t have classes till the afternoon might visit the bar and get Xanax, sometimes chasing that tranquilizer with alcohol — what can be a deadly combination.

When 2015 came, so did news about a high school classmate, a former cross-country track star who became hooked on opioids after hurting his back and blowing out his ACL.

His sister, Callie, had helped him get sober, letting him live with her for six months.

Callie Culbertson, the older sister of Symmes Culbertson, graduated in December from LSU with a degree in animal science, history and psychology. She knows of eight young people from her hometown of Greenville, South Carolina, who have died of drug overdoses. (Photo: SCOTT CLAUSE/USA TODAY Network)

Afterward, she kept in touch by telephone. One morning she learned on Facebook that he had overdosed — news that stunned her because she had just spoken to him the night before.

She and Culbertson attended the funeral, and she couldn’t believe that so many people attending were high, doing the same drugs that killed her friend.

Since that funeral, she knows of eight people from her hometown who have died of overdoses.

“Everybody knows somebody this has touched,” she said. “The problem is no one is changing.”

‘He only took five’

Culbertson returned to LSU, and the next funeral of someone he knew took place just a few months later.

The environment has become “so accepting of the drugs,” he said. “If you don’t enjoy them, then you’re the a–hole — at least if you speak up about it.”

More funerals followed, and last January, he got a call that a friend of his had just overdosed.

Culbertson had just seen his friend the night before, taking Xanax in a bar. “We were with him at midnight,” he said.

When it was obvious he needed help getting home, friends took him there. He never woke up.

Word came that he had died of fentanyl, a drug up to 50 times stronger than heroin, and that fentanyl may have been mixed with the Xanax pills.

After this death, Culbertson said some slowed down in their drug taking, but no one quit.

Months later, he heard of a classmate back home who had been hooked on opioids before secretly moving to heroin and overdosing.

On Oct. 14, hours after LSU defeated Auburn University in football, Culbertson and his friends met at a bar.

After midnight, a friend informed him that he had just stolen a bottle of liquor from the bar, and that he was going back to his place to celebrate with his girlfriend.

The next morning, a friend called him in tears, letting him know their friend was dead.

“That’s crazy,” Culbertson replied. “He only took five (Xanax) sticks last night.”

As soon as he hung up, he realized the insanity of his own words, nonchalantly saying that his friend had taken five Xanax bars.

“And I thought that was completely normal,” he said. “And that’s what has come to scare me — the culture here is so accepting of it that even me, who doesn’t do any of this stuff, it’s normalized to me. My thinking had gotten as distorted as anybody engaging in the culture.”

He wore the dark suit for his friend’s funeral in New Orleans and returned home to write out an idea for a short film, based on what he had experienced.

The next day, he pitched his idea to his film class. His movie proposal, “Only the Good,” resonated with his fellow students.

“I just wanted to tell the story about my peers that shows everybody thinks they’re having a good time, and while that’s true 90 percent of the time, there’s that 10 percent of the time where you not only do, you die from it, but it devastates the lives of the people that care about you.”

Turning a blind eye

Rovero would like to see learning about medicine safety start in kindergarten, saying schools and colleges need to do a better job of educating students.

“Colleges should be educating students about how addictive and dangerous these drugs can be, especially mixed with other drugs and alcohol, and about the risk factors and signs of addiction and overdose,” she said.

Students should be trained to aid those in trouble, she said. “Parents should work with their administrators to have resident assistants have a naloxone rescue kit on hand in dorm settings, just in case, and everyone with a kit needs to be trained to use it.”

All incoming LSU freshman receive orientation regarding alcohol, drug use and sexual violence prevention. University officials say they continue to work with students to identify and reduce high-risk drinking, providing addiction programs and services, including the Anxiety and Addictive Behaviors Clinic.

Culbertson praised LSU for its all of its efforts, including education, outreach and support groups.

But there is a huge hurdle, he said. “There’s not much a support group can do when people aren’t looking for support. Nobody feels like they have a problem.”

The problem is one of perception, he said. “Students don’t really identify themselves as drug addicts, and everybody else is turning a blind eye.”

Source: https://www.clarionledger.com/story/news/2018/02/05

New Hampshire’s Heroin Crisis Takes Toll with Record Overdose Deaths 2:24

LONDONDERRY, New Hampshire — Nearly a decade later, Susan Allen-Samuel still vividly remembers the moment that she first realized her son Joe was a heroin addict.

“It took my breath away,” Allen-Samuel told NBC News.

Allen-Samuel says that she began to notice all the metal spoons — typically used by users to melt down the heroin — in her kitchen were disappearing. She says she suspected heroin but admits that she couldn’t fully accept that Joe had been caught up in what she calls the “heroin epidemic” sweeping New Hampshire. “I was that person: ‘It’s not gonna happen, I’m a good mom,'” said Allen Samuel. “Wow, I got a wake-up call.”

At the time, Joe was just a teenager. He had recently switched from abusing opiates in pill form— primarily pain killers like OxyContin – to using heroin. The reason, he says, was purely financial. One OxyContin pill can cost as much as $80 on the black market. Joe says he was spending roughly $400 a day on his addiction. “They [the pills] were so expensive,” said Joe, 26. “You can’t afford a habit.”

At just $10-15 a bag, heroin was cheaper and more readily available. A short-drive to nearby Lawrence, Massachusetts — just across the state border — and he and his friends could purchase the drug on just about every street corner. Three overdoses and two arrests later, Joe’s life was forever altered by the deadly drug known as the “Big H.”

A State at the Center of a Heroin Crisis

The lush, rolling hills and idyllic red barns here can transform you to another time. Every town’s main street sprinkled with mom-and-pop shops and glistening white church steeples provide a backdrop to the scene of a Norman Rockwell painting, the personification of New England nostalgia.

In 2016, however, New Hampshire finds itself on the front lines of a heroin crisis that, critics warn, is unravelling the state’s social fabric. The numbers, alone, are daunting.

Last year, there were roughly 400 drug-overdose related deaths in New Hampshire — the most in the state’s history. With a population of roughly 1.4 million, the Granite State has one of the highest per-capita rates of addiction in the country.

As the problem has worsened over the last decade, however, access to substance abuse treatment has not improved. According to a 2014 report from the U.S. Department of Health and Human Services, the state is second to last — ahead of only Texas — in access to treatment programs. New Hampshire does not fund any methadone treatment programs and relies on a network of privately-run for-profit clinics to treat the thousands of addicts across the state. “There’s a stigma out there for users,” said Diane St. Onge, director of the Manchester Comprehensive Health Center — one of only eight clinics in the state that provides methadone treatment for heroin addiction. “We need more treatment options. People’s lives are at stake.”

In 2013, St. Onge’s clinic had 250 patients. Today, it has 540 patients and a two-week long waiting list. On a recent weekday, the clinic’s waiting room was teeming with weary

patients, most appearing middle-aged, and young children whose parents were there to receive their daily dose of methadone, the drug that reduces the withdrawal symptoms in people addicted to heroin or other narcotic drugs.

Outside, amid the political paraphernalia and live-shots being set up by crews ahead of Tuesday’s New Hampshire primary, patients sat on benches waiting to go inside. The juxtaposition was striking.

A Town under Siege

Situated along the I-93 interstate between the state’s two largest cities of Manchester and Nashua, the small town of Londonderry is at the center of a drug-trafficking route where heroin cuts across socio-economic and political lines.

Ed Daniels has worked with the Londonderry Fire Department for 11 years. For most of that time, he says, he saw one or two overdose cases a year. He says he now sees at least one every shift. He says the victims he treats come from all demographics. “There’s no rhyme or reason to it,” said Daniels.

Daniels says the numbers began to spike last summer and have continued to rise, unabated. He blames the increase on fentanyl — an extremely potent pain killer drug that is now commonly cut with heroin to produce a more intense high — and feels, at times, that there is little long-term that he can do for his patients. “They can leave the hospital,” said Daniels. “[But] once they have the addiction, where can they go for help?”

For Londonderry Fire Department Chief Darren O’Brien, who has lived his entire life in Londonderry, “it’s hard to see what’s going on in a community you grew up in.” O’Brien noted that there were 82 reported overdoses last year — nearly three times the 31 reported cases in 2014. “I’m hoping we can get a handle on it,” he said.

Joe’s heroin addiction lasted nearly a decade, a time that Allen-Samuel says she was fearful to come home to confront her son. “It’s a hell of a ride, it’s devastating,” she said. Allen-Samuel tried everything to help Joe. On one occasion, after he had been placed in jail for a minor offense, she had officers keep him there for months knowing that he’d likely not have access to any drugs inside. Meanwhile, she says, Joe’s childhood friends were dying one-by-one from overdose.

Joe says he had periods of sobriety but ultimately relapsed. It was not until his second stint in jail, he says, where he vowed to fight back. “That was probably my lowest point,” he said. He sought treatment and, ultimately, got clean.

He says losing his closest friends was motivation for him to be there for his girlfriend and young children. He has been sober for more than two years. “I’m just thankful,” said Joe. “[Before] I wasn’t able to be a dad. I’m glad I’m able to be here and experience it now.”

For Allen-Samuel, the unfolding crisis in New Hampshire should be an impetus for reform. Heroin addiction, she says, is a disease that should be dealt with the same way society treats cancer or any other deadly illness. “Our families are dying,” said Allen-Samuel. “What’s going on in our community is a war.” Source: http://www.nbcnews.com/nightly-news/our-families-are-dying-new-hampshire-s-heroin-crisis-n510661?cid=sm_fb Feb.2016

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