Wilkinson ST1, Stefanovics E, Rosenheck RA.
An increasing number of states have approved posttraumatic stress disorder (PTSD) as a qualifying condition for medical marijuana, although little evidence exists evaluating the effect of marijuana use in PTSD. We examined the association between marijuana use and PTSD symptom severity in a longitudinal, observational study.
From 1992 to 2011, veterans with DSM-III/-IV PTSD (N = 2,276) were admitted to specialized Veterans Affairs treatment programs, with assessments conducted at intake and 4 months after discharge. Subjects were classified into 4 groups according to marijuana use: those with no use at admission or after discharge ("never-users"), those who used at admission but not after discharge ("stoppers"), those who used at admission and after discharge ("continuing users"), and those using after discharge but not at admission ("starters"). Analyses of variance compared baseline characteristics and identified relevant covariates. Analyses of covariance then compared groups on follow-up measures of PTSD symptoms, drug and alcohol use, violent behavior, and employment.
After we adjusted for relevant baseline covariates, marijuana use was significantly associated with worse outcomes in PTSD symptom severity (P < .01), violent behavior (P < .01), and measures of alcohol and drug use (P <.01) when compared with stoppers and never-users. At follow-up, stoppers and never-users had the lowest levels of PTSD symptoms (P < .0001), and starters had the highest levels of violent behavior (P < .0001). After adjusting for covariates and using never-users as a reference, starting marijuana use had an effect size on PTSD symptoms of +0.34 (Cohen d = change/SD), and stopping marijuana use had an effect size of -0.18.
In this observational study, initiating marijuana use after treatment was associated with worse PTSD symptoms, more violent behavior, and alcohol use. Marijuana may actually worsen PTSD symptoms or nullify the benefits of specialized, intensive treatment. Cessation or prevention of use may be an important goal of treatment.
(c) Copyright 2015 Physicians Postgraduate Press, Inc.
Overwhelming evidence points to chronic alterations in sleep from chronic use of addictive substances that may be distinct from some or all of the acute effects of those substances. Interestingly, the effects of chronic use on sleep are similar among both CNS stimulants and depressants. Decreased sleep time, increased sleep latency and wake time after sleep onset, and deficiency in slow-wave sleep generation appear to be common to chronic use of alcohol, cocaine, cannabis, and opiates. REM sleep is also affected by acute and chronic use, but may be more sensitive to the pattern or quantity of recent use and time from last use, as results vary more among studies. Also linking these abnormalities are connections with ongoing use and relapse. However, treatment with typical sleep promoting agents that increase sleep time or efficiency by increasing light sleep may be counterproductive. Agents that address deficiency in slow-wave sleep generation and alterations in REM sleep may prove to be more useful in addressing the connection between chronically-altered sleep physiology and ongoing use and relapse, but substantial research still needs to be done to explore this possibility.
Shi, Yuyan and Lenzi, Michela and An, Ruopeng (2015) Cannabis liberalization and adolescent cannabis use: a cross-national study in 38 countries. ,Public Library of Science.PLoS ONE DOI: 10.1371/journal.pone.0143562 - URL
Aims: To assess the associations between types of cannabis control policies at country level and prevalence of adolescent cannabis use.
Setting, participants and design: Multilevel logistic regressions were performed on 172,894 adolescents 15 year of age who participated in the 2001/2002, 2005/2006, or 2009/2010 cross-sectional Health Behaviour in School-Aged Children (HBSC) survey in 38 European and North American countries.
Measures: Self-reported cannabis use status was classified into ever use in life time, use in past year, and regular use. Country-level cannabis control policies were categorized into a dichotomous measure (whether or not liberalized) as well as 4 detailed types (full prohibition, depenalization, decriminalization, and partial prohibition). Control variables included individual-level sociodemographic characteristics and country-level economic characteristics.
Findings: Considerable intra-class correlations (.15-.19) were found at country level. With respect to the dichotomized cannabis control policy, adolescents were more likely to ever use cannabis, use in past year, and use regularly. Although boys were substantially more likely to use cannabis, the correlation between cannabis liberalization and cannabis use was smaller in boys than in girls. With respect to detailed types of policies, depenalization was associated with higher odds of past-year use and regular use, and partial prohibition was associated with higher odds of regular use. The correlation between cannabis liberalization and regular use was only significant after the policy had been introduced for more than 5 years.
Conclusions: Cannabis liberalization with depenalization and partial prohibition policies was associated with higher levels of regular cannabis use among adolescents. The correlations were heterogeneous between genders and between short- and long-terms
The warning from scientists in the UK, US, Europe and Australia reflects a growing consensus that frequent use of the drug can increase the risk of psychosis in vulnerable people, and comes as the UN prepares to convene a special session on the global drugs problem for the first time since 1998. The meeting in New York next week aims to unify countries in their efforts to tackle issues around illicit drug use…
“It’s not sensible to wait for absolute proof that cannabis is a component cause of psychosis,” said Sir Robin Murray, professor of psychiatric research at King’s College London. “There’s already ample evidence to warrant public education around the risks of heavy use of cannabis, particularly the high-potency varieties. For many reasons, we should have public warnings.”
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Carter RC1, Wainwright H2, Molteno CD3, Georgieff MK4, Dodge NC5, Warton F6, Meintjes EM6, Jacobson JL3,6,5, Jacobson SW3,6,5.
Animal studies have demonstrated adverse effects of prenatal alcohol exposure on placental development, but few studies have examined these effects in humans. Little is known about effects of prenatal exposure to methamphetamine, marijuana, and cigarette smoking on placental development.
Placentas were collected from 103 Cape Coloured (mixed ancestry) pregnant women recruited at their first antenatal clinic visit in Cape Town, South Africa. Sixty-six heavy drinkers and 37 nondrinkers were interviewed about their alcohol, cigarette smoking, and drug use at 3 antenatal visits. A senior pathologist, blinded to exposure status, performed comprehensive pathology examinations on each placenta using a standardized protocol. In multivariable regression models, effects of prenatal exposure were examined on placental size, structure, and presence of infections and meconium.
Drinkers reported a binge pattern of heavy drinking, averaging 8.0 drinks/occasion across pregnancy on 1.4 d/wk. 79.6% smoked cigarettes; 22.3% used marijuana; and 17.5% used methamphetamine. Alcohol exposure was related to decreased placental weight and a smaller placenta-to-birthweight ratio. By contrast, methamphetamine was associated with larger placental weight and a larger placenta-to-birthweight ratio. Marijuana was also associated with larger placental weight. Alcohol exposure was associated with increased risk of placental hemorrhage. Prenatal alcohol, drug, and cigarette use were not associated with chorioamnionitis, villitis, deciduitis, or maternal vascular underperfusion. Alcohol and cigarette smoking were associated with a decreased risk of intrauterine passing of meconium, a sign of acute fetal stress and/or hypoxia; methamphetamine, with an increased risk.
This is the first human study to show that alcohol, methamphetamine, and marijuana were associated with distinct patterns of pathology, suggesting different mechanisms mediating their effects on placental development. Given the growing body of evidence linking placental abnormalities to neurodevelopmental deficits, these findings may be important in the long-term teratogenic effects of prenatal alcohol and drug exposure.