949 resultados para Consommateurs de cannabis


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Cannabis is one of the most commonly used illicit drugs, and its effects have traditionally been seen as less harmful than outcomes associated with the highly prevalent use of alcohol and other illicit substances (e.g., cocaine and amphetamines), and injecting drugs. Consequently, less attention has been focused on developing and evaluating interventions in this area. However, current research supports the idea that cannabis does pose a number of acute and chronic health risks to the individual and to society. The authors review findings concerning the physiological and neurological effects of cannabis, prevalence of use, and studies concerning its possible role as a "gateway" drug. Diagnostic criteria for cannabis dependence and abuse are discussed, with a focus on whether a cannabis withdrawal syndrome exists and if so how it can be diagnosed. There is strong support for a link between cannabis and the development and exacerbation of psychosis and other mental health conditions (e.g., anxiety, depression). Further research is needed to determine the underlying neurochemical processes and their possible contribution to etiology, as well as the social factors that contribute to the increasing use of cannabis by young people. In addition there is a need for systematic evaluation using randomized controlled trials to determine effective prevention and treatment strategies. A number of public health programs that address cannabis use are reviewed along with available evidence for their effectiveness.

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Although cannabis is the most commonly used illicit drug, duration of cannabis use is typically short, with many of those who initiate cannabis use ceasing use by their late twenties. In this paper we analyze data from a volunteer Australian cohort of 6265 male and female twins to examine whether the duration of cannabis use is an informative phenotype for future genetic analyses. Genetic modeling indicated: (a) moderate genetic influences on duration of cannabis use in both males (41%; 95% CI = 31–51) and females (55%; 95% CI = 46–63); (b) strong genetic influences on cannabis dependence in both males (72%, 95% CI = 61–81) and females (62%, 95% CI = 48–74); (c) no evidence of shared environmental influences on duration of cannabis use or on cannabis dependence in either males or females. Importantly, this model fitting indicated that a substantial component of genetic influences (rg = .90, 95% CI = .77–.99 (males); .70, 95% CI = .57–.83 (females)) on duration of cannabis use was shared with those influencing liability to cannabis dependence. While there were high genetic correlations in both women and men, lifetime duration of cannabis may be uniquely informative in assessing components of liability to cannabis use.

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Objective: To assess whether cannabis use in adolescence and young adulthood is a contributory cause of schizophreniform psychosis in that it may precipitate psychosis in vulnerable individuals. Method: We reviewed longitudinal studies of adolescents and young adults that examined the relations between self-reported cannabis use and the risk of diagnosis with a psychosis or of reporting psychotic symptoms. We also reviewed studies that controlled for potential confounders, such as other forms of drug use and personal characteristics that predict an increased risk of psychosis. We assessed evidence for the biological plausibility of a contributory causal relation. Results: Evidence from 6 longitudinal studies in 5 countries shows that regular cannabis use predicts an increased risk of a schizophrenia diagnosis or of reporting symptoms of psychosis. These relations persisted after controlling for confounding variables, such as personal characteristics and other drug use. The relation did not seem to be a result of cannabis use to self-medicate symptoms of psychosis. A contributory causal relation is biologically plausible because psychotic disorders involve disturbances in the dopamine neurotransmitter systems with which the cannabinoid system interacts, as demonstrated by animal studies and one human provocation study. Conclusion: It is most plausible that cannabis use precipitates schizophrenia in individuals who are vulnerable because of a personal or family history of schizophrenia.

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Objective: To explore the implications for mental health services, for health education about the risks of cannabis use, and for public policy toward cannabis use of observational evidence that cannabis use is a contributory cause of psychosis. Method: Using comparative analyses of similar evidence for the harmful effects of alcohol, tobacco, and amphetamine use, we considered the relation between observational evidence and action on cannabis. We examined arguments on the grounds of public health prudence for discouraging cannabis use by young individuals. With the assumption that the relation may be causal, we considered recommendations for policy in mental health services, health education, and public policy toward cannabis. Results: The observational evidence and biological plausibility of the hypothesis that cannabis is a contributory cause of psychosis is at least as strong as evidence for causal relations between heavy alcohol and amphetamine use and psychosis. On public health grounds, there is a good case for discouraging cannabis use among adolescents and young adults. It remains uncertain how best to discourage use and at whom campaigns to reduce cannabis use should be targeted. Conclusions: We should discourage young adults seeking treatment in mental health services from using cannabis and inform them of the probable mental health risks of cannabis use, especially of early and frequent use. We must exercise caution in liberalizing cannabis laws in ways that may increase young individuals' access to cannabis, decrease their age of first use, or increase their frequency of cannabis use. We should consider the feasibility of reducing the availability of high-potency cannabis products.

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Background: Cannabis use appears to exacerbate psychotic symptoms and increase risk of psychotic relapse. However, the relative contribution of cannabis use compared with other risk factors is unclear. The influence of psychotic symptoms on cannabis use has received little attention. Aims: To examine the influence of cannabis use on psychotic symptom relapse and the influence of psychotic symptom severity on relapse in cannabis use in the 6 months following hospital admission. Method: At baseline, 84 participants with recent-onset psychosis were assessed and 81 were followed up weekly for 6 months, using telephone and face-to-face interviews. Results: A higher frequency of cannabis use was predictive of psychotic relapse, after controlling for medication adherence, other substance use and duration of untreated psychosis. An increase in psychotic symptoms was predictive of relapse to cannabis use, and medication adherence reduced cannabis relapse risk. Conclusions: The relationship between cannabis use and psychosis may be bidirectional, highlighting the need for early intervention programmes to target cannabis use and psychotic symptom severity in this population. Declaration of interest: None. Funding detailed in Acknowledgements.

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Since the early 1970s, when cannabis first began to be widely used [1], the proportion of young people who have used cannabis has steeply increased and the age of first use has declined [2, 3]. Most cannabis users now start in the mid-to-late teens [1], an important period of psychosocial transition when misadventures can have large adverse effects on a young person's life chances.

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Cannabis sativa is the most frequently used of all illicit drugs in the United States. Cannabis has been used throughout history for its stems in the production of hemp fiber, for its seed for oil and food, and for its buds and leaves as a psychoactive drug. Short tandem repeats (STRs), were chosen as molecular markers because of their distinct advantages over other genetic methods. STRs are co-dominant, can be standardized such that reproducibility between laboratories can be easily achieved, have a high discrimination power and can be multiplexed. ^ In this study, six STR markers previously described for Cannabis were multiplexed into one reaction. The multiplex reaction was able to individualize 98 Cannabis samples (14 hemp and 84 marijuana, authenticated as originating from 33 of the 50 United States) and detect 29 alleles averaging 4.8 alleles per loci. The data did not relate the samples from the same state to each other. This is the first study to report a single reaction six-plex and apply it to the analysis of almost 100 Cannabis samples of known geographic collection site. ^

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Microsatellite markers were developed for Cannabis sativa L. (marijuana) to estimate the level of polymorphism, usefulness for DNA typing (genotype identification), and to measure the genetic relationships between the different plants. Twelve different oligonucleotide probes were used to screen an enriched microsatellite library of Cannabis sativa in which 49% of the clones contained microsatellite sequences. Characterization of microsatellite loci in Cannabis revealed that GA/CT was the most abundant class of isolated microsatellites representing 50% overall. Eleven polymorphic SSR markers were developed, derived from dinucleotide motifs and eight from trinucleotide motifs. A total of 52 alleles were detected averaging 4.7 alleles/locus. The expected heterozygosity of the eleven loci ranged between 0.368 and 0.710 and the common probability of identical genotypes was 1.8 x 107. The loci identified 27 unique profiles of the 41 Cannabis samples. The eleven microsatellite markers developed in this study were found to be useful for DNA fingerprinting and for assessing genetic relationships in Cannabis.

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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.