There is growing evidence of a link between the use of marijuana and mental disease.
Marijuana use at a young age significantly increased the risk of psychosis in young adulthood, Australian investigators reported.
Young adults who reported a longer duration since first exposure to marijuana had a two- to fourfold greater prevalence of three different psychosis-related outcomes, John McGrath, MD, PhD, of the Queensland Center for Mental Health Research in Wacol, and colleagues concluded in an article published online in Archives of General Psychiatry.
Several prospective-cohort studies have demonstrated an association between early marijuana use and an increased risk of psychosis. On the basis of such studies, reviews of the issue have generally concluded that early use of marijuana, or cannabis, is a modifiable risk factor for psychosis-related outcomes, the authors wrote.http://www.medpagetoday.com/Psychiatry/Addictions/18722
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Marijuana use at a young age significantly increased the risk of psychosis in young adulthood, Australian investigators reported.
Young adults who reported a longer duration since first exposure to marijuana had a two- to fourfold greater prevalence of three different psychosis-related outcomes, John McGrath, MD, PhD, of the Queensland Center for Mental Health Research in Wacol, and colleagues concluded in an article published online in Archives of General Psychiatry.
Several prospective-cohort studies have demonstrated an association between early marijuana use and an increased risk of psychosis. On the basis of such studies, reviews of the issue have generally concluded that early use of marijuana, or cannabis, is a modifiable risk factor for psychosis-related outcomes, the authors wrote.
More info from another article:
Several lines of evidence support the potential biologic plausibility of these links between cannabis use and psychosis. First, exogenous (eg, Δ-9-tetrahydrocannabinol) and endogenous cannabinoids (eg, anandamide) exert their effects (such as modulating the release of neurotransmitters including dopamine and glutamate) by interactions with specific cannabinoid (CB1) receptors that are distributed in brain regions implicated in schizophrenia. Second, several studies have shown an increased CB1 receptor density in brain regions of interest in schizophrenia, including the dorsolateral prefrontal cortex and the anterior cingulate cortex.[17,18] Third, other studies report elevated levels of endogenous cannabinoids in the blood and cerebrospinal fluid of patients with schizophrenia.[19-21] Fourth, acute, controlled administration of Δ-9-tetrahydrocannabinol causes both patients and controls to experience transient increases in cognitive impairments and schizophrenia-like positive and negative symptoms.[22] In summarizing these and many other findings, Fernandez-Espejo and colleagues[23] have suggested that the endocannabinoid system is altered in schizophrenia and that dysregulation of this system, perhaps induced by exogenous cannabis, can interact with neurotransmitter systems in a way so that a "cannabinoid hypothesis" can be integrated with other neurobiologic hypotheses (eg, those involving dopamine and glutamate).
Conclusion
In sum, a growing body of clinical and epidemiologic research suggests significant but complex links between cannabis use and psychosis. Concurrently, ongoing neurobiologic research is revealing findings in the endocannabinoid system that appear to support the biologic plausibility of such links. It should be noted that much of the research conducted to date does not allow for causal determinations. Ongoing research of varying designs will undoubtedly enlighten the field.
http://www.medscape.com/viewarticle/719139Conclusion
In sum, a growing body of clinical and epidemiologic research suggests significant but complex links between cannabis use and psychosis. Concurrently, ongoing neurobiologic research is revealing findings in the endocannabinoid system that appear to support the biologic plausibility of such links. It should be noted that much of the research conducted to date does not allow for causal determinations. Ongoing research of varying designs will undoubtedly enlighten the field.