Cannabis and psychosis

Abstract

There has been considerable debate about the reasons for the association observed between cannabis use and psychosis in both clinical and general population samples. Among the hypotheses proposed to explain the association are the following: 1) common factors explain the co-occurrence; 2 cannabis causes psychosis that would not have occurred in the absence of cannabis use; 3) cannabis precipitates psychosis among persons who were vulnerable to developing the disorders; 4) cannabis use worsens or prolongs psychosis among those who have already developed the disorder; and 5) that persons with psychosis are more likely to become regular or problematic cannabis users than persons without psychosis. This article evaluates the evidence on each of these hypotheses, including recent research on the role of the cannabinoid receptor system in schizophrenia. The evidence suggests that common factors do not explain the comorbidity between cannabis use and psychosis, and it is unlikely that cannabis use causes psychosis among persons who would otherwise not have developed the disorder. The evidence is more consistent with the hypotheses that cannabis use may precipitate psychosis among vulnerable individuals, increase the risk of relapse among those who have already developed the disorder, and may be more likely to lead to dependence in persons with schizophrenia.

The CB receptor agonist WIN 55,212-2 fails to elicit disruption of prepulse inhibition of the startle in Sprague-Dawley rats

“…Interestingly, such an interpretation would complement clinical observations suggesting that genetic factors play a role in determination of effects and rewarding properties of cannabis in humans (Lyons et al 1997) and would also confirm clinical evidence according to which cannabis may precipitate psychosis only in vulnerable individuals (Degenhardt and Hall 2002). Independent of the neurobiological issue, however, clinical inferences can be drawn from our data that temper Schneider and Koch's interpretation of disruptive effects of WIN on sensorimotor gating.…”

Who Seeks Treatment for Dual Disorders? Observations from a Dual Disorder Clinic at the National Drug Dependence Treatment Centre in India Over a 12 Year Period

“…Cannabis was associated with the emergence of psychotic disorders, the mechanisms of which might have several facets (29,30). The likelihood of a psychotic patient consuming alcohol or opiates was lower, probably a reflection of cannabis playing a prominent role in the genesis of psychosis.…”

No changes in densities of cannabinoid receptors in the superior temporal gyrus in schizophrenia

“…[1,2] . These psychiatric effects of cannabis are likely to be mediated by cannabinoid CB1 receptor, since many of the psychological effects of marijuana are reversed by SR141716A, a selective CB1 receptor antagonist [3] .…”

“…These psychiatric effects of cannabis are likely to be mediated by cannabinoid CB1 receptor, since many of the psychological effects of marijuana are reversed by SR141716A, a selective CB1 receptor antagonist [3] . In addition, cannabis consumption may precipitate psychosis among vulnerable individuals, and provoke relapse and exacerbates symptoms among those who have already developed schizophrenia [1,4] . Following the finding of central cannabinoid receptors and endogenous cannabinoids [5,6] , a cannabinoid hypothesis has been proposed [7,8] .…”