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Cannabis and psychosis: what is the link?

Mohamed Ben Amar, Stéphane Potvin

Journal of psychoactive drugs June 1, 2007 DOI: 10.1080/02791072.2007.10399871 via PubMed

Summary

AI-generated from the abstract

Cannabis consumption appears to increase the risk of psychotic symptoms, but whether it causes psychosis remains uncertain. A review of ten epidemiological studies found that three supported a causal link between cannabis use and diagnosed psychosis, five suggested chronic use increases psychotic symptoms without leading to diagnosed psychosis, and two found no causal relationship. Heavy consumption, prolonged use, early exposure, and underlying psychotic vulnerability may contribute. Potential neurobiological mechanisms involve dopamine, endocannabinoids, and brain growth factors. Uncertainty persists due to challenges in measuring cannabis use and psychosis, possible reverse causality, and residual confounding factors.

Study at a glance

Characteristics Systematic review Longitudinal Peer reviewed
Key finding Evidence suggests cannabis use increases the risk of psychotic symptoms, but the causal nature of the association with diagnosed psychosis remains unclear.

Abstract

Growing evidence supports the hypothesis that cannabis consumption is a risk factor for the development of psychotic symptoms. Nonetheless, controversy remains about the causal nature of the association. This review takes the debate further through a critical appraisal of the evidence. An electronic search was performed, allowing to identify 622 studies published until June 1st 2005. Longitudinal studies and literature reviews were selected if they addressed specifically the issues of the cannabis/psychosis relationship or possible mechanisms involved. Ten epidemiological studies were relevant: three supported a causal relationship between cannabis use and diagnosed psychosis; five suggested that chronic cannabis intake increases the frequency of psychotic symptoms, but not of diagnosed psychosis; and two showed no causal relationship. Potential neurobiological mechanisms were also identified, involving dopamine, endocannabinoids, and brain growth factors. Although there is evidence that cannabis use increases the risk of developing psychotic symptoms, the causal nature of this association remains unclear. Contributing factors include heavy consumption, length and early age of exposure, and psychotic vulnerability. This conclusion should be mitigated by uncertainty arising from cannabis use assessment, psychosis measurement, reverse causality and control of residual confounding.

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