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Cannabis use and the risk of developing a psychotic disorder.

Wayne Hall, Louisa Degenhardt

World psychiatry : official journal of the World Psychiatric Association (WPA) January 1, 2008 DOI: 10.1002/j.2051-5545.2008.tb00158.x via PubMed

Summary

AI-generated from the abstract

Regular cannabis use during adolescence and young adulthood predicts an increased risk of schizophrenia and psychotic symptoms, even after controlling for confounding factors like other drug use and personal characteristics. This relationship does not appear to be explained by self-medication for psychosis. A contributory causal role is biologically plausible because psychotic disorders involve disturbances in the dopamine system, which interacts with the cannabinoid system, as supported by animal studies and a human provocation study. The most plausible hypothesis is that cannabis use precipitates schizophrenia in individuals already vulnerable due to personal or family history.

Study at a glance

Characteristics Review Longitudinal Peer reviewed
Population Adolescents and young adults
Keywords Cannabis, psychosis Adolescents Dopamine Educational interventions Schizophrenia
Key finding Regular cannabis use predicts an increased risk of schizophrenia and psychotic symptoms, persisting after controlling for confounders, and is not explained by self-medication.

Abstract

WE BRIEFLY REVIEW THE EVIDENCE THAT CANNABIS USE IN ADOLESCENCE AND YOUNG ADULTHOOD IS A CONTRIBUTORY CAUSE OF SCHIZOPHRENIFORM PSYCHOSES, BY SUMMARISING LONGITUDINAL STUDIES THAT: a) have examined relationships between cannabis use and the risk of psychosis or psychotic symptoms; and b) have controlled for potential confounders, such as other forms of drug use and personal characteristics that predict an increased risk of psychosis. There is now reasonable evidence from longitudinal studies that regular cannabis use predicts an increased risk of schizophrenia and of reporting psychotic symptoms. These relationships have persisted after controlling for confounding variables such as personal characteristics and other drug use. The relationships did not seem to be explained by cannabis being used to self-medicate symptoms of psychosis. A contributory causal relationship is biologically plausible because psychotic disorders involve disturbances in the dopamine neurotransmitter system with which the cannabinoid system interacts, as has been shown by animal studies and a human provocation study. We briefly explore the clinical and public health implications of the most plausible hypothesis, that cannabis use precipitates schizophrenia in persons who are vulnerable because of a personal or family history of schizophrenia.

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