Epidemiological, neurobiological, and genetic clues to the mechanisms linking cannabis use to risk for nonaffective psychosis.
Epidemiological studies have shown that the association between cannabis and psychosis is robust and consistent across different samples, with compelling evidence for a dose-response relationship. Because longitudinal work indicates that cannabis use precedes psychotic symptoms, it seems reasonable to assume a causal relationship. However, more work is needed to address the possibility of gene-environment correlation (for example, genetic risk for psychosis causing onset of cannabis use). Moreover, knowledge about underlying biological mechanisms linking cannabis use and psychosis is still relatively limited. In order to understand how cannabis use may lead to an increased risk for psychosis, in the present article we (a) review the epidemiological, neurobiological, and genetic evidence linking cannabinoids and psychosis, (b) assess the quality of the evidence, and finally (c) try to integrate the most robust findings into a neurodevelopmental model of cannabis-induced psychosis and identify the gaps in knowledge that are in need of further investigation.
Department of Psychiatry and Psychology, School of Mental Health and Neuroscience, European Graduate School of Neuroscience (EURON), South Limburg Mental Health Research and Teaching Network (SEARCH), Maastricht University Medical Center, Maastricht, The Netherlands; email: ruud.vanwinkel@maastrichtuniversity.nl.
Ruud
R
van Winkel
Rebecca
R
Kuepper
D017668:Age of Onset; D001921:Brain / Q000503:physiopathology*; D015984:Causality; D063388:Endocannabinoids / Q000502:physiology; D059647:Gene-Environment Interaction; D006801:Humans; D008385:Marijuana Smoking / Q000453:epidemiology* / Q000235:genetics / Q000503:physiopathology; D011618:Psychotic Disorders / Q000453:epidemiology* / Q000235:genetics / Q000503:physiopathology; D012307:Risk Factors
D063388:Endocannabinoids