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June 5, 2019

Insights Into the Pathophysiology of Endocannabinoid Signaling in Schizophrenia

Author Affiliations
  • 1Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania
  • 2Veterans Integrated Service Network 4 Mental Illness Research Education and Clinical Center, Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, Pennsylvania
  • 3Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania
JAMA Psychiatry. 2019;76(9):887-888. doi:10.1001/jamapsychiatry.2019.0844

Changes in state laws that have made cannabis more available for medical indications or recreational use have raised concerns about potential unintended negative societal consequences of cannabis use. For example, epidemiologic studies have reported associations between cannabis use and schizophrenia, including a greater risk of developing the disorder, an earlier age at onset, more severe symptoms, and more frequent hospitalizations.1 Furthermore, a 2018 large-scale genome-wide association study2 reported that genetic risk for schizophrenia is also associated with a causal positive risk for cannabis use, suggesting a deleterious interaction in which individuals at risk for the disorder are more likely to start using cannabis during susceptible periods of life such as adolescence, leading to more adverse consequences.2 Consequently, understanding the pathophysiologic mechanism(s) by which cannabis use may affect the onset and course of schizophrenia requires an understanding of the status of the neural target of cannabis, the endogenous cannabinoid (endocannabinoid) system, in individuals with schizophrenia.

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