Cannabis and Psychosis: A Genetically-Informed Perspective скачать в хорошем качестве

Cannabis and Psychosis: A Genetically-Informed Perspective

February 26, 2026 At the February CMCR Investigators’ Meeting, Emma Johnson, Ph.D., Assistant Professor of Psychiatry at Washington University School of Medicine, presented a genetically informed perspective on the relationship between cannabis use and psychosis. She examined whether associations between cannabis use and schizophrenia reflect causal effects, shared genetic liability, or both. Drawing on large genomewide association studies (GWAS), Dr. Johnson reviewed evidence that cannabis use behaviors are complex and polygenic. Both lifetime cannabis use and cannabis use disorder (CUD) show moderate genetic correlations with schizophrenia, suggesting overlapping genetic risk. Cross-trait analyses identified overlapping genetic regions linked to schizophrenia, cannabis use disorder, and tobacco use, many of which involve genes that are active in the brain. However, shared genetic liability does not rule out causal effects. Epidemiologic data continue to support dose-response relationships, particularly for heavy, high-potency, or early-onset use. Dr. Johnson emphasized that causal and genetic vulnerability models are not mutually exclusive. She then presented new findings from the All of Us Research Program. Lifetime and more frequent cannabis use were associated with psychotic-like experiences, including perceptual distortions and referential ideation. Modest evidence suggested that schizophrenia polygenic risk may amplify some associations. However, individuals with higher genetic risk were also more likely to use cannabis, indicating gene–environment correlation that complicates interpretation. Finally, Dr. Johnson highlighted the importance of accounting for polysubstance use, noting independent associations of methamphetamine and tobacco use with certain psychotic-like symptoms. In closing, she argued that the cannabis–psychosis relationship likely reflects both shared genetic architecture and independent exposure effects. Larger, better-phenotyped studies will be essential to clarify mechanisms and guide clinical and public health decision-making.