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Abstract

Cohort studies and meta-analyses have documented a robust association between cannabis use, heavy use, and misuse with future risk of schizophrenia. Despite adjusting for covariates, including current psychotic symptoms, other psychopathology, and social integration, the ability of these models to determine the degree to which cannabis causes schizophrenia is limited and dependent on their ability to capture all relevant confounders. When evaluating efforts to reduce cannabis use as a means of preventing schizophrenia, the proportion of this association that is causal is critical.