Exposure to cannabis increases the risk for psychoses ranging from transient psychotic states to chronic recurrent psychosis. Greater dose and earlier age of exposure raise the risk. For some psychosis outcomes, evidence supports some causality criteria, but reverse causality and confounders cannot be ruled out. Cannabis is neither necessary nor sufficient to cause psychosis; it is likely one of multiple causal components. In those with established psychosis, cannabis negatively affects the illness course and expression. Emerging evidence suggests alterations in the endocannabinoid system in psychotic disorders. Delaying or eliminating cannabis exposure could potentially reduce psychosis rates, especially in high-risk individuals.
Heavy, chronic cannabis use that begins early and is not accompanied by other drugs is associated with more psychosis-relevant symptoms and poorer cognitive performance. Users averaged over 30,000 lifetime cannabis exposures and scored higher on the Schizotypal Personality Questionnaire (mean 24 vs. 13) and lower on a composite cognitive test (mean -0.23 vs. +0.28) compared to matched non-user controls. Moderate to large deficits appeared in attention, psychomotor speed, working memory, cognitive flexibility, visuo-spatial processing, and verbal memory. A subsample of users also showed worse outcomes than their non-using siblings.