Youth at clinical high-risk for psychosis report more lifetime, past-six-month, and baseline cannabis use than healthy controls, along with greater frequency, severity, and rates of cannabis use disorder. Among high-risk youth, those who use cannabis show higher baseline grandiosity and lower social anhedonia at 12 months. Cannabis use severity was unrelated to clinical status at two years and did not distinguish those who later developed psychosis from those who did not. The small number of cannabis users in the high-risk group limited statistical power.
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.