In positing mechanisms that link cannabis use to psychosis, the role of reverse causation has been largely eliminated (31; 54–56). In contrast, the causal hypothesis has received significant attention. Causation has been strongly asserted on account of longitudinal studies showing a persisting association between cannabis use and psychosis even after accounting for confounders as well as preexisting psychotic symptoms (57–60). Unfortunately, these studies have had limited ability to control for genetic factors as twin studies adequately powered to study psychotic illness are rare. Additionally, the causal mechanisms that underpin this relationship are likely to be complex. Persuasive support for this arises from the observation that during periods of increasing cannabis use, rates of psychosis have remained fairly constant (61; 62). If cannabis use caused psychosis, a significantly higher rate of the latter would be expected.
