Consensus paper of the WFSBP task force on cannabis, cannabinoids and psychosis
D. D’souza, M. Diforti, S. Ganesh, T. George, Wayne Hall, C. Hjorthøj, O. Howes, M. Keshavan, Robin M. Murray, Timothy Nguyen, G. Pearlson, M. Ranganathan, A. Selloni, N. Solowij, E. Spinazzola
World Journal of Biological Psychiatry March 22, 2022 DOI: 10.1080/15622975.2022.2038797 via Semantic Scholar
Summary
AI-generated from the abstractExposure 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.
Study at a glance
| Characteristics | Review Peer reviewed |
|---|---|
| Keywords | Medicine Psychology |
| Key finding | Exposure to cannabis increases the risk for psychoses, with greater dose and earlier age of exposure raising the risk, but cannabis is neither necessary nor sufficient to cause psychosis. |
Abstract
Abstract Objectives The liberalisation of cannabis laws, the increasing availability and potency of cannabis has renewed concern about the risk of psychosis with cannabis. Methods The objective of the WFSBP task force was to review the literature about this relationship. Results Converging lines of evidence suggest that exposure to cannabis increases the risk for psychoses ranging from transient psychotic states to chronic recurrent psychosis. The greater the dose, and the earlier the age of exposure, the greater the risk. For some psychosis outcomes, the evidence supports some of the criteria of causality. However, alternate explanations including reverse causality and confounders cannot be conclusively excluded. Furthermore, cannabis is neither necessary nor sufficient to cause psychosis. More likely it is one of the multiple causal components. In those with established psychosis, cannabis has a negative impact on the course and expression of the illness. Emerging evidence also suggests alterations in the endocannabinoid system in psychotic disorders. Conclusions Given that exposure to cannabis and cannabinoids is modifiable, delaying or eliminating exposure to cannabis or cannabinoids, could potentially impact the rates of psychosis related to cannabis, especially in those who are at high risk for developing the disorder.