Cannabis and Psychosis: a Critical Overview of the Relationship.
Current psychiatry reports February 1, 2016 DOI: 10.1007/s11920-015-0657-y via PubMed
Summary
AI-generated from the abstractA review of recent research on cannabis and psychosis examines two competing hypotheses: cannabis as a contributing cause of psychosis and a shared vulnerability between cannabis use and psychosis. The evidence suggests that cannabis does not in itself cause a psychotic disorder. Instead, both early and heavy cannabis use are more likely in individuals who already have a vulnerability to psychosis. The role of early and heavy cannabis use as a prodromal sign, along with other problem behaviors such as early or heavy use of cigarettes or alcohol and poor school performance, merits further examination. Future studies focusing solely on the cannabis-psychosis association will be of little value in understanding psychosis.
Study at a glance
| Characteristics | Review Peer reviewed |
|---|---|
| Topics | Cannabis |
| Keywords | Cognition Mental illness Psychotic disorder Schizophrenia |
| Key finding | Cannabis does not in itself cause a psychosis disorder; early and heavy use are more likely in individuals with a vulnerability to psychosis. |
Abstract
Interest in the relationship between cannabis use and psychosis has increased dramatically in recent years, in part because of concerns related to the growing availability of cannabis and potential risks to health and human functioning. There now exists a plethora of scientific articles addressing this issue, but few provide a clear verdict about the causal nature of the cannabis-psychosis association. Here, we review recent research reports on cannabis and psychosis, giving particular attention to how each report provides evidence relating to two hypotheses: (1) cannabis as a contributing cause and (2) shared vulnerability. Two primary kinds of data are brought to bear on this issue: studies done with schizophrenic patients and studies of first-episode psychosis. Evidence reviewed here suggests that cannabis does not in itself cause a psychosis disorder. Rather, the evidence leads us to conclude that both early use and heavy use of cannabis are more likely in individuals with a vulnerability to psychosis. The role of early and heavy cannabis use as a prodromal sign merits further examination, along with a variety of other problem behaviors (e.g., early or heavy use of cigarettes or alcohol and poor school performance). Future research studies that focus exclusively on the cannabis-psychosis association will therefore be of little value in our quest to better understand psychosis and how and why it occurs.