‘Gone to pot’: pharmacological evidence supporting the contribution of cannabinoid receptor function to psychosis
CRC Press eBooks June 25, 2004 DOI: 10.3109/9780203397978-21 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Commentary Peer reviewed |
|---|---|
| Citations | 1 |
| Key points | Argues that although cannabis has been associated with psychosis since at least 1845, the precise nature of this association remains unclear because existing evidence comes mainly from naturalistic studies limited by small or poorly selected samples, non-standardized assessments, self-reported psychosis, unconfirmed cannabis use, and retrospective designs that cannot establish prior psychiatric status. Proposes that laboratory studies could address some of these limitations. |
Abstract
The association between cannabis and psychosis is not a new one. It was described as far back as 1845 that use of hashish was associated with acute psychotic reactions that sometimes could last up to days.1 Since then several other studies support an association between cannabis and psychosis (reviewed in reference 2). However, the precise nature of the association remains unclear. The existing literature is based mainly on naturalistic studies. These data have limitations including inadequate patient selection and sample size, poorly defined inclusion criteria, absence of standardized assessments, a reliance on self-report of psychosis, lack of a urine toxicology to confirm cannabis use and exclude other drug use, and crude information about dose-response relations. Most importantly, some naturalistic studies cannot, because of their retrospective nature, confirm the psychiatric health status of individuals who later go on to develop psychosis. Some of these limitations can be addressed in laboratory studies.