The first, and perhaps most obvious, possibility is that cannabis may cause psychosis. Plausible neurophysiological mechanisms that might mediate such an effect have been described. Broadly, psychosis may be a disorder of dopamine metabolism and cannabis is one of many substances that appear to influence dopamine metabolism (Hall & Solowij, 1998).

Cannabis use could also cause psychosis through social mechanisms: aspects of the social environment have also been proposed as causes of schizophrenia (Maki et al, 2005); and cannabis use may give entry to social situations that the user would not be in were it not for their use of the drug. However, as Austin Bradford Hill suggested in his original essay on causal attribution and as has been reiterated more recently, apparent mechanistic plausibility is generally the weakest test of any causal hypothesis (Hill, 1965; Petitti, 2004).

It is seldom difficult to mobilise a broadly plausible mechanism through which even the most unlikely causal relations might arise. Similarly, the precise mechanism through which demonstrably causal relations do arise is frequently the subject of continuing discussion (Bellosta et al, 2000; Beckman & Creager, 2006).

Psychosis might cause cannabis use

It is also possible that psychosis may cause cannabis use, an idea variously referred to as the ‘reverse causality’ or ‘self-medication’ hypothesis. Some aspect of the experience of psychosis may increase the likelihood that a person will use cannabis, through social, neurochemical or other mechanisms. More narrowly, people who are psychotic may use cannabis to in some way ameliorate the unpleasant aspects of their experience (Macleod, 2007). It seems unlikely that this self-medication would be directed at positive psychotic symptoms in themselves, since acute cannabis intoxication increases rather than decreases unusual thoughts and perceptions. Cannabis use, however, may have other effects valued by users, either effects of the drug itself or those arising out of the social milieu surrounding use (Gregg et al, 2007).

John Macleod

John Macleod’s clinical interest in problem drug use dates from his work in Edinburgh in the 1990s as a general practitioner and as medical officer for a street sex-workers’ outreach project. Supported by the Wellcome Trust, he trained in epidemiology at the London School of Hygiene and Tropical Medicine, after which he worked as a GP in Birmingham, where he undertook epidemiological research at the University. He is now Reader in Clinical Epidemiology and Primary Care at the University of Bristol (Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Road, Bristol BS8 2PR, UK. Email: .(JavaScript must be enabled to view this email address)). He is involved in ongoing studies of the causes and consequences of drug use based in Edinburgh and Bristol.

References

_{Advisory Council on the Misuse of Drugs (2006) Pathways to Problems . Home Office.}

Ames, B. N. & Gold, L. S. (1997) The causes and prevention of cancer: gaining perspective. Environmental Health Perspectives,105 (suppl. 4), 865–873.

Amos, A., Wiltshire, S., Bostock, Y., et al (2004) ‘You can’t go without a fag ... you need it for your hash’: a qualitative exploration of smoking, cannabis and young people. Addiction, 99, 77–81.

Andreasson, S., Allebeck, P., Engstrom, A., et al (1987) Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. Lancet, ii, 1483–1486.

Anthony, J. C., Neumark, Y. D. & Van Etten, M. L. (2000) Do I do what I say? A perspective on self-report methods in drug dependence epidemiology. In The Science of Self-report: Implications for Research and Practice (eds A. A. Stone, J. S. Turkkan, C. A. Bachrach, et al), pp. 175–198. Lawrence Erlbaum.

Arseneault, L., Cannon, M., Poulton, R., et al (2002) Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study. BMJ, 325, 1212–1213.