Hostname: page-component-586b7cd67f-t7fkt Total loading time: 0 Render date: 2024-11-28T14:27:00.583Z Has data issue: false hasContentIssue false

Correspondence

Published online by Cambridge University Press:  26 February 2008

MARTA DI FORTI
Affiliation:
Institute of Psychiatry, De Crespigny Park, London, UK (Email: [email protected])
Rights & Permissions [Opens in a new window]

Abstract

Type
Correspondence
Copyright
Copyright © 2008 Cambridge University Press

Letter to the Editor: Why do psychotic patients take cannabis?

In spite of the strictures of Macleod (Reference Macleod2007), previous research is generally in line with the report recently published by Degenhardt et al. (Reference Degenhardt, Tennant, Gilmour, Schofield, Nash, Hall and McKay2007), which provides further evidence to challenge the hypothesis that psychotic patients take cannabis to ameliorate their symptoms. For example, in both the population-based study of Henquet et al. (Reference Henquet, Krabbendam, Spauwen, Kaplan, Lieb, Wittchen and van Os2005) and in the large Dunedin birth cohort sample (Arseneault et al. Reference Arseneault, Cannon, Poulton, Murray, Caspi and Moffitt2002), psychotic symptoms failed to predict later cannabis use. Furthermore, the longitudinal cohort study from Christchurch, New Zealand specifically attempted to distinguish between the causal and self-medication hypotheses of cannabis use. The findings were that cannabis use increased risk of later psychosis, but the development of psychotic symptoms tended to decrease the subsequent consumption of cannabis (Fergusson et al. Reference Fergusson, Horwood and Ridder2005).

However, in contrast with the above studies, Ferdinand et al. (Reference Ferdinand, van der Ende, Bongers, Selten, Huizink and Verhulst2005) found that cannabis use predicted not only future psychotic symptoms in individuals who did not have such symptoms before they began using cannabis but also the reverse; the presence of psychotic symptoms in those who had never used cannabis predicted future cannabis use.

All the above studies have tried to disentangle self-medication, cannabis and psychosis, by applying sophisticated statistical techniques to longitudinal data. However, those studies did not directly ask psychotic patients or pre-psychotic patients why they smoked cannabis.

We know from the study of Arendt et al. (Reference Arendt, Rosenberg, Fjordback, Brandholdt, Foldager, Sher and Munk-Jørgensen2007), in which cannabis-dependent subjects were actually asked why they used cannabis, that the most frequently reported reasons for using cannabis are relaxation, pleasure seeking and the experience of being ‘high’. These reasons are similar to those given by cannabis users in the general population. Such effects may be particularly sought after in those with psychotic or quasi-psychotic symptoms. Kapur et al. (Reference Kapur, Mizrahia and Lia2005) asked a series of chronically treated psychotic patients how their antipsychotic medication affected their psychosis. Among the most common reported effects was that the medication ‘helps me stop thinking’ so that ‘the symptoms do not bother me so much’. It is possible that from the patients' viewpoint cannabis use is beneficial in decreasing preoccupation with psychotic symptoms while not decreasing or even increasing them on objective measures.

Thus, the evidence of worsening of psychotic symptoms when using cannabis is not incompatible with the self-medication hypothesis, if what patients achieve when smoking cannabis is a detachment, as Kapur would call it, from their symptoms, even when they are rated as more severe on objective measures such as the BPRS.

Declaration of Interest

None.

References

Arendt, M, Rosenberg, R, Fjordback, L, Brandholdt, J, Foldager, L, Sher, L, Munk-Jørgensen, P (2007). Testing the self-medication hypothesis of depression and aggression in cannabis-dependent subjects. Psychological Medicine 37, 935945.Google Scholar
Arseneault, L, Cannon, M, Poulton, R, Murray, R, Caspi, A, Moffitt, T (2002). Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study. British Medical Journal 325, 12121213.Google Scholar
Degenhardt, L, Tennant, C, Gilmour, S, Schofield, D, Nash, L, Hall, W, McKay, D (2007). The temporal dynamics of relationships between cannabis psychosis and depression among young adults with psychotic disorders: findings from a 10-month prospective study. Psychological Medicine 37, 927934.Google Scholar
Ferdinand, F, van der Ende, J, Bongers, I, Selten, J-P, Huizink, A, Verhulst, FC (2005). A cannabis psychosis pathway independent of other types of psychopathology. Schizophrenia Research 292, 289295.Google Scholar
Fergusson, DM, Horwood, LJ, Ridder, EM (2005). Tests of causal linkages between cannabis use and psychotic symptoms. Addiction 100, 354366.Google Scholar
Henquet, C, Krabbendam, L, Spauwen, J, Kaplan, C, Lieb, R, Wittchen, HU, van Os, J (2005). Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. British Medical Journal 330, 1114.Google Scholar
Kapur, S, Mizrahia, R, Lia, M (2005). From dopamine to salience to psychosis: linking biology, pharmacology and phenomenology of psychosis. Schizophrenia Research 79, 5968.Google Scholar
Macleod, J (2007). Cannabis use and symptom experience amongst people with mental illness: a commentary on Degenhardt et al. Psychological Medicine 37, 913916.Google Scholar