Evidence for the effectiveness of treatment or secondary prevention of psychotic illness such as schizophrenia is often disappointing. This situation reflects our limited understanding of the aetiology of psychosis.

There is good evidence that both genetic and environmental factors are implicated but the precise identity of these is unclear. Cannabis use is one candidate as a possible, modifiable environmental influence on both incidence and prognosis of psychosis.

Evidence supporting this candidature is exclusively observational, and its strength has perhaps been overestimated and problems related to its interpretation underestimated by some. Nevertheless the possibility that cannabis does cause psychosis remains. Because of this, and because there are other good public health reasons to prevent cannabis use, interventions targeting use need to be evaluated.

This evaluation, along with other imaginative approaches to future research, is needed to further our understanding of the determinants of mental illness and how we can most effectively improve the population’s mental health.

Psychosis is a symptom of severe mental illness characterised by impairment of thought and perception, leading to disconnection from objective reality. Several severe mental illness phenotypes (e.g. bipolar disorder and severe depression) involve psychosis but, contemporary arguments about the classification of mental illness aside, the quintessential psychotic illness is schizophrenia. Schizophrenia is estimated to be the fourth most important cause of life-years lost through disability in the world and it has been described as the ‘leading unsolved disease afflicting humans’ (Carpenter, 2003). There is good evidence that both genetic and environmental factors contribute to the aetiology of schizophrenia, but which genes, what aspects of the environment and whether these interact in important ways remains unclear (Ma"ki et al, 2005). Many environmental exposures have been proposed as causes of schizophrenia, with the initial hope and enthusiasm accompanying the emergence of these hypothesised causes later turning to disappointment and scepticism as subsequent evidence fails to support their candidacy.

An association between cannabis use and psychosis was first observed several decades ago (Negrete, 1988). More recently, results from several large population-based prospective observational studies have reported associations between a range of cannabis use phenotypes and a variety of measures of psychotic experience (Macleod et al, 2004a).

In the largest (and oldest) of these studies, cannabis use in late adolescence was associated with an increased risk of a subsequent diagnosis of schizophrenia (Andreasson et al, 1987).

It is important that clinicians and population health scientists consider the meaning of this evidence and its implications for both policy and clinical practice. This task is made more pressing by the fact that cannabis use is now widespread. Since the late 1960s cannabis use has increased substantially in most high-income countries (Hickman et al, 2007).

The increase may now be levelling off, but this is hardly a reason for complacency. Cannabis is now well established as the third most widely used psychoactive drug (after alcohol and tobacco) in Europe, the USA and Australasia (Advisory Council on the Misuse of Drugs, 2006).

In the UK around half of adolescents will use cannabis at least once and about a fifth of them will use it regularly (monthly or more frequently) in young adulthood. Prior assumptions that most of these will subsequently ‘grow out of’ this pattern of use have no firm evidential basis. Irrespective of any direct effects of cannabis use on physical or mental health, use exposes users to risks of criminalisation, as in most jurisdictions cannabis use is illegal.

Against this background we can now consider the competing, although not necessarily mutually exclusive, reasons why an association between cannabis use and psychosis might be apparent.

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.

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