Cannabis and psychosis
BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.332.7534.172 (Published 19 January 2006) Cite this as: BMJ 2006;332:172All rapid responses
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I understood that the high incidence of schizophrenia in
afrocaribbeans was linked to their cultural use of smoking cannabis. I
qualified in 1960. Am I out of date?
Competing interests:
None declared
Competing interests: No competing interests
Recent studies and clinical experience have shown that at least half
of all UK teenagers use some cannabis. Colleagues from countries which
abjure alcohol report high levels of recreational cannabis use. Certain
Caribbean countries use cannabis regularly. How come the incidence of
psychosis is the same for all these populations?
Many but not all in our secure unit use cannabis, but so do many more
outside it. Cannabis appears to worsen psychosis in the mentally ill but
not in their mentally stable peers.
Competing interests:
None declared
Competing interests: No competing interests
Cannabis and brain disorder
I am afraid the logic of Fergusson at al1 will not do. They suggest that it is better to reach interim conclusions about the relationship between cannabis and psychosis despite the uncertain evidence. This is contrary to the scientific principle of starting from the null hypothesis. The null hypothesis should only be overturned if there is sufficient evidence.
Moreover, the argument they use to tip the balance in favour of a causal association depends on biased evidence about the neurobiological basis of psychotic disorders, such as schizophrenia. They suggest that the dopamine system is known to have a key role in the development of psychotic symptoms. However, unequivocal evidence of a hyperactivity of dopaminergic neurotransmission in schizophrenia has not been found.2 It is pure speculation for Fergusson et al to suggest that repeated A9-tetrahydrocannabinol exposure may lead to permanent changes in transmitter function. Let's wait to see if the Val/Val variant of the COMT gene really increases the strength of association of cannabis and psychosis.3 Many behavioural genetic studies have not been replicated,4 and this finding needs to be confirmed. The effects of cannabis on dopamine processing in the brain do not necessarily cause psychosis, as dopamine activity may be normal in psychosis.
The problem of interpretation arises because of the hypothesis of brain abnormality as the primary cause of mental disorder.5 I am not saying that cannabis does not cause emotional problems; nor that people do not use it to deal with their emotional problems. Cannabis use is likely to be a proxy measure for poor premorbid adjustment associated with psychosis. Focusing on cannabis as a potential aetiological factor should not but may avoid understanding of the psychosocial origins of psychosis.
1. Fergusson DM, Poulton R, Smith PF, Boden JM. Cannabis and psychosis. BMJ 2006;332: 172-5.[Full Text]
2. Reynolds, G.P. Beyond the dopamine hypothesis. The neurochemical pathology of schizophrenia. British Journal of Psychiatry 1989;155: 305-16
3. Caspi A, Moffitt T, Cannon M, McClay J, Murray R, Harrington H, et al. Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-o-methyltransferase gene: Longitudinal evidence of a gene x environment interaction. Biol Psychiatry 2005;57: 1117-27
4. Moldin, S.O. The maddening hunt for madness genes. Nature Genetics, 1997;17: 127-9
5. Double D. The limits of psychiatry. BMJ 2002;324: 900-4 [Full text]
Competing interests:
None declared
Competing interests: No competing interests