Cannabis and psychosis: Let's start from the null hypothesis

EDITOR—Fergusson at al say that it is better to reach interim conclusions about the relation between cannabis and psychosis despite the uncertain evidence.1 This is contrary to the scientific principle of starting from the null hypothesis. The null hypothesis should be overturned only 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. The authors say 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 exposure to Δ⁹-tetrahydrocannabinol 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.