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French

ID: <

10.7202/008536ar

>

·

DOI: <

10.7202/008536ar

>

Where these data come from
Schizophrenia and cannabinoids: Clinical, experimental and biological data

Abstract

In the ongoing debate regarding the legal status of cannabis, much emphasis has been put on the consequences of this psychoactive substance. Much less attention has been paid, however, to the very nature of cannabis intoxication. Interestingly, following a close review of the literature, it appears that cannabis pharmacology shares much in common with schizophrenia.Being a dysleptic, cannabis has psychotomimetic properties. According to the circumstances, it produces effects that remind diverse schizophrenic dimensions. Acutely, cannabis disrupts cognition similarly to what is observed in schizophrenia. Chronically, its effects (the controversial amotivational syndrome) show resemblance with the negative symptoms of this psychopathology. Among its adverse effects, cannabis can induce, in rare occasions, a transient psychosis that mimics the positive symptoms of schizophrenia.Incidentally, schizophrenic patients seem to be particularly sensitive to cannabis. In fact, they are six times more likely to develop a cannabis disorder, compared to the general population. Different models try to explain this particular comorbidity, the principal one being the self-medication model. Against this hypothesis however, the data currently available demonstrates that cannabis consumption increases the rates of relapses and hospitalisations of schizophrenic patients.On the biological level, some disturbances of the endogenous cannabinoid system in schizophrenic patients have been shown recently. Along these observations, the scientific community was hoping that the blockade of the CB1 receptor, the principal cannabinoid receptor, would act as an antipsychotic. However, rimonabant, a CB1 antagonist, has failed in a phase II clinical study. Researchers now shift their attention to uptake inhibitors of anandamide, the best known endocannabinoid.

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