Arseneault et al (Reference Arseneault, Cannon and Witton2004) very accurately reviewed recent epidemiological data and concluded that cannabis use should now be considered as a component cause leading to psychosis. Yet at least two unanswered questions remain. How can cannabis lead to psychosis? Are some subjects specifically vulnerable to the psychotogenic effect of cannabis?
Several studies, including the Dunedin study, have suggested that adolescents are more vulnerable to cannabis (Reference Arseneault, Cannon and WittonArseneault et al, 2004). Interestingly, the effects of cannabis on cognitive function also seem more pronounced in adolescents (Reference Ehrenreich, Rinn and KunertEhrenreich et al, 1999; Reference Pope, Gruber and HudsonPope et al, 2003). This difference might also reflect pre-existing differences in cognitive ability between groups.
Cannabis interferes with endocannabinoid systems, known to be involved in neurodevelopment. In rats, chronic cannabinoid treatment during puberty induces behavioural and cognitive changes that are not found when the treatment is done in adulthood (Reference Schneider and KochSchneider & Koch, 2003).
Together, these observations are compatible with the idea that cannabis consumption could alter the last steps of brain maturation, leading to cognitive dysfunction and, in turn, enhancing the risk of psychosis. On the other hand, we recently suggested that genetic variants of the cannabinoid receptor type 1 could be associated with a specific sensitivity to cannabis (Reference Krebs, Leroy and DuauxKrebs et al, 2002). Further studies are now needed to identify subjects ‘highly sensitive’ to the psychotogenic effect of cannabis, by coupling genetic analysis and cognitive testing to prospective follow-up.
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