Cannabis consumption and the risk of psychosis
Alice Mulè, Lucia Sideli, Giuseppe Colli, Laura Ferraro, Caterina La Cascia, Crocettarachele Sartorio, Fabio Seminerio, Giada Tripoli, Marta Di Forti, Daniele La Barbera, Robin Murray
Evidence-based Psychiatric Care, 2017, 3, 25-31
Enfin, un article récent (novembre 2018) explorant la co-occurence “consommation de cannabis / troubles “psychotique””, qui plus est international (anglo-italien), et comprenant, parmi les signataires, les célèbres Robin Murray du Kings Collège londonien, et Marta Di Forti de l’Université de Palerme, qui énonce clairement l’incapacité épidémiologique à établir un lien de causalité entre “consommation de cannabis et éclosion de troubles “psychotique”” !!! :
“Conclusions : The findings suggest that cannabis exposure, and especially daily cannabis consumption, is associated with the risk for psychosis; however, the retrospective study design does not allow drawing firm conclusions about causality.”
La cause de cette co-occurence peut effectivement être “imaginée” par rapport à une perturbation neurophysiologique des liens entre système endocannabinoide et “production” de psychose, mais, là encore, la recherche scientifique échoue à faire un lien de causalité incontestable, et la question du “terrain génétique” causal ou favorisant est loin d’être explicitée.
Par contre, l’hypothèse clinique de l’automédication” (encore plus chez les patients traités par des médicaments neuroleptiques et “antipsychotiques”) reste, au vu de la “science clinique”, une hypothèse principale étiologique de cette co-occurence.
Bien évidemment, nous ne remettons pas en cause le fait que la consommation de cannabis puisse constituer un paramètre “causal”, parmi d’autres, vis à vis de l’éclosion de “bouffées délirantes aiguës”, bien connues de longue date, au plan clinique, mais nous contestons ce lien causaliste “principal” soutenu par des chercheurs comme Robin Murray et al., entre consommation de cannabis et “éclosion” indiscutable, ou “création” de pathologies complexes comme la schizophrénie, dont l’étiologie, comprise aussi bien dans une perspective métapsychologique et psychodynamique, que comme “maladie neurodéveloppementale”, se “construit” dans la prime enfance.
Dr Christian Sueur
cf également, des mêmes auteurs :
Objectives : Cannabis is the most widely used illicit drug globally and its use has been linked to an increased risk for psychotic disorders. An association between cannabis consumption and psychotic symptoms was consistently reported by several studies. This case-control study aimed to widen the current findings about the impact of cannabis exposure on the risk of psychosis, by investigating the pattern of cannabis consumption in a sample of first-episode of psychosis (FEP) patients compared to healthy controls.
Material and methods : 68 individuals who presented for the first time to mental health services of Palermo (Italy) with an ICD-10 diagnosis of psychotic disorders and 74 healthy were enrolled as part of the Sicilian Genetics and Psychosis study. Psychopathological assessment and diagnosis were carried out by the Schedule for Clinical Assessment in Neuropsychiatry (SCAN). Socio-demographic data were collected by the modified version of the Medical Research Council (MRC) socio-demographic scale. All participants were interviewed using the Cannabis Experience Questionnaire – Modified Version to obtain a detailed assessment of lifetime patterns of cannabis and other illicit drug consumption. Logistic regression was applied to investigate the relationships between various aspects of cannabis use (lifetime use, age at first use, duration, and frequency of use) and case-control status while controlling for potential confounders.
Results : Patients started cannabis consumption about 3 years earlier than the control group (t = 3.1, p = 0.002) and were 8 times more likely to having started using cannabis before 15 years (adjusted OR = 8.0, 95% CI 2.4-27) than controls. Furthermore cases were more likely to smoke more frequently than controls (adjusted OR = 4.4, 95% CI 1.08-18). We did not find a difference in duration of cannabis use between cases and controls.
Conclusions : The findings suggest that cannabis exposure, and especially daily cannabis consumption, is associated with the risk for psychosis; however, the retrospective study design does not allow drawing firm conclusions about causality.
Key words : cannabis, schizophrenia, psychosis, tetrahydrocannabinol, drug and schizophrenia
Cannabis exposure has been associated to an increased risk of developing psychosis. Cannabis is the most popular illicit drug worldwide, and although most people who smoke cannabis do not become psychotic, evidence from the literature supports an association between cannabis use and an increased risk of developing a psychotic disorder 1 2.
The main psychoactive component, which is responsible of the psychotogenic effect of cannabis, is Δ9-tetrahydrocannabinol (Δ9-THC). The other main constituent of cannabis is cannabidiol (CBD) which has antianxiety and antipsychotic properties 3 4. Recently, high potency varieties of cannabis, such as “skunk” (sensimilla), have become available in the market over much of Europe. Such varieties of cannabis contain a high concentration of THC and a lower proportion of CBD which seems to “balance” the psychotogenic effect of the former 3 4.
Cannabis intoxication can cause brief psychotic episodes or may exacerbate pre-existing psychotic symptoms 5 6. It has been shown that healthy people who are administered THC intravenously were more likely to develop transient psychotic-like experiences and that THC worsens psychotic symptoms in people suffering from psychosis 7. THC exerts its psychotogenic role by modulating the dopamine neurotransmission, which is involved in development of psychotic symptoms.
The first report suggesting that cannabis might be a risk factor for psychosis was the Swedish Conscript study. This was a 15 year follow-up of a cohort of 45.570 conscripts into the armed forces. The risk of schizophrenia was 2.3 fold higher among subjects who had used cannabis by 18 years and there was a dose response relationship, as the risk of developing schizophrenia was even higher in those who had smoked cannabis more frequently 8. Subsequently, a series of cohort studies have shown that cannabis use generally predates psychosis 9-13. For instance, the Dunedin cohort study reported that children and adolescents who had used cannabis by the age of 15 years were 4.5 times more likely to develop schizophreniform psychosis at the age of 26 years 9. van Os et al. reported a three times higher risk of developing psychotic symptoms in the general population associated to cannabis consumption 12. Two meta-analyses concluded that cannabis consumption was associated with approximately two-fold increased risk of developing a psychotic disorder 1 2.
Individuals who showed any evidence of psychosis proneness appear especially vulnerable, as those who started using cannabis in early adolescence. A meta-analysis by Large et al. supported the association between cannabis consumption and an earlier age at first presentation of psychosis 14. Other studies confirmed that cannabis use is associated to an earlier age at first presentation of schizophrenia and that there is an interaction between cannabis use and gender difference in age at first presentation, in the way that the difference by gender in age at first presentation is reduced in cannabis users 15.
Furthermore, recent evidence shows that high potency cannabis and higher frequency of use are associated with a higher risk of developing psychosis 3. However, only a small proportion of cannabis users develop psychotic symptoms or schizophrenia. Cannabis users who develop psychosis may have an underlying genetic susceptibility, and some gene polymorphisms have been associated to an increased risk to develop psychosis 16-21; nevertheless, these results need to be further replicated.