Cannabis consumption around puberty has long been discussed as an inducer drug of schizophrenia or, alternatively, as desperate self-medication during psychotic episodes or during the disease prodrome. Nowadays, it is quite safe to say that despite some truth to both views, cannabis can induce schizophrenia in predisposed individuals, dose-dependently lead to earlier disease onset, and act as trigger of psychotic relapses. But it can also result in amotivational behavior, social withdrawal or cognitive deficits upon peripubertal use. Here, a specific and highly relevant responsibility of psychiatry arises, and awareness among essentially all clinicians and in the general public needs to grow. Legalizing cannabis may not send the right message to the public.
Robin Murray, a leading pioneer in this field, will give us an update on the long-term relationship between cannabis and psychoses. Beat Lutz will motivate the audience to understand the basics of the brain cannabinoid system. Hannelore Ehrenreich will speak about juvenile cannabis consumption as risk factor of behavioural abnormalities and mental illness. Delineating an important and urgent task for psychiatry, bill Honer will talk about cannabis use and its consequences after its legal release in Canada.
Cannabis and psychosis: news from a long-term relationship
Robin Murray, London (United Kingdom)
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Robin Murray, London (United Kingdom)
Both genetic and environmental factors are involved in causing psychotic conditions like schizophrenia. 11 out of 13 longitudinal prospective studies of young people in the general population have shown that those who use marijuana (cannabis) have a significantly greater risk of developing psychosis than non-users; the other two showed a trend. Of course, only a minority of cannabis users will develop psychosis. Some people appear genetically susceptible, and those who start using in their early teens appear also particularly vulnerable.
Our experimental studies demonstrate that IV administration of tetrahydrocannibinol (THC), the active ingredient of cannabis, can induce a transient psychosis in normal volunteers However, pretreatment with cannibidiol (CBD), before administering the THC, largely blocked the psychotogenic effects of THC. This fits with the clinical evidence that CBD has antipsychotic properties and the clinical evidence that high THC and low CBD varieties of cannabis carry a greater risk of psychosis than traditional marijuana, which has not only lower THC concentration but also substantial CBD.
We have recently studied cannabis use and its risk-increasing effect on psychosis in 16 centres across Europe in the EU-GEI study. Not only did the frequency of use differ widely but so did the potency of the cannabis used with the highest THC concentration cannabis being reported from Holland and England; he latter appeared to have the greatest effect on the incidence of psychosis. Use of stimulants such as amphetamine was also associated with psychosis. Use of synthetic cannabinoids was less common but is now being reported to be associated with an even greater risk of acute psychotic reactions.
Juvenile cannabis consumption as risk factor of behavioural abnormalities and mental illness
Hannelore Ehrenreich, Göttingen (Germany)
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Hannelore Ehrenreich, Göttingen (Germany)
Background: Pre-adult exposure to environmental risk factors shapes individual behavior and contributes to mental illness. We reported previously that accumulated environmental risk dramatically decreases age at schizophrenia onset. Risk factors in this study were urbanicity, migration, physical and sexual abuse as primary, and cannabis or alcohol as secondary hits. In a follow-up evaluation, also including healthy subjects, we discovered that high-risk subjects had up to 50% probability of later development of violent aggression and criminal conduct, independent of mental disease.
Methods: We determined in 6 independent samples (4 schizophrenia, 2 general population samples) pre-adult environmental risk exposure. As proxies of violent aggression, highly intercorrelated measures were applied: (1) violent aggression severity score (VASS); (2) ranking of aggression by independent raters; (3) conviction for battery, sexual assault, manslaughter, murder, or forensic history; (4) established psychopathy and aggression-hostility scores.
Results: Frequent environmental factors, when accumulated, were a major risk for early schizophrenia onset (up to -9 years; p=2.9x10-10; OR=10) in contrast to a complete lack of effect of polygenic GWAS risk scores. Specifically cannabis reduced age-at-prodrome dose-dependently with unprecedented significance (p=3.8x10-20). In schizophrenic as well as healthy subjects, all single risk factors by themselves were marginally associated with higher risk of violent aggression, whereas their accumulation strongly predicted it (OR=10.5). Histone-deacetylase1 mRNA as ‘umbrella mediator’ of epigenetic processes was increased in PBMC of high-risk subjects, suggesting epigenetic alterations.
Conclusions: We provide sound evidence of a disease-independent disastrous relationship between well-defined pre-adult environmental hits and violent aggression. Considering prevention measures, we should bear in mind that cannabis is among the avoidable risks.