The recent proposal by the Liberal Democrats in the UK to legalise cannabis in a standardised format follows America’s legalisation accross a few of its states. However, fear of Mary Jane continues due to it’s implications in the causal pathway to psychosis. I recently presented on the strength of this evidence, and whether we have enough data to implicate the substance as being a factor toward the development of psychosis.
Cannabis is comprised of two main chemicals: deltra-tetrahydrocannabinol, or THC for short, and Cannabidiol (CBD). These two compounds are the two main chemical building blocks of the of the cannabis plant, and remarkably important to hold in mind. THC is often described as the ‘active’ compound which produces psychological effects, as well as stimulating your appetite, whereas CBD is implicated in antipsychotic, anxiolytic, and neuroprotective effects.
Most studies which draw a link between cannabis and psychosis fail to distinguish between these two chemicals. So while a given risk is calculated upon these data, samples are often drawn from cultures where cannabis is illegal, and so the risks may be bias due to the prevalent use of ‘Skunk’ in the population. Usually high-THC Skunk is smoked in most high-economically developed areas because because of the high-yield and relatively faster growth times of the plants. Indeed when looking at THC alone, we do see a dose-response relationship between THC concentration and psychotic symptoms.
Alongside this, despite a recent pop publication to the contrary, genetics plays a part in psychological development, and this includes the interaction between cannabis and psychosis. Research has suggested that those who smoke cannabis and develop psychosis may share similar genetic relationships, or indeed genetic markers associated with smoking cannabis may also be associated with genetic risk for developing psychosis. This poses the question as to whether genetic vulnerability in those who develop psychosis are also predisposing them to smoking cannabis? It is quite difficult to separate the two.
This genetic relationship is also confounded by other factors in itself. When we look at cannabis in relation to other causal factors of psychosis, and even other drugs such as tobacco, the risk begins to diminish. Smoking tobacco has begun to show its head in research toward the development of psychotic symptoms, and when adjusting for tobacco use in research, often the risk of psychosis linked with cannabis drops. Alongside tobacco use, various other factors have been suggested to contribute to developing psychosis, and produce confounders in the causal chain, such as Socio Economic Status (SES), childhood trauma, and other drugs use. Indeed, tobacco and alcohol were implicated in exacerbating anxiety and affective symptoms, which have been suggested to drive core symptoms, poor prognosis, and distress in psychosis.
So does cannabis cause psychosis? Somewhat. But most often in relation to genetic, SES, childhood trauma, smoking, and other drugs use factors. We need to take a bigger picture approach to cannabis and risk of psychosis, however not deny the link between high THC content and symptoms of the condition, as well as multiple other vulnerabilities that may contribute. Taking a look at the Disability Adjusted Living Years (DALYs) as a result of cannabis use in psychosis, the data shows that cannabis plays quite minimal role (0.03% globally). This figure is also adjusted for the increase in population and cannabis use, i.e. the risk has stayed the same, even though the population, and hence usage, has increased. DALYs figures increase slightly in higher economically developed countries, but again, this may be due to the large proportion of high THC skunk in most of the countries included. When compared to other drugs such as Opoids and Alcohol, cannabis accounted for fewer DALYs. This isn’t to say there’s a reason to ignore the link, as 2 million DALYs globally were attributed to cannabis dependence, which is a considerable amount alone. In the context of those it affects negatively, further investigation is required.
Research needs a more refined definition of cannabis, so we know what we’re measuring. Instead of making sweeping statements as to whether one specific thing may be causing psychosis (such as all genetics, or definitely not genetics at all), we must observe the web of vulnerability as a collective model into what may cause this enigmatic condition. Certainly there are no easy, straight forward answers.
What does this mean for public policy? Well, certainly approaching the issue from a scientific angle is remarkably important, as well as being aware about the current link between high THC skunk and psychotic symptoms. As evidence toward the use of CBD for multiple medical and psychological issues increase (notably, alleviating psychotic symptoms), we might look at this enigmatic compound with great potential for therapeutic purposes, as well understanding it’s potential risks.