With the recent study from King’s College London linking “skunk” to diagnosis of psychotic disorders, I thought it would be a good time to examine the link between cannabis and psychosis in detail.
I have previously written about cannabis and psychosis while talking gangs and drugs, but we didn’t look at the evidence base.
As I was writing this post, I realised that I’ve also waded into the fields of statistics and research methodology. Hopefully, this will provide some clarity the next time a newspaper starts talking about odds and risk in healthcare.
First, let’s get some definitions on the table.
Psychosis, in essence, is the inability to distinguish what is real and what is not. It is most often talked about it terms of schizophrenia. You can read more detail about it here.
Cannabis is a group of flowering plants native to Central and South Asia. To get biological, there are three main species – Cannabis sativa, Cannabis indica, and Cannabis ruderalis. However, the cross-breeding produces all kinds of different sub-species.
Sativa is the most prevalent and the one used for hemp production. Skunk is a hybrid of sativa and indica and contains two-three times higher concentrations of tetrahydrocannabinol (THC), the main psychoactive chemical in cannabis. UK police seizures indicate that skunk is now the prevalent form of cannabis in the UK.
Cannabis and psychosis: the evidence
People have been looking at cannabis in relation to its mind-altering effects ever since they discovered it could be ingested, which is why a number of ancient cultures used it in religious rituals.
However, scientific research didn’t kick off until the 20th century (before which we used to give morphine and cocaine to babies). The key thing about research is this: you have to know what the researchers were looking for. Research can only answer the specific questions asked – remember that as we take a wander through the history of cannabis and psychosis research:
The most famous study of cannabis and psychosis is known as the Swedish conscript study, published in 1987. Firstly, it was HUGE – 45,570 military recruits followed up for fifteen years. Cohort studies don’t get much better than that.
What’s a cohort study, you cry? It’s when a group of people are followed up over a long time to see what happens to them. It is only observational not interventional – you find what’s there and don’t try to influence the outcome. It is a good research method for looking at causal association – the question of “does x increase the risk for y?”. It’s the method that was used to look at links beteween smoking and lung cancer. However, in defiance of the Latin phrase, “after it therefore because of it” is not always true.
What they found was interesting – “high consumers” of cannabis were six times more likely to develop schizophrenia than non-users. And by “high consumers”, they meant people who had smoked cannabis more than fifty times. Ever. That could be only once a week for a year.
Two points also worth noting:
One – psychosis does not equal schizophrenia. However, this was 1987 and “schizophrenia” was used fairly liberally. We might now recognise schizoaffective disorder, drug-induced psychosis and mania separately.
Two – this was self-reported. Therefore, it’s likely that people underestimated their usage. All told, this is pretty good evidence for a link between cannabis and psychosis.
To reinforce these findings, a Lancet 2007 meta-analysis – i.e. looking at the whole body of research – explored the assocation between cannabis and psychosis. Note here that we’re including studies which didn’t look at cause and effect, but looked at where x and y appear together (though they only included longitudinal studies). The study found that there was a significant association between cannabis and all psychosis (not just schizophrenia) which went beyond the transient intoxication effects. It also concluded there is a dose response – like smoking and lung cancer, the more you smoke cannabis, the more likely you are to develop psychosis.
Skunk and psychosis
Which brings us to the King’s College study. First question – what were their questions? The full title of the study is “Proportion of patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case-control study”.
So, we’re not looking at schizophrenia here but “first episode psychosis”. This is relatively new term arising from the movement for early intervention in psychosis, which is the idea that we prevent long-term disability by throwing in a lot of support at the beginning of the illness. First episode psychosis can be just a one-off episode, or can be the start of schizophrenia, schizoaffective disorder, or bipolar affective disorder.
You will also have caught the word “attributable”, so it seems we’re thinking causation again. However, the methods used can only conclude an association. The introduction goes on to say that the researchers hypothesise that the frequency of use and the potency of cannabis increases risk – i.e. a dose response. They think we should focus more of types of cannabis used, using alcohol as a comparison – it’s not enough to know someone drinks twice a week, but how much they drink per session and what they drink (wine, beer, spirits) matters to the outcome.
“Case control” is a type of study where people with a problem – in this case, first episode psychosis – are compared directly to individuals without that problem but otherwise similar. This helps reduce confounders, factors that could potentially influence the outcome, like gender, ethnicity or socioeconomic status.
Their findings support an increased association between users of skunk and psychosis, and a stronger association for daily use. Media reporting has focussed on this figure of 24% new cases of psychosis related to skunk. The study has calculated this as a population attributable fraction. This means that if you eliminated skunk from the population of South London, you would prevent almost a quarter of first episode psychosis cases in this area. However, this would be unlikely to be the same for Cardiff or the Scottish Highlands.
Conclusions about cannabis and psychosis
With the research evidence we have to date, we can conclude:
– Cannabis and psychosis are strongly associated
– Cannabis has a dose-related association with psychosis – i.e. the more you smoke and the more potent the cannabis, the more like you are to have psychosis
– If we eliminated all cannabis, we would significantly reduce psychosis
This is obviously just the tip of the iceberg. We have not considered how cannabis affects people who already have a diagnosis of psychosis. We also haven’t looked into what influence other drugs might have on the illness.
As my role with Freudian Script is to look at fictional portrayals of mental health, we don’t see a lot of cannabis and psychosis. The amotivational and appetite-inducing side effects are well-covered, but the “stoner movie” subgenre focussses on the comedy not calamity associated with cannabis use.
What are your impressions of cannabis and psychosis? What does this research add to the public debate around drugs? Should Hollywood make more films about psychotic stoners? Let me know in the comments!