The debate over whether or not cannabis causes schizophrenia is one that has been raging since the dawn of prohibition. We’ve all seen the ludicrous “this is your brain on drugs” adverts, and heard the stark warnings from politicians about how smoking ‘skunk’ will ‘mess with your mind’. But what is the truth? As always, it’s not easy to say, and certainly can’t be summed up with a media-friendly sound bite.
A recent publication in the journal ‘Nature’ written by Matthew Hill, a cannabinoid neuropharmacologist at The Hotchkiss Brain Institute, University of Calgary, Alberta, Canada, attempted to shed some light on many of the common misconceptions about the issue.
In it, Hill points out that despite what we’re often told “the nature of this relationship [between cannabis use and schizophrenia] is still a matter of debate and is not as clear as some researchers or policymakers would suggest.”
Instead, he argues, the relationship is far more complex and nuanced than if it were simply causal. As he points out, if cannabis were in fact a cause of schizophrenia, then an increase in its use would necessarily have to lead to an increase in diagnoses of schizophrenia. However this simply isn’t the case.
Before the 1960’s, cannabis use in much of Europe and North America was extremely rare, but since that time it has seen an explosion in popularity. In certain regions over 20% of the adolescent population now use the drug. In stark contrast to this, schizophrenia rates have remained stable and in some cases have even declined. Not only that, the rate of cannabis usage in a country doesn’t seem to have any bearing on schizophrenia rates compared to other countries. Broadly speaking, despite wild variations in cannabis usage, schizophrenia rates are fairly regular throughout the world.
What this means is that the idea that ‘cannabis causes schizophrenia’ cannot be true. If it was, there’d be an uptick. However, as Hill points out, it’s not as simple as saying that there’s no relationship between the two either. Studies have suggested that heavy, prolonged use of cannabis (especially in adolescence) does seem to speed up the onset of the disease, but only in those individuals who would have developed it anyway.
However, as is always the case in science, not everyone agrees with Hill’s take on the issue. In response to his article, Matthew Large, Marta Di Forti and Robin Murray have now offered up a rebuttal in the very same journal – Nature – in which Hill’s piece was published.
In their rebuttal, Large, Di Forti, and Murray claim that Hill’s “contention that the increased societal use of cannabis over time is not reflected in increased rates of schizophrenia has been tested only once to our knowledge — and that study came to the opposite conclusion.”
This is surprising, since these three eminent scientists seem to be conveniently forgetting a study which even I, a lowly writer, am very much aware of. A 2009 meta-analysis undertaken by Keele University found, and I quote, that “In terms of the model set out in the Introduction, the expected rise in diagnoses of schizophrenia and psychoses did not occur over a 10 year period. This study does not therefore support the specific causal link between cannabis use and the incidence of psychotic disorders”
The Keele study even goes on to mention 3 other studies which came to the same conclusion, none of which were mentioned by Large, Di Forti, and Murray.
The other ‘argument’ put forward by these three in their response to Matthew Hill which deserves a mention is that “Deaths from cardiac disease are declining in many countries despite increased obesity, but that does not mean that obesity is unrelated to cardiac disease.”
This is a complete red herring and really a distortion of the facts used to serve their own argument. They’re correct that deaths from cardiac disease have fallen, but when looking at schizophrenia’s relationship with cannabis we are not talking about deaths. We are talking about diagnoses. Diagnoses of cardiac disease do, obviously, increase with obesity levels, but the reason deaths do not is that we are getting ever better at treating cardiac disease. Frankly, if I were one of these three scientists I’d probably be pretty embarrassed by what I’d just put my name to.
The point of all of this is not to settle the argument one way or the other. I am certainly not qualified to do that. But what can be taken from all of this is that the cannabis/schizophrenia relationship is a complex one. It is undeniably a relationship that exists, but exactly why and in what sense we don’t yet fully understand.
The problem is, we don’t seem able to extricate ourselves from the stigma and politics which have enveloped the issue to simply focus on the cold, hard, science of it. Even renowned scientists like Robin Murray are guilty of twisting things to suit their agenda, and no doubt scientists on the other side of the argument have done the same. Until we can remove the emotion from the issue we are not likely to get any real answers any time soon, and the great cannabis and schizophrenia debate will continue to rage.