Regular readers will recall the confused mess that is this government’s cannabis policy. There has been a drop in cannabis consumption since it was downgraded from Class B to C, but nevertheless they want to put it back up to Class B again. Yes, we know all about the argument that what you ingest is entirely your business, it being your body and all that but morals are always trumped by politics.

In the comments section to our last piece the general consensus was that the policy was driven either by a craven servility to the Murdoch press or, as a daring alternative, a bending to Daily Mail woo woo. The general consensus however was that it was Puritanism, that awful fear that someone, somewhere, might be enjoying themselves and that this situation cannot be allowed to continue. We’re arguing over whose Puritanism, not whether.

There was one vaguely respectable argument that could be put forward on the prohibitionist’s side, that of cannabis induced schizophrenia. This has been increasing even as the general incidence of schizophrenia has been stable (or even falling, depending upon who you ask). That the rise was on the order of 500 people a year means it’s not a very important point, not when compared to 3 million regular tokers, but there are still those who will buy the argument that people should be stopped from harming themselves, even if the risks are very low.

There is certainly a correlation, but we should still want to know about causation before we take any further action. For it is possible, and it is a view advanced by some (like myself last time), that those who are about to become schizophrenic dose themselves on cannabis as they are known to on alcohol and any other substance that comes to hand to still the voices. Or perhaps there’s a milder version, that cannabis induced psychosis isn’t in fact cannabis induced at all, but is simply coincidental: that it’s an early marker of schizophrenia rather than something brought on by cannabis itself.

When we try to test this we also want to be very careful indeed about our sample groups. We really don’t want to be making the mistake that the World Health Organisation has been making with HIV testing in sub-Saharan Africa. Testing pregnant women to give you the incidence of a sexually transmitted disease in the general population really ain't all that clever: you’re testing the one group of the population where you have actual proof that they’ve been partaking in unprotected sex. It might be useful to get an idea of scale, but it's just not going to be all that accurate.

Fortunately, all of this is just what some scientists have done (sadly, the full paper is not online for free access). We know that there is a genetic predisposition to schizophrenia (more accurately to three different conditions that we'll, for convenience sake, group together here). If we’re lucky we can also find a decent data set which we have indeed got, some 2.25 million Danes born between 1955 and 1990, and we know both their own treatments for either cannabis induced psychosis or for those varied schizophrenic type diseases. We can also track their familial relationships and see which of them did or didn’t suffer in these manners. Excellent, we can now try to test our correlation. Do people who have had cannabis induced psychotic episodes then go on to develop schizophrenia at a higher rate than their genetic predisposition (as evidenced by their familial incidence of schizophrenia) would lead us to believe they would?

Well, looking at the 609 who had treatment for such pot induced freakouts and those 6,476 who were treated for the full blown nastiness, well, umm, no. Formally:

In terms of estimated rate ratios, persons who develop cannabis-induced psychosis are as predisposed to schizophrenia spectrum disorder and other psychiatric disorders as those who develop schizophrenia spectrum disorder without a history of cannabis-induced psychosis.