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Cannabis of different types has been shown to be differentially associated with psychosis (Photo by Chris Jackson/Getty Images
Cannabis of different types has been shown to be differentially associated with psychosis. Photograph: Chris Jackson/Getty
Cannabis of different types has been shown to be differentially associated with psychosis. Photograph: Chris Jackson/Getty

So smoking skunk causes psychosis, but milder cannabis doesn't?

This article is more than 9 years old

Research that looks at different potencies of cannabis could advance our understanding of the relationship between the drug and psychosis

The Mail on Sunday has shouted that ‘cannabis TRIPLES psychosis risk’ and that skunk is to blame for ‘1 in 4 of all new serious mental disorders’. Is this what the study they cite shows? Well, no, but it’s really interesting research which could advance our understanding of the relationship between cannabis and psychosis.

The research compares a group of first-episode psychosis patients in South London with a group from the general population in the same area. Not only did the authors ask participants about the frequency of their cannabis use, but also about the type of cannabis they used– specifically whether it was skunk, or hash.

They found that those with psychosis were much more likely to have used skunk every day, than to have never used cannabis. Conversely, people who smoked hash every day were no more likely to have psychosis than people who never tried cannabis.

But does this mean cannabis triples psychosis risk? The headline reported in the Mail came from a ‘population attributable fraction’ that the paper calculated: the number of cases of psychosis that would be prevented if all skunk use was removed, assuming that cannabis causes psychosis. The authors of the study estimated this to be 24%. However, the authors clearly point out that they cannot be sure the association seen in their study is causal.

There’s lots of consistent evidence associating cannabis use with psychosis and schizophrenia, but as the saying goes, correlation isn’t causation. For all sorts of reasons, you can’t randomly assign one group of teenagers to use cannabis, and another not to. This means you have to observe what people choose to do, and the people who choose to smoke cannabis might be different in a variety of other ways, which could be the cause of the increase in psychosis risk. Although you can control for these in analyses, you can never be sure you’ve adequately adjusted for them.

This study uses a case-control design. This type of study can lead to bias if the control population is not adequately selected. In this article, the controls were selected from people who lived in the same area of London. However, the authors noted some difference between the cases and controls, in particular those with psychosis were more likely to be male, more likely to be white Caucasian, and more likely to be heavy smokers. Psychosis is more common in men, and more common in ethnic minorities (in particular those of migrant status). The authors accounted for these differences and adjusted for other potential confounders, but there could be others that weren’t measured.

Another drawback of case control studies is that the exposure measure (cannabis use) has to be assessed retrospectively. This can lead to biased findings if having psychosis might affect likelihood to over- or under- report former drug use. Given that an association was found with skunk but not hash, perhaps this is unlikely to be a problem, but again the authors can’t be sure.

For all the caveats though, this study is really important. It’s the first of its kind to try and separate out different cannabis potencies in this way. Past cannabis research has mainly focused on the effects of THC – which has been shown in randomized trials to induce transient psychotic experiences. However, recent evidence has hinted that cannabidiol (CBD), another cannabinoid, might be protective against psychosis. Skunk commonly has higher levels of THC than hash (government reports suggest 15% in skunk and 5% in hash), but skunk often only contains traces of CBD, while hash tends to have roughly equivalent CBD and THC.

Skunk and hash use were self-reported in this study, so we have to assume that participants knew what they were smoking, and can only guess at the true levels of THC and CBD in the cannabis being used. Ideally, samples would have been taken and the precise levels of these cannabinoids assessed, but this isn’t practical in studies of this size and design.

If it is the case that skunk use is causing an increased risk of psychosis, does this mean that it’s responsible for one in four of all serious mental disorders, as the Mail claims? Ignoring that this paper was specifically about psychosis, not ‘serious mental disorders’ more generally, perhaps in certain high risk populations the impact of cannabis could be this high, for example in those with a genetic predisposition to psychosis, but it’s a big leap to conclude that from one study.

This new research is an important step on the road to understanding the nature of the association between cannabis and psychosis, but once again media exaggeration or misrepresentation of the findings could risk the message being ignored by the people most likely to benefit from it. Just in the same way that a pint of beer of an evening is likely to have a different health impact to a pint of vodka, the same could be true for skunk compared to hash. I look forward to more research investigating this.

Update: When I wrote this, only the Mail had covered the research. However, the Guardian also ran with the headline ‘skunk triples risk of serious psychotic episode’, and the Telegraph with ‘super strong cannabis responsible for a quarter of new psychosis cases’. So apologies to the Mail for singling them out!

Suzi Gage has just completed a PhD investigating associations between cannabis use and psychotic experiences in the Children of the 90s cohort in Bristol, and has published a review on the topic, as well as her findings.

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