“Teen Pot Use Linked To Psychoses“, “Teen pot smokers at high risk of mental illness“,”Study finds cannabis use is ‘crazy-making’” are the headlines being produced about some new research that finds a link between cannabis use and psychosis
But are the headlines justified? Well, headlines like this are rarely justified. A more interesting question worth asking is, does pot cause psychosis? And does this current study point to a causal link?
Two things are worth thinking about. Firstly, the researchers are careful to point out that the relationship between pot smoking and psychosis is complicated, meaning that inferring a causal connection is difficult. Secondly, some research done in the UK last year puts the case for a causal connection on very shaky ground.
The author’s caveats
The authors state in their conclusion that their study does suggest that smoking pot early is associated with higher rates of psychosis.
This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults.
Whether there is a causal link, however, is not entirely clear. As the authors emphasise, the connection between smoking pot and psychosis is very complicated since it is clear “since those with early-onset psychotic symptoms were also likely to report early cannabis use”.
The nature of the relationship between psychosis and cannabis use is by no means simple… Those individuals who were vulnerable to psychosis (ie, those who had isolated psychotic symptoms) were more likely to commence cannabis use, which could then subsequently contribute to an increased risk of conversion to a nonaffective psychotic disorder.
So it seems clear that people who are likely to develop psychosis are also more likely to smoke pot. Moreover, the authors continue:
Analyses that incorporated adjustments for depressive and anxiety-related disorders led to a reduction in the strength of the association between cannabis use and psychosis-related outcomes. This suggests that depression and/or anxiety disorders may mediate or moderate the pathways between cannabis use and psychosis-related outcomes. We plan to further explore these issues in more detail in future studies.
A previous study: pot doesn’t cause psychosis
In the face of some research published last year, I think the case for a causal link between smoking pot and developing psychotic symptoms requires some very strong evidence.
This study examined the medical records of 600,000 patients aged between 16 and 44, and failed to find any link between smoking pot and schizophrenia.
If smoking pot causes psychotic symptoms, massive increases in pot smoking within a population should correspond to an increase in psychosis.
A previous study found that pot smoking increased four-fold in the UK between 1972 and 2002 and 18 fold among under 18s. Now, if smoking pot causes psychosis, then we should expect to see an associated increase in the rates of psychosis.
But rather than finding an increase in psychotic symptoms, the authors found that the incidence was stable or declining.
In conclusion, this study did not find any evidence of increasing schizophrenia or psychoses in the general population from 1996 to 2005.
And since schizophrenia and psychosis did not increase, the authors conclude that “the causal models linking cannabis with schizophrenia/psychoses” are not supported by their study.
Given the limitations of studies that attempt to show a causal link and the strong evidence provided by the UK study, it doesn’t seem that claims of a causal link are justified.
Frisher, M., Crome, I., Martino, O., & Croft, P. (2009). Assessing the impact of cannabis use on trends in diagnosed schizophrenia in the United Kingdom from 1996 to 2005 Schizophrenia Research, 113 (2-3), 123-128 DOI: 10.1016/j.schres.2009.05.031
McGrath, J., Welham, J., Scott, J., Varghese, D., Degenhardt, L., Hayatbakhsh, M., Alati, R., Williams, G., Bor, W., & Najman, J. (2010). Association Between Cannabis Use and Psychosis-Related Outcomes Using Sibling Pair Analysis in a Cohort of Young Adults Archives of General Psychiatry DOI: 10.1001/archgenpsychiatry.2010.6
Great article Michael.
What struck me first and foremost was that the report was purely about young people. I think many folks comprehend that smoking dope is probably not healthy for under 21 year olds and the issue is not in contention. The major issue is whether cannabis in moderation is relatively harmless for adults who don’t have a negative reaction to it’s effects. The report does not answer this vital question or even really address it. And that’s the point … it wasn’t about adult cannabis use.
Most of the trash media didn’t distinguish between the two age groups whilst some of the more credible news bureaux did. It seems the bulk of the media are still content to push drug hysteria and moral panic when possible. No wonder the issue is still contentious to the public when their major source of information is the MSM.
That’s a good point. It seems like what evidence there is for a link between cannabis and psychosis is all about young people.
Alex Wodak made some predictably sensible comments on the issue. In Australian Doctor magazine, he made the following comments.
“Dr Alex Wodak, director of the Alcohol and Drug Service at St Vincent’s Hospital in Sydney, said policies regarding cannabis should be based on the assumption that it caused psychosis, even though the absolute risk was very small. However, the contribution that alcohol and amphetamines made to mental illness ‘dwarfs any contribution that cannabis might make’.”
Actually, it appears even narrower than that. Most of the better-controlled studies finding a link found it in those who began using before 18, especially before 15. The link was strongest in those who progressed to heavy or very heavy use before 18. Though a few studies found no connection with age at all for whatever reason. I am not aware of any study that found that using cannabis at 18 is any more risky than using it at 21, all else being equal.
And we still don’t know if the relationship is causal.