The disconnect between the science on cannabis and public health campaigns

Abstract

The review of cannabis-induced psychosis by Ian Hamilton in Addiction 1 raised key issues that warrant further exploration. In focusing upon the literature up to the turn of the 21st century, the author omitted the subsequent explosion of scientific inquiry into a causal relationship between cannabis use and chronic psychotic disorders. The author pointed towards one type of relevant research, citing the seminal dose–response work of Andréasson 2 while disregarding recent publications on this topic 3, 4, as well as other important criteria which have been applied to test causation: prospective studies on the timing of use and psychosis 5; age of onset of schizophrenia in users versus non-users 6; percentage exhibiting psychotic symptoms from clinically administered ∆9-tetrahydrocannabinol 7; conversion from temporary to chronic psychosis from cannabis versus other drugs 8; likelihood of cannabis use in those with a family history of psychosis 9; cannabis-induced psychosis without such a family history 10; rates of psychosis in siblings discordant for cannabis 11; course of recovery from psychotic breaks in non-users versus those who used and quit, or continued use 12; and whether family history of psychosis affects recovery from cannabis-induced psychotic breaks 13. Collectively, this literature supports cannabis having a causal impact on chronic psychotic disorders. The second key issue is the rarity of the outcome. A disease is considered rare in the United States if it afflicts one person per 1500 (Rare Disease Act) or, in Europe, one per 2000 (European Commission on Public Health). As the recent literature supports a fourfold increase in risk for chronic psychosis in heavy users 14, and given that the life-time morbid risk for schizophrenia is, on average, 0.7% 15, the outcome would be rare by no generally accepted standard. It appears plausible that in asserting cannabis-induced psychosis to be relatively rare, the author was influenced by the publication of Hickman 16 reporting on the number needed to abstain from using the lower-strength cannabis prevalent in the last century in order to prevent one case of schizophrenia [number needed to prevent (NNP)], and showing that 2800 was the NNP for males aged 20–24 years. What is often not understood is that the NNP was per year, i.e. to prevent one schizophrenia case per year in each age group studied 17. If treatment programs are geared towards a couple of decades of prevention, the NNP for today's cannabis across the age groups/genders combined can be estimated to be far fewer than 100 individuals. The author raised a third key issue, that being the reason for lack of acceptance of a causal impact of cannabis on psychosis, correctly placing some blame on the outcome being difficult to discern at the population level. Indeed, discernable impacts on whole populations depend upon tracking both the variable and the outcome; on the population size interacting with the variable; and on whether there are changes in untracked variables over time that influence outcome. The involvement of gene–environment interactions and the failure to identify a mechanism for how cannabis induces psychosis have also been cited by some scientists as reasons for downplaying the likelihood of a causal basis. Conversely, cannabis use causing chronic psychosis should be no different than carcinogens causing cancer, where an agent suspected of being a carcinogen based on dose–responsive cancer rates in large case–control or prospective studies will move from the category of suspected carcinogen to known carcinogen if it is also shown to cause cancerous or pre-cancerous lesions in the laboratory. Whether or not genes influence the development of the cancer is considered a moot point in that designation, as all cancers involve some type of gene–environment interaction. With tobacco smoking, 72–84% of individuals (depending on where they live) can smoke for most of their lives without developing lung cancer 18. Despite the reasons for differential susceptibility not being well understood and the exact mechanism of the carcinogenesis still being determined, large public health campaigns have been directed against tobacco use for more than half a century. In contrast, no widely broadcast public health advisories or Surgeon General's warnings have been issued about the mental health impact of cannabis, at a time when it is undoubtedly the most well-studied and well-replicated finding for an environmental factor promoting psychotic outcomes. None.