The scientific literature on the dangers of marijuana is a bit thin. The first report on possible harmful effects of cannabis use is the oft-cited Swedish Army study, where conscripts who reported a heavy use of cannabis in adolescence were six times more likely to be diagnosed with schizophrenia in adulthood than non-users (1). There have been a few other studies suggesting that adolescent cannabis use is a risk factor for psychosis (e.g. 2). The most damning evidence is a longitudinal study by Dutch researchers that found a dose-response relationship between reported cannabis use and psychotic symptoms over a three-year period (3). And now a group has asked that cannabis use be included as a risk factor for psychotic illness in the Global Burden of Disease. (The article is in PLoS, so available for free. Isn't PLoS the greatest thing ever?)
From the article:
As the quoted section above alludes to, there is no firm evidence that cannabis use causes psychosis. Could adolescents who are at risk for schizophrenia be self-medicating through use of marijuana? I do not think any of the studies have examined whether those heavy users who showed some type of psychosis later in life also had family histories of psychoses. Are those who experience psychotic symptoms self-medicating with marijuana (use of the drug is more common with those who report psychoses), similar to the abuse of nicotine among schizophrenics? Or is the marijuana use really causing psychosis or compounding its effects in a small population?
Some commentators may well argue that it is premature to conclude that the relationships between cannabis use and psychosis are causal, which raises the question of what the standard of proof should be causal inference. Some may argue for “proof beyond reasonable doubt,” the standard implicitly used in the last iteration of the GBD. It is rare, however, to meet this standard of proof for noncommunicable diseases other than smoking-related diseases. What has changed since the last iteration of the GBD? The broad approach to all risk factors has been to set the standard of proof at “more likely than not,” rather than “beyond reasonable doubt.” If the latter was the standard of proof, then no adverse health consequences of cannabis would be considered apart from dependence.
If we had treatments that resulted in complete, immediate, and sustained remission for all individuals who develop psychosis, then the role of cannabis as an aetiological agent may attract less attention. But schizophrenia remains a poorly understood group of disorders. Even our best treatments are suboptimal. In the absence of better treatments, the most effective way to reduce the disability associated with schizophrenia is to prevent its occurrence when we can. Thus, when considering potential risk factors for schizophrenia, we argue that candidates that offer the opportunity for public health interventions should be accorded more attention (e.g., education about the potential risks of cannabis use). Even exposures that may account for a small attributable fraction of those with the disorder warrant scrutiny.
Either way, consider yourself forewarned the next time someone says marijuana use is "safe" and passes you a joint. And don't do drugs.
1. Andreasson S, Allebeck P, Engström A, et al. Cannabis and schizophrenia: a longitudinal study of Swedish conscripts. Lancet 1987;11:1483-5.
2. Arseneault L, Cannon M, Poulton R, et al. Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study. BMJ 2002;325:1212-3.
3. (2002) Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol 156:319–27