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New York State Practitioner Education Medical Use of Marijuana 2-hr Required Course
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Section 5.0: Cannabis Use and Mental Health
Part 1
Cannabis Use and Mental Health Disorders
Any clinical discussion on medical cannabis is limited by the relative paucity of randomized controlled trials. Only a small number of clinical studies involving the therapeutic use of cannabis have been carried out to date. And, of those studies, only short term adverse effects associated with cannabis use have been evaluated.
In general, the medical literature on physiological effects and adverse effects of cannabis use pertains to recreational cannabis use much more so than medicinal cannabis use. As such, the information presented in this section comes mostly from studies involving recreational cannabis users who often use tobacco and alcohol, as well as other drugs (prescription and illicit drugs).
Therefore, when recommending medical cannabis, it is essential to realize that the effects may not mirror the published studies and, analogous to any prescription medication recommendation, decisions must be made on an individualized basis with appropriate follow-up.
This section is comprised of two parts. The first part reviews the literature evaluating the mental health effects of cannabis use, while the second part addresses cannabis use disorder.
This discussion focuses on the association between cannabis use and mental health disorders. The difficulty has been in deciding whether there is a causal relationship between exposure to cannabis and the development of these mental health disorders.
Regular cannabis use has been associated with psychotic symptoms (disordered thinking, hallucinations and delusions) and with diagnosed psychotic disorders, such as schizophrenia, in which persons report severe psychotic symptoms over months, and often experience substantial social disability, a loss of motivation, disturbed behavior and cognitive deficits (1).
A 15-year follow up of over 50,000 Swedish male conscripts found that those who had tried cannabis by age 18 were 2.4 times more likely to be diagnosed with schizophrenia than those who had not (2). The risk increased with the frequency of cannabis use and remained significant after adjustment for limited confounding variables.
A 27-year follow up of the same cohort (3) also found a dose-response relationship between frequency of cannabis use at age 18 and risk of schizophrenia during the follow up that persisted after statistically controlling for confounding factors. Zammit et al.'s findings have been supported by longitudinal studies of the relationship between cannabis use and psychotic symptoms in the Netherlands (4), Germany (5) and New Zealand (6,7).
A meta-analysis of these longitudinal studies reported a pooled odds ratio of 1.4 [95% confidence interval (CI): 1.20 - 1.65] of psychotic symptoms or psychotic disorder among those who had ever used cannabis (8). The risk of psychotic symptoms or psychotic disorders was higher in regular users (odds ratio of 2.09 [95% CI: 1.54 - 2.84]). Reverse causation was addressed in most of these studies by excluding cases reporting psychotic symptoms at baseline or by statistically adjusting for pre-existing psychotic symptoms. A common causal hypothesis was harder to exclude because the association between cannabis use and psychosis was attenuated after statistical adjustment for potential confounders and no study assessed all major confounders.
There is conflicting evidence on whether the incidence of schizophrenia has increased as cannabis use has increased among young adults, as would occur if the relationship were causal. An Australian study did not find clear evidence of increased psychosis incidence despite steep increases in cannabis use during the 1980s and 1990s (9). A similar study (10) suggested that it was too early to detect any increased incidence in Britain in the 1990s. A British (11) and a Swiss study (12) reported conflicting findings (1).
The interpretation of data on the incidence of psychoses has been complicated by changes in diagnostic criteria, the availability of psychiatric services for psychosis, and the quality of data on the treated incidence of psychosis. If causality is assumed, the risk of developing psychosis roughly doubles from around 7 in 1000 in non-users (13) to 14 in 1000 for regular users. A doubling of risk is important in persons with an affected first degree relative, for whom the risk would increase from around 10% (14) to 20%. It is nonetheless difficult to reduce the population incidence of psychosis by preventing cannabis uptake: approximately 5000 men aged 20-24 years would have to avoid smoking cannabis to prevent one case of schizophrenia (1,10)
Less consistent and weaker relationships have been reported between cannabis use and depression (8,15). In a follow up of the Swedish cohort described above, there was an increased risk of depression (1.5 times) in those who reported the heaviest cannabis use at age 18, but this association disappeared after adjustment for confounding variables (16). Fergusson and Horwood found a dose-response relationship between frequency of cannabis use by age 16 and depressive disorder, but the relationship was no longer statistically significant after adjusting for confounders. Note: The 2017 report on the health effects of cannabis and cannabinoids prepared by the National Academies of Sciences, Engineering, and Medicine concludes "cannabis use does not appear to increase the likelihood of developing depression" (17).
A meta-analysis of these studies (8) found an association between cannabis use and depressive disorders, but the authors argued that these studies had not controlled for confounders, and had not convincingly excluded the possibility that depressed young people are more likely to use cannabis. Similar conclusions were reached by a combined analysis of data from four Australian birth cohorts (18).
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