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Mental health[edit | edit source]
Several studies correlate cannabis use with the development of anxiety, psychosis, and depression. For example, a 2005 study associated daily cannabis use with an increased risk of psychosis by a factor of 1.6-1.8, and suggested that cannabis causes psychosis in this relationship. However, others offer the opposite direction of causality, or consider cannabis to only form parts of the "causal constellation." This research denies that cannabis use inflicts mental health problems that would not have occurred in its absence. Many researchers at least partially attribute the correlation between cannabis use and mental illness to self-medication. Indeed, as much as 60% of the mentally ill are suspected to be substance abusers, and many seem to prefer cannabis and alcohol.
The suggested increase in psychotic episodes and the development of psychosis is relatively modest, and these occurrences are rare to begin with. Dr. Stanley Zammit of Bristol and Cardiff universities reported, "Even if cannabis did increase the risk of psychosis, most people using the drug would not get ill...Nevertheless, we would still advise people to avoid or limit their use of this drug, especially if they start to develop any mental health symptoms or if they have relatives with psychotic illnesses." In a 2007 review of available data, Zammit and colleagues found a dose-dependent correlation between cannabis use and psychotic illness. They concluded that the heaviest cannabis users are 40% more likely than non-users to suffer a psychotic illness, while the aforementioned 2005 study suggested a 60-80% increased risk.
The BEACH study (Bettering the Evaluation and Care of Health) conducted by the Australian General Practice Statistics and Classification Centre suggested that "cannabis smokers are more likely to suffer depression, anxiety and psychosis." The report continues that of the number of patients who mentioned cannabis use to their general practitioner, 48% had a psychological problem, including 19% with depression, 9% with psychosis and 6% with anxiety. However, the study also noted that few cannabis users actually tell their doctors of their use, which could potentially bias the results of the study.
Acute Psychosis[edit | edit source]
Much of the evidence for cannabis-induced acute psychosis is based on case reports in which heavy cannabis use has preceded the onset of a psychotic episode, which then remits upon abstinence.
Chronic Psychosis[edit | edit source]
A large, unselected population-based study, published in British Journal of Psychiatry (2008), examined cannabis use and prodromal symptoms of psychosis at age 15–16 years and concluded that cannabis use was associated with prodromal symptoms of psychosis in adolescence.
Cannabis use during adolescence increases the risk of developing schizophrenia in adulthood due to interference with brain development. In adults with a genetic risk cannabis abuse can cause psychosis or may worsen the progress of schizophrenia.
In a recent study at the Institute of Psychiatry at King's College London, scientists have confirmed a link between potent cannabis use ("skunk" cannabis, which accounts for 80 per cent of street seizures of the drug in the UK) and transient psychotic symptoms in healthy people. After testing 22 healthy males in their late 20s by injecting them with THC, with a control dummy injection administered to a percentage of the sample group, a link was found between the chemical and psychosis, "in which hallucinations leave sufferers unable to know what is real and what is imagined". Dr Paul Morrison, who led the team, concluded, "these findings confirm that THC can induce a transient acute psychological reaction in psychiatrically well individuals". In addition, it was found that the extent of the psychotic reaction was not related to "the degree of anxiety or cognitive impairment" in the sample group. Further research is needed into the chemical makeup of skunk cannabis as it is believed stronger strains have virtually no traces of CBD (cannabidiol), which appears to counteract the damaging effects of THC. However, there is likely to be wide variation in the THC and CBD levels (and ratios) since numerous (perhaps even hundreds) of different strains of cannabis have been marketed by dealers as "skunk", some of which are descended from the original 1980s Amsterdam variety.
The largest longitudinal study examining the link between cannabis and psychosis was undertaken by Andreasson and colleagues and followed 45,570 male Swedish Army conscripts for 15 years. After controlling for other factors such as parental mental illness or a pre-existing psychotic illness at conscription, the study found that the odds of developing schizophrenia later in life were "1.5 times higher for those who had used cannabis 1-10 times and 2.3 times more likely for those who had used cannabis 10 times or more". Further to criticism that the study did not control for the use of other potentially psychotogenic substances such as amphetamines, a follow-up study re-analysed the data and ruled out this argument, finding that cannabis use remained predictive of schizophrenia in a dose-dependent manner even after accounting for other substance use and premorbid social integration.
A 2005 meta analysis of available data which evaluated several hypotheses regarding the correlation of cannabis and psychosis found that there is no support for the hypothesis that cannabis can cause cases of psychosis which would not have occurred otherwise, however further study is needed to explore the correlation between cannabis and other types of psychosis patients. Studies have shown that a risk does exist in some individuals with a predisposition to mental illness to develop symptoms of psychosis. The risk was found to be directly related to high dosage and frequency of use, early age of introduction to the drug, and was especially pronounced for those with a predisposition for mental illness. These results have been questioned as being biased by failing to account for medicinal versus recreational usage — critics contend it could be a causal relationship, or it could be that people who are susceptible to mental problems tend to smoke cannabis, or it could be connected to the criminalization of cannabis. Another important question is whether the observed symptoms of mental illness are actually connected to development of a permanent mental disorder; cannabis may trigger latent conditions, or be part of a complex coordination of causes of mental illness, referred to in psychology as the diathesis-stress model. People with developed psychological disorders are known to self-medicate their symptoms with cannabis as well, although one study has claimed that those with a predisposition for psychosis did not show a statistically significant increase in likelihood of cannabis use four years later.
- See also: Correlation does not imply causation
Some studies conclude that there is a correlation of cannabis use and some symptoms of psychosis, but do not necessarily support the notion that cannabis use is a sufficient or necessary cause for psychosis. It might be a component cause, part of a complex constellation of factors leading to psychosis, or it might be a correlation without forward causality at all.
For example, a review of the evidence by Louise Arsenault, et al., in 2004 reports that on an individual level, cannabis use confers an overall twofold increase in the relative risk of later schizophrenia, assuming a causal relationship. This same research also states that "There is little dispute that cannabis intoxication can lead to acute transient psychotic episodes in some individuals". The study synthesizes the results of several studies into a statistical model. The study does not correct for the use of other illicit drugs, and relies on self-reporting of cannabis dosage. The study also does not determine if the cannabis use preceded or followed the mental health problem.
Similarly, the landmark study, in 1987, of 50,000 Swedish Army conscripts, mentioned above, found that those who admitted at age 18 to having taken cannabis on more than 50 occasions, were six times more likely to develop schizophrenia in the following 15 years. In fact, psychosis cases were restricted to patients requiring a hospital admission. These findings have not been replicated in another population based sample. As the study did not control for symptoms preexisting onset of cannabis use, the use of other illicit drugs, the study does not resolve the correlation versus causality question but has fueled a major debate within the scientific community. This study also used self reporting for cannabis dosage.
A 2005 study found that "the onset of schizotypal symptoms generally precedes the onset of cannabis use. The findings do not support a causal link between cannabis use and schizotypal traits". A schizotypal personality disorder is a personality disorder different from schizophrenia, though there is some evidence that the former may predispose to the latter. A 2007 British study concluded, "We found few appreciable differences in symptomatology between schizophrenic patients who were or were not cannabis users. There were no differences in the proportion of people with a positive family history of schizophrenia between cannabis users and non-users. This argues against a distinct schizophrenia-like psychosis caused by cannabis."
Research based on the Dunedin Multidisciplinary Health and Development Study has found that those who begin regular use of cannabis in early adolescence (from age 15, median 25 days per year by age 18) and also fit a certain genetic profile (specifically, the Val/Val variant of the COMT gene) are five times more likely to develop psychotic illnesses than individuals with differing genotypes, or those who do not use cannabis. The study was noted for having controlled for preexisting symptoms, but is open to the criticism that it cannot control for late adolescent onset of psychotic illness. Also, the study was on a cohort population, so there is no way to correlate a change in the rate of adolescent use with a change in the rate of incidence of schizophrenia in the study population. These points undermine its value in resolving the correlation versus causality question.
A study that inversely correlated cerebrospinal anandamide (an endogenous cannabinoid) levels with severity of schizophrenia (i.e., that anandamide was released in order to suppress psychosis) suggests that cannabis use may be an effect of schizophrenia or its predisposition, as opposed to a cause.
Cannabis use does not appear to be causally related to the incidence of schizophrenia, but its use is highly likely to precipitate psychotic disorders in persons who are vulnerable to developing psychosis; and cannabis use is also likely to worsen the course of the disorder among those who have already developed it.
See also[edit | edit source]
References[edit | edit source]
- (2008) Cannabis and Mental Health: Put into Context, Australian Government Department of Health and Ageing. URL accessed 17 October 2009.
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- "Cannabis 'raises psychosis risk'". BBC News (2007-07-27). Retrieved on 2007-11-03.
- The BEACH Project. URL accessed on 17 October 2009.
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- Degenhardt L, Hall W, Lynskey M (2001). Comorbidity between cannabis use and psychosis: Modelling some possible relationships. Technical Report No. 121.
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- Avshalom Caspi, Terrie E. Moffitt, Mary Cannon, Joseph McClay, Robin Murray, HonaLee Harrington, Alan Taylor, Louise Arseneault, Ben Williams, Antony Braithwaite, Richie Poulton, and Ian W. Craig (18 January 2005). Moderation of the Effect of Adolescent-Onset Cannabis Use on Adult Psychosis by a Functional Polymorphism in the catechol-O-Methyltransferase Gene: Longitudinal Evidence of a Gene X Environment Interaction. Society of Biological Psychiatry 57 (10): 1117–27.
- Giuffrida A, Leweke FM, Gerth CW, et al. (2004). Cerebrospinal anandamide levels are elevated in acute schizophrenia and are inversely correlated with psychotic symptoms. Neuropsychopharmacology 29 (11): 2108–14., New Scientist
- Earlier onset of schizophrenia linked to pot. Webmd.com. URL accessed on 2012-10-09.
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Further reading[edit | edit source]
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