This study performed a reanalysis of the 1969 Swedish conscript study:
An association between use of cannabis in adolescence and subsequent risk of schizophrenia was previously reported in a follow up of Swedish conscripts. Arguments were raised that this association may be due to use of drugs other than cannabis and that personality traits may have confounded results. We performed a further analysis of this cohort to address these uncertainties while extending the follow up period to identify additional cases.The followup study found that reanalysis of the data with more modern statistical techniques, as well as additional followup data from those conscripts, found that the association was still present:
Prodromal: a person who has early symptoms of the disease. This is an issue because people with mental illness are more likely to self-medicate using alcohol, marijuana, and other drugs. The conclusion that marijuana users were more likely to develop schizophrenia turned out to be true even for those persons who exhibited no prodromal symptoms before beginning marijuana use.Results: Cannabis was associated with an increased risk of developing schizophrenia in a dose dependent fashion both for subjects who had ever used cannabis (adjusted odds ratio for linear trend of increasing frequency 1.2, 95% confidence interval 1.1 to 1.4, P<0.001), and for subjects who had used only cannabis and no other drugs (adjusted odds ratio for linear trend 1.3, 1.1 to 1.5, P<0.015). The adjusted odds ratio for using cannabis >50 times was 6.7 (2.1 to 21.7) in the cannabis only group. Similar results were obtained when analysis was restricted to subjects developing schizophrenia after five years after conscription, to exclude prodromal cases.
Conclusions: Cannabis use is associated with an increased risk of developing schizophrenia, consistent with a causal relation. This association is not explained by use of other psychoactive drugs or personality traits relating to social integration.["Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study," British Medical Journal (2002) 325:1199]
This study performed a longitudinal study in New Zealand and found that:
Firstly, cannabis use is associated with an increased risk of experiencing schizophrenia symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for. … Secondly, early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18). The youngest cannabis users may be most at risk because their cannabis use becomes longstanding. ["Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study," British Medical Journal (2002) 325:1212]This paper, from the British Journal of Psychiatry in 2004, also concluded that marijuana roughly doubles the risk of schizophrenia. From the abstract:
On an individual level, cannabis use confers an overall twofold increase in the relative risk for later schizophrenia. At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship. Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis. ["Causal association between cannabis and psychosis: examination of the evidence," British Journal of Psychiatry (2004) 184:110-117]
This metastudy examined existing published studies of mental illness and marijuana:
Results On an individual level, cannabis use confers an overall twofold increase in the relative risk for later schizophrenia. At the population level, elimination of cannabis use would reduce the incidence of schizophrenia by approximately 8%, assuming a causal relationship. Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis.
Conclusions Cases of psychotic disorder could be prevented by discouraging cannabis use among vulnerable youths. Research is needed to understand the mechanisms by which cannabis causes psychosis. ["Causal association between cannabis and psychosis: examination of the evidence," British Journal of Psychiatry (2004) 184: 110-117]
There’s unquestionably a genetic component. This Schizophrenia Bulletin (2008) paper tells us:
Cannabis use is considered a contributory cause of schizophrenia and psychotic illness. However, only a small proportion of cannabis users develop psychosis. This can partly be explained by the amount and duration of the consumption of cannabis and by its strength, but also by the age at which individuals are first exposed to cannabis. Genetic factors, in particular, are likely to play a role in the short- and the long-term effects cannabis may have on psychosis outcome. … Evidence suggests that mechanisms of gene-environment interaction are likely to underlie the association between cannabis and psychosis. ["Gene-Environment Interplay Between Cannabis and Psychosis," Schizophrenia Bulletin (2008), 34:6 1111-1121]Recent studies continue to recognize a causal connection:
Cross-sectional studies document an association between cannabis use and psychotic symptoms, and longitudinal studies suggest that early exposure to cannabis confers a close to two-fold increase in the risk of developing schizophrenia. Pharmacological studies show that cannabinoids can induce a full range of transient positive, negative, and cognitive symptoms in healthy individuals that are similar to those seen in schizophrenia. There is considerable evidence that in individuals with an established psychotic disorder such as schizophrenia, exposure to cannabis can exacerbate symptoms, trigger relapse, and worsen the course of the illness. Only a very small proportion of the general population exposed to cannabis develop a psychotic illness. It is likely that cannabis exposure is a ‘component cause’ that interacts with other factors to ‘cause’ schizophrenia or other psychotic disorder, but is neither necessary nor sufficient to do so alone. ["Cannabinoids and psychosis," International Review of Psychiatry (2009), 21:2 152-162]
This study published in 2009 sought to identify age relationships to psychotic symptoms and substance abuse. While it found no correlation of frequency of use of marijuana or tobacco and psychotic symptoms, it did find that increase in frequency of marijuana and tobacco use was correlated to onset of psychotic symptoms--suggesting that increases in dosage might be the factor. From the abstract:
RESULTS: Whereas classifying participants according to maximum frequency of use prior to onset (none, ever, weekly, or daily) revealed no significant effects of cannabis or tobacco use on risk of onset, analysis of change in frequency of use prior to onset indicated that progression to daily cannabis and tobacco use was associated with an increased risk of onset of psychotic symptoms. Similar or even stronger effects were observed when onset of illness or prodromal symptoms was the outcome. A gender-by-daily-cannabis-use interaction was observed; progression to daily use resulted in a much larger increased relative risk of onset of psychosis in females than in males.
CONCLUSIONS: Pre-onset cannabis use may hasten the onset of psychotic as well as prodromal symptoms. Age at onset is a key prognostic factor in schizophrenia, and discovering modifiable predictors of age at onset is crucial. ["Association of Pre-Onset Cannabis, Alcohol, and Tobacco Use With Age at Onset of Prodrome and Age at Onset of Psychosis in First-Episode Patients," American Journal of Psychiatry (2009), 166:1251-1257]Here's a study published 2010 that used siblings to attempt to reduce unmeasured confounding variables:
A chapter from The Handbook of Neuropsychiatric Biomarkers, Endophenotypes and Genes (2009) concludes that there is evidence for brain structure changes in heavy marijuana users that are similar in nature to those measureable in schizophrenics. From the abstract:Results Duration since first cannabis use was associated with all 3 psychosis-related outcomes. For those with duration since first cannabis use of 6 or more years, there was a significantly increased risk of (1) nonaffective psychosis (adjusted odds ratio, 2.2; 95% confidence interval, 1.1-4.5), (2) being in the highest quartile of Peters et al Delusions Inventory score (adjusted odds ratio, 4.2; 95% confidence interval, 4.2-5.8), and (3) hallucinations (adjusted odds ratio, 2.8; 95% confidence interval, 1.9-4.1). Within sibling pairs, duration since first cannabis use and higher scores on the Peters et al Delusions Inventory remained significantly associated.
Conclusions Early cannabis use is associated with psychosis-related outcomes in young adults. The use of sibling pairs reduces the likelihood that unmeasured confounding explains these findings. This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults. ["Association Between Cannabis Use and Psychosis-Related Outcomes Using Sibling Pair Analysis in a Cohort of Young Adults," Archives of General Psychiatry (May 2010), 67:5]
While previous research failed to identify structural brain abnormalities in human cannabis users, more recent studies using high resolution imaging techniques combined with more robust delineations of specifi c brain regions in very heavy cannabis users have revealed evidence of dose-related alterations in regions implicated in schizophrenia. Moreover, these regional brain volumetric reductions are of similar magnitude to those seen in schizophrenia. We discuss the association between cannabis use and the development of cognitive defi cits and psychiatric symptoms in relation to structural brain alterations. We propose that long term heavy cannabis use leads to structural brain changes and associated deleterious functional (cognitive and mental health) sequelae that resemble schizophrenia. These changes may occur not only in individuals who are vulnerable to the development of such disorders, but also in nonvulnerable individuals if cannabis is used heavily for prolonged periods. ["Structural Brain Alterations in Cannabis Users: Association with Cognitive Deficits and Psychiatric Symptoms," ch. 27, The Handbook of Neuropsychiatric Biomarkers, Endophenotypes and Genes (2009)]
The American Psychiatric Association's May 21, 2010 Psychiatric News reports on upcoming research about to be published, showing that marijuana use both increases psychotic symptoms, and psychotic symptoms increase use of marijuana:
Marijuana use among individuals with schizophrenia is associated with more severe positive psychotic symptoms over time, according to a 10-year longitudinal study posted online May 15 on AJP in Advance.
Researchers found that changes in cannabis use at four follow-up points over the 10-year period were associated with similar direction changes in positive psychotic symptoms of delusions and hallucinations over time; if subjects stopped using cannabis, their symptoms decreased, and if they started or increased use, their symptoms increased. This remained true even after controlling for gender, age, socioeconomic status, other drug use, antipsychotic medication use, and other symptoms.