An overview of systematic reviews on cannabis and psychosis: Discussing apparently conflicting results

Department of Epidemiology, Local Health Unit Roma E, Roma, Italy.
Drug and Alcohol Review (Impact Factor: 1.55). 05/2010; 29(3):304-17. DOI: 10.1111/j.1465-3362.2009.00132.x
Source: PubMed


Cross-sectional surveys have revealed that cannabis is the most widely used illicit substance in Western countries. Cannabis intoxication can lead to acute, transient psychotic symptoms and the short-term exacerbation of pre-existing psychotic symptoms. However, controversy exists about whether cannabis can actually cause long-term psychosis.
We summarised the findings of systematic reviews on the association between cannabis use and psychosis, searching MEDLINE, EMBASE and CINAHL up to August 2007. We assessed the methodological quality, selected the better quality reviews and analysed reasons for discordant results.
We included five systematic reviews. Four of the reviews performed a meta-analysis and showed a consistent association between cannabis use and psychosis; the fifth review considered psychological problems more broadly, did not perform a meta-analysis and reported an inconsistent association. The reasons for discordance were: different outcomes (psychosis vs. psychological problems), different inclusion criteria for primary studies and different methods for summarising the results.
This overview shows a consistent association between cannabis use and psychotic symptoms, though it is not possible to draw firm conclusions about a causal relationship. Reverse causality and residual confounding cannot be excluded. An interaction with other environmental and genetic factors is difficult to ascertain.
We conclude that there is insufficient knowledge to determine the level of risk associated with cannabis use in relation to psychotic symptoms and that more information is needed on both the risks of cannabis use and the benefits of preventive interventions to support evidence-based approaches in this area.

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    • "A growing body of evidence indicates that environmental risk factors play a role in the aetiology of psychotic syndromes (van Os et al. 2010). Exposure to an urban environment (Vassos et al. 2012), early childhood trauma (Varese et al. 2012) and cannabis use (Minozzi et al. 2010) are consistently associated with psychotic outcome in rigorously designed epidemiological studies, including prospective studies, in both clinical and general populations. Confirming the shared vulnerability theory of psychopathology , environmental factors, particularly cannabis use and trauma, are also associated with affective disorders, albeit less pronounced (Bovasso, 2001; Moore et al. 2007; Breetvelt et al. 2010; Nanni et al. 2012; Kedzior & Laeber, 2014). "
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    ABSTRACT: Evidence suggests that in affective, non-psychotic disorders: (i) environmental exposures increase risk of subthreshold psychotic experiences (PEs) and strengthen connectivity between domains of affective and subthreshold psychotic psychopathology; and (ii) PEs are a marker of illness severity. In 3021 adolescents from the Early Developmental Stages of Psychopathology cohort, we tested whether the association between PEs and presence of DSM-IV mood disorder (MD)/obsessive-compulsive disorder (OCD) would be moderated by risk factors for psychosis (cannabis use, childhood trauma and urbanicity), using the interaction contrast ratio (ICR) method. Furthermore, we analysed whether the interaction between environment and PEs was mediated by non-psychotic psychopathology. The association between PEs and MD/OCD was moderated by urbanicity (ICR = 2.46, p = 0.005), cannabis use (ICR = 3.76, p = 0.010) and, suggestively, trauma (ICR = 1.91, p = 0.063). Exposure to more than one environmental risk factor increased the likelihood of co-expression of PEs in a dose-response fashion. Moderating effects of environmental exposures were largely mediated by the severity of general non-psychotic psychopathology (percentage explained 56-68%, all p < 0.001). Within individuals with MD/OCD, the association between PEs and help-seeking behaviour, as an index of severity, was moderated by trauma (ICR = 1.87, p = 0.009) and urbanicity (ICR = 1.48, p = 0.005), but not by cannabis use. In non-psychotic disorder, environmental factors increase the likelihood of psychosis admixture and help-seeking behaviour through an increase in general psychopathology. The findings are compatible with a relational model of psychopathology in which more severe clinical states are the result of environment-induced disturbances spreading through a psychopathology network.
    No preview · Article · Mar 2015 · Psychological Medicine
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    • "A long history of empirical evidence shows an association between cannabis use and symptoms of psychosis (for reviews, see D'Souza, 2007; Minozzi et al. 2010). Three main inferences may be drawn from this extensive body of research. "
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    ABSTRACT: Background: Although cannabis abuse (CA) is known to be associated with schizophrenia, the causal nature of this association is unclear, with prodromal effects complicating its interpretation. Method: From Swedish national registry databases, we used a co-relative case-control design with full-sibling, half-sibling and first-cousin comparisons, alongside a general Swedish population sample. Using ICD codes, 5456 individuals with an initial diagnosis of schizophrenia (2000-2010) were matched with five schizophrenia-free controls. We further identified first-cousin, half-sibling and full-sibling pairs discordant for CA and statistically extrapolated results for discordant monozygotic (MZ) twins. Results: Within the general Swedish population, CA was strongly associated with later schizophrenia [odds ratio (OR) 10.44, 95% confidence interval (CI) 8.99-12.11]. This association was substantially attenuated both by increasing temporal delays between CA exposure and schizophrenia diagnosis and by controlling for increasing degrees of familial confounding. Extrapolated discordant MZ pairs suggested that fully controlling for confounding familial factors reduced the association between CA and later schizophrenia to more modest levels (ORs of approximately 3.3 and 1.6 with 3- and 7-year temporal delays respectively). Opiate, sedative, cocaine/stimulant and hallucinogen abuse were also strongly associated with subsequent schizophrenia in the general population. After controlling for familial confounding, only cocaine/stimulant exposure remained associated. Conclusions: CA has an appreciable causal impact on future risk for schizophrenia. However, population-based estimates of cannabis-schizophrenia co-morbidity substantially overestimate their causal association. Predictions of the cases of schizophrenia that might be prevented by reduced cannabis consumption based on population associations are therefore likely to be considerably overestimated.
    Full-text · Article · Jul 2014 · Psychological Medicine
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    ABSTRACT: Psychotic syndromes can be understood as disorders of adaptation to social context. Although heritability is often emphasized, onset is associated with environmental factors such as early life adversity, growing up in an urban environment, minority group position and cannabis use, suggesting that exposure may have an impact on the developing 'social' brain during sensitive periods. Therefore heritability, as an index of genetic influence, may be of limited explanatory power unless viewed in the context of interaction with social effects. Longitudinal research is needed to uncover gene-environment interplay that determines how expression of vulnerability in the general population may give rise to more severe psychopathology.
    Full-text · Article · Nov 2010 · Nature
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