The association between cannabis abuse and subsequent schizophrenia: a Swedish national co-relative control study.
G N Giordano, H Ohlsson, Kristina Sundquist, Jan Sundquist, K S Kendler
Psychological Medicine January 2015 DOI: 10.1017/s0033291714001524 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Co-relative case-control study Peer reviewed |
|---|---|
| Sample size | 5,456 |
| Population | Swedish national registry individuals with an initial schizophrenia diagnosis (2000-2010) and matched schizophrenia-free controls, plus first-cousin, half-sibling, and full-sibling pairs discordant for cannabis abuse |
| Topics | Cannabis |
| Keywords | Causality Co-relative design Cocaine Schizophrenia |
| Key findings | Cannabis abuse is associated with later schizophrenia in the general population (OR 10.44), but this association is substantially attenuated by longer temporal delays and by controlling for familial confounding, with extrapolated discordant monozygotic twin comparisons suggesting fully controlled ORs of approximately 3.3 and 1.6 at 3 and 7 years. The authors argue that cannabis has an appreciable causal impact on schizophrenia risk, but that population-based estimates substantially overestimate the causal association. |
Abstract
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. 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. 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. 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.
Comparable studies
Other observational and cohort studies on cannabis, most cited first.
| Study | Year | Design | Participants |
|---|---|---|---|
| High-potency cannabis and the risk of psychosis People with first episode of psychosis and healthy controls from the local population | 2009 | Case-control study | n = 454 |
| Ayahuasca-Assisted Therapy for Addiction: Results from a Preliminary Observational Study in Canada Rural aboriginal population | 2013 | Observational study | |
| Impaired cognitive performance in drug free users of recreational ecstasy (MDMA) Otherwise healthy young people | 2000 | Observational | |
| Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study Individuals from the general population in Germany aged 14-24 at baseline | 2011 | Observational cohort | n = 1,923 |
| Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders: follow-up study of 535 incident cases Patients treated for cannabis-induced psychotic symptoms in Denmark between 1994 and... | 2005 | Observational cohort | n = 535 |
Citations in the library
Cited by 12
- Repeated Exposure to the “Spice” Cannabinoid JWH-018 Induces Tolerance and Enhances Responsiveness to 5-HT1A Receptor Stimulation in Male Rats Frontiers in Psychiatry February 27, 2018
- From heavy cannabis use to psychosis: is it time to take action? Irish Journal of Psychological Medicine May 27, 2021
- Development and initial validation of the cannabis-related psychosis risk literacy scale (CPRL): a multinational psychometric study BMC Psychiatry April 19, 2024
- Assessing evidence supporting cannabis harm reduction practices for adolescents at clinical high-risk for psychosis: a review and clinical implementation tool. Psychological Medicine 2024
- Cannabis and Psychosis: An Overview of The Relationship Revista Portuguesa de Psiquiatria e Saúde Mental September 30, 2023
and 7 more in the library
Cites 7
- Causal association between cannabis and psychosis: examination of the evidence The British Journal of Psychiatry January 30, 2004
- High-potency cannabis and the risk of psychosis The British Journal of Psychiatry November 30, 2009
- An overview of systematic reviews on cannabis and psychosis: Discussing apparently conflicting results Drug and Alcohol Review May 1, 2010
- Are Cannabis Use Disorders Associated with an Earlier Age at Onset of Psychosis? A Study in First Episode Schizophrenia Schizophrenia Research May 14, 2010
- Assessing evidence for a causal link between cannabis and psychosis: a review of cohort studies. The International journal on drug policy 2010
and 2 more in the library