Zammit · BMJ (Clinical research ed.) 2002 · historical cohort study · n=50087

Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study.

Cited 875 times in the scientific literature.

Level 3 - non-randomized controlled study

Historical cohort study with longitudinal register follow-up

PubMed 12446534 · doi:10.1136/bmj.325.7374.1199 · record verified 2026-08-26

What was done

Extended follow-up of a nationwide historical cohort of 50,087 Swedish males conscripted in 1969–1970 (>97% of the male population aged 18–20). Baseline self-reported data on cannabis and other drug use, along with social and psychological characteristics, were linked via national records to hospital admissions for ICD-8/9 schizophrenia and other psychoses. Analyses assessed dose-response trends, restricted to cannabis-only users, and excluded cases diagnosed within five years of conscription to reduce prodromal bias.

What was found

Cannabis exposure was associated with an increased risk of schizophrenia in a dose-dependent fashion: - In subjects who had ever used cannabis, adjusted odds ratio (aOR) for the linear trend of increasing frequency was 1.2 (95% CI 1.1 to 1.4, P < 0.001). - In subjects who used only cannabis and no other drugs, aOR for linear trend was 1.3 (95% CI 1.1 to 1.5, P < 0.015). - In the cannabis-only group, using cannabis >50 times had an aOR of 6.7 (95% CI 2.1 to 21.7). - Similar results remained after restricting analysis to subjects developing schizophrenia more than five years after conscription.

Why it matters

It demonstrates that the link between adolescent cannabis use and subsequent schizophrenia is dose-dependent and persists after controlling for other drug use and personality traits related to social integration.

Limits

The cohort included only young Swedish men, limiting generalizability to females and other populations. Drug use was measured solely by baseline self-report at age 18–20 without tracking post-conscription exposure changes, and residual confounding from unmeasured genetic or early environmental vulnerabilities remains possible.

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