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Study breakdown

Cannabis Likely Contributes to Schizophrenia Development, Especially in Adolescents

Systematic ReviewStrong evidence
The takeaway

A systematic review and causation analysis found cannabis use is likely causal for schizophrenia development, with an overall odds ratio of 2.88 and double the risk for adolescent users.

Mental health professionals, policymakers on cannabis regulation, parents of adolescents, psychosis researchers.

OR 2.88 for schizophrenia risk

What the researchers found

Analysis of 18 qualifying studies (10 included in forest plot) found all reported increased risk for psychosis-like events or schizophrenia with cannabis use, with 9 of 10 reaching significance. The overall odds ratio was 2.88 (CI 2.24-3.70). Adolescent use carried roughly double the risk compared to adult use. Hill causality criteria indicated a high likelihood of causal contribution.

Why it matters

While the association between cannabis and psychosis has been extensively documented, this study goes further by systematically applying formal causation criteria. The Hill analysis suggests this is not merely correlation but likely a genuine causal contribution, particularly concerning given the twofold higher risk during adolescence when brain development is ongoing.

The numbers in context

18 studies met search criteria. 10 included in forest plot. Overall OR 2.88 (CI 2.24-3.70). Twofold higher risk for adolescent use. 9 of 10 studies showed significant increase. All 18 studies reported increased risk.

How the study worked

Systematic literature review following PRISM guidelines. Epidemiological studies and randomized clinical trials investigating cannabis-psychosis links were identified. Ten studies were included in a forest plot analysis. Confounder analysis used funnel plots. The Hill causality criteria (nine criteria for inferring causation from epidemiological evidence) were applied to estimate the likelihood of a causal relationship.

What this study cannot tell us

Funnel plot indicated potential confounder effects. Cannot rule out shared genetic vulnerability or reverse causation entirely. Included studies varied in cannabis exposure definitions and outcome measures. Most studies were observational, inherently limiting causal inference despite Hill criteria application.

How to read the evidence

Strong: systematic review with formal causation analysis, consistent findings across 18 studies, and clear dose-response and age-dependent relationships.

When this study was published

2025 study

The bigger picture

This analysis adds to growing evidence that cannabis is not just associated with but likely contributes to schizophrenia. The stronger effect during adolescence points to a window of vulnerability during brain development. As cannabis potency increases and legalization expands access, the public health implications of this causal relationship become more pressing.

Questions still open

  • Is there a THC potency threshold below which schizophrenia risk is not elevated? Can the adolescent vulnerability window be more precisely defined? Would genetic screening identify individuals at highest risk from cannabis exposure?

Common questions

Does cannabis cause schizophrenia?
This systematic review applied formal causation criteria and concluded cannabis likely contributes to schizophrenia development, with an overall 2.88-fold increased risk. However, most cannabis users never develop schizophrenia, suggesting individual vulnerability plays a key role.
Is the risk higher for teenagers?
Yes. Adolescent cannabis use carried roughly double the risk compared to adult use, likely because the brain is still developing during this period and is more vulnerable to disruption.

Read the original research

Does Cannabis Use Contribute to Schizophrenia? A Causation Analysis Based on Epidemiological Evidence.

Biomolecules, 15(3)

Citation

Pourebrahim, Sepehr; Ahmad, Tooba; Rottmann, Elisabeth; Schulze, Johannes; Scheller, Bertram. (2025). Does Cannabis Use Contribute to Schizophrenia? A Causation Analysis Based on Epidemiological Evidence.. Biomolecules, 15(3). https://doi.org/10.3390/biom15030368

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