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Youth

Cannabis Use Contributes to Schizophrenia, Especially in Adolescents

Strategic Insights

— 1 min read

A recent study has revealed a direct link between cannabis use and an increased risk of developing psychosis-like events and schizophrenia, particularly in adolescents. The study analyzed 18 epidemiological studies and randomized clinical trials to investigate the association between cannabis use and psychotic symptoms or schizophrenia. The results showed that cannabis use increased the risk of developing psychosis-like events or schizophrenia by 2.88 times, with a significant increase in risk if use occurred during adolescence.

Key Takeaways:

  • The odds ratio of developing psychosis-like events or schizophrenia was 2.88, indicating a significant increase in risk.
  • Cannabis use during adolescence increased the risk of developing psychosis-like events or schizophrenia by two times.
  • The Hill criteria indicated a high likelihood for the contribution of cannabis to schizophrenia development.
  • The study found that the "exogenous cannabinoid hypothesis" for acute effects and the "shared vulnerability" hypothesis were not supported.
  • The researchers suggested that cannabinoids may have two major psychotic effects: acute psychotic sensations comparable to other hallucinogenic drugs and altered synaptic plasticity during adolescence.
  • The study found a strong age effect, with adolescents showing a much higher odds ratio (26.7) after adjusting for confounders.

Statistics:

  • Odds ratio of developing psychosis-like events or schizophrenia: 2.88
  • Risk increase with cannabis use during adolescence: 2 times
  • Number of studies that met the criteria: 10 out of 18
  • Percentage of studies with a significant increase in risk: 90% (9 out of 10 studies)
  • Odds ratio for adolescents after adjusting for confounders: 26.7

Sources:

  • Pourebrahim S, Ahmad T, Rottmann E, et al. Does cannabis use contribute to schizophrenia? A causation analysis based on epidemiological evidence. Biomolecules. 2025 Mar 4: 15(3):368. https://doi-org.sdpl.idm.oclc.org/10.3390/biom15030368

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