Cannabis Genetic Response Tool

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Explore genetic variants studied in relation to cannabis use

Important — Please Read

This is vibe coded SLOP and results may not be correct. This tool displays genetic variants that have been discussed in scientific research. It is for educational and informational purposes only and is not a medical test, diagnosis, or risk assessment. Results should not be used to make health, treatment, or lifestyle decisions.

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Supports 23andMe, AncestryDNA, and similar formats

Your Results Summary

Below are your genotypes at variants that have been studied in published research. Evidence quality varies - each variant has been labeled to help you understand how robust the findings are.

Putting This In Context

What This Doesn't Tell You

  • Your actual probability of developing psychosis
  • Whether cannabis is "safe" or "unsafe" for you
  • How different products, doses, or frequencies might affect you

Non-Genetic Risk Factors (Often More Important)

  • Family history — First-degree relative with schizophrenia/psychosis is a major risk factor
  • Age of first use — Adolescent use (especially before 15) carries higher risk
  • Frequency & potency — Daily use of high-THC products increases risk substantially
  • Personal history — Previous psychotic symptoms, even brief ones
  • Childhood trauma — Associated with increased vulnerability
  • Sex — Males show higher rates of cannabis-related psychotic disorder in most studies, and some genetic effects appear sex-dependent

How To Interpret Gene-Environment Research

Most of these genetic variants only show effects in people who use cannabis frequently (daily or near-daily). Studies generally don't find the same associations with occasional use. The "risk alleles" don't cause psychosis on their own — they may increase vulnerability in the context of heavy use.

Why Single Variants Tell A Limited Story

This tool looks at individual genetic variants one at a time. Modern research has largely moved toward polygenic risk scores that aggregate thousands of variants across the genome, because each individual SNP explains very little risk on its own. Studies using polygenic approaches find that cannabis use and schizophrenia genetic liability have independent effects, and that gene-environment interaction at the polygenic level is complex. Additionally, Mendelian randomization studies suggest that some of the association between cannabis and psychosis may reflect shared genetic liability — people genetically predisposed to schizophrenia may also be more likely to use cannabis — rather than a purely causal cannabis → psychosis pathway.

Key Research Papers

    This list is auto-generated from the studies referenced in the SNP database (plus a small set of featured background papers).

    🔒 Privacy First All processing happens locally in your browser. Your genetic data never leaves your device and is not stored anywhere.