This tool lets you explore genetic variants that have been studied in relation to cannabis use. It parses raw DNA data from services like 23andMe and AncestryDNA and shows you your genotypes at specific locations that researchers have investigated.
Why This Exists
Cannabis is increasingly legal and accessible, but not everyone responds to it the same way. A small percentage of users develop severe adverse effects such as psychosis, and researchers have been trying to understand why. Genetics appears to play a role — for example certain gene variants may increase vulnerability to cannabis-induced psychosis, particularly with heavy use.
This information exists in academic papers, but it's not easily accessible to regular people. This tool is an attempt to bridge that gap — to let curious individuals see their own genotypes at these studied variants and read plain-language summaries of the research.
What This Tool Is Not
This is not a clinical risk prediction tool. It cannot tell you whether you will or won't develop a specific positive or negative outcome of using cannabis. The science is still evolving, effect sizes are modest, and genetics is just one piece of a complex puzzle that includes family history, age of first use, frequency, potency, trauma history, and other factors.
Specifically, this tool:
- Does not provide medical advice
- Does not calculate a "risk score" or probability
- Does not account for gene-gene interactions or polygenic risk
- Does not consider your personal or family psychiatric history
- Is not a substitute for genetic counseling
The Science
The tool covers four categories of genetic variants studied in relation to cannabis response:
- Cannabis-psychosis interaction variants (AKT1, COMT, DRD2, BDNF) — These have been specifically studied for whether they moderate the relationship between cannabis use and psychosis risk. AKT1 rs2494732 is the most consistently replicated finding; COMT Val158Met was influential early on but has multiple null replications; DRD2 and BDNF variants have smaller evidence bases, sometimes with sex-specific or combination effects.
- Endocannabinoid system variants (FAAH, CNR1, MGLL) — These affect the body's own cannabinoid signaling. They are more commonly studied for dependence and withdrawal phenotypes than for psychosis directly.
- Dopamine pathway variants (DRD2 C957T, DAT1) — Relevant to schizophrenia biology generally, with limited cannabis-specific interaction evidence.
- THC metabolism (CYP2C9) — CYP2C9*3 carriers break down THC significantly slower, leading to higher blood levels from the same dose. This is the most pharmacologically straightforward finding in the tool, with strong evidence from controlled studies.
We've labeled each variant with an evidence tier (strong, moderate, preliminary) based on replication across studies. "Strong" doesn't mean definitive — it means the finding has been reproduced more consistently than others.
Important Context
Modern research has largely moved toward polygenic risk scores that aggregate thousands of variants, because each individual SNP explains very little risk on its own. This tool looks at variants one at a time — a useful educational lens, but not how the genetics of complex traits actually work. Additionally, Mendelian randomization studies suggest some of the association between cannabis and psychosis reflects shared genetic liability (people predisposed to schizophrenia may be more likely to use cannabis) rather than a purely one-directional causal pathway.
Key Research Papers
- Di Forti M, et al. (2012). Confirmation that the AKT1 (rs2494732) genotype influences the risk of psychosis in cannabis users. Biological Psychiatry.
- Caspi A, et al. (2005). Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the COMT gene. Biological Psychiatry.
- Colizzi M, et al. (2015). Interaction between functional genetic variation of DRD2 and cannabis use on risk of psychosis. Schizophrenia Bulletin.
- Hindocha C, et al. (2020). Do AKT1, COMT and FAAH influence reports of acute cannabis intoxication experiences? Translational Psychiatry.
- Sachse-Seeboth C, et al. (2009). Interindividual variation in the pharmacokinetics of Δ9-THC as related to genetic polymorphisms in CYP2C9. Clinical Pharmacology & Therapeutics.
- Carvalho C & Vieira-Coelho MA (2022). Cannabis induced psychosis: A systematic review on the role of genetic polymorphisms. Pharmacological Research.
- Gage SH, et al. (2017). Association between cannabis and psychosis: epidemiologic evidence. Psychological Medicine. (Mendelian randomization)
- Wainberg M, et al. (2021). Cannabis, schizophrenia genetic risk, and psychotic experiences. Translational Psychiatry. (Polygenic risk scores)
- NASEM (2017). The Health Effects of Cannabis and Cannabinoids. National Academies Press.
Privacy
Your genetic data never leaves your device. All parsing happens locally in your browser using JavaScript. We don't upload, store, or transmit your data anywhere. There's no backend server, no analytics tracking your genotypes, no database of results.
Who Made This
Disclaimer
This tool is for educational and informational purposes only. It is not intended to diagnose, treat, or prevent any disease or condition. The information provided should not be used as a substitute for professional medical advice, diagnosis, or treatment. Always consult with a qualified healthcare provider or genetic counselor before making decisions based on genetic information.
The developer of this tool is not responsible for any actions taken based on the information provided.