Genetic associations studied in cannabis-use patterns

Addiction Risk

Cannabis use research studies inherited differences in initiation and frequency of cannabis use.

GWAS work has identified variants linked to lifetime cannabis use, with overlap with risk tolerance and other substance use traits.

This result reflects research-level variation in cannabis use traits and is not a diagnosis of cannabis use disorder.

Social environment, age of first use, mental health, peers, legal context, and access all strongly shape actual cannabis use.

All traits Compare samples

Selected sample: Demo Report
Report markers: 8 SNP entries
Genes: 0
Research: 1 study

Important Medical Disclaimer

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Research summary

What this trait studies

Research summary, not an individual result

This trait is presented as population-level genetic research rather than an individual Low/High verdict, because the science behind it is either too preliminary, too easily misread as a diagnosis, or too sensitive to responsibly reduce to a single badge.

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Explore the evidence

Behind this report

Review the genes, tested markers and supporting research.

SNPs tested

These are the unique genetic markers analyzed for this trait. Genotypes showing "--" were not identified in your DNA file. Report marker totals can include repeated study entries; this table shows each SNP once.

Genotypes and reported variant frequencies
SNP	Genotype	Variant allele	Frequency
rs2875907	AG		35.20%
rs9919557	--		61.40%
rs9773390	--		93.30%
rs10085617	--		41.60%
rs10499	--	A	65.10%
rs1448602	--		75.57%
rs17761723	--	T	34.60%
rs7651996	--	T	47.70%

DNA Genics reports genotypes based on the 'positive' strand of the human genome reference sequence (build 37/HG19). Other companies may use the opposite strand, so genotypes may need conversion for comparison.

Research studies

The following peer-reviewed scientific studies support the genetic associations analyzed in this report.

GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal influence of schizophrenia

Evidence

Very strong scientific evidence

2018 Sep Nat Neurosci

Authors: Pasman JA, Verweij KJH, Gerring Z, Stringer S, Sanchez-Roige S, Treur JL, Abdellaoui A, Nivard MG, Baselmans BML, Ong JS, Ip HF, van der Zee MD, Bartels M, Day FR, Fontanillas P, Elson SL, , de Wit H, Davis LK, MacKillop J, , , Derringer JL, Branje SJT, Hartman CA, Heath AC, van Lier PAC, Madden PAF, Mägi R, Meeus W, Montgomery GW, Oldehinkel AJ, Pausova Z, Ramos-Quiroga JA, Paus T, Ribases M, Kaprio J, Boks MPM, Bell JT, Spector TD, Gelernter J, Boomsma DI, Martin NG, MacGregor S, Perry JRB, Palmer AA, Posthuma D, Munafò MR, Gillespie NA, Derks EM, Vink JM

Study sample: 184,756 individuals (european ancestry)