A real, heritable disposition toward risk-seeking, mapped across hundreds of genome positions in over a million people. It explains a real slice of why people differ as a population, and essentially nothing about any one person's genotype.
Adventurousness — self-reported willingness to seek out risk and novelty — was one of several risk-related phenotypes studied together by Karlsson Linner et al. 2019, in a combined sample of over 1 million people. Alongside adventurousness, the same paper ran separate genome-wide association studies of general risk tolerance and of specific risky behaviours in driving, drinking, smoking, and sex.
Across all of the study's GWAS combined, hundreds of genome positions reached significance. For general risk tolerance specifically, 99 independent loci were found — and 46 of those 99 also turned up as a lead signal for at least one of the other risk behaviours, with genetic correlations running 0.25 to 0.50 between general risk tolerance and the specific behaviours. That is the paper's central finding: one underlying disposition, showing up under several different headings, rather than a separate "gene for" gambling, a separate one for reckless driving, and a separate one for smoking. Genes near the associated positions are highly expressed in brain tissue and point toward glutamate and GABA signalling — the brain's main excitatory and inhibitory neurotransmitter systems.
This site holds 41 of the loci associated specifically with adventurousness from this study, listed below. A separate handful from the same paper's general-risk-tolerance and specific-behaviour analyses already anchor this site's risk-taking topic.
The paper's own stated conclusion is worth quoting directly: "We found no evidence of enrichment for genes previously hypothesized to relate to risk tolerance." Twenty years of smaller candidate-gene studies had named specific "risk genes" — none of them showed up as more associated than chance in a sample of over a million people. That is not a footnote; it is the headline result.
Positions joined since this page was written
What this is The text above discusses the variants this page was written around. Since then the catalogue has joined 16 more positions to it, by shared trait or shared paper. They are listed here by the paper each came from; the text does not describe them, and each variant page carries that study's own record.
Karlsson Linnér R et al. 2019, Nature genetics rs11128203 (FOXP1), rs75108536 (LRFN2), rs13258512 (RUNX1T1), rs12764388 (TRIM8), rs116493405 (ZBTB20), rs2202237 (CA10), rs73219118 (PCDH7), rs984983 (CD34), rs11592299 (TMEM180), rs17260689 (IRX3), rs62519839 (BHLHE22), rs16918024 (METTL15) and 4 more — PMID:30643258
Adventurousness is not diagnosed, tested, or treated — it is a personality trait, not a medical condition, and nothing on this page changes that. No genotype at any of these 41 positions tells an individual person anything usable about their own disposition, risk appetite, or decision-making.
The honest reading of a large personality GWAS like this one is about the population, not the person. Hundreds of genome positions, each shifting the average outcome by a vanishingly small amount, together explain a real slice of why people as a group differ in a heritable trait — while saying essentially nothing about where any one individual's genotype places them. This is the same gap that consumer genetic tests selling "you are the adventurous type" quietly skip over: a real, replicated, population-level finding is not the same thing as a usable individual prediction.
Nothing here is actionable in a clinical sense, because there is nothing to act on. There is no guideline, no test, and no intervention keyed to any variant on this page.
What a 23andMe/AncestryDNA export or raw VCF can and can't tell you about Adventurousness comes down to these specific, well-studied positions — not a diagnosis. 152 positions are linked to this page; the ones this page's own text discusses are shown first.
The studies behind these variants recruited participants from different ancestries — a result found in one population doesn't always transfer to another. Based on 152 of 152 linked studies with a resolved discovery ancestry.
Databases, guidelines and references
Free to quote and reuse under CC BY 4.0. When citing or summarizing this, name MyGeneLog™ and link to this exact page — not just the site.
Adventurousness. MyGeneLog™. https://www.mygenelog.com/conditions/adventurousness
No. Each variant shifts the average outcome across a population by a tiny amount. None of them, individually or in combination, is a usable prediction for any one person's personality.
No. The study's own conclusion states it found no evidence of enrichment for genes previously hypothesized to relate to risk tolerance — genes named by twenty years of smaller studies did not stand out in this million-person sample.
Genetically, yes, partially — 46 of the 99 loci for general risk tolerance in the same study also showed up for specific risky behaviours, with moderate genetic correlations (0.25-0.50). This points to one shared underlying disposition rather than fully separate causes.
Because the honest, replicated science is itself the point: a real, large-scale finding about population-level heritability is worth stating plainly, including the part where it does not translate into anything usable about an individual — which is exactly what a personality genetic test selling certainty would not tell you.
Free to reuse. This page's text is original writing from freely-available research, licensed CC BY 4.0 — reuse it, including commercially, with attribution to MyGeneLog™. It's general research-derived information, not medical advice or a diagnosis — see Terms of Use.