Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Know Your Genetic Metabolism Profile: Variants in ADH1B and ALDH2 affect how your body processes alcohol. People who clear acetaldehyde slowly accumulate more of this toxic, carcinogenic byproduct when they drink, which is associated with higher risk of alcohol-related cancers. Understanding your metabolism profile can inform healthier drinking limits. National Institute on Alcohol Abuse and Alcoholism
Follow Low-Risk Drinking Guidelines: The NIAAA defines low-risk drinking as no more than 4 drinks on any day and 14 per week for men, and no more than 3 on any day and 7 per week for women. Many people are at lower risk drinking less than this, and some should not drink at all. If you have elevated genetic risk, consider reducing intake further or abstaining. NIAAA
Address Stress Without Alcohol: Using alcohol as a coping mechanism for stress is a key pathway to problematic use. Build alternative stress management strategies: regular exercise, mindfulness meditation, social connection, and professional support. These approaches address stress without reinforcing reward-seeking neural circuits. American Psychological Association
Be Aware of Family History: Having a first-degree relative with alcohol use disorder roughly doubles your own risk. If you have both elevated genetic risk scores and a positive family history, consider discussing preventive strategies with a healthcare provider and maintaining heightened awareness of consumption patterns. Mayo Clinic
Seek Help Early If Patterns Change: Increasing tolerance, difficulty controlling intake, drinking to avoid withdrawal symptoms, and neglecting responsibilities are warning signs. Evidence-based treatments for AUD - including naltrexone, acamprosate, CBT, and mutual support groups - are highly effective, especially when initiated early. Substance Abuse and Mental Health Services Administration
How much of this is genetic?
Genetics explains 49% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Verhulst, Neale & Kendler 2015, Psych Med
Background and further reading
Alcohol use disorder (AUD) is a medical condition characterised by an impaired ability to stop or control alcohol use despite adverse consequences. It lies on a spectrum from mild to severe, and is shaped by how the body metabolises ethanol, reward and stress circuitry in the brain, and social context. In the United States, an estimated 10.3% of adults (about 27 million people) met criteria for past-year AUD in 2024, and roughly one in three adults will meet criteria at some point in their lives [1]. Genetic variation contributes substantially to individual differences in consumption patterns, tolerance, and vulnerability to problematic use.
Genetic Basis: A meta-analysis of twin and adoption studies estimates the heritability of AUD at about 49% [2]. The best-characterised genetic influences involve the alcohol-metabolising enzymes encoded by ADH1B and ALDH2. The ADH1B variant rs1229984, which speeds the conversion of ethanol to the toxic intermediate acetaldehyde, and the ALDH2*2 allele (rs671, common in East Asian populations) that impairs acetaldehyde clearance, both raise acetaldehyde levels and produce an unpleasant facial-flushing reaction that is associated with reduced heavy drinking and lower risk of AUD [4][5]. Beyond these larger-effect variants, the trait is highly polygenic: a cross-ancestry study of problematic alcohol use in more than one million people identified 110 independent risk variants, implicating genes involved in metabolism, synaptic function, and brain signalling [3].
Environmental Factors: Because heritability is around half, non-genetic factors account for the remaining variation in AUD liability [2]. Key influences include cultural drinking norms, alcohol availability and pricing, peer behavior, stress exposure, and adverse childhood experiences. Early age at first drink is associated with later problematic use, and gene-environment interplay is common: inherited risk is more likely to translate into heavy drinking in permissive social settings and may be buffered by social structure and strong family bonds [1]. These associations describe population-level patterns and do not determine any individual's outcome.
The published research behind your score, and the variants it draws on.
12 published scores from 5 studies
The alcohol use disorder score combines 12 polygenic scores drawn from 5 published studies.
These traits are influenced by some of the same genes and variants as this one
Content updated August 2026.
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