What you carry at this position in your DNA and what research says about it.
Alcoholism Risk: 10/10 evidence, 28 publications.
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Sample genotype (not yours): G/G
Typical Alcoholism Risk
Alcohol is metabolized at a normal rate, resulting in a typical risk profile for alcohol dependence and related liver conditions. Standard therapeutic responses to alcohol treatment medications like naltrexone are expected.
What this genotype means: Typical alcohol metabolism rate; Standard risk of alcohol use disorder; Typical response to naltrexone.
Sample genotype (not yours): A/A
Lowest Alcoholism Risk
Alcohol is metabolized at an exceptionally fast rate, creating a strong natural deterrent against heavy drinking. This genotype provides the highest level of protection against alcohol use disorder and liver disease, but is linked to a poorer response to naltrexone.
What this genotype means: Extremely fast alcohol metabolism; Lowest risk of alcohol use disorder; Reduced response to naltrexone.
Sample genotype (not yours): G/A
Lower Alcoholism Risk
Alcohol is metabolized much faster than typical, which can cause rapid sedation and naturally discourages excessive drinking. This protective effect significantly lowers the risk of alcohol use disorder and liver disease, though it may reduce the effectiveness of naltrexone.
What this genotype means: Faster alcohol metabolism; Significantly lower risk of alcohol use disorder; Potentially reduced response to naltrexone.
Gene function and biological role
Gene Function: The ADH1B gene encodes a crucial subunit of alcohol dehydrogenase, an enzyme primarily responsible for metabolizing ethanol into acetaldehyde in the liver [1]. This enzyme represents the first and rate-limiting step of alcohol clearance in the body [1]. Variations in this gene can significantly alter the speed at which alcohol is broken down, directly influencing how much acetaldehyde accumulates after drinking [1]. Higher levels of acetaldehyde can cause rapid, uncomfortable physical reactions that naturally deter heavy drinking [1]. Consequently, ADH1B is one of the most well-studied genes associated with the risk of developing alcohol use disorders [2].
Variant Impact: This missense variant, rs2066702, causes an amino acid substitution from arginine to cysteine at position 370 of the ADH1B enzyme, defining the ADH1B*3 allele [3]. This structural change significantly alters the enzyme's kinetic properties, dramatically increasing its rate of alcohol metabolism [3]. Because the enzyme processes alcohol much faster, acetaldehyde levels rise rapidly after drinking, leading to increased sedation and other physical responses [1]. This rapid response acts as a natural protective mechanism against excessive drinking [1]. The variant is highly prevalent in populations of African ancestry but remains rare in other groups [4].
Key Insight: The ADH1B*3 variant increases the rate of alcohol breakdown by up to 30 times compared to the typical enzyme, leading to rapid sedation that naturally discourages heavy drinking.
Location: ADH1B. Chromosome 4 · 4q23 · 99.3 Mb
Estimated prevalence by population
Global 90.1%; European 99.7%; African 65.9%; East Asian 99.9%; South Asian 99.8%; Americas 96.6%; Ashkenazi 98.7%; Finnish > 99.9%; Middle Eastern 98.6%; Amish 100.0%.
Estimated GG genotype frequency.
Global 9.0%; European 0.3%; African 30.6%; East Asian 0.1%; South Asian 0.2%; Americas 3.4%; Ashkenazi 1.3%; Finnish < 0.1%; Middle Eastern 1.4%; Amish 0.0%.
Estimated GA genotype frequency.
Global 1.0%; European < 0.1%; African 3.5%; East Asian < 0.1%; South Asian < 0.1%; Americas < 0.1%; Ashkenazi < 0.1%; Finnish < 0.1%; Middle Eastern < 0.1%; Amish 0.0%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Neurology & Mental Health
Addiction & Reward
Alcohol Use Disorder. Evidence: 10/10. Source: PMID 30940813. Typical Risk.
Alcohol Consumption. Evidence: 9/10. Source: PMID 31151762. Typical Consumption.
Naltrexone Response. Evidence: 5/10. Source: PMID 34680127. Typical Response.
Organ Systems
Liver Function & Disease
Alcoholic Liver Disease. Evidence: 8/10. Source: PMID 39024449. Typical Risk.
Cardiovascular & Metabolic
Hypertension
Diastolic Blood Pressure. Evidence: 8/10. Source: PMID 39024449. Typical.
Showing effects for A/A genotype
Alcohol Use Disorder. Evidence: 10/10. Source: PMID 30940813. Lowest Risk.
Alcohol Consumption. Evidence: 9/10. Source: PMID 31151762. Lowest Consumption.
Naltrexone Response. Evidence: 5/10. Source: PMID 34680127. Poorer Response.
Alcoholic Liver Disease. Evidence: 8/10. Source: PMID 39024449. Lowest Risk.
Diastolic Blood Pressure. Evidence: 8/10. Source: PMID 39024449. Slightly Lower.
Showing effects for G/A genotype
Alcohol Use Disorder. Evidence: 10/10. Source: PMID 30940813. Reduced Risk.
Alcohol Consumption. Evidence: 9/10. Source: PMID 31151762. Lower Consumption.
Alcoholic Liver Disease. Evidence: 8/10. Source: PMID 39024449. Reduced Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Normal alcohol dehydrogenase activity means ethanol is processed at a standard pace, preventing the rapid accumulation of acetaldehyde [1]. Because there is no rapid buildup of acetaldehyde to cause immediate discomfort or sedation, there is no innate genetic deterrent against heavy drinking [1]. Large-scale genomic studies show that this typical baseline is associated with standard rates of alcohol consumption and alcohol use disorder [2]. It is also linked to typical baseline risks for alcoholic liver disease and standard diastolic blood pressure levels [3]. When treating alcohol dependence, standard clinical responses to the opioid antagonist naltrexone are typically observed [4].
Typical alcohol metabolism rate; Standard risk of alcohol use disorder; Typical response to naltrexone.
Sample genotype: AA (Homozygous)
Having two copies of the accelerated variant maximizes the conversion rate of alcohol to acetaldehyde [1]. The rapid accumulation of acetaldehyde typically causes immediate physical feedback, such as pronounced sedation, which strongly discourages heavy drinking [2]. Large-scale population studies demonstrate that this genotype is highly protective, resulting in the lowest rates of alcohol consumption and alcohol use disorder [3]. This robust protection also correlates with a significantly reduced risk of alcoholic liver disease and lower diastolic blood pressure [4]. On the other hand, pharmacogenomic research indicates that this metabolic profile is associated with a less effective response to naltrexone therapy [5].
Extremely fast alcohol metabolism; Lowest risk of alcohol use disorder; Reduced response to naltrexone.
Sample genotype: GA (Heterozygous)
Carrying one copy of the protective variant accelerates the breakdown of alcohol into acetaldehyde [1]. This rapid conversion often triggers swift physiological responses, such as increased sedation and mild discomfort, which serve as a natural barrier to overconsumption [2]. Multiple genetic studies confirm that this accelerated metabolism is strongly associated with lower overall alcohol intake and a reduced risk of developing alcohol use disorder [3]. The protective effect extends to a lower risk of alcoholic liver disease and slightly lower diastolic blood pressure [4]. However, clinical trials suggest that this accelerated metabolism profile is associated with a poorer response to naltrexone treatment for alcohol dependence [5].
Faster alcohol metabolism; Significantly lower risk of alcohol use disorder; Potentially reduced response to naltrexone.
Variants with shared genetic architecture
rs1229984 · ADH1B Gene · Chr 4 · Alcohol Sensitivity and Risk
rs1042026 · ADH1B Gene · Chr 4 · Alcohol Health Risks
rs1799971 · OPRM1 Gene · Chr 6 · Opioid and Pain Response
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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