What you carry at this position in your DNA and what research says about it.
Alcohol Sensitivity and Risk: 10/10 evidence, 104 publications.
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Sample genotype (not yours): T/T
Strong Protection Against Alcohol Dependence
Two copies of the fast-metabolizing allele provide powerful protection against alcohol abuse and related cancers. However, this genotype is also linked to a higher risk of gout.
What this genotype means: Strong protection against alcohol dependence; Significantly lower risk of esophageal and throat cancers; Lower average blood pressure and LDL cholesterol.
Sample genotype (not yours): C/C
Typical Alcohol Metabolism and Higher Dependence Risk
Two copies of the slow-metabolizing allele represent the typical global baseline, which is associated with a higher risk of alcohol dependence and related cancers. However, this genotype is protective against gout.
What this genotype means: Typical global rate of alcohol clearance; Higher risk of alcohol use disorder and dependence; Higher risk of esophageal and throat cancers.
Sample genotype (not yours): T/C
Moderate Protection Against Alcohol Dependence
One copy of the fast-metabolizing allele provides moderate protection against alcohol abuse and related cancers. There is also a slightly increased risk of developing gout.
What this genotype means: Moderate protection against alcohol dependence; Lower risk of esophageal and throat cancers; Slightly lower average blood pressure and LDL.
Gene function and biological role
Gene Function: The ADH1B gene encodes alcohol dehydrogenase 1B, a key enzyme responsible for metabolizing ethanol into acetaldehyde in the liver [1]. This enzyme represents the first and most critical step in clearing alcohol from the body [1]. Variations in this gene dictate how rapidly or slowly this conversion occurs, directly influencing how alcohol makes a person feel [2]. Fast-acting versions of the enzyme cause a rapid buildup of acetaldehyde, which can lead to unpleasant symptoms like facial flushing, nausea, and a rapid heart rate [2]. Consequently, these genetic differences are strong determinants of habitual drinking behavior and the long-term risk of developing alcohol dependence [3].
Variant Impact: The rs1229984 variant is a missense mutation in the ADH1B gene that alters the amino acid at position 48 from histidine to arginine [1]. This single amino acid change dramatically alters the enzyme's metabolic rate, with the histidine-encoding T allele producing a highly active enzyme that oxidizes alcohol up to 100 times faster than the arginine-encoding C allele [1]. Because the T allele converts alcohol to toxic acetaldehyde so rapidly, carriers experience immediate, uncomfortable side effects after drinking [2]. This rapid accumulation acts as a natural deterrent against heavy drinking, significantly reducing the likelihood of alcohol abuse [2]. Conversely, the slow-metabolizing C allele allows alcohol to linger, making drinking more tolerable but increasing the risk of overconsumption and related health issues [3].
Key Insight: The same genetic variant that protects against alcohol addiction by making drinking unpleasant also significantly lowers the risk of several cancers, but paradoxically increases the risk of gout.
Location: ADH1B. Chromosome 4 · 4q23 · 99.3 Mb
Origin Story: The protective T allele has undergone strong positive selection in East Asian populations, where its frequency is exceptionally high, likely coinciding with the historical expansion of rice domestication and early agriculture of fermented beverages.
Estimated prevalence by population
Global 2.0%; European 0.1%; African < 0.1%; East Asian 49.5%; South Asian 0.2%; Americas 0.5%; Ashkenazi 7.2%; Finnish < 0.1%; Middle Eastern 4.6%; Amish 1.0%.
Estimated TT genotype frequency.
Global 8.0%; European 6.9%; African 2.4%; East Asian 41.7%; South Asian 7.8%; Americas 12.7%; Ashkenazi 39.3%; Finnish 0.6%; Middle Eastern 33.7%; Amish 18.1%.
Estimated TC genotype frequency.
Global 90.0%; European 93.0%; African 97.6%; East Asian 8.8%; South Asian 92.0%; Americas 86.8%; Ashkenazi 53.5%; Finnish 99.4%; Middle Eastern 61.7%; Amish 80.8%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Neurology & Mental Health
Addiction & Reward
Alcohol Use Disorder. Evidence: 10/10. Source: PMID 30940813. Highly Decreased Risk.
Cancer & Oncology
Gastrointestinal Cancers
Esophageal Cancer. Evidence: 10/10. Source: PMID 19698717. ~0.56x Lower Risk.
Cardiovascular & Metabolic
Hypertension
Blood Pressure. Evidence: 10/10. Source: PMID 30595370. Lower Blood Pressure.
Gout & Uric Acid
Gout. Evidence: 10/10. Source: PMID 33832965. ~1.5x Higher Risk.
Obesity & Body Composition
Body Mass Index. Evidence: 10/10. Source: PMID 28892062. Lower BMI.
Lipids & Cholesterol
LDL Cholesterol. Evidence: 9/10. Source: PMID 32154731. Lower LDL.
Showing effects for C/C genotype
Alcohol Use Disorder. Evidence: 10/10. Source: PMID 30940813. Typical Risk.
Esophageal Cancer. Evidence: 10/10. Source: PMID 19698717. Typical Risk.
Blood Pressure. Evidence: 10/10. Source: PMID 30595370. Typical/Higher BP.
Gout. Evidence: 10/10. Source: PMID 33832965. Typical Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 28892062. Typical/Higher BMI.
LDL Cholesterol. Evidence: 9/10. Source: PMID 32154731. Typical/Higher LDL.
Showing effects for T/C genotype
Alcohol Use Disorder. Evidence: 10/10. Source: PMID 30940813. Decreased Risk.
Blood Pressure. Evidence: 10/10. Source: PMID 30595370. Slightly Lower BP.
Gout. Evidence: 10/10. Source: PMID 33832965. Slightly Higher Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 28892062. Slightly Lower BMI.
LDL Cholesterol. Evidence: 9/10. Source: PMID 32154731. Slightly Lower LDL.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Two copies of the T allele result in an exceptionally rapid conversion of alcohol into acetaldehyde [1]. This rapid buildup of acetaldehyde triggers immediate discomfort, such as facial flushing and nausea, making heavy drinking highly unpleasant [2]. Consequently, this genotype is strongly protective against alcohol use disorder, alcohol dependence, and alcoholic liver disease [3]. It also significantly reduces the risk of developing esophageal, oral, and throat cancers [4]. On the cardiovascular front, this genotype is associated with lower blood pressure, lower body mass index, and healthier LDL cholesterol levels [5]. However, the T allele is also linked to elevated serum urate levels, which increases the risk of developing gout [6]. This gout risk is particularly pronounced in individuals who continue to consume alcohol despite their natural sensitivity [7].
Strong protection against alcohol dependence; Significantly lower risk of esophageal and throat cancers; Lower average blood pressure and LDL cholesterol; Increased risk of elevated uric acid and gout.
Sample genotype: CC (Homozygous)
Two copies of the C allele result in a standard, slower rate of alcohol metabolism [1]. Because alcohol is cleared slowly, acetaldehyde levels rise gradually, making drinking more tolerable and less likely to cause immediate unpleasant symptoms like flushing [2]. While this makes social drinking easier, it lacks the natural genetic barrier against overconsumption, leading to a higher risk of alcohol use disorder and dependence [3]. Over time, higher alcohol consumption in this group is linked to an increased risk of esophageal, oral, and throat cancers [4]. This genotype is also associated with higher average blood pressure, higher body mass index, and elevated LDL cholesterol levels [5]. On the positive side, the absence of the T allele keeps serum urate levels lower, resulting in a typical or reduced risk of gout [6]. Maintaining a moderate alcohol intake is highly recommended to mitigate these risks [7].
Typical global rate of alcohol clearance; Higher risk of alcohol use disorder and dependence; Higher risk of esophageal and throat cancers; Lower risk of elevated uric acid and gout.
Sample genotype: TC (Heterozygous)
One copy of the T allele leads to a moderately accelerated conversion of alcohol into acetaldehyde [1]. This intermediate metabolic rate can cause mild flushing or discomfort after drinking, acting as a partial natural deterrent against heavy alcohol consumption [2]. As a result, this genotype is associated with a significantly reduced risk of alcohol dependence and alcohol use disorder compared to the typical genotype [3]. It also offers substantial protection against esophageal, oral, and throat cancers [4]. Additionally, carriers tend to have lower average blood pressure, lower body mass index, and lower LDL cholesterol levels [5]. However, the presence of the T allele also slightly increases serum urate levels, which can elevate the risk of gout [6]. This risk is highly dependent on lifestyle factors, especially alcohol intake [7].
Moderate protection against alcohol dependence; Lower risk of esophageal and throat cancers; Slightly lower average blood pressure and LDL; Slightly increased risk of elevated uric acid and gout.
Variants with shared genetic architecture
rs2066702 · ADH1B Gene · Chr 4 · Alcoholism Risk
rs1042026 · ADH1B Gene · Chr 4 · Alcohol Health Risks
rs11940694 · KLB Gene · Chr 4 · Alcohol Consumption and Gout
Functional validity, role, and implications of heavy alcohol consumption genetic loci.
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
Diversity and scale: Genetic architecture of 2068 traits in the VA Million Veteran Program.
Content updated August 2026.
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