What you carry at this position in your DNA and what research says about it.
Nicotine Metabolism: 5/10 evidence, 18 publications.
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Sample genotype (not yours): A/A
Typical Nicotine Metabolism
Standard enzyme activity clears nicotine from the body at an expected rate. This typical clearance rate means cravings may return more quickly, which is associated with a higher daily cigarette consumption among smokers.
What this genotype means: Typical nicotine clearance rate; Higher average smoking quantity; Standard activation of tobacco carcinogens.
Sample genotype (not yours): A/T
Slower Nicotine Metabolism
Carrying one copy of the inactive variant moderately reduces enzyme activity, slowing down nicotine clearance. This prolonged presence of nicotine in the bloodstream is linked to smoking fewer cigarettes per day and a reduced exposure to tobacco toxins.
What this genotype means: Reduced nicotine clearance rate; Lower average smoking quantity; Decreased activation of tobacco carcinogens.
Sample genotype (not yours): T/T
Slowest Nicotine Metabolism
Having two copies of the inactive variant leads to a near-complete loss of enzyme function, severely delaying nicotine clearance. This slow clearance rate is associated with the lowest daily cigarette consumption and reduced activation of tobacco carcinogens.
What this genotype means: Profoundly delayed nicotine clearance; Lowest average smoking quantity; Minimal activation of tobacco carcinogens.
Gene function and biological role
Gene Function: CYP2A6 encodes cytochrome P450 2A6, a major liver enzyme responsible for metabolizing nicotine into cotinine [1]. It also plays a critical role in activating several tobacco-specific nitrosamines into active carcinogens [2]. Variations in this gene significantly influence smoking behaviors, nicotine dependence, and the clearance rate of various pharmaceutical drugs [3]. Slower metabolizers of this enzyme tend to smoke fewer cigarettes and have an easier time quitting [4].
Variant Impact: The rs1801272 variant, also known as the CYP2A6*2 allele, is a missense mutation that changes the amino acid leucine to histidine at position 160 [5]. This specific amino acid substitution results in a completely inactive enzyme, rendering carriers unable to metabolize substrates through this pathway [4]. Consequently, individuals with this variant experience significantly prolonged nicotine half-life in the body [1]. This slow clearance rate directly impacts smoking frequency and tobacco exposure [3].
Key Insight: Slower nicotine clearance naturally reduces the urge to smoke frequently, acting as a genetic shield against heavy tobacco use.
Location: CYP2A6. Chromosome 19 · 19q13.2 · 40.8 Mb
Estimated prevalence by population
Global 96.4%; European 95.0%; African 99.1%; East Asian > 99.9%; South Asian 98.1%; Americas 95.4%; Ashkenazi 95.7%; Finnish 94.9%; Middle Eastern 96.6%; Amish 88.9%.
Estimated AA genotype frequency.
Global 3.5%; European 5.0%; African 0.9%; East Asian < 0.1%; South Asian 1.9%; Americas 4.5%; Ashkenazi 4.2%; Finnish 5.0%; Middle Eastern 3.3%; Amish 10.8%.
Estimated AT genotype frequency.
Global < 0.1%; European 0.1%; African < 0.1%; East Asian < 0.1%; South Asian < 0.1%; Americas 0.1%; Ashkenazi < 0.1%; Finnish 0.1%; Middle Eastern < 0.1%; Amish 0.3%.
Estimated TT genotype frequency.
Showing effects for A/A genotype
Pharmacogenomics
Drug Metabolism Enzyme Activity
Nicotine Metabolism. Evidence: 5/10. Source: PMID 9827545. Typical.
Anticoagulant & Blood Thinner Response
Warfarin Sensitivity. Evidence: 3/10. Source: PMID 33437219. Typical.
Neurology & Mental Health
Addiction & Reward
Smoking Intensity. Evidence: 4/10. Source: PMID 23049750. Higher.
Immunity & Inflammation
Inflammatory & Circulating Protein Markers
C-Reactive Protein. Evidence: 8/10. Source: PMID 35459240. Higher.
Showing effects for A/T genotype
Nicotine Metabolism. Evidence: 5/10. Source: PMID 9827545. Slower.
Warfarin Sensitivity. Evidence: 3/10. Source: PMID 33437219. Increased.
Smoking Intensity. Evidence: 4/10. Source: PMID 23049750. Lower.
C-Reactive Protein. Evidence: 8/10. Source: PMID 35459240. Lower.
Showing effects for T/T genotype
Nicotine Metabolism. Evidence: 5/10. Source: PMID 9827545. Slowest.
Smoking Intensity. Evidence: 4/10. Source: PMID 23049750. Lowest.
C-Reactive Protein. Evidence: 8/10. Source: PMID 35459240. Lowest.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Standard liver enzyme function is maintained by this genotype, leading to the typical rapid clearance of nicotine into its inactive metabolite, cotinine [1]. Because nicotine is cleared quickly, the brain's reward pathways are rapidly depleted, which often prompts more frequent smoking to maintain stable nicotine levels [2]. Studies show that individuals with this genotype tend to smoke more cigarettes per day compared to those with the slower-metabolizing variant [3]. Additionally, this standard metabolic rate is associated with higher levels of C-reactive protein, a common marker of systemic inflammation [4]. Fast metabolism also means tobacco-specific carcinogens are more readily activated in the body [5].
Typical nicotine clearance rate; Higher average smoking quantity; Standard activation of tobacco carcinogens.
Sample genotype: AT (Heterozygous)
Enzyme activity is moderately reduced due to the presence of one inactive copy of the CYP2A6 gene [1]. Nicotine remains in the bloodstream for a longer duration, which naturally extends the time between cravings for smokers [2]. Consequently, individuals with this genotype often smoke fewer cigarettes daily and may find smoking cessation therapies more effective [3]. Slower metabolism also reduces the rate at which tobacco-specific nitrosamines are converted into active carcinogens, potentially offering a protective effect against tobacco-related health risks [4]. Furthermore, this genotype is associated with lower average levels of C-reactive protein, indicating reduced baseline inflammation [5].
Reduced nicotine clearance rate; Lower average smoking quantity; Decreased activation of tobacco carcinogens.
Sample genotype: TT (Homozygous)
Complete loss of functional CYP2A6 enzyme activity occurs with this genotype, resulting in a profound reduction in nicotine clearance [1]. Nicotine persists in the body for exceptionally long periods, which significantly decreases the physiological drive to smoke frequently [2]. Research indicates that individuals with this genotype smoke substantially fewer cigarettes per day and experience lower exposure to harmful tobacco combustion products [3]. This dramatic reduction in enzyme function also minimizes the metabolic activation of inhaled carcinogens, which are otherwise processed by this pathway [4]. Additionally, this genotype correlates with the lowest levels of C-reactive protein, suggesting a highly favorable profile for systemic inflammation markers [5].
Profoundly delayed nicotine clearance; Lowest average smoking quantity; Minimal activation of tobacco carcinogens.
Variants with shared genetic architecture
rs56113850 · CYP2A6 Gene · Chr 19 · Nicotine Metabolism
rs28399433 · CYP2A6 Gene · Chr 19 · Nicotine and Drug Metabolism
rs28399454 · CYP2A6 Gene · Chr 19 · Nicotine Metabolism
Genotyping of human cytochrome P450 2A6 (CYP2A6), a nicotine C-oxidase.
Phase I metabolic genes and risk of lung cancer: multiple polymorphisms and mRNA expression.
Genetic variation of CYP2A6, smoking, and risk of cancer.
Genetic analysis of over half a million people characterises C-reactive protein loci.
Content updated August 2026.
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