What you carry at this position in your DNA and what research says about it.
Blood Thinner Sensitivity: 8/10 evidence, 79 publications.
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Sample genotype (not yours): G/G
Typical Blood Thinner Sensitivity and Lower Cardiovascular Risk
A typical response to blood thinners is expected, because enzyme activity is normal. There is no elevated genetic risk for arterial calcification or lupus associated with this variant.
What this genotype means: Typical response to standard warfarin doses; Lower risk of bleeding complications on blood thinners; Typical baseline risk of aortic calcification.
Sample genotype (not yours): A/A
High Blood Thinner Sensitivity and Elevated Cardiovascular Risk
Significantly greater sensitivity to blood thinners, with a risk of severe bleeding. There is an elevated genetic risk for arterial calcification and lupus.
What this genotype means: Significantly greater sensitivity to warfarin; High risk of over-anticoagulation and bleeding; Elevated risk of aortic calcification.
Sample genotype (not yours): G/A
Increased Blood Thinner Sensitivity and Moderate Cardiovascular Risk
Greater sensitivity to blood thinners, with a higher bleeding risk. There is a moderately increased genetic risk for arterial calcification and lupus.
What this genotype means: Greater sensitivity to warfarin and other blood thinners; Increased risk of over-anticoagulation and bleeding; Moderately elevated risk of aortic calcification.
Gene function and biological role
Gene Function: The VKORC1 gene encodes vitamin K epoxide reductase complex subunit 1, an enzyme essential for recycling vitamin K in the body. This recycling process is critical for activating proteins that control blood clotting and bone mineralization [1]. Because it is the direct target of coumarin-based anticoagulants like warfarin, variations in this gene heavily influence how people respond to blood thinners [2]. Reduced activity of this enzyme can lead to a shortage of active vitamin K, affecting both cardiovascular health and bone density [3].
Variant Impact: The rs9934438 variant, also known as 1173C>T, is an intronic change in the VKORC1 gene that alters its expression levels. This molecular change directly impacts the availability of the active enzyme, thereby modifying sensitivity to oral anticoagulants [4]. The presence of the variant allele is strongly linked to a lower requirement for warfarin and related medications [5]. Beyond drug response, this genetic marker has been associated with differences in arterial calcification and susceptibility to autoimmune conditions [3].
Key Insight: Carrying the A allele of this variant makes you highly sensitive to common blood thinners like warfarin, meaning standard doses could cause dangerous bleeding. Surprisingly, this same genetic change is also linked to a higher risk of calcium buildup in your major arteries.
Location: VKORC1. Chromosome 16 · 16p11.2 · 31.1 Mb
Estimated prevalence by population
Global 49.3%; European 38.7%; African 81.1%; East Asian 1.1%; South Asian 67.5%; Americas 37.1%; Ashkenazi 25.0%; Finnish 37.2%; Middle Eastern 22.3%; Amish 31.2%.
Estimated GG genotype frequency.
Global 37.7%; European 47.0%; African 17.9%; East Asian 19.1%; South Asian 29.3%; Americas 47.6%; Ashkenazi 50.0%; Finnish 47.6%; Middle Eastern 49.8%; Amish 49.3%.
Estimated GA genotype frequency.
Global 13.0%; European 14.3%; African 1.0%; East Asian 79.7%; South Asian 3.2%; Americas 15.3%; Ashkenazi 25.0%; Finnish 15.2%; Middle Eastern 27.8%; Amish 19.5%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Anticoagulant Response. Evidence: 8/10. Source: PMID 16201835. Typical Sensitivity.
Cardiovascular & Metabolic
Vascular Health & Aneurysm
Arterial Calcification. Evidence: 3/10. Source: PMID 18218987. Typical Risk.
Immunity & Inflammation
Autoimmune Diseases
Lupus. Evidence: 3/10. Source: PMID 23124848. Typical Risk.
Organ Systems
Bone, Joint & Connective Tissue Health
Bone Mineral Density. Evidence: 3/10. Source: PMID 21179439. Typical BMD.
Showing effects for A/A genotype
Anticoagulant Response. Evidence: 8/10. Source: PMID 16201835. High Sensitivity.
Arterial Calcification. Evidence: 3/10. Source: PMID 18218987. 1.19x Increased Risk.
Lupus. Evidence: 3/10. Source: PMID 23124848. Increased Risk.
Bone Mineral Density. Evidence: 3/10. Source: PMID 21179439. Slightly Higher BMD.
Showing effects for G/A genotype
Anticoagulant Response. Evidence: 8/10. Source: PMID 16201835. Increased Sensitivity.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Normal levels of the VKORC1 enzyme are produced, maintaining standard vitamin K recycling. When prescribed blood thinners like warfarin, standard therapeutic doses are generally necessary to achieve effective anticoagulation [1]. There is a lower risk of accidental over-anticoagulation or major bleeding complications compared to carriers of the variant allele [2]. Additionally, this genotype is associated with a lower baseline risk of developing calcium deposits in the abdominal aorta [3]. Research also indicates a typical, non-elevated risk for systemic lupus erythematosus in Asian populations [4]. Bone mineral density is expected to be within the typical range for your demographic group. Unexpected sensitivity is less likely.
Typical response to standard warfarin doses; Lower risk of bleeding complications on blood thinners; Typical baseline risk of aortic calcification.
Sample genotype: AA (Homozygous)
Enzyme activity is substantially decreased because of two copies of the variant allele. A substantial reduction in enzyme levels leads to extreme sensitivity to vitamin K antagonists, meaning warfarin produces a very strong effect [1]. Standard dosing regimens present a high risk of rapid over-anticoagulation and major bleeding complications [2]. Calcium deposits are more likely to develop in the abdominal aorta due to altered vitamin K-dependent protein activation [3]. Furthermore, studies in Asian cohorts show a significantly higher risk of developing systemic lupus erythematosus [4]. Some evidence suggests a potential correlation with slightly higher bone mineral density in specific populations. Healthcare providers frequently adjust initial anticoagulant therapies downward when this genetic profile is known.
Significantly greater sensitivity to warfarin; High risk of over-anticoagulation and bleeding; Elevated risk of aortic calcification.
Sample genotype: GA (Heterozygous)
Enzyme production is moderately reduced due to the presence of one copy of the variant allele. When taking medications like warfarin, acenocoumarol, or phenprocoumon, the effect is typically stronger, with a risk of excessive blood thinning [1]. Initiating standard doses can significantly increase the risk of over-anticoagulation and serious bleeding events [2]. Beyond medication response, carrying this variant is associated with a 19% increased risk of calcium buildup in the abdominal aorta [3]. In Asian populations, it is also linked to an elevated susceptibility to systemic lupus erythematosus [4]. Slightly higher bone mineral density has been observed in some demographic groups with this variant. Medical professionals often utilize genetic testing to tailor blood thinner dosages more safely. Awareness of this sensitivity helps in understanding potential drug interactions and dietary vitamin K influences.
Greater sensitivity to warfarin and other blood thinners; Increased risk of over-anticoagulation and bleeding; Moderately elevated risk of aortic calcification.
Variants with shared genetic architecture
rs2359612 · VKORC1 Gene · Chr 16 · Cardiovascular Risk
rs2884737 · VKORC1 Gene · Chr 16 · Warfarin Sensitivity
rs61742245 · VKORC1 Gene · Chr 16 · Warfarin Resistance
A C1173T dimorphism in the VKORC1 gene determines coumarin sensitivity and bleeding risk.
Content updated August 2026.
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