What you carry at this position in your DNA and what research says about it.
Vitamin K and Bone Health: 8/10 evidence, 42 publications.
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Sample genotype (not yours): C/C
Typical Vitamin K Recycling and Bone Density
Efficient recycling of vitamin K supports normal bone mineralization and typical bone density. Standard clinical guidelines apply if taking blood thinners.
What this genotype means: Efficient vitamin K recycling; Typical bone mineral density; Greater warfarin sensitivity.
Sample genotype (not yours): C/T
Typical Bone Density with Altered Medication Response
Vitamin K recycling remains sufficient to support typical bone density. Reduced response to certain blood thinners.
What this genotype means: Typical bone mineral density; Reduced warfarin response; Increased risk of irinotecan-induced neutropenia.
Sample genotype (not yours): T/T
Lower Vitamin K Recycling and Higher Medication Requirements
Reduced efficiency in recycling vitamin K is linked to lower bone density. Typically reduced response to blood thinners.
What this genotype means: Lower bone mineral density; Reduced response to blood thinners; Increased risk of irinotecan-induced neutropenia.
Gene function and biological role
Gene Function: The VKORC1 gene encodes the vitamin K epoxide reductase complex subunit 1 enzyme, which is responsible for recycling vitamin K in the body. This recycling process converts inactive vitamin K back into its active form, which is essential for blood clotting and bone mineralization. Without sufficient active vitamin K, key proteins like osteocalcin cannot bind calcium to strengthen bones. The enzyme is also the primary target of anticoagulant medications like warfarin, which work by inhibiting its recycling activity.
Variant Impact: The rs7294 variant is located in the 3 prime untranslated region of the VKORC1 gene, a region critical for regulating gene expression. This genetic change is a regulatory polymorphism that alters the stability of the messenger RNA and affects how much enzyme is produced. Because it modifies the abundance of the VKORC1 enzyme, it directly impacts the rate of vitamin K recycling. These changes in enzyme levels also alter how sensitive the body is to vitamin K-inhibiting medications.
Key Insight: This single genetic variant acts as a bridge between how your body builds bone density and how it responds to common blood thinners.
Location: VKORC1. Chromosome 16 · 16p11.2 · 31.1 Mb
Estimated prevalence by population
Global 36.4%; European 38.1%; African 29.3%; East Asian 79.8%; South Asian 8.4%; Americas 36.0%; Ashkenazi 49.0%; Finnish 38.7%; Middle Eastern 56.5%; Amish 46.1%.
Estimated CC genotype frequency.
Global 46.6%; European 47.3%; African 49.7%; East Asian 19.1%; South Asian 41.2%; Americas 48.0%; Ashkenazi 42.0%; Finnish 47.0%; Middle Eastern 37.3%; Amish 43.6%.
Estimated CT genotype frequency.
Global 17.0%; European 14.7%; African 21.0%; East Asian 1.1%; South Asian 50.5%; Americas 16.0%; Ashkenazi 9.0%; Finnish 14.3%; Middle Eastern 6.2%; Amish 10.3%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Organ Systems
Bone, Joint & Connective Tissue Health
Bone Mineral Density. Evidence: 3/10. Source: PMID 19436136. Typical Density.
Pharmacogenomics
Anticoagulant & Blood Thinner Response
Warfarin Dosage. Evidence: 8/10. Source: PMID 15358623. Higher Sensitivity.
Acenocoumarol Dosage. Evidence: 5/10. Source: PMID 29479633. Typical Response.
Chemotherapy Response
Irinotecan Toxicity. Evidence: 5/10. Source: PMID 38344867. Typical Risk.
Showing effects for C/T genotype
Warfarin Dosage. Evidence: 8/10. Source: PMID 15358623. Higher Tolerance.
Acenocoumarol Dosage. Evidence: 5/10. Source: PMID 29479633. Higher Tolerance.
Irinotecan Toxicity. Evidence: 5/10. Source: PMID 38344867. Higher Toxicity Risk.
Showing effects for T/T genotype
Bone Mineral Density. Evidence: 3/10. Source: PMID 19436136. Lower Density.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Efficient recycling of vitamin K ensures that the body has a steady supply of the active cofactor needed to activate osteocalcin, a protein vital for binding calcium to the bone matrix. This process helps maintain typical bone mineral density over time. In cardiovascular care, this genotype is associated with typical sensitivity to vitamin K antagonists. Clinical data show that individuals with this genotype are generally more sensitive to warfarin than those carrying the T allele. Standard dosing algorithms often utilize this genetic marker to optimize therapeutic initiation.
Efficient vitamin K recycling; Typical bone mineral density; Greater warfarin sensitivity.
Sample genotype: CT (Heterozygous)
Sufficient enzyme activity is maintained to support normal calcium binding in the bones, preserving typical bone mineral density. However, the presence of one T allele alters the expression of the VKORC1 enzyme, which impacts sensitivity to medications. Clinical studies indicate that individuals with this genotype typically respond less strongly to anticoagulants like warfarin, acenocoumarol and phenprocoumon. There is also a noted association with an increased risk of severe neutropenia when undergoing chemotherapy with irinotecan.
Typical bone mineral density; Reduced warfarin response; Increased risk of irinotecan-induced neutropenia.
Sample genotype: TT (Homozygous)
Reduced efficiency in the VKORC1 enzyme limits the continuous recycling of vitamin K, which can lower the levels of active vitamin K available for bone-building proteins. Over time, this reduced activation of osteocalcin is associated with lower bone mineral density. When taking vitamin K antagonists like warfarin, the altered enzyme expression means the drug is typically significantly less effective. A similarly reduced response is observed for other blood thinners such as acenocoumarol and phenprocoumon. Additionally, this genotype is linked to a higher risk of bone marrow suppression during irinotecan chemotherapy.
Lower bone mineral density; Reduced response to blood thinners; Increased risk of irinotecan-induced neutropenia.
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
Content updated August 2026.
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