What you carry at this position in your DNA and what research says about it.
Blood Clot Risk: 6/10 evidence, 56 publications.
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Sample genotype (not yours): G/G
Typical Blood Clotting Risk
Standard levels of prothrombin protein are maintained, resulting in a typical baseline risk for blood clots. No inherited elevation in clotting activity is present from this genetic marker.
What this genotype means: Typical baseline risk of deep vein thrombosis; Standard prothrombin levels in circulation.
Sample genotype (not yours): A/A
Highly Elevated Blood Clot Risk
Significantly higher prothrombin levels substantially increase the risk of serious clotting events. Proactive management and avoiding supplemental estrogens are critical for vascular safety.
What this genotype means: Over 6-fold higher risk of venous thromboembolism; Substantially increased risk of deep vein thrombosis and pulmonary embolism.
Sample genotype (not yours): G/A
Moderately Increased Blood Clot Risk
Elevated prothrombin levels increase the likelihood of developing deep vein clots or pulmonary embolisms. Extra caution is warranted during high-risk events like surgery, pregnancy, or hormone therapy.
What this genotype means: Approximately 2.8-fold higher risk of venous thromboembolism; Elevated risk of clotting when taking estrogen-containing medications.
Gene function and biological role
Gene Function: Coagulation factor II, commonly known as prothrombin, is a critical protein in the blood clotting cascade. Produced by the liver, it is enzymatically cleaved to form active thrombin, which converts soluble fibrinogen into insoluble fibrin strands to seal blood vessels. Precise regulation of this pathway prevents both excessive bleeding and dangerous, spontaneous clotting. Variations in the gene encoding this protein can alter its expression levels or activity, directly shifting the body's delicate hemostatic balance.
Variant Impact: Located in the 3 prime untranslated region of the F2 gene, this specific single nucleotide change is widely known as the prothrombin G20210A mutation. The genetic alteration swaps a guanine for an adenine, which enhances the efficiency of mRNA processing. This molecular gain-of-function leads to increased accumulation of prothrombin messenger RNA. Consequently, the body produces elevated levels of plasma prothrombin, significantly predisposing the system to hypercoagulability and spontaneous clot formation.
Key Insight: This variant does not change the structure of the clotting protein itself, but rather acts like a volume booster, causing the body to produce too much of it. The risk of clotting is heavily amplified when combined with estrogen-containing medications like birth control pills.
Location: F2. Chromosome 11 · 11p11.2 · 46.7 Mb
Estimated prevalence by population
Global 98.1%; European 97.3%; African 99.5%; East Asian 100.0%; South Asian 99.8%; Americas 97.0%; Ashkenazi 94.3%; Finnish 99.0%; Middle Eastern 94.0%; Amish 100.0%.
Estimated GG genotype frequency.
Global 1.9%; European 2.7%; African 0.5%; East Asian 0.0%; South Asian 0.2%; Americas 3.0%; Ashkenazi 5.7%; Finnish 1.0%; Middle Eastern 5.9%; Amish 0.0%.
Estimated GA genotype frequency.
Global < 0.1%; European < 0.1%; African < 0.1%; East Asian 0.0%; 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
Cardiovascular & Metabolic
Coagulation & Clotting
Venous Thromboembolism. Evidence: 10/10. Source: PMID 26908601. Typical Risk.
Deep Vein Thrombosis. Evidence: 10/10. Source: PMID 26908601. Typical Risk.
Pulmonary Embolism. Evidence: 9/10. Source: PMID 26908601. Typical Risk.
Contraceptive Clot Risk. Evidence: 6/10. Source: PMID 12069454. Typical Risk.
Showing effects for A/A genotype
Venous Thromboembolism. Evidence: 10/10. Source: PMID 26908601. ~6.7x Increased Risk.
Deep Vein Thrombosis. Evidence: 10/10. Source: PMID 26908601. Highly Increased Risk.
Pulmonary Embolism. Evidence: 9/10. Source: PMID 26908601. Highly Increased Risk.
Contraceptive Clot Risk. Evidence: 6/10. Source: PMID 12069454. Highly Increased Risk.
Showing effects for G/A genotype
Venous Thromboembolism. Evidence: 10/10. Source: PMID 26908601. ~2.8x Increased Risk.
Deep Vein Thrombosis. Evidence: 10/10. Source: PMID 26908601. Increased Risk.
Pulmonary Embolism. Evidence: 9/10. Source: PMID 26908601. Increased Risk.
Contraceptive Clot Risk. Evidence: 6/10. Source: PMID 12069454. Increased Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Baseline levels of prothrombin circulate in the bloodstream, supporting normal wound healing without genetic hypercoagulability. Spontaneous blood clots in the deep veins or lungs remain at the standard population rate. Standard medical guidelines apply for situations like surgery, long-distance travel, or the use of estrogen-containing medications. No inherited risk for prothrombin-related thrombophilia is passed down to offspring. Maintaining a healthy weight and staying active during long periods of immobility are effective ways to support overall vascular health.
Typical baseline risk of deep vein thrombosis; Standard prothrombin levels in circulation.
Sample genotype: AA (Homozygous)
Excessive amounts of prothrombin circulate in the blood, creating a highly hypercoagulable state. The risk of experiencing a venous thromboembolic event is estimated to be over 6-fold higher than typical baseline levels. Serious complications such as deep vein thrombosis, pulmonary embolism, or cerebral vein thrombosis are much more common. Estrogen-containing medications, including combined oral contraceptives, pose a severe risk and are generally avoided. Close clinical monitoring is typically recommended during high-risk scenarios like major surgeries, prolonged immobility, or pregnancy. Genetic counseling may be beneficial, as this highly elevated risk profile is consistently passed on to offspring.
Over 6-fold higher risk of venous thromboembolism; Substantially increased risk of deep vein thrombosis and pulmonary embolism.
Sample genotype: GA (Heterozygous)
Production of prothrombin is elevated due to more efficient messenger RNA processing. This elevation leads to an estimated 2.8-fold increase in the risk of developing venous thromboembolism. The likelihood of deep vein thrombosis and pulmonary embolism is notably higher than in the general population. Combining this genetic profile with oral contraceptives further escalates the risk of venous clots. Pregnancy also presents a period of heightened risk, sometimes associated with recurrent pregnancy loss. Preventive measures, such as compression stockings during long flights or temporary blood thinners during major surgeries, are often discussed with healthcare providers.
Approximately 2.8-fold higher risk of venous thromboembolism; Elevated risk of clotting when taking estrogen-containing medications.
Variants with shared genetic architecture
rs5896 · F2 Gene · Chr 11 · Blood Clotting and Medication
rs710446 · KNG1 Gene · Chr 3 · Blood Clot Risk
rs5985 · F13A1 Gene · Chr 6 · Blood Clotting Risk
Content updated August 2026.
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