What you carry at this position in your DNA and what research says about it.
Triglycerides and Heart Risk: 8/10 evidence, 23 publications.
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Sample genotype (not yours): A/A
Typical Triglyceride Levels and Heart Risk
This genotype represents the typical genetic baseline for lipid metabolism. It is associated with normal lipoprotein lipase activity, typical triglyceride levels, and standard cardiovascular risk.
What this genotype means: Standard fat clearance rate; Typical cardiovascular risk profile.
Sample genotype (not yours): A/G
Higher Triglycerides and Elevated Blood Clot Risk
Carrying one copy of the variant G allele is linked to reduced lipoprotein lipase activity, which can lead to higher triglyceride levels and lower HDL cholesterol. It is also associated with an increased risk of blood clots and coronary artery disease.
What this genotype means: Slower clearance of dietary fats; Increased risk of deep vein blood clots; Slightly elevated risk of heart disease.
Sample genotype (not yours): G/G
Significantly Higher Triglycerides and Blood Clot Risk
Carrying two copies of the variant G allele is linked to significantly reduced lipoprotein lipase activity, leading to elevated triglycerides and lower HDL cholesterol. This genotype is associated with a higher risk of venous thromboembolism and coronary artery disease.
What this genotype means: Markedly slower clearance of dietary fats; Substantially increased risk of deep vein blood clots; Elevated risk of heart disease.
Gene function and biological role
Gene Function: The LPL gene encodes lipoprotein lipase, a crucial enzyme responsible for breaking down dietary fats in the bloodstream [1]. It primarily hydrolyzes triglycerides found in chylomicrons and very-low-density lipoproteins, releasing free fatty acids for energy use or storage [1]. This process is essential for maintaining healthy lipid levels and preventing fat accumulation in blood vessels [1]. Reduced activity of this enzyme can lead to elevated circulating triglycerides and lower high-density lipoprotein levels [2]. Consequently, LPL plays a central role in cardiovascular health, insulin sensitivity, and metabolic regulation [3].
Variant Impact: This missense variant, also known as Asn291Ser or N291S, alters a single amino acid in the lipoprotein lipase enzyme [4]. The substitution of serine for asparagine occurs near the ligand-binding site, which impairs the enzyme's catalytic efficiency [4]. Because the enzyme cannot clear fats from the blood as effectively, carriers of the variant G allele tend to have higher triglycerides and lower HDL cholesterol [2]. This metabolic shift is also linked to an increased susceptibility to blood clots in the veins and coronary artery disease [5]. The variant is relatively uncommon, found in about one to two percent of people of European and Latino ancestry [6].
Key Insight: This variant reduces the efficiency of a key fat-clearing enzyme, which simultaneously raises triglycerides and lowers protective HDL cholesterol. It is also linked to a significantly higher risk of deep vein blood clots.
Location: LPL. Chromosome 8 · 8p21.3 · 20.0 Mb
Estimated prevalence by population
Global 97.5%; European 96.3%; African 99.4%; East Asian 100.0%; South Asian 99.5%; Americas 96.8%; Ashkenazi 97.9%; Finnish 95.6%; Middle Eastern 98.6%; Amish 100.0%.
Estimated AA genotype frequency.
Global 2.5%; European 3.7%; African 0.6%; East Asian 0.0%; South Asian 0.5%; Americas 3.2%; Ashkenazi 2.1%; Finnish 4.4%; Middle Eastern 1.4%; Amish 0.0%.
Estimated AG 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 GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 8/10. Source: PMID 24507774. Typical.
HDL Cholesterol. Evidence: 10/10. Source: PMID 24507774. Typical.
Coagulation & Clotting
Venous Thromboembolism. Evidence: 3/10. Source: PMID 16651467. Typical Risk.
Heart Disease
Coronary Artery Disease. Evidence: 7/10. Source: PMID 36474045. Typical Risk.
Metabolic Syndrome & Insulin Resistance
Insulin Sensitivity. Evidence: 3/10. Source: PMID 28502509. Typical.
Showing effects for A/G genotype
Triglycerides. Evidence: 8/10. Source: PMID 24507774. Elevated.
HDL Cholesterol. Evidence: 10/10. Source: PMID 24507774. Lower.
Venous Thromboembolism. Evidence: 3/10. Source: PMID 16651467. ~3x Higher Risk.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 36474045. Slightly Higher Risk.
Insulin Sensitivity. Evidence: 3/10. Source: PMID 28502509. Reduced.
Showing effects for G/G genotype
Triglycerides. Evidence: 8/10. Source: PMID 24507774. Significantly Elevated.
HDL Cholesterol. Evidence: 10/10. Source: PMID 24507774. Significantly Lower.
Venous Thromboembolism. Evidence: 3/10. Source: PMID 16651467. ~3x or Higher Risk.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 36474045. Higher Risk.
Insulin Sensitivity. Evidence: 3/10. Source: PMID 28502509. Significantly Reduced.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Maintaining typical lipoprotein lipase activity helps keep blood lipids within a healthy range [1]. Having two copies of the common A allele means the enzyme functions at its standard capacity, efficiently clearing triglycerides from the bloodstream [1]. Studies show this genotype is associated with typical levels of high-density lipoprotein cholesterol and normal insulin sensitivity [2]. The risk of developing coronary artery disease or venous thromboembolism remains at the general population baseline [3]. No special dietary or lifestyle modifications are suggested beyond standard healthy living guidelines [1]. This genetic profile is highly common, occurring in over ninety-eight percent of the global population [4].
Standard fat clearance rate; Typical cardiovascular risk profile.
Sample genotype: AG (Heterozygous)
Carrying one copy of the G allele reduces the overall efficiency of lipoprotein lipase, leading to slower clearance of dietary fats [1]. Clinical studies have linked this heterozygous state to significantly higher plasma triglyceride levels and lower HDL cholesterol [2]. The altered lipid clearance also impairs whole-body insulin sensitivity, which can affect metabolic health [1]. Furthermore, this genotype is associated with an elevated risk of coronary artery disease [3]. Research has also identified a roughly three-fold increase in the risk of developing idiopathic venous thromboembolism, or blood clots in the veins [4]. Managing cardiovascular risk factors through a balanced diet, regular exercise, and avoiding smoking is particularly beneficial for individuals with this genetic profile [5].
Slower clearance of dietary fats; Increased risk of deep vein blood clots; Slightly elevated risk of heart disease.
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele leads to a more pronounced reduction in lipoprotein lipase activity [1]. This homozygous state is associated with significantly elevated plasma triglycerides and lower levels of protective HDL cholesterol [2]. Slower fat clearance from the bloodstream can impair insulin sensitivity and alter overall lipid metabolism [1]. These metabolic changes contribute to a higher risk of developing coronary artery disease [3]. Additionally, having two copies of the variant is linked to a substantially increased risk of venous thromboembolism, where blood clots form in the deep veins [4]. Focus on a heart-healthy lifestyle, including a low-fat diet and regular physical activity, is highly relevant for managing these risks [5].
Markedly slower clearance of dietary fats; Substantially increased risk of deep vein blood clots; Elevated risk of heart disease.
Variants with shared genetic architecture
rs10096633 · LPL Gene · Chr 8 · Triglycerides and Heart Health
rs115849089 · LPL Gene · Chr 8 · Triglyceride Levels
rs12678919 · LPL Gene · Chr 8 · Cholesterol and Lipids
Content updated August 2026.
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