What you carry at this position in your DNA and what research says about it.
Cholesterol and Lipids: 10/10 evidence, 15 publications.
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Sample genotype (not yours): T/T
Typical Lipid Levels and Cardiovascular Risk
Standard lipoprotein lipase activity maintains typical baseline levels of triglycerides and HDL cholesterol. There is no inherited reduction in cardiovascular risk from this specific genetic marker.
What this genotype means: Typical baseline triglyceride levels; Standard baseline HDL cholesterol levels.
Sample genotype (not yours): C/C
Highly Favorable Lipids and Lowest Cardiovascular Risk
Carrying two copies of the beneficial variant maximizes lipoprotein lipase activity, leading to significantly higher HDL and lower triglycerides. This genotype offers the strongest genetic protection against cardiovascular disease.
What this genotype means: Lowest baseline triglyceride levels; Highest HDL good cholesterol levels; Strongest genetic protection against coronary artery disease.
Sample genotype (not yours): T/C
Favorable Lipid Profile and Lower Cardiovascular Risk
Carrying one copy of the beneficial variant is linked to higher HDL cholesterol and lower triglycerides. This enhanced lipid clearance provides a protective effect against heart disease.
What this genotype means: Lower circulating triglycerides; Higher HDL good cholesterol levels; Reduced risk of coronary artery disease.
Gene function and biological role
Gene Function: The LPL gene encodes lipoprotein lipase, a key enzyme found on the surface of blood vessels in muscles and fatty tissues [1]. This enzyme plays a critical role in lipid metabolism by breaking down circulating fats, particularly triglycerides, carried in lipoproteins [1] [2]. By hydrolyzing these fats, lipoprotein lipase releases free fatty acids that cells can use for energy or store for future use [2]. This process also generates lipid remnants that are essential for assembling high-density lipoprotein, commonly known as HDL or good cholesterol [2]. Consequently, lipoprotein lipase activity is a major determinant of blood lipid levels and overall cardiovascular health [1].
Variant Impact: An intron change within the LPL gene, rs325 is in perfect linkage disequilibrium with the well-known S447X nonsense mutation [1]. This genetic linkage means that the minor C allele of rs325 serves as an exact proxy for the S447X gain-of-function variant [1] [3]. The S447X mutation truncates the lipoprotein lipase protein by two amino acids, which enhances its enzymatic activity and stability [1]. Increased activity of this enzyme accelerates the clearance of triglyceride-rich particles from the bloodstream [3]. As a result, this genetic variation is strongly associated with a highly favorable blood lipid profile and reduced cardiovascular risk [1].
Key Insight: This variant is in perfect linkage with a rare genetic truncation that actually makes the lipoprotein lipase enzyme work faster and more efficiently.
Location: LPL. Chromosome 8 · 8p21.3 · 20.0 Mb
Estimated prevalence by population
Global 82.8%; European 80.8%; African 86.4%; East Asian 79.3%; South Asian 81.6%; Americas 84.7%; Ashkenazi 80.1%; Finnish 82.6%; Middle Eastern 80.6%; Amish 71.5%.
Estimated TT genotype frequency.
Global 16.4%; European 18.2%; African 13.1%; East Asian 19.5%; South Asian 17.4%; Americas 14.7%; Ashkenazi 18.8%; Finnish 16.5%; Middle Eastern 18.3%; Amish 26.1%.
Estimated TC genotype frequency.
Global 0.8%; European 1.0%; African 0.5%; East Asian 1.2%; South Asian 0.9%; Americas 0.6%; Ashkenazi 1.1%; Finnish 0.8%; Middle Eastern 1.0%; Amish 2.4%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 10/10. Source: PMID 20864672. Typical Levels.
Triglycerides. Evidence: 10/10. Source: PMID 30670697. Typical Levels.
VLDL Cholesterol. Evidence: 9/10. Source: PMID 34610981. Typical Levels.
Chylomicron Lipids. Evidence: 6/10. Source: PMID 34610981. Typical Levels.
Heart Disease
Cardiovascular Health. Evidence: 6/10. Source: PMID 20864672. Typical Risk.
Nutrition & Metabolism
Macronutrient Metabolism
Circulating Fatty Acids. Evidence: 9/10. Source: PMID 38448586. Typical Levels.
Showing effects for C/C genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 20864672. Highest Levels.
Triglycerides. Evidence: 10/10. Source: PMID 30670697. Lowest Levels.
VLDL Cholesterol. Evidence: 9/10. Source: PMID 34610981. Lowest Levels.
Chylomicron Lipids. Evidence: 6/10. Source: PMID 34610981. Lowest Levels.
Cardiovascular Health. Evidence: 6/10. Source: PMID 20864672. Lowest Risk.
Circulating Fatty Acids. Evidence: 9/10. Source: PMID 38448586. Lowest Levels.
Showing effects for T/C genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 20864672. Higher Levels.
Triglycerides. Evidence: 10/10. Source: PMID 30670697. Lower Levels.
VLDL Cholesterol. Evidence: 9/10. Source: PMID 34610981. Lower Levels.
Chylomicron Lipids. Evidence: 6/10. Source: PMID 34610981. Lower Levels.
Cardiovascular Health. Evidence: 6/10. Source: PMID 20864672. Lower Risk.
Circulating Fatty Acids. Evidence: 9/10. Source: PMID 38448586. Lower Levels.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Standard lipoprotein lipase function is maintained by this genotype, resulting in typical baseline levels of circulating lipids [1]. Without the gain-of-function variation, the clearance rate of triglyceride-rich lipoproteins remains at the population average [1] [2]. This typical metabolic rate is reflected in standard levels of VLDL cholesterol and circulating fatty acids [3]. Baseline levels of HDL cholesterol are also typical, as the standard rate of lipid breakdown provides a normal supply of components for HDL assembly [1]. While this genotype does not elevate cardiovascular risk, it lacks the protective, lipid-lowering benefits associated with the minor variant [1]. Maintaining a heart-healthy diet and regular physical activity remains important for managing long-term lipid profiles [4].
Typical baseline triglyceride levels; Standard baseline HDL cholesterol levels.
Sample genotype: CC (Homozygous)
Maximum lipoprotein lipase activity is achieved with two copies of this beneficial variant [1]. This double dose of the gain-of-function change drives highly efficient clearance of triglyceride-rich lipoproteins from circulation [1] [2]. Consequently, individuals with this genotype typically exhibit the lowest levels of triglycerides and VLDL cholesterol [2] [3]. The highly active enzyme also maximizes the generation of lipid components needed to assemble HDL, leading to significantly elevated good cholesterol levels [1]. These optimal lipid dynamics provide robust, lifelong protection against plaque buildup in the arteries and coronary artery disease [1]. Research across multiple ancestries confirms that this genetic profile is highly advantageous for cardiovascular health [2].
Lowest baseline triglyceride levels; Highest HDL good cholesterol levels; Strongest genetic protection against coronary artery disease.
Sample genotype: TC (Heterozygous)
Enhanced lipoprotein lipase activity is inherited through this single copy of the beneficial variant [1]. This gain-of-function effect accelerates the breakdown of triglyceride-rich particles in the bloodstream, leading to lower circulating triglycerides [1] [2]. The rapid processing of these fats also provides more lipid remnants to build high-density lipoprotein, resulting in higher HDL cholesterol levels [1]. Additionally, carriers of this variant show reduced levels of VLDL cholesterol and fewer circulating fatty acids [3] [4]. These combined lipid improvements contribute to a significantly lower risk of coronary artery disease over time [1]. The protective benefits of this genotype are well-documented across diverse global populations [2].
Lower circulating triglycerides; Higher HDL good cholesterol levels; Reduced risk of coronary artery 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
Genetic variants influencing circulating lipid levels and risk of coronary artery disease.
Genetic analyses of diverse populations improves discovery for complex traits.
Multi-ancestry study of blood lipid levels identifies four loci interacting with physical activity.
Genome-wide characterization of circulating metabolic biomarkers.
Content updated August 2026.
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