What you carry at this position in your DNA and what research says about it.
Lipid and Cholesterol Levels: 8/10 evidence, 20 publications.
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Sample genotype (not yours): C/C
Typical Cholesterol and Triglyceride Levels
This genotype represents the most common genetic baseline for lipid metabolism. Blood levels of HDL cholesterol and triglycerides are expected to be within the typical range for your demographic.
What this genotype means: Typical blood triglyceride levels; Standard HDL cholesterol levels; Baseline risk of metabolic syndrome.
Sample genotype (not yours): A/A
Optimal HDL and Lowest Triglycerides
Carrying two copies of the protective A allele provides the maximum genetic benefit for lipid clearance. This genotype is linked to the highest levels of good HDL cholesterol and the lowest triglyceride levels.
What this genotype means: Highest average HDL cholesterol levels; Lowest average blood triglyceride levels; Significantly reduced risk of metabolic syndrome.
Sample genotype (not yours): C/A
Higher HDL and Lower Triglycerides
Carrying one copy of the protective A allele is associated with improved lipid clearance. This typically results in higher levels of good HDL cholesterol and lower circulating triglycerides.
What this genotype means: Increased HDL cholesterol levels; Reduced blood triglyceride levels; Lower risk of metabolic syndrome.
Gene function and biological role
Gene Function: The LPL gene encodes lipoprotein lipase, an enzyme essential for breaking down lipids in the bloodstream [1]. Produced primarily in fat and muscle tissues, this enzyme sits on the walls of blood vessels where it processes triglyceride-rich lipoproteins [1]. By breaking down these fats, lipoprotein lipase provides energy to muscles and allows fat tissue to store excess nutrients [2]. This process also generates the building blocks for high-density lipoprotein, commonly known as good cholesterol [2]. Efficient functioning of this enzyme is a cornerstone of healthy cardiovascular and metabolic systems [3].
Variant Impact: The rs10503669 variant is located near the LPL gene on chromosome 8 and is in near-perfect linkage disequilibrium with the functional S447X mutation [1]. This genetic change acts as a gain-of-function variation, resulting in a truncated but highly stable and active lipoprotein lipase enzyme [1]. Because the enzyme remains active longer, it clears circulating triglycerides from the bloodstream at an accelerated rate [3]. This rapid clearance directly boosts the production of cardioprotective HDL cholesterol particles [3]. Consequently, this variant is one of the most well-replicated genetic influences on blood lipid profiles across diverse human populations [4].
Key Insight: The protective A allele is in near-perfect linkage with a gain-of-function mutation that makes the lipid-clearing enzyme more stable.
Location: LPL. Chromosome 8 · 8p21.3 · 20.0 Mb
Estimated prevalence by population
Global 83.7%; European 81.3%; African 88.4%; East Asian 79.5%; South Asian 82.0%; Americas 85.7%; Ashkenazi 81.1%; Finnish 83.2%; Middle Eastern 81.7%; Amish 71.5%.
Estimated CC genotype frequency.
Global 15.5%; European 17.7%; African 11.3%; East Asian 19.4%; South Asian 17.1%; Americas 13.7%; Ashkenazi 17.9%; Finnish 16.1%; Middle Eastern 17.3%; Amish 26.1%.
Estimated CA genotype frequency.
Global 0.8%; European 1.0%; African 0.4%; East Asian 1.2%; South Asian 0.9%; Americas 0.5%; Ashkenazi 1.0%; Finnish 0.8%; Middle Eastern 0.9%; Amish 2.4%.
Estimated AA genotype frequency.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 8/10. Source: PMID 18193043. Typical.
Triglycerides. Evidence: 8/10. Source: PMID 18193043. Typical.
Hypertriglyceridemia. Evidence: 4/10. Source: PMID 31910446. Typical Risk.
Metabolic Syndrome & Insulin Resistance
Metabolic Syndrome. Evidence: 6/10. Source: PMID 30382898. Typical Risk.
Showing effects for A/A genotype
HDL Cholesterol. Evidence: 8/10. Source: PMID 18193043. Highest Levels.
Triglycerides. Evidence: 8/10. Source: PMID 18193043. Lowest Levels.
Hypertriglyceridemia. Evidence: 4/10. Source: PMID 31910446. Lowest Risk.
Metabolic Syndrome. Evidence: 6/10. Source: PMID 30382898. Lowest Risk.
Showing effects for C/A genotype
HDL Cholesterol. Evidence: 8/10. Source: PMID 18193043. Higher Levels.
Triglycerides. Evidence: 8/10. Source: PMID 18193043. Lower Levels.
Hypertriglyceridemia. Evidence: 4/10. Source: PMID 31910446. Lower Risk.
Metabolic Syndrome. Evidence: 6/10. Source: PMID 30382898. Lower Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Carrying two copies of the common C allele means lipoprotein lipase enzyme activity operates at standard baseline levels [1]. Without the gain-of-function A allele, there is no genetically driven acceleration in triglyceride clearance [1]. Consequently, blood triglyceride levels and HDL cholesterol levels are likely to follow typical population averages [2]. While this genotype does not carry the protective lipid-lowering benefits of the A allele, it does not inherently increase cardiovascular risk beyond standard baseline factors [2]. Maintaining a balanced diet and regular exercise remains the primary way to support healthy lipid levels [3].
Typical blood triglyceride levels; Standard HDL cholesterol levels; Baseline risk of metabolic syndrome.
Sample genotype: AA (Homozygous)
Having two copies of the A allele means all produced lipoprotein lipase enzymes are in the highly active, stable form [1]. This leads to exceptionally rapid clearance of triglycerides from the blood [1]. Consequently, this genotype is strongly associated with the highest average levels of cardioprotective HDL cholesterol and the lowest triglyceride levels [2]. The risk of metabolic syndrome, hypertriglyceridemia, and related cardiovascular complications is significantly reduced compared to the general population [2].
Highest average HDL cholesterol levels; Lowest average blood triglyceride levels; Significantly reduced risk of metabolic syndrome.
Sample genotype: CA (Heterozygous)
Having one copy of the A allele introduces a highly efficient, gain-of-function version of the lipoprotein lipase enzyme [1]. This enhanced enzyme clears triglycerides from the bloodstream more rapidly than the standard version [1]. As a result, individuals with this genotype often exhibit significantly higher HDL cholesterol and lower overall triglycerides [2]. Studies show this lipid profile is associated with a lower risk of developing metabolic syndrome and hypertriglyceridemia [2]. The protective effect can be further optimized by lifestyle factors, such as moderate physical activity and a diet rich in unsaturated fats [3].
Increased HDL cholesterol levels; Reduced blood triglyceride levels; Lower risk of metabolic syndrome.
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
Newly identified loci that influence lipid concentrations and risk of coronary artery disease.
Evaluation of seven common lipid associated loci in a large Indian sib pair study.
Genetic analyses of diverse populations improves discovery for complex traits.
Content updated August 2026.
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