What you carry at this position in your DNA and what research says about it.
Blood Triglyceride Levels: 10/10 evidence, 22 publications.
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Sample genotype (not yours): T/T
Typical Triglyceride and HDL Cholesterol Levels
Standard LPL enzyme regulation allows microRNA-410 to bind normally and limit LPL production. This results in typical levels of triglycerides and HDL cholesterol.
What this genotype means: Standard LPL enzyme activity; Typical baseline cardiovascular risk profile.
Sample genotype (not yours): C/C
Optimal Lipid Profile and Reduced Cardiovascular Risk
Carrying two copies of the protective C allele maximizes LPL enzyme production by completely blocking microRNA-410 suppression. This leads to the lowest triglyceride levels and highest HDL cholesterol.
What this genotype means: Maximally increased LPL enzyme expression; Significantly lowered circulating triglycerides; Significantly elevated HDL cholesterol.
Sample genotype (not yours): T/C
Favorable Lipid Profile and Lower Triglycerides
Carrying one copy of the protective C allele disrupts microRNA-410 binding, leading to higher LPL enzyme levels. This results in lower triglycerides and higher HDL cholesterol.
What this genotype means: Increased LPL enzyme expression; Lowered circulating triglycerides; Elevated HDL cholesterol.
Gene function and biological role
Gene Function: The LPL gene provides instructions for making lipoprotein lipase, an enzyme critical for clearing fats from the bloodstream [1]. This enzyme is primarily produced in fat tissue and muscles, where it breaks down triglycerides carried by lipoproteins [1]. Once broken down, these fatty acids are used by muscles for energy or stored in fat tissue [1]. Efficient LPL activity is essential for maintaining healthy blood lipid levels and preventing the accumulation of fat in blood vessels [2]. When LPL activity is compromised, triglyceride levels can rise significantly, increasing the risk of cardiovascular disease [2].
Variant Impact: Located in the 3 prime untranslated region of the LPL gene, rs13702 is a regulatory change that controls gene expression. The major T allele contains a binding site for microRNA-410, a small regulatory molecule that suppresses LPL production [1]. The minor C allele disrupts this microRNA-410 binding site, preventing the microRNA from silencing the gene [1]. This disruption results in increased LPL enzyme production, effectively acting as a gain-of-function variant that enhances the clearance of triglycerides and raises protective HDL cholesterol [1].
Key Insight: This variant is a rare example of a functional microRNA-disrupting mutation that acts as a natural gain-of-function, boosting LPL enzyme levels to improve lipid clearance.
Location: LPL. Chromosome 8 · 8p21.3 · 20.0 Mb
Estimated prevalence by population
Global 43.1%; European 49.9%; African 23.7%; East Asian 63.2%; South Asian 57.3%; Americas 49.2%; Ashkenazi 31.8%; Finnish 54.8%; Middle Eastern 41.8%; Amish 31.4%.
Estimated TT genotype frequency.
Global 43.4%; European 41.5%; African 50.0%; East Asian 32.6%; South Asian 36.8%; Americas 41.9%; Ashkenazi 49.2%; Finnish 38.4%; Middle Eastern 45.7%; Amish 49.3%.
Estimated TC genotype frequency.
Global 13.5%; European 8.6%; African 26.3%; East Asian 4.2%; South Asian 5.9%; Americas 8.9%; Ashkenazi 19.1%; Finnish 6.7%; Middle Eastern 12.5%; Amish 19.3%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 10/10. Source: PMID 21386085. Typical.
HDL Cholesterol. Evidence: 10/10. Source: PMID 21386085. Typical.
VLDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. Typical.
Apolipoprotein B. Evidence: 10/10. Source: PMID 32203549. Typical.
Heart Disease
Coronary Artery Disease. Evidence: 8/10. Source: PMID 33020668. Typical Risk.
Showing effects for C/C genotype
Triglycerides. Evidence: 10/10. Source: PMID 21386085. Significantly Lowered.
HDL Cholesterol. Evidence: 10/10. Source: PMID 21386085. Significantly Elevated.
VLDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. Significantly Lowered.
Apolipoprotein B. Evidence: 10/10. Source: PMID 32203549. Significantly Lowered.
Coronary Artery Disease. Evidence: 8/10. Source: PMID 33020668. Significantly Lowered.
Showing effects for T/C genotype
Triglycerides. Evidence: 10/10. Source: PMID 21386085. Lowered.
HDL Cholesterol. Evidence: 10/10. Source: PMID 21386085. Elevated.
VLDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. Lowered.
Apolipoprotein B. Evidence: 10/10. Source: PMID 32203549. Lowered.
Coronary Artery Disease. Evidence: 8/10. Source: PMID 33020668. Lowered Risk.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Standard regulation of the LPL gene occurs when microRNA-410 binds to its target site in the 3 prime untranslated region, keeping enzyme levels at a baseline level [1]. This baseline activity is associated with typical concentrations of circulating triglycerides and HDL cholesterol [1]. Large-scale genomic studies show that this genotype is the most common globally, representing the standard baseline for lipid metabolism [2]. While it does not elevate cardiovascular risk on its own, it lacks the protective lipid-lowering effects observed in carriers of the C allele [2]. Maintaining a balanced diet and regular exercise remains important for supporting optimal lipid clearance [3]. Dietary factors, particularly the intake of polyunsaturated fatty acids, can interact with this genetic background to influence overall lipid trends [4]. This baseline status means that standard cardiovascular prevention guidelines apply without genetic modifications.
Standard LPL enzyme activity; Typical baseline cardiovascular risk profile.
Sample genotype: CC (Homozygous)
Complete disruption of the microRNA-410 binding site on both chromosomes maximizes the production of the LPL enzyme [1]. This robust enzyme activity drives highly efficient breakdown and clearance of circulating fats [1]. Individuals with this genotype exhibit the most favorable lipid profiles, characterized by very low triglycerides and elevated HDL cholesterol [1]. These optimal lipid levels provide strong protection against the development of coronary artery disease [2]. Additionally, this genetic profile is associated with lower levels of atherogenic particles like VLDL [3]. The lipid-lowering benefits of this genotype are particularly pronounced when combined with a healthy intake of polyunsaturated fatty acids [4]. This makes dietary quality an exceptionally powerful tool for managing cardiovascular wellness in these individuals [4]. Having two copies of this protective variant represents a highly efficient natural defense against lipid accumulation.
Maximally increased LPL enzyme expression; Significantly lowered circulating triglycerides; Significantly elevated HDL cholesterol.
Sample genotype: TC (Heterozygous)
Disruption of the microRNA-410 binding site on one chromosome allows for increased expression of the LPL gene [1]. This gain-of-function effect enhances the clearance of triglyceride-rich lipoproteins from the bloodstream [1]. Clinical data show that individuals with this genotype have significantly lower fasting triglyceride levels and higher HDL cholesterol compared to those with the T/T genotype [1]. These improved lipid parameters contribute to a reduced risk of developing coronary artery disease [2]. Furthermore, the beneficial effects of this genotype on triglycerides are enhanced by diets rich in unsaturated fats, such as the Mediterranean diet [3]. This interaction suggests that dietary choices can synergize with genetic advantages to optimize cardiovascular health [3].
Increased LPL enzyme expression; Lowered circulating triglycerides; Elevated HDL cholesterol.
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
A large electronic-health-record-based genome-wide study of serum lipids.
Content updated August 2026.
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