What you carry at this position in your DNA and what research says about it.
Triglyceride Levels: 10/10 evidence, 78 publications.
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Sample genotype (not yours): G/G
High Triglycerides and Elevated Heart Risk
Two copies of the G allele lead to significantly reduced apolipoprotein A-V levels, resulting in a marked increase in circulating triglycerides. This lipid accumulation is associated with a substantially higher risk of early-onset heart disease and metabolic syndrome.
What this genotype means: Significantly elevated fasting triglyceride levels; Increased risk of early-onset coronary artery disease; Higher susceptibility to metabolic syndrome.
Sample genotype (not yours): A/A
Typical Triglyceride Levels and Heart Risk
Two copies of the A allele support normal production of apolipoprotein A-V, promoting efficient clearance of triglycerides from the bloodstream. This genotype is associated with typical cardiovascular risk and an optimal response to statin medications.
What this genotype means: Typical fasting triglyceride levels; Standard baseline risk of coronary artery disease; Optimal response to common statin medications.
Sample genotype (not yours): G/A
Moderately Elevated Triglycerides and Heart Risk
One copy of the G allele moderately reduces apolipoprotein A-V levels, leading to elevated circulating triglycerides. This genotype is associated with an intermediate increase in the risk of early-onset heart disease and metabolic syndrome.
What this genotype means: Moderately elevated fasting triglyceride levels; Slightly increased risk of early-onset coronary artery disease; Moderate susceptibility to metabolic syndrome.
Gene function and biological role
Gene Function: The APOA5 gene encodes apolipoprotein A-V, a specialized protein produced in the liver that plays a critical role in regulating plasma triglyceride levels [1]. Apolipoprotein A-V acts as a potent modulator of lipid metabolism by accelerating the breakdown of triglyceride-rich lipoproteins [2]. It achieves this by stimulating the activity of lipoprotein lipase, an enzyme responsible for clearing fats from the bloodstream [2]. Additionally, apolipoprotein A-V helps inhibit the liver's production and secretion of very low-density lipoproteins [1]. Consequently, functional variations in this gene directly influence circulating lipid profiles and cardiovascular health [1].
Variant Impact: The rs662799 variant is located in the promoter region upstream of the APOA5 gene, where it directly influences how efficiently the gene is transcribed and translated [1]. The G allele reduces ribosomal translation efficiency, leading to significantly lower levels of apolipoprotein A-V [1]. With less apolipoprotein A-V available, the body cannot efficiently activate lipoprotein lipase to clear fats from the blood [1]. This molecular deficit results in a marked accumulation of circulating triglycerides and an altered lipid profile [1]. Conversely, the common A allele maintains normal protein expression and supports healthy lipid clearance [2].
Key Insight: The G allele of this variant acts like a dimmer switch, reducing the production of a key fat-clearing protein and causing triglycerides to linger in the bloodstream.
Location: APOA5. Chromosome 11 · 11q23.3 · 116.8 Mb
Estimated prevalence by population
Global 1.3%; European 0.4%; African 1.4%; East Asian 9.1%; South Asian 3.6%; Americas 1.8%; Ashkenazi 0.8%; Finnish 0.6%; Middle Eastern 1.4%; Amish 0.4%.
Estimated GG genotype frequency.
Global 17.7%; European 12.2%; African 21.2%; East Asian 42.1%; South Asian 30.7%; Americas 23.1%; Ashkenazi 16.1%; Finnish 14.6%; Middle Eastern 21.0%; Amish 12.1%.
Estimated GA genotype frequency.
Global 81.0%; European 87.3%; African 77.4%; East Asian 48.8%; South Asian 65.7%; Americas 75.1%; Ashkenazi 83.1%; Finnish 84.8%; Middle Eastern 77.6%; Amish 87.5%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 10/10. Source: PMID 31910446. Elevated.
Heart Disease
Heart Disease. Evidence: 7/10. Source: PMID 32469254. ~2x Higher Risk.
Metabolic Syndrome & Insulin Resistance
Metabolic Syndrome. Evidence: 9/10. Source: PMID 29212154. Increased Risk.
Pharmacogenomics
Lipid-Lowering Drug Response
Statin Response. Evidence: 5/10. Source: PMID 29695967. Reduced Response.
Nutrition & Metabolism
Macronutrient Metabolism
Weight Response to Dietary Fat. Evidence: 4/10. Source: PMID 29404214. Less Weight Gain.
Showing effects for A/A genotype
Triglycerides. Evidence: 10/10. Source: PMID 31910446. Typical.
Heart Disease. Evidence: 7/10. Source: PMID 32469254. Typical Risk.
Metabolic Syndrome. Evidence: 9/10. Source: PMID 29212154. Typical Risk.
Statin Response. Evidence: 5/10. Source: PMID 29695967. Optimal Response.
Weight Response to Dietary Fat. Evidence: 4/10. Source: PMID 29404214. Typical Weight Gain.
Showing effects for G/A genotype
Triglycerides. Evidence: 10/10. Source: PMID 31910446. Moderately Elevated.
Heart Disease. Evidence: 7/10. Source: PMID 32469254. ~1.4x Higher Risk.
Metabolic Syndrome. Evidence: 9/10. Source: PMID 29212154. Moderately Increased.
Statin Response. Evidence: 5/10. Source: PMID 29695967. Slightly Reduced.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
A double dose of the G allele severely impairs the translation of apolipoprotein A-V, leading to a profound reduction in its circulating levels [1]. This deficiency hinders the activation of lipoprotein lipase, causing triglycerides to accumulate in the bloodstream rather than being cleared efficiently [1]. Multiple genome-wide association studies have linked this genotype to a near-doubling of early-onset coronary artery disease risk [2]. It also significantly increases the likelihood of developing metabolic syndrome, a cluster of conditions that elevate cardiovascular risk [3]. Interestingly, some research suggests that this genotype may experience less weight gain on high-fat diets compared to other genotypes, though the cardiovascular risks remain the primary concern [4]. Standard lipid-lowering therapies like statins may also show reduced efficacy in individuals with this genetic profile [5].
Significantly elevated fasting triglyceride levels; Increased risk of early-onset coronary artery disease; Higher susceptibility to metabolic syndrome.
Sample genotype: AA (Homozygous)
Having two copies of the common A allele ensures optimal ribosomal translation and normal levels of apolipoprotein A-V [1]. This protein level allows for the healthy activation of lipoprotein lipase, which efficiently clears triglycerides and other fats from circulation [1]. As a result, this genotype is strongly associated with typical fasting triglyceride levels and a lower baseline risk of coronary artery disease compared to G allele carriers [2]. It also provides a protective baseline against metabolic syndrome [3]. Furthermore, clinical trials have demonstrated that individuals with this genetic profile show a highly favorable response to common statin medications, achieving significant reductions in lipid levels [4]. However, typical weight gain patterns are observed on high-fat diets, making balanced nutrition important for maintaining long-term metabolic health [5].
Typical fasting triglyceride levels; Standard baseline risk of coronary artery disease; Optimal response to common statin medications.
Sample genotype: GA (Heterozygous)
Carrying a single G allele partially reduces the production of apolipoprotein A-V, which in turn limits the body's ability to clear triglycerides from the bloodstream [1]. This partial deficiency typically results in moderately elevated fasting triglyceride levels [1]. Clinical studies indicate that this intermediate lipid profile correlates with a roughly 1.4-fold increase in the risk of early-onset coronary artery disease [2]. It also moderately raises the susceptibility to metabolic syndrome, particularly when combined with a high-carbohydrate or high-fat diet [3]. On the positive side, carriers of this allele may experience slightly less weight gain when consuming high-fat diets [4]. However, maintaining a heart-healthy lifestyle remains crucial to offset the genetic predisposition to elevated lipids [1]. Response to common statin medications may also be slightly less pronounced compared to those with the typical genotype [5].
Moderately elevated fasting triglyceride levels; Slightly increased risk of early-onset coronary artery disease; Moderate susceptibility to metabolic syndrome.
Variants with shared genetic architecture
rs2266788 · APOA5 Gene · Chr 11 · Triglyceride Levels
rs3135506 · APOA5 Gene · Chr 11 · Triglyceride and Lipid Levels
rs651821 · APOA5 Gene · Chr 11 · Triglyceride Levels
Genome-wide association study of metabolic syndrome in Korean populations.
Content updated August 2026.
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