What you carry at this position in your DNA and what research says about it.
Triglyceride and Lipid Levels: 10/10 evidence, 53 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): G/G
Typical Lipid and Triglyceride Levels
Two copies of the common G allele are associated with typical triglyceride clearance and standard cholesterol profiles. This genotype represents the baseline genetic influence on blood lipid levels.
What this genotype means: Typical triglyceride clearance; Standard HDL cholesterol levels; Baseline cardiovascular lipid profile.
Sample genotype (not yours): C/C
Elevated Triglycerides and Altered Lipid Profile
Two copies of the C allele are associated with significantly higher triglyceride levels and lower HDL cholesterol. This genetic profile can notably impact your cardiovascular lipid balance.
What this genotype means: Significantly higher fasting triglycerides; Lower circulating HDL cholesterol; Increased total and non-HDL cholesterol.
Sample genotype (not yours): G/C
Slightly Elevated Triglycerides
Carrying one copy of the C allele is linked to slightly higher triglyceride levels and a minor reduction in HDL cholesterol. This can modestly influence your overall cardiovascular lipid profile.
What this genotype means: Modestly higher fasting triglycerides; Slightly lower HDL cholesterol; Slightly higher total cholesterol.
Gene function and biological role
Gene Function: The APOA5 gene provides instructions for making apolipoprotein A-V, a specialized protein that plays a crucial role in regulating blood lipid levels. This protein is primarily produced in the liver and associates with lipoprotein particles in the bloodstream, where it acts as a powerful accelerator for triglyceride clearance [1]. By interacting with lipoprotein lipase, apolipoprotein A-V helps break down circulating fats so they can be cleared from circulation [2]. Genetic variations that alter the structure or abundance of this protein can significantly impact how efficiently the body processes dietary fats. Consequently, this gene is a major genetic determinant of plasma triglyceride concentrations and overall cardiovascular lipid profiles.
Variant Impact: This missense variant, known as p.Ser19Trp or S19W, changes the 19th amino acid of the apolipoprotein A-V protein from serine to tryptophan. This structural alteration occurs within the signal peptide region of the protein, which is critical for its proper secretion from liver cells into the bloodstream. Because the tryptophan substitution impairs the secretion of apolipoprotein A-V, carriers of the altered allele have lower circulating levels of this protective protein [3]. The reduction in functional apolipoprotein A-V leads to a decreased rate of triglyceride breakdown, resulting in higher levels of circulating fats [4]. This specific molecular change is widely studied across diverse populations for its consistent impact on blood lipid profiles.
Key Insight: A single amino acid change in the signal peptide of the APOA5 protein slows down its secretion, directly leading to a measurable buildup of triglycerides in the bloodstream.
Location: APOA5. Chromosome 11 · 11q23.3 · 116.8 Mb
Estimated prevalence by population
Global 87.5%; European 87.8%; African 88.0%; East Asian 100.0%; South Asian 92.0%; Americas 78.6%; Ashkenazi 87.3%; Finnish 89.3%; Middle Eastern 86.2%; Amish 77.5%.
Estimated GG genotype frequency.
Global 12.0%; European 11.8%; African 11.6%; East Asian 0.0%; South Asian 7.8%; Americas 20.1%; Ashkenazi 12.3%; Finnish 10.4%; Middle Eastern 13.3%; Amish 21.1%.
Estimated GC genotype frequency.
Global 0.5%; European 0.4%; African 0.4%; East Asian 0.0%; South Asian 0.2%; Americas 1.3%; Ashkenazi 0.4%; Finnish 0.3%; Middle Eastern 0.5%; Amish 1.4%.
Estimated CC genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
Total Cholesterol. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
Apolipoprotein B. Evidence: 8/10. Source: PMID 33462484. Typical Levels.
Showing effects for C/C genotype
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Highly Elevated.
Total Cholesterol. Evidence: 10/10. Source: PMID 29507422. Higher Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Lower Levels.
Apolipoprotein B. Evidence: 8/10. Source: PMID 33462484. Higher Levels.
Showing effects for G/C genotype
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Increased Levels.
Total Cholesterol. Evidence: 10/10. Source: PMID 29507422. Slightly Higher.
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Slightly Lower.
Apolipoprotein B. Evidence: 8/10. Source: PMID 33462484. Slightly Higher.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Having the G/G genotype means carrying two copies of the most common version of the APOA5 gene. This genetic profile supports the normal secretion of apolipoprotein A-V from the liver, facilitating the efficient breakdown of circulating fats [1]. Large-scale genomic studies consistently show that individuals with this baseline genotype maintain typical levels of triglycerides and total cholesterol [2]. Additionally, this genotype is associated with standard levels of HDL cholesterol, often referred to as the beneficial cholesterol [3]. Because this is the most common genetic baseline, it does not elevate your risk for lipid-related cardiovascular concerns beyond typical population averages.
Typical triglyceride clearance; Standard HDL cholesterol levels; Baseline cardiovascular lipid profile.
Sample genotype: CC (Homozygous)
Having the C/C genotype means both copies of your APOA5 gene carry the S19W alteration, which significantly impairs the secretion of apolipoprotein A-V into the bloodstream [1]. With very low levels of this crucial lipid-clearing protein, the body processes circulating fats much more slowly [2]. Research shows that individuals with two copies of the C allele are highly likely to have elevated fasting triglycerides and higher total cholesterol [3]. This genotype is also strongly linked to lower levels of protective HDL cholesterol [4]. While ClinVar notes that this variant alone is benign and does not directly cause severe inherited hypertriglyceridemia syndromes, it is a well-established genetic risk factor that significantly increases the likelihood of developing elevated blood lipids when combined with a high-fat diet or other lifestyle factors [5].
Significantly higher fasting triglycerides; Lower circulating HDL cholesterol; Increased total and non-HDL cholesterol.
Sample genotype: GC (Heterozygous)
Carrying one copy of the C allele means some of the apolipoprotein A-V produced by the liver is structurally altered, which slightly reduces its secretion into the bloodstream [1]. This mild reduction in functional protein levels leads to a modest decrease in the rate at which triglycerides are cleared from your blood [2]. Large population studies indicate that individuals with the G/C genotype tend to have slightly higher fasting triglycerides and total cholesterol compared to those with the G/G genotype [3]. There is also a small associated reduction in HDL cholesterol levels [4]. While this genotype is not a direct cause of severe lipid disorders, it represents a genetic nudge toward higher circulating fats, making dietary and lifestyle habits more influential.
Modestly higher fasting triglycerides; Slightly lower HDL cholesterol; Slightly higher total cholesterol.
Variants with shared genetic architecture
rs2266788 · APOA5 Gene · Chr 11 · Triglyceride Levels
rs651821 · APOA5 Gene · Chr 11 · Triglyceride Levels
rs662799 · APOA5 Gene · Chr 11 · Triglyceride Levels
Two independent apolipoprotein A5 haplotypes influence human plasma triglyceride levels.
Mapping the proteo-genomic convergence of human diseases.
A large electronic-health-record-based genome-wide study of serum lipids.
Genetic analyses of diverse populations improves discovery for complex traits.
Polygenic determinants of severe hypertriglyceridemia.
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com