What you carry at this position in your DNA and what research says about it.
Cholesterol and Lipids: 10/10 evidence, 23 publications.
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Sample genotype (not yours): G/G
Typical Lipid Profile and Oxidized LDL Levels
Standard levels of circulating lipids and oxidized LDL characterize this genetic profile. It represents the most common genetic baseline across most populations.
What this genotype means: Typical circulating lipid levels; Standard response to fenofibrate therapy.
Sample genotype (not yours): A/A
Highly Favorable Lipid Profile and Enhanced Drug Response
The lowest levels of oxidized LDL and triglycerides are associated with this genetic profile. It also predicts an enhanced response to certain lipid-lowering medications.
What this genotype means: Lowest levels of oxidized LDL; Greater triglyceride reduction with fenofibrate.
Sample genotype (not yours): G/A
Favorable Lipid Profile and Lower Oxidized LDL
A single copy of the A allele is linked to slightly lower triglycerides and reduced oxidized LDL levels. This profile offers a modest natural advantage for cardiovascular health.
What this genotype means: Slightly lower triglyceride levels; Reduced oxidized LDL levels.
Gene function and biological role
Gene Function: The APOB gene provides instructions for making apolipoprotein B, a primary protein component of low-density lipoprotein (LDL) and other lipid-transporting particles [1]. This protein acts as a crucial structural scaffold that allows cholesterol and triglycerides to travel through the watery environment of the bloodstream [1]. It also serves as a ligand for LDL receptors, enabling cells throughout the body to bind and internalize cholesterol particles [2]. Variations in this gene can alter how efficiently lipids are cleared from circulation or how susceptible they are to chemical modifications [3]. Consequently, APOB is a major genetic determinant of cardiovascular health and blood lipid profiles [2].
Variant Impact: The rs676210 variant is a missense mutation in the APOB gene that changes the amino acid proline to leucine at position 2739 of the apolipoprotein B protein [2]. This structural alteration is predicted to modify the three-dimensional shape of the protein, directly influencing how LDL particles interact with their environment [2]. Specifically, this change affects the susceptibility of LDL particles to chemical oxidation in the arterial walls [2]. The variant is also strongly associated with variations in circulating levels of triglycerides, LDL, and HDL cholesterol [4]. Additionally, this genetic change has been shown to influence how individuals respond to lipid-lowering medications like fenofibrate [3].
Key Insight: This genetic variant is the single strongest genetic driver of oxidized LDL levels in the bloodstream, explaining up to 11 percent of its variation.
Location: APOB. Chromosome 2 · 2p24.1 · 21.0 Mb
Estimated prevalence by population
Global 60.6%; European 61.4%; African 72.1%; East Asian 7.2%; South Asian 22.5%; Americas 59.7%; Ashkenazi 65.8%; Finnish 54.4%; Middle Eastern 48.6%; Amish 59.9%.
Estimated GG genotype frequency.
Global 32.7%; European 33.9%; African 25.7%; East Asian 39.2%; South Asian 49.9%; Americas 35.1%; Ashkenazi 30.6%; Finnish 38.7%; Middle Eastern 42.2%; Amish 35.0%.
Estimated GA genotype frequency.
Global 6.6%; European 4.7%; African 2.3%; East Asian 53.6%; South Asian 27.6%; Americas 5.2%; Ashkenazi 3.6%; Finnish 6.9%; Middle Eastern 9.2%; Amish 5.1%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
Oxidized LDL Levels. Evidence: 6/10. Source: PMID 23247145. Higher Levels.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
LDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Typical Levels.
Pharmacogenomics
Lipid-Lowering Drug Response
Fenofibrate Response. Evidence: 5/10. Source: PMID 20724655. Typical Response.
Showing effects for A/A genotype
Oxidized LDL Levels. Evidence: 6/10. Source: PMID 23247145. Lowest Levels.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Lower Levels.
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Higher Levels.
LDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Lower Levels.
Fenofibrate Response. Evidence: 5/10. Source: PMID 20724655. Enhanced Response.
Showing effects for G/A genotype
Oxidized LDL Levels. Evidence: 6/10. Source: PMID 23247145. Lower Levels.
Triglycerides. Evidence: 10/10. Source: PMID 29507422. Slightly Lower.
HDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Slightly Higher.
LDL Cholesterol. Evidence: 10/10. Source: PMID 29507422. Slightly Lower.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
The presence of two G alleles represents the most common genetic profile globally, serving as the standard baseline for lipid metabolism. Studies show that this genotype is associated with typical levels of circulating triglycerides, LDL, and HDL cholesterol [1]. However, the G allele is also linked to higher levels of oxidized LDL compared to carriers of the A allele [2]. Oxidized LDL is a modified form of cholesterol that is more prone to accumulating in arterial walls, which is a key early step in plaque formation [2]. Despite this association, large-scale clinical cohorts have found that this variant alone does not significantly alter the overall risk of major cardiovascular events [2]. Individuals with this genotype also exhibit a standard, typical response to lipid-lowering medications like fenofibrate [3].
Typical circulating lipid levels; Standard response to fenofibrate therapy.
Sample genotype: AA (Homozygous)
Two copies of the A allele provide the most pronounced benefits for lipid metabolism at this genetic locus. Individuals with this genotype exhibit the lowest levels of oxidized LDL and circulating triglycerides, as well as higher HDL cholesterol. The structural change from proline to leucine at position 2739 of the apolipoprotein B protein significantly reduces the susceptibility of LDL to oxidation [1]. This is highly favorable because oxidized LDL is a primary driver of vascular inflammation and plaque accumulation [1]. Furthermore, clinical studies show that individuals with this genotype experience a significantly greater reduction in triglycerides when treated with fenofibrate [2]. This enhanced drug response makes the genotype highly relevant for personalized lipid management strategies [2].
Lowest levels of oxidized LDL; Greater triglyceride reduction with fenofibrate.
Sample genotype: GA (Heterozygous)
A single copy of the A allele is associated with a more favorable circulating lipid profile. Research indicates that carriers of this genotype tend to have slightly lower triglycerides and LDL cholesterol, alongside slightly higher HDL cholesterol [1]. Crucially, the presence of the A allele significantly reduces the levels of oxidized LDL in the bloodstream [2]. Because oxidized LDL is highly reactive and contributes to arterial plaque buildup, having lower levels is generally considered protective for vascular health [2]. This structural change in the apolipoprotein B protein appears to make LDL particles less susceptible to chemical oxidation [2]. While this genotype provides a modest lipid-lowering benefit, it does not drastically change overall cardiovascular disease risk on its own [2]. Response to standard lipid-lowering therapies like fenofibrate remains typical [3].
Slightly lower triglyceride levels; Reduced oxidized LDL levels.
Variants with shared genetic architecture
rs1042034 · APOB Gene · Chr 2 · Cholesterol and Lipids
rs1367117 · APOB Gene · Chr 2 · Cholesterol Levels
rs4665710 · APOB Gene · Chr 2 · Blood Lipid Levels
Apolipoprotein B genetic variants modify the response to fenofibrate: a GOLDN study.
A large electronic-health-record-based genome-wide study of serum lipids.
Content updated August 2026.
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