What you carry at this position in your DNA and what research says about it.
LDL Cholesterol: 10/10 evidence, 11 publications.
You're viewing every possible genotype for this variant.
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Sample genotype (not yours): G/G
Typical LDL Cholesterol Levels
Blood lipid profiles tend to remain within normal ranges. This genotype is associated with the lowest levels of LDL and total cholesterol.
What this genotype means: Typical circulating levels of LDL and total cholesterol; Lower baseline risk of lipid accumulation in blood vessels.
Sample genotype (not yours): A/A
Elevated LDL Cholesterol Levels
Carrying two copies of the A allele is associated with the highest levels of LDL and total cholesterol. This profile increases the risk of lipid accumulation in the cardiovascular system.
What this genotype means: Highest circulating levels of LDL and total cholesterol; Increased risk of arterial plaque accumulation.
Sample genotype (not yours): G/A
Moderately Elevated LDL Cholesterol
Carrying one copy of the A allele is linked to moderately higher LDL and total cholesterol levels. This increase can contribute to a higher risk of lipid buildup in blood vessels.
What this genotype means: Moderately higher circulating levels of LDL and total cholesterol; Slightly increased risk of arterial plaque buildup over time.
Gene function and biological role
Gene Function: Apolipoprotein B, encoded by the APOB gene, is the primary protein component of low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) particles [1]. It acts as a structural scaffold that allows these lipid-carrying particles to travel through the bloodstream [1]. By binding to specific receptors on cell surfaces, it guides the clearance of cholesterol from circulation [2]. When this process is disrupted, cholesterol can accumulate in the blood vessels, contributing to plaque buildup [2].
Variant Impact: The rs934197 variant is located in the upstream region of the APOB gene, where it influences how actively the gene is expressed rather than altering the protein structure itself [3]. This regulatory change directly impacts the abundance of circulating apolipoprotein B proteins [3]. Higher expression levels lead to an increased concentration of cholesterol-carrying particles in the bloodstream [4]. Consequently, this single nucleotide change is a major genetic determinant of circulating LDL and total cholesterol levels [4].
Key Insight: This variant regulates how much APOB protein is produced rather than changing the protein itself, directly influencing the number of cholesterol-carrying particles in your blood.
Location: APOB. Chromosome 2 · 2p24.1 · 21.0 Mb
Estimated prevalence by population
Global 57.8%; European 46.5%; African 76.2%; East Asian 77.2%; South Asian 73.3%; Americas 48.8%; Ashkenazi 64.5%; Finnish 52.7%; Middle Eastern 70.0%; Amish 45.2%.
Estimated GG genotype frequency.
Global 35.5%; European 43.4%; African 22.2%; East Asian 21.3%; South Asian 24.6%; Americas 42.1%; Ashkenazi 31.6%; Finnish 39.8%; Middle Eastern 27.3%; Amish 44.1%.
Estimated GA genotype frequency.
Global 6.8%; European 10.1%; African 1.6%; East Asian 1.5%; South Asian 2.1%; Americas 9.1%; Ashkenazi 3.9%; Finnish 7.5%; Middle Eastern 2.7%; Amish 10.8%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
LDL Cholesterol. Evidence: 10/10. Source: PMID 31719535. Typical.
Total Cholesterol. Evidence: 10/10. Source: PMID 34610981. Typical.
VLDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. Typical.
IDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. Typical.
Lipoprotein(a) Levels. Evidence: 10/10. Source: PMID 33730874. Typical.
Pharmacogenomics
Lipid-Lowering Drug Response
Fenofibrate Response. Evidence: 3/10. Source: PMID 20724655. Typical Response.
Showing effects for A/A genotype
LDL Cholesterol. Evidence: 10/10. Source: PMID 31719535. +0.34 mmol/L.
Total Cholesterol. Evidence: 10/10. Source: PMID 34610981. +0.27 mmol/L.
VLDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. +0.32 mmol/L.
IDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. +0.34 mmol/L.
Lipoprotein(a) Levels. Evidence: 10/10. Source: PMID 33730874. Increased.
Fenofibrate Response. Evidence: 3/10. Source: PMID 20724655. Altered Response.
Showing effects for G/A genotype
LDL Cholesterol. Evidence: 10/10. Source: PMID 31719535. +0.17 mmol/L.
Total Cholesterol. Evidence: 10/10. Source: PMID 34610981. +0.135 mmol/L.
VLDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. +0.16 mmol/L.
IDL Cholesterol. Evidence: 10/10. Source: PMID 34610981. +0.17 mmol/L.
Lipoprotein(a) Levels. Evidence: 10/10. Source: PMID 33730874. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Carrying two copies of the common G allele is associated with lower circulating levels of low-density lipoprotein (LDL) and total cholesterol [1]. Because this genotype does not elevate gene expression, fewer cholesterol-carrying particles are released into the bloodstream [1]. Studies show that individuals with this profile typically maintain healthier lipid ratios compared to those carrying the A allele [2]. This natural baseline helps minimize the risk of arterial plaque accumulation over time [2]. Research also indicates that this genetic profile is linked to lower levels of very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) [3]. Maintaining these lower lipid fractions is a key factor in long-term cardiovascular health [2]. While diet and lifestyle remain crucial, this genetic background provides a favorable starting point for lipid management [1].
Typical circulating levels of LDL and total cholesterol; Lower baseline risk of lipid accumulation in blood vessels.
Sample genotype: AA (Homozygous)
Carrying two copies of the A allele is associated with the highest circulating levels of LDL and total cholesterol [1]. This genetic profile significantly increases the expression of the APOB gene, resulting in a high abundance of cholesterol-transporting particles [2]. Research indicates that each A allele raises LDL cholesterol by about 0.17 mmol/L, leading to a pronounced cumulative effect for those with two copies [1]. This elevation is also observed in other lipid fractions, such as VLDL and IDL cholesterol [3]. The continuous presence of elevated atherogenic particles in the bloodstream increases the risk of arterial plaque buildup [2]. While this variant is not a direct cause of severe familial hypercholesterolemia, it represents a notable genetic driver of high cholesterol [1].
Highest circulating levels of LDL and total cholesterol; Increased risk of arterial plaque accumulation.
Sample genotype: GA (Heterozygous)
Carrying one copy of the A allele is associated with a moderate increase in circulating LDL and total cholesterol levels [1]. This genetic change enhances the expression of the APOB gene, leading to a higher concentration of lipid-carrying particles in the blood [2]. Clinical studies have shown that each copy of the A allele raises LDL cholesterol by approximately 0.17 mmol/L [1]. This elevation extends to other atherogenic particles, including very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL) [3]. Over time, higher levels of these particles can increase the likelihood of plaque formation in the arteries [2]. Although this variant is classified as benign for severe familial hypercholesterolemia, it still influences everyday lipid levels [1].
Moderately higher circulating levels of LDL and total cholesterol; Slightly increased risk of arterial plaque buildup over time.
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
Genome-wide characterization of circulating metabolic biomarkers.
The power of genetic diversity in genome-wide association studies of lipids.
Content updated August 2026.
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