What you carry at this position in your DNA and what research says about it.
Saturated Fat Sensitivity: 8/10 evidence, 10 publications.
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Sample genotype (not yours): G/G
Higher Obesity Risk with Saturated Fat but Lower Heart Risk
High sensitivity to dietary saturated fat increases weight gain when fat intake is high. However, significant protection against coronary artery disease is also present.
What this genotype means: Increased obesity risk on high saturated fat diets; Lower risk of coronary artery disease; Higher HDL cholesterol levels.
Sample genotype (not yours): A/A
Typical Saturated Fat Response and Heart Risk
A standard response to dietary saturated fat and a typical baseline risk for heart disease characterize this profile. Weight gain is not disproportionately triggered by saturated fat.
What this genotype means: Typical response to dietary saturated fat; Standard baseline risk for coronary artery disease; Typical HDL cholesterol levels.
Sample genotype (not yours): G/A
Gene function and biological role
Gene Function: The APOA2 gene encodes apolipoprotein A-II, which is the second most abundant protein component of high-density lipoprotein (HDL) particles [1]. This protein plays a critical role in lipid metabolism, stabilizing HDL particles and regulating how the body processes triglycerides and other fats [2]. It also influences the activity of enzymes involved in fat clearance and interacts with pathways that control appetite and satiety [3]. Variations in this gene can alter the amount of apolipoprotein A-II produced, which in turn affects how the body responds to dietary fats [4].
Variant Impact: Located in the promoter region of the APOA2 gene, rs5082 directly influences how much apolipoprotein A-II protein is synthesized [3]. Carrying the G allele (often reported as the C allele on the opposite strand) reduces the transcription rate of the gene, leading to lower circulating levels of apolipoprotein A-II [4]. This reduction in protein levels alters the body's postprandial response to fat, meaning how lipids are processed after a meal [5]. Interestingly, this molecular change creates a unique interaction with dietary saturated fat, affecting both weight management and cardiovascular markers [6].
Key Insight: The obesity risk associated with this variant is entirely dependent on diet, appearing only when daily saturated fat intake exceeds 22 grams.
Location: APOA2. Chromosome 1 · 1q23.3 · 161.2 Mb
Estimated prevalence by population
Global 10.9%; European 15.2%; African 5.3%; East Asian 0.8%; South Asian 6.3%; Americas 8.4%; Ashkenazi 14.6%; Finnish 14.4%; Middle Eastern 13.5%; Amish 17.3%.
Estimated GG genotype frequency.
Global 42.2%; European 47.6%; African 35.6%; East Asian 16.6%; South Asian 37.6%; Americas 41.1%; Ashkenazi 47.2%; Finnish 47.1%; Middle Eastern 46.5%; Amish 48.6%.
Estimated GA genotype frequency.
Global 46.9%; European 37.2%; African 59.1%; East Asian 82.5%; South Asian 56.1%; Americas 50.6%; Ashkenazi 38.2%; Finnish 38.5%; Middle Eastern 40.0%; Amish 34.1%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Obesity & Body Composition
Obesity. Evidence: 3/10. Source: PMID 17446329. Higher Risk.
Appetite Regulation. Evidence: 3/10. Source: PMID 17446329. Lower Satiety.
Heart Disease
Heart Disease. Evidence: 3/10. Source: PMID 18179799. ~43% Lower Risk.
Lipids & Cholesterol
HDL Cholesterol. Evidence: 8/10. Source: PMID 35213538. Higher Levels.
Showing effects for A/A genotype
Obesity. Evidence: 3/10. Source: PMID 17446329. Typical Risk.
Appetite Regulation. Evidence: 3/10. Source: PMID 17446329. Typical Satiety.
Heart Disease. Evidence: 3/10. Source: PMID 18179799. Typical Risk.
HDL Cholesterol. Evidence: 8/10. Source: PMID 35213538. Typical Levels.
Showing effects for G/A genotype
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
A fascinating genetic trade-off exists here between weight management and cardiovascular health. When consuming a diet high in saturated fat, defined as 22 grams or more per day, carriers of this genetic profile have a significantly higher risk of obesity [1]. This susceptibility is driven by altered appetite regulation, as this genetic profile is associated with higher levels of the hunger hormone ghrelin and increased overall food intake [1]. However, when saturated fat intake is kept low, there is no elevated risk of weight gain [2]. On the positive side, this profile is strongly protective against heart disease, showing an estimated 43% lower risk of coronary artery disease [3]. It is also associated with higher levels of protective HDL cholesterol and larger HDL particle sizes [4]. Managing saturated fat intake allows individuals to bypass the weight-gain risk while retaining the cardiovascular benefits.
Increased obesity risk on high saturated fat diets; Lower risk of coronary artery disease; Higher HDL cholesterol levels.
Sample genotype: AA (Homozygous)
Representing the most common genetic profile globally, this configuration serves as the standard baseline for this gene. It is associated with a typical response to dietary fats, meaning that saturated fat does not trigger the same exaggerated weight gain seen in other genetic profiles [1]. Baseline risks for obesity and coronary artery disease remain at standard population levels [2]. Levels of HDL cholesterol and other circulating lipids are typical, showing no strong genetic elevation or reduction [3]. Because there is no heightened sensitivity, standard nutritional guidelines for balanced fat intake apply normally [4]. This profile provides a stable, baseline metabolic response without the unique trade-offs of the homozygous minor genotype.
Typical response to dietary saturated fat; Standard baseline risk for coronary artery disease; Typical HDL cholesterol levels.
Sample genotype: GA (Heterozygous)
Carrying one copy of each allele results in a typical response to dietary fats, meaning that saturated fat does not trigger the same exaggerated weight gain seen in other genetic profiles [1]. Baseline risks for obesity and coronary artery disease remain at standard population levels [2]. Levels of HDL cholesterol and other circulating lipids are typical, showing no strong genetic elevation or reduction [3]. Because there is no heightened sensitivity, standard nutritional guidelines for balanced fat intake apply normally [4]. This profile provides a stable, baseline metabolic response without the unique trade-offs of the homozygous minor genotype.
Variants with shared genetic architecture
rs116843064 · ANGPTL4 Gene · Chr 19 · Heart Disease Risk
rs1800437 · GIPR Gene · Chr 19 · Heart and Metabolic Health
rs663129 · MC4R Gene · Chr 18 · Weight and Heart Health
Genome-wide characterization of circulating metabolic biomarkers.
Content updated August 2026.
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