What you carry at this position in your DNA and what research says about it.
Heart and Lipid Health: 10/10 evidence, 24 publications.
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Sample genotype (not yours): G/G
Higher Cardiovascular and Lipid Risk
Two copies of the G allele are linked to lower HDL, higher triglycerides, and an elevated risk of heart disease.
What this genotype means: Lower HDL cholesterol; Higher triglycerides; Elevated heart disease risk.
Sample genotype (not yours): A/A
Favorable Lipid Profile and Lower Heart Risk
Two copies of the A allele are linked to higher protective HDL, lower triglycerides, and reduced heart disease risk.
What this genotype means: Higher protective HDL cholesterol; Lower circulating triglycerides; Reduced risk of heart disease.
Sample genotype (not yours): G/A
Typical Cardiovascular and Lipid Profile
A combination of one G and one A allele is linked to average lipid levels and standard baseline heart risk.
What this genotype means: Typical cholesterol levels; Standard heart disease risk; Average body fat distribution.
Gene function and biological role
Gene Function: The DNAH10 gene encodes dynein axonemal heavy chain 10, a protein primarily involved in cellular structure and movement. While historically studied for its role in ciliated cells, modern genomic research has linked variation in this region to metabolic regulation and adipose tissue function [1]. It is highly expressed in subcutaneous fat tissue, where it influences how the body stores and distributes lipids [2]. Researchers have found that cellular knockdown of DNAH10 significantly reduces lipid accumulation in fat cells, suggesting a direct role in adipocyte development [2]. This gene sits within a critical genomic region that helps determine whether body fat is stored in a metabolically healthy or unhealthy manner [1] [2].
Variant Impact: The rs7133378 variant is an intronic change located within the DNAH10 gene. This specific genetic marker acts as a key regulator of local gene expression in subcutaneous fat tissue, particularly affecting nearby genes like CCDC92 [2]. It is widely recognized as a classic favorable adiposity variant, meaning it uncouples higher body fat from the typical negative metabolic consequences [3]. The change alters how fat cells store lipids, shifting storage toward subcutaneous depots rather than harmful visceral areas around internal organs [2] [3]. Consequently, this single nucleotide change has a profound cascading effect on circulating cholesterol, triglycerides, and overall cardiovascular risk [3].
Key Insight: This variant is a prime example of favorable adiposity, where having genetically higher body fat and BMI actually pairs with a healthier heart and a highly protective cholesterol profile.
Location: DNAH10. Chromosome 12 · 12q24.31 · 123.9 Mb
Estimated prevalence by population
Global 40.9%; European 45.5%; African 22.2%; East Asian 75.7%; South Asian 60.4%; Americas 45.9%; Ashkenazi 36.8%; Finnish 53.8%; Middle Eastern 31.9%; Amish 35.9%.
Estimated GG genotype frequency.
Global 44.3%; European 43.9%; African 49.8%; East Asian 22.6%; South Asian 34.7%; Americas 43.7%; Ashkenazi 47.7%; Finnish 39.1%; Middle Eastern 49.2%; Amish 48.0%.
Estimated GA genotype frequency.
Global 14.8%; European 10.6%; African 27.9%; East Asian 1.7%; South Asian 5.0%; Americas 10.4%; Ashkenazi 15.5%; Finnish 7.1%; Middle Eastern 19.0%; Amish 16.1%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 10/10. Source: PMID 33619380. Lower HDL.
Triglycerides. Evidence: 10/10. Source: PMID 33619380. Higher Triglycerides.
Heart Disease
Coronary Artery Disease. Evidence: 7/10. Source: PMID 36474045. ~1.03x Risk.
Obesity & Body Composition
Body Fat Percentage. Evidence: 10/10. Source: PMID 30593698. Lower Body Fat.
Showing effects for A/A genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 33619380. Higher HDL.
Triglycerides. Evidence: 10/10. Source: PMID 33619380. Lower Triglycerides.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 36474045. Lower Risk.
Body Fat Percentage. Evidence: 10/10. Source: PMID 30593698. Higher Body Fat.
Showing effects for G/A genotype
HDL Cholesterol. Evidence: 10/10. Source: PMID 33619380. Typical HDL.
Triglycerides. Evidence: 10/10. Source: PMID 33619380. Typical Levels.
Coronary Artery Disease. Evidence: 7/10. Source: PMID 36474045. Typical Risk.
Body Fat Percentage. Evidence: 10/10. Source: PMID 30593698. Typical Body Fat.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Inheriting two copies of the G allele is associated with an unfavorable metabolic and lipid profile. Large-scale genomic studies show that this genotype leads to lower levels of protective HDL cholesterol and higher levels of circulating triglycerides [1] [2]. Additionally, this genetic makeup is linked to a higher waist-to-hip ratio, indicating a tendency to store fat viscerally around internal organs rather than safely under the skin [3]. This unfavorable fat distribution pattern directly contributes to an increased risk of developing coronary artery disease [4]. Even though this genotype is associated with a slightly lower overall body mass index and body fat percentage, the underlying metabolic health is less optimal [1] [2]. Maintaining a heart-healthy diet and regular physical activity can help mitigate these genetic lipid risks.
Lower HDL cholesterol; Higher triglycerides; Elevated heart disease risk.
Sample genotype: AA (Homozygous)
Possessing two copies of the A allele is linked to a highly favorable metabolic profile, characterized by higher HDL cholesterol and lower triglycerides [1] [2]. This genotype represents a classic favorable adiposity profile, where fat is preferentially stored in safe subcutaneous depots rather than around vital organs [2] [3]. As a result, this genetic signature is associated with a lower waist-to-hip ratio and a reduced risk of coronary artery disease [3] [4]. Interestingly, this protective cardiovascular state occurs despite a genetic predisposition to a slightly higher overall body fat percentage and body mass index [1] [2]. The body effectively uncouples excess weight from the typical metabolic complications, keeping blood vessels healthier [2]. This natural metabolic advantage provides a strong foundation for long-term cardiovascular wellness.
Higher protective HDL cholesterol; Lower circulating triglycerides; Reduced risk of heart disease.
Sample genotype: GA (Heterozygous)
Possessing one G allele and one A allele typically results in an intermediate metabolic profile. This heterozygous state balances the lipid-lowering and lipid-raising tendencies of both variants, leading to average levels of HDL cholesterol and triglycerides [1] [2]. Cardiovascular risk remains at the standard population baseline, with no significant genetic push toward or away from coronary artery disease [3]. Body fat distribution and overall body mass index also tend to fall within the typical average range [1] [4]. Because this genotype represents the middle ground, lifestyle factors such as diet, exercise, and stress management will play the dominant role in shaping long-term cardiovascular outcomes. Standard cardiovascular screenings and routine lipid panels are sufficient for monitoring health.
Typical cholesterol levels; Standard heart disease risk; Average body fat distribution.
Variants with shared genetic architecture
rs964184 · ZPR1 Gene · Chr 11 · Triglyceride and Heart Risk
rs1045241 · TNFAIP8 Gene · Chr 5 · Lipids and Body Fat
rs268 · LPL Gene · Chr 8 · Triglycerides and Heart Risk
A scalable variational inference approach for increased mixed-model association power.
Genome-wide discovery of genetic loci that uncouple excess adiposity from its comorbidities.
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
A Large Multiethnic Genome-Wide Association Study of Adult Body Mass Index Identifies Novel Loci.
Content updated August 2026.
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