What you carry at this position in your DNA and what research says about it.
Cardiovascular Lipid Levels: 8/10 evidence, 5 publications.
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Sample genotype (not yours): A/A
Lower Cholesterol and Lower Coronary Risk
Lower total and LDL cholesterol levels characterize this profile, which helps reduce overall cardiovascular risk. A slight elevation in triglycerides is also associated with this genetic pattern.
What this genotype means: Lower LDL and total cholesterol levels; Reduced risk of coronary artery disease; Slightly higher triglyceride levels.
Sample genotype (not yours): A/G
Intermediate Cholesterol Levels and Moderate Coronary Risk
A balanced lipid profile is typical here, with intermediate levels of both cholesterol and triglycerides. Cardiovascular risk falls close to the population average.
What this genotype means: Intermediate LDL and total cholesterol levels; Average risk of coronary artery disease; Moderate triglyceride levels.
Sample genotype (not yours): G/G
Higher Cholesterol and Higher Coronary Risk
Elevated levels of total cholesterol, LDL cholesterol, and apolipoprotein B are associated with this profile, increasing cardiovascular risk. Conversely, triglyceride levels tend to be lower.
What this genotype means: Higher LDL and total cholesterol levels; Increased risk of coronary artery disease; Lower triglyceride levels.
Gene function and biological role
Gene Function: The FADS3 gene encodes fatty acid desaturase 3, an enzyme belonging to the fatty acid desaturase family [1]. This family of enzymes regulates the unsaturation of fatty acids by introducing double bonds into fatty acyl chains [1]. FADS3 is clustered with its family members FADS1 and FADS2 on chromosome 11 [1]. Unlike FADS1 and FADS2, which have well-characterized roles in polyunsaturated fatty acid synthesis, the precise biochemical activity of FADS3 has been more elusive, though it is known to act as a sphingoid base desaturase [1]. It plays a significant role in regulating the human plasma sphingolipidome and lipid homeostasis [2].
Variant Impact: The rs1000778 variant is an intron variant located within the FADS3 gene. This genetic variation is associated with significant changes in circulating lipid levels, including cholesterol fractions and triglycerides [3]. It also influences the levels of various blood metabolites, such as sphingomyelins and phosphatidylcholines [2]. Studies suggest that this variant may alter the splicing or expression of FADS3, thereby affecting downstream lipid processing [1]. These metabolic shifts can ultimately influence cardiovascular health and coronary artery disease susceptibility [1].
Key Insight: This variant showcases a classic lipid trade-off, where the same genetic copy that lowers LDL cholesterol actually raises triglycerides.
Location: FADS3. Chromosome 11 · 11q12.2 · 61.9 Mb
Estimated prevalence by population
Global 20.0%; European 6.4%; African 48.7%; East Asian 9.6%; South Asian 13.5%; Americas 23.3%; Ashkenazi 5.8%; Finnish 5.1%; Middle Eastern 15.3%; Amish 3.6%.
Estimated AA genotype frequency.
Global 40.5%; European 37.9%; African 42.2%; East Asian 42.7%; South Asian 46.5%; Americas 49.9%; Ashkenazi 36.6%; Finnish 34.9%; Middle Eastern 47.6%; Amish 30.7%.
Estimated AG genotype frequency.
Global 39.4%; European 55.7%; African 9.1%; East Asian 47.7%; South Asian 39.9%; Americas 26.8%; Ashkenazi 57.6%; Finnish 60.0%; Middle Eastern 37.1%; Amish 65.7%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Cardiovascular & Metabolic
Lipids & Cholesterol
LDL Cholesterol. Evidence: 6/10. Source: PMID 33462484. Lower LDL.
Triglycerides. Evidence: 8/10. Source: PMID 33462484. Higher Triglycerides.
Total Cholesterol. Evidence: 6/10. Source: PMID 33462484. Lower Cholesterol.
Heart Disease
Coronary Artery Disease. Evidence: 3/10. Source: PMID 21040914. Lower Risk.
Diabetes & Glycemic Traits
HbA1c. Evidence: 6/10. Source: PMID 33462484. Lower HbA1c.
Showing effects for A/G genotype
LDL Cholesterol. Evidence: 6/10. Source: PMID 33462484. Slightly Higher LDL.
Triglycerides. Evidence: 8/10. Source: PMID 33462484. Slightly Higher.
Total Cholesterol. Evidence: 6/10. Source: PMID 33462484. Slightly Higher.
Coronary Artery Disease. Evidence: 3/10. Source: PMID 21040914. Slightly Higher Risk.
HbA1c. Evidence: 6/10. Source: PMID 33462484. Slightly Higher HbA1c.
Showing effects for G/G genotype
LDL Cholesterol. Evidence: 6/10. Source: PMID 33462484. Higher LDL.
Triglycerides. Evidence: 8/10. Source: PMID 33462484. Lower Triglycerides.
Total Cholesterol. Evidence: 6/10. Source: PMID 33462484. Higher Cholesterol.
Coronary Artery Disease. Evidence: 3/10. Source: PMID 21040914. Higher Risk.
HbA1c. Evidence: 6/10. Source: PMID 33462484. Higher HbA1c.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Genetic analysis indicates that inheriting two copies of the A allele is associated with lower circulating levels of total cholesterol, LDL cholesterol, and apolipoprotein B [1]. These lipid markers are key components of cardiovascular health, and lower levels generally correlate with a reduced risk of coronary artery disease [2]. Interestingly, this same genetic pattern is linked to higher circulating triglycerides [1]. This inverse relationship between cholesterol fractions and triglycerides is a common feature of FADS gene cluster variants [2]. Blood sugar regulation may also be slightly more favorable, as indicated by lower average HbA1c levels [1]. Maintaining a balanced diet rich in healthy fats can help manage the associated triglyceride levels while maximizing cardiovascular benefits.
Lower LDL and total cholesterol levels; Reduced risk of coronary artery disease; Slightly higher triglyceride levels.
Sample genotype: AG (Heterozygous)
Carrying one copy of each allele results in intermediate levels of circulating lipids, balancing the opposing effects of the A and G variants [1]. Total cholesterol, LDL cholesterol, and apolipoprotein B levels are typically moderate, falling between the high levels of the G/G genotype and the low levels of the A/A genotype [1]. Similarly, triglyceride levels are only slightly elevated compared to the G/G baseline [1]. This intermediate profile generally translates to an average risk of coronary artery disease [2]. Metabolic markers such as HbA1c and various sphingolipids also remain within typical ranges. Standard cardiovascular wellness strategies, including regular exercise and a fiber-rich diet, are highly effective for maintaining healthy lipid ratios.
Intermediate LDL and total cholesterol levels; Average risk of coronary artery disease; Moderate triglyceride levels.
Sample genotype: GG (Homozygous)
Inheriting two copies of the G allele is linked to higher circulating levels of total cholesterol, LDL cholesterol, and apolipoprotein B [1]. These elevated lipid fractions are well-established risk factors for the development of coronary artery disease [2]. Conversely, this genetic pattern is associated with lower circulating triglycerides, representing a distinct metabolic trade-off [1]. Average HbA1c levels also tend to be slightly higher, suggesting a minor impact on long-term blood sugar regulation [1]. The G allele is also associated with altered levels of sphingomyelins and other complex cell membrane lipids [3]. Given the increased cardiovascular risk, focusing on heart-healthy lifestyle choices, such as limiting saturated fats and monitoring lipid panels, is particularly beneficial.
Higher LDL and total cholesterol levels; Increased risk of coronary artery disease; Lower triglyceride levels.
Variants with shared genetic architecture
rs174455 · FADS3 Gene · Chr 11 · Gout Risk
rs7115739 · FADS3 Gene · Chr 11 · Triglyceride and Lipid Levels
rs174448 · FADS3 Gene · Chr 11 · Omega-3 and Triglycerides
Genetics of 35 blood and urine biomarkers in the UK Biobank.
Content updated August 2026.
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