What you carry at this position in your DNA and what research says about it.
Omega Fatty Acid Conversion: 8/10 evidence, 30 publications.
You're viewing every possible genotype for this variant.
None of these is your result. Use the genotype toggle to compare them, then sign up and upload your DNA to see which one is yours.
Sample genotype (not yours): T/T
Higher Cholesterol and Increased Aortic Stenosis Risk
Efficient conversion of plant-based omega fats comes with a trade-off of higher blood lipids. This genotype is linked to elevated total cholesterol and an increased risk of heart valve calcification.
What this genotype means: Elevated total cholesterol and triglycerides; Higher risk of aortic valve calcification; Highly efficient conversion of plant-based omega fats.
Sample genotype (not yours): C/C
Lower Cardiovascular Risk but Inefficient Omega Conversion
Excellent protection against high cholesterol and heart valve calcification is paired with very low efficiency in processing plant-based omega fats.
What this genotype means: Significantly lower total cholesterol and triglycerides; Lowest risk of aortic valve calcification; Very poor conversion of plant-based omega-3 and omega-6 fats.
Sample genotype (not yours): T/C
Balanced Lipid Levels and Moderate Omega Conversion
A single copy of the protective C allele helps maintain balanced cholesterol and triglyceride levels. This intermediate profile offers a favorable middle ground between cardiovascular risk and fatty acid conversion efficiency.
What this genotype means: Moderate, balanced blood lipid levels; Reduced risk of aortic stenosis compared to T/T; Adequate conversion of plant-based fatty acids.
Gene function and biological role
Gene Function: The FADS1 gene encodes fatty acid desaturase 1, a critical enzyme in the metabolism of polyunsaturated fatty acids. This enzyme regulates the rate-limiting step that converts plant-derived short-chain omega-3 and omega-6 fatty acids into active, long-chain forms like eicosapentaenoic acid (EPA) and arachidonic acid (ARA) [1]. Through this conversion process, FADS1 directly influences cell membrane composition, lipid profiles, and inflammatory signaling pathways [2]. Variations in this gene can significantly alter enzyme activity, impacting blood cholesterol, triglyceride levels, and overall cardiovascular health [3]. Consequently, FADS1 is a major genetic determinant of how the body processes dietary fats and manages systemic inflammation [4].
Variant Impact: The rs174547 variant is an intronic change located within the FADS1 gene that acts as a major regulator of enzyme expression. The major T allele is associated with high FADS1 expression and elevated desaturase activity, leading to rapid conversion of plant-based fats into long-chain fatty acids [1]. Conversely, the minor C allele significantly reduces FADS1 expression, resulting in lower desaturase activity and a reduced rate of fatty acid conversion [2]. This functional difference creates distinct metabolic profiles, where the T allele promotes higher levels of arachidonic acid and circulating lipids, while the C allele maintains lower lipid levels [5]. Because of these widespread metabolic effects, this single nucleotide polymorphism is strongly linked to variations in blood cholesterol, heart valve calcification, and resting heart rate [4].
Key Insight: The T/T genotype is highly efficient at converting plant-based oils into active omega fats, but this same high efficiency increases the risk of cholesterol buildup and heart valve calcification.
Location: FADS1. Chromosome 11 · 11q12.2 · 61.8 Mb
Origin Story: The ancestral C allele was predominant among hunter-gatherers who consumed diets rich in animal meats and fish, which already contained preformed long-chain fatty acids. With the transition to agriculture and plant-heavy diets, natural selection favored the T allele, which allowed early farmers to efficiently synthesize essential long-chain fats directly from plant sources.
Estimated prevalence by population
Global 52.9%; European 44.1%; African 85.0%; East Asian 19.9%; South Asian 67.3%; Americas 26.3%; Ashkenazi 51.0%; Finnish 33.6%; Middle Eastern 42.7%; Amish 58.8%.
Estimated TT genotype frequency.
Global 36.7%; European 44.6%; African 14.4%; East Asian 49.4%; South Asian 29.5%; Americas 50.0%; Ashkenazi 40.8%; Finnish 48.7%; Middle Eastern 45.3%; Amish 35.7%.
Estimated TC genotype frequency.
Global 10.4%; European 11.3%; African 0.6%; East Asian 30.7%; South Asian 3.2%; Americas 23.8%; Ashkenazi 8.2%; Finnish 17.7%; Middle Eastern 12.0%; Amish 5.4%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Heart Disease
Aortic Valve Stenosis. Evidence: 6/10. Source: PMID 32186652. Increased Risk.
Lipids & Cholesterol
Total Cholesterol. Evidence: 10/10. Source: PMID 27790247. Higher Levels.
Triglycerides. Evidence: 10/10. Source: PMID 19060906. Lower Levels.
Nutrition & Metabolism
Macronutrient Metabolism
Omega-3 Conversion. Evidence: 8/10. Source: PMID 21414826. Highly Efficient.
Showing effects for C/C genotype
Aortic Valve Stenosis. Evidence: 6/10. Source: PMID 32186652. ~24% Lower Risk.
Total Cholesterol. Evidence: 10/10. Source: PMID 27790247. Lower Levels.
Triglycerides. Evidence: 10/10. Source: PMID 19060906. Higher Levels.
Omega-3 Conversion. Evidence: 8/10. Source: PMID 21414826. Low Efficiency.
Showing effects for T/C genotype
Aortic Valve Stenosis. Evidence: 6/10. Source: PMID 32186652. ~12% Lower Risk.
Total Cholesterol. Evidence: 10/10. Source: PMID 27790247. Moderate Levels.
Triglycerides. Evidence: 10/10. Source: PMID 19060906. Moderate Levels.
Omega-3 Conversion. Evidence: 8/10. Source: PMID 21414826. Moderate Efficiency.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
High desaturase activity in this genotype ensures that plant-based omega-3 and omega-6 fatty acids are rapidly converted into active long-chain forms like EPA and arachidonic acid [1]. While this efficient conversion is beneficial for plant-based diets, it also leads to higher levels of pro-inflammatory arachidonic acid and circulating lipids [2]. Large-scale genetic studies have consistently linked this genotype to elevated total cholesterol [3]. Furthermore, the increased production of arachidonic acid is associated with a higher risk of developing aortic valve calcification and aortic stenosis [4].
Elevated total cholesterol and triglycerides; Higher risk of aortic valve calcification; Highly efficient conversion of plant-based omega fats.
Sample genotype: CC (Homozygous)
Low desaturase activity in this genotype significantly reduces the conversion of plant-based short-chain fatty acids into active long-chain forms [1]. This inefficient conversion leads to lower levels of pro-inflammatory arachidonic acid, which provides strong natural protection against cardiovascular issues [2]. Studies show that this genotype is associated with the lowest levels of total cholesterol and LDL cholesterol [3]. Additionally, carrying two copies of the protective C allele reduces the risk of aortic stenosis by up to 24% [4]. However, because the synthesis of EPA and DHA from plant sources like flaxseed is highly restricted, relying solely on a vegetarian diet may lead to a deficit in active omega-3s [5].
Significantly lower total cholesterol and triglycerides; Lowest risk of aortic valve calcification; Very poor conversion of plant-based omega-3 and omega-6 fats.
Sample genotype: TC (Heterozygous)
Possessing one copy of each allele results in moderate fatty acid desaturase activity, balancing the benefits and risks of both extremes. This intermediate enzyme activity allows for a reasonable rate of converting plant-based omega-3 and omega-6 fats into active long-chain forms [1]. At the same time, the presence of the protective C allele helps keep total cholesterol lower than the T/T genotype [2]. Research indicates that each copy of the C allele reduces the odds of developing aortic stenosis by approximately 12% [3]. This balanced genetic profile generally supports healthy lipid levels without severely compromising the body's ability to synthesize essential long-chain fats.
Moderate, balanced blood lipid levels; Reduced risk of aortic stenosis compared to T/T; Adequate conversion of plant-based fatty acids.
Variants with shared genetic architecture
rs174546 · FADS1 Gene · Chr 11 · Fatty Acid Metabolism
rs174554 · FADS1 Gene · Chr 11 · Omega Fat Conversion
rs174545 · FADS1 Gene · Chr 11 · Fatty Acid Metabolism
Polymorphisms in FADS1 and FADS2 alter desaturase activity in young Caucasian and Asian adults.
Common variants at 30 loci contribute to polygenic dyslipidemia.
Association of FADS1/2 Locus Variants and Polyunsaturated Fatty Acids With Aortic Stenosis.
Content updated September 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com