What you carry at this position in your DNA and what research says about it.
Omega-3 and Heart Health: 5/10 evidence, 19 publications.
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Sample genotype (not yours): T/T
High Omega-3 Conversion but Higher Cardiovascular Risk
This genotype allows highly efficient conversion of plant-based fats into active omega-3s. However, it also increases the production of inflammatory compounds, raising cardiovascular risk.
What this genotype means: Highly efficient conversion of plant-based omega-3s; Elevated levels of inflammatory arachidonic acid; Increased baseline risk of cardiovascular events.
Sample genotype (not yours): C/C
Low Omega-3 Conversion but Lower Cardiovascular Risk
This genotype significantly reduces the conversion of plant-based fats into active omega-3s, requiring direct dietary supplementation. However, it lowers the production of inflammatory compounds, reducing heart risk.
What this genotype means: Inefficient conversion of plant-based omega-3s; Reduced levels of inflammatory arachidonic acid; Lower baseline risk of coronary artery disease.
Sample genotype (not yours): T/C
Typical Omega-3 Conversion and Balanced Cardiovascular Risk
This genotype provides a balanced, intermediate rate of fatty acid conversion. It offers a moderate ability to process plant-based fats without excessively raising inflammatory markers.
What this genotype means: Moderate conversion of plant-based fatty acids; Typical baseline levels of arachidonic acid; Average cardiovascular risk profile.
Gene function and biological role
Gene Function: Fatty acid desaturase 1 is a key enzyme responsible for the rate-limiting step in the biosynthesis of long-chain polyunsaturated fatty acids [1]. It converts precursor plant-based fatty acids into biologically active forms like arachidonic acid and eicosapentaenoic acid [2]. This enzyme plays a central role in regulating systemic lipid levels, cellular membrane composition, and the production of inflammatory signaling molecules [3]. Genetic variations in this gene significantly alter how efficiently an individual processes dietary fats [4].
Variant Impact: The rs174561 variant is located in the regulatory region of the FADS1 gene, directly influencing its expression levels [5]. The major T allele is associated with high desaturase activity, leading to rapid conversion of precursor fats [2]. In contrast, the minor C allele significantly reduces enzyme activity, slowing down the synthesis of long-chain fatty acids [4]. This molecular difference creates a distinct trade-off between omega-3 synthesis efficiency and cardiovascular inflammation risk [1].
Key Insight: Your ability to convert plant-based omega-3s into brain-healthy EPA depends heavily on this variant. The genotype that makes you highly efficient at processing plant fats also increases your baseline risk for cardiovascular inflammation.
Location: FADS1. Chromosome 11 · 11q12.2 · 61.8 Mb
Origin Story: The ancestral T allele, which allows highly efficient conversion of plant-based fatty acids, is thought to have been strongly selected for as early human populations transitioned to agricultural diets rich in plant seed oils but low in marine foods.
Estimated prevalence by population
Global 56.5%; European 49.2%; African 86.2%; East Asian 21.0%; South Asian 70.0%; Americas 29.0%; Ashkenazi 60.8%; Finnish 36.6%; Middle Eastern 45.8%; Amish 62.7%.
Estimated TT genotype frequency.
Global 34.8%; European 41.9%; African 13.2%; East Asian 49.7%; South Asian 27.3%; Americas 49.7%; Ashkenazi 34.4%; Finnish 47.8%; Middle Eastern 43.7%; Amish 33.0%.
Estimated TC genotype frequency.
Global 8.7%; European 8.9%; African 0.5%; East Asian 29.3%; South Asian 2.7%; Americas 21.3%; Ashkenazi 4.9%; Finnish 15.6%; Middle Eastern 10.4%; Amish 4.3%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Nutrition & Metabolism
Macronutrient Metabolism
Omega-3 Conversion. Evidence: 3/10. Source: PMID 23160180. High Efficiency.
Arachidonic Acid Levels. Evidence: 3/10. Source: PMID 20562440. Elevated Levels.
Cardiovascular & Metabolic
Heart Disease
Cardiovascular Risk. Evidence: 3/10. Source: PMID 21793953. Increased Risk.
Lipids & Cholesterol
Triglycerides. Evidence: 5/10. Source: PMID 34503513. Lower Levels.
Showing effects for C/C genotype
Omega-3 Conversion. Evidence: 3/10. Source: PMID 23160180. Low Efficiency.
Arachidonic Acid Levels. Evidence: 3/10. Source: PMID 20562440. Reduced Levels.
Cardiovascular Risk. Evidence: 3/10. Source: PMID 21793953. Decreased Risk.
Triglycerides. Evidence: 5/10. Source: PMID 34503513. Higher Levels.
Showing effects for T/C genotype
Omega-3 Conversion. Evidence: 3/10. Source: PMID 23160180. Moderate Efficiency.
Arachidonic Acid Levels. Evidence: 3/10. Source: PMID 20562440. Typical Levels.
Cardiovascular Risk. Evidence: 3/10. Source: PMID 21793953. Typical Risk.
Triglycerides. Evidence: 5/10. Source: PMID 34503513. Typical Levels.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Individuals with the T/T genotype possess highly active FADS1 enzymes, enabling them to efficiently convert plant-derived alpha-linolenic acid into active eicosapentaenoic acid [1]. This makes plant-based sources of omega-3s, such as flaxseeds and chia seeds, highly effective for maintaining healthy omega-3 levels [2]. However, this rapid conversion rate also applies to omega-6 fatty acids, leading to elevated levels of arachidonic acid [3]. Arachidonic acid is a direct precursor to pro-inflammatory eicosanoids, which can promote vascular inflammation [4]. Consequently, this highly active metabolism is linked to an increased baseline risk of coronary artery disease and ischemic stroke [5]. To balance this risk, managing the dietary ratio of omega-6 to omega-3 fatty acids is highly recommended [5].
Highly efficient conversion of plant-based omega-3s; Elevated levels of inflammatory arachidonic acid; Increased baseline risk of cardiovascular events.
Sample genotype: CC (Homozygous)
Individuals carrying the C/C genotype have significantly reduced FADS1 enzyme activity, resulting in a limited ability to synthesize long-chain omega-3s from plant sources [1]. Precursor plant fats like alpha-linolenic acid accumulate in the blood rather than being converted to active EPA and DHA [2]. Consequently, relying solely on plant-based omega-3s can lead to low systemic levels of these crucial fatty acids [3]. To compensate, direct dietary intake of EPA and DHA from fish, fish oil, or microalgae supplements is highly beneficial [1]. On the positive side, this slow conversion rate also limits the production of arachidonic acid from omega-6 fats [4]. Because arachidonic acid drives inflammatory pathways, having lower levels of this compound is associated with a reduced risk of coronary artery disease and stroke [5]. However, this genotype is also linked to slightly higher baseline triglyceride levels [6].
Inefficient conversion of plant-based omega-3s; Reduced levels of inflammatory arachidonic acid; Lower baseline risk of coronary artery disease.
Sample genotype: TC (Heterozygous)
Carrying one copy of each allele results in intermediate FADS1 desaturase activity, representing the most common metabolic profile globally [1]. Individuals with the T/C genotype convert plant-based omega-3 fatty acids into active EPA at a moderate rate [2]. While they can utilize plant-based fats, they may still benefit from direct sources of EPA and DHA like fish or algae oil to optimize their lipid profile [3]. On the omega-6 side, the production of arachidonic acid is kept at a typical, balanced level [4]. This moderate conversion rate avoids the high inflammatory risk associated with the T/T genotype while maintaining better synthesis than the C/C genotype [5]. Overall, cardiovascular risk and lipid levels remain close to the population average [6].
Moderate conversion of plant-based fatty acids; Typical baseline levels of arachidonic acid; Average cardiovascular risk profile.
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
Genetic variation in lipid desaturases and its impact on the development of human disease.
Comprehensive analysis of the impact of SNPs and CNVs on human microRNAs and their regulatory genes.
Content updated August 2026.
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