What you carry at this position in your DNA and what research says about it.
Fatty Acid Metabolism: 9/10 evidence, 18 publications.
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Sample genotype (not yours): A/A
Efficient Omega Fatty Acid Conversion but Higher LDL Cholesterol
High enzyme activity ensures efficient conversion of plant-based fats into active omega-3 and omega-6 forms. However, this metabolic efficiency is also associated with higher circulating levels of LDL cholesterol.
What this genotype means: Efficient conversion of plant-based omega fats; Higher baseline LDL cholesterol; Lower baseline triglycerides.
Sample genotype (not yours): A/G
Typical Lipid and Fatty Acid Balance
Moderate enzyme activity provides a balanced rate of fatty acid conversion. Circulating levels of cholesterol, triglycerides, and active omega fats generally remain near the population average.
What this genotype means: Typical conversion of plant-based omega fats; Average baseline LDL cholesterol; Average baseline triglycerides.
Sample genotype (not yours): G/G
Lower LDL Cholesterol but Reduced Omega Fatty Acid Conversion
Reduced enzyme activity limits the conversion of plant-based fats into active omega-3 and omega-6 forms. While this profile naturally lowers LDL cholesterol, it is linked to higher triglycerides and a greater need for direct dietary omegas.
What this genotype means: Reduced conversion of plant-based omega fats; Lower baseline LDL cholesterol; Higher baseline triglycerides.
Gene function and biological role
Gene Function: The FADS1 gene encodes delta-5 desaturase, a key enzyme responsible for the biosynthesis of highly unsaturated fatty acids [1]. This enzyme catalyzes the rate-limiting step that converts short-chain plant-derived fatty acids into long-chain polyunsaturated fatty acids [1]. These long-chain fats, including arachidonic acid and eicosapentaenoic acid, are critical structural components of cell membranes [2]. They also serve as precursors for signaling molecules that regulate inflammatory responses and cardiovascular health [2]. Variations in this gene directly influence how efficiently the body processes dietary fats [1].
Variant Impact: The rs174553 variant is an intronic change within the FADS1 gene that alters the expression levels of delta-5 desaturase [1]. Having the major A allele maintains high enzymatic activity, leading to rapid conversion of precursor fats into active long-chain fatty acids [1]. Conversely, the minor G allele significantly reduces desaturase activity, resulting in lower circulating levels of arachidonic acid and omega-3 products [2]. This reduction in enzyme activity shifts the overall lipid profile, lowering low-density lipoprotein cholesterol while raising triglycerides [3]. Consequently, this single nucleotide polymorphism acts as a major genetic determinant of blood lipid composition and fatty acid balance [1].
Key Insight: This variant acts as a metabolic trade-off, where genotypes that lower LDL cholesterol also reduce the body's ability to synthesize active omega-3 fats from plants.
Location: FADS1. Chromosome 11 · 11q12.2 · 61.8 Mb
Estimated prevalence by population
Global 52.9%; European 44.1%; African 85.0%; East Asian 20.0%; South Asian 67.4%; Americas 26.3%; Ashkenazi 51.0%; Finnish 33.6%; Middle Eastern 42.7%; Amish 59.1%.
Estimated AA genotype frequency.
Global 36.7%; European 44.6%; African 14.4%; East Asian 49.4%; South Asian 29.4%; Americas 50.0%; Ashkenazi 40.9%; Finnish 48.7%; Middle Eastern 45.3%; Amish 35.6%.
Estimated AG genotype frequency.
Global 10.4%; European 11.3%; African 0.6%; East Asian 30.6%; South Asian 3.2%; Americas 23.7%; Ashkenazi 8.2%; Finnish 17.7%; Middle Eastern 12.0%; Amish 5.3%.
Estimated GG genotype frequency.
Showing effects for A/A genotype
Nutrition & Metabolism
Macronutrient Metabolism
Omega-6 Conversion. Evidence: 3/10. Source: PMID 18936223. Efficient.
Omega-3 Conversion. Evidence: 3/10. Source: PMID 18936223. Efficient.
Cardiovascular & Metabolic
Lipids & Cholesterol
LDL Cholesterol. Evidence: 9/10. Source: PMID 35213538. Higher.
Triglycerides. Evidence: 8/10. Source: PMID 38448586. Lower.
Showing effects for A/G genotype
Omega-6 Conversion. Evidence: 3/10. Source: PMID 18936223. Typical.
Omega-3 Conversion. Evidence: 3/10. Source: PMID 18936223. Typical.
LDL Cholesterol. Evidence: 9/10. Source: PMID 35213538. Typical.
Triglycerides. Evidence: 8/10. Source: PMID 38448586. Typical.
Showing effects for G/G genotype
Omega-6 Conversion. Evidence: 3/10. Source: PMID 18936223. Reduced.
Omega-3 Conversion. Evidence: 3/10. Source: PMID 18936223. Reduced.
LDL Cholesterol. Evidence: 9/10. Source: PMID 35213538. Lower.
Triglycerides. Evidence: 8/10. Source: PMID 38448586. Higher.
What this genotype means for the people who carry it
Sample genotype: AA (Homozygous)
Efficient synthesis of long-chain polyunsaturated fatty acids is maintained by this genotype due to high delta-5 desaturase activity [1]. Plant-derived precursor oils are rapidly converted into essential active fats like arachidonic acid and eicosapentaenoic acid [2]. These lipids play vital roles in maintaining cell membrane fluidity, supporting cognitive function, and regulating immune responses [1]. While this active conversion is highly beneficial, it also correlates with elevated total and low-density lipoprotein cholesterol levels [3]. Conversely, circulating triglycerides and very-low-density lipoproteins tend to remain lower [4]. Individuals with this profile typically do not require high dietary intake of pre-formed animal-sourced omega fatty acids to maintain adequate cellular levels [2]. However, monitoring cardiovascular lipid markers remains important due to the naturally higher LDL baseline [3].
Efficient conversion of plant-based omega fats; Higher baseline LDL cholesterol; Lower baseline triglycerides.
Sample genotype: AG (Heterozygous)
Intermediate delta-5 desaturase activity is characteristic of this heterozygous genotype, resulting in a balanced lipid profile [1]. Precursor fatty acids from dietary sources are converted into active long-chain forms at a moderate, typical rate [2]. This ensures a steady baseline supply of crucial cellular fats like arachidonic acid and eicosapentaenoic acid under normal dietary conditions [2]. Circulating levels of low-density lipoprotein cholesterol and triglycerides generally align with standard population averages [3]. Because the metabolic rate is intermediate, the body retains a flexible response to dietary fat intake [1]. Obtaining a mix of both plant-based precursors and pre-formed marine-sourced omega-3 fatty acids supports optimal lipid balance [2]. No extreme deviations in cardiovascular risk markers are typically driven by this genetic baseline [3].
Typical conversion of plant-based omega fats; Average baseline LDL cholesterol; Average baseline triglycerides.
Sample genotype: GG (Homozygous)
Significantly reduced delta-5 desaturase activity limits the endogenous synthesis of active long-chain polyunsaturated fatty acids [1]. Precursor fats from plant oils accumulate in the blood because they cannot be efficiently converted into arachidonic acid or eicosapentaenoic acid [2]. This metabolic bottleneck results in lower circulating levels of these essential active fats in both blood plasma and breast milk [2]. On the positive side, this slower conversion rate is strongly associated with lower low-density lipoprotein cholesterol levels [3]. However, it also leads to higher circulating triglycerides and very-low-density lipoproteins [4]. To compensate for the reduced internal synthesis, obtaining pre-formed omega-3 and omega-6 fatty acids directly from marine or animal sources is highly beneficial [2]. This dietary strategy bypasses the genetic bottleneck to support cellular and cardiovascular health [1].
Reduced conversion of plant-based omega fats; Lower baseline LDL cholesterol; Higher baseline triglycerides.
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.
Genome-wide characterization of circulating metabolic biomarkers.
Content updated August 2026.
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