What you carry at this position in your DNA and what research says about it.
Fatty Acid Metabolism: 8/10 evidence, 20 publications.
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Sample genotype (not yours): T/T
Higher Risk of Asthma and Inflammatory Conditions
Carrying two copies of the T allele is linked to highly efficient fatty acid conversion but also increases susceptibility to inflammatory and respiratory issues.
What this genotype means: Highly efficient conversion of dietary fats; Increased risk of asthma and nasal polyps; Lower circulating HDL cholesterol.
Sample genotype (not yours): C/C
Lower Risk of Asthma and Inflammatory Conditions
Carrying two copies of the C allele protects against respiratory inflammation and supports higher HDL cholesterol, though fatty acid conversion is slower.
What this genotype means: Slower conversion of plant-based fats; Lower risk of asthma and nasal polyps; Higher circulating HDL cholesterol.
Sample genotype (not yours): T/C
Slightly Higher Risk of Asthma and Inflammation
Carrying one copy of the T allele results in intermediate fatty acid conversion and a modest increase in inflammatory risks.
What this genotype means: Moderate conversion of dietary fats; Slightly elevated risk of respiratory inflammation; Typical HDL cholesterol levels.
Gene function and biological role
Gene Function: The MYRF gene encodes myelin regulatory factor, a transcription factor vital for central nervous system myelination. However, genetic variants within the MYRF gene region, including rs174535, act as powerful expression quantitative trait loci for the neighboring FADS1 and FADS2 genes [1]. These fatty acid desaturase genes control the rate-limiting steps in the synthesis of long-chain polyunsaturated fatty acids from dietary precursors [2]. Consequently, variations in this region heavily influence systemic lipid profiles and inflammatory pathways [1].
Variant Impact: The rs174535 variant is a synonymous change located within the MYRF gene, meaning it does not alter the encoded amino acid sequence of the MYRF protein. Instead, it serves as a genetic marker strongly linked to the expression levels of the nearby FADS1 and FADS2 desaturase enzymes [1]. The T allele is associated with increased expression of these enzymes, leading to highly efficient conversion of short-chain fatty acids into long-chain polyunsaturated fatty acids [2]. Conversely, the C allele reduces this conversion efficiency, altering circulating lipid levels and inflammatory responses [1].
Key Insight: While the T allele allows your body to convert plant-based omega-3 fats into active forms more efficiently, it also increases the production of pro-inflammatory arachidonic acid, raising the risk of asthma and nasal polyps.
Location: MYRF. Chromosome 11 · 11q12.2 · 61.8 Mb
Estimated prevalence by population
Global 46.8%; European 43.3%; African 65.2%; East Asian 19.5%; South Asian 64.0%; Americas 24.4%; Ashkenazi 50.0%; Finnish 33.4%; Middle Eastern 41.3%; Amish 58.8%.
Estimated TT genotype frequency.
Global 41.6%; European 45.0%; African 31.1%; East Asian 49.3%; South Asian 32.0%; Americas 50.0%; Ashkenazi 41.4%; Finnish 48.8%; Middle Eastern 45.9%; Amish 35.7%.
Estimated TC genotype frequency.
Global 11.7%; European 11.7%; African 3.7%; East Asian 31.2%; South Asian 4.0%; Americas 25.6%; Ashkenazi 8.6%; Finnish 17.8%; Middle Eastern 12.8%; Amish 5.4%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Nutrition & Metabolism
Macronutrient Metabolism
Fatty Acid Conversion. Evidence: 5/10. Source: PMID 31991592. Highly Efficient.
Organ Systems
Respiratory Health
Asthma. Evidence: 8/10. Source: PMID 30929738. ~1.1x Higher Risk.
Nasal Polyps. Evidence: 6/10. Source: PMID 30643255. ~1.3x Higher Risk.
Liver Function & Disease
Liver Enzyme Levels. Evidence: 8/10. Source: PMID 35654975. Elevated ALT.
Cardiovascular & Metabolic
Lipids & Cholesterol
HDL Cholesterol. Evidence: 7/10. Source: PMID 35213538. Lower Levels.
Showing effects for C/C genotype
Fatty Acid Conversion. Evidence: 5/10. Source: PMID 31991592. Slower Conversion.
Asthma. Evidence: 8/10. Source: PMID 30929738. Typical Risk.
Nasal Polyps. Evidence: 6/10. Source: PMID 30643255. Typical Risk.
Liver Enzyme Levels. Evidence: 8/10. Source: PMID 35654975. Typical ALT.
HDL Cholesterol. Evidence: 7/10. Source: PMID 35213538. Higher Levels.
Showing effects for T/C genotype
Fatty Acid Conversion. Evidence: 5/10. Source: PMID 31991592. Moderate Efficiency.
Asthma. Evidence: 8/10. Source: PMID 30929738. Slightly Higher Risk.
Nasal Polyps. Evidence: 6/10. Source: PMID 30643255. Slightly Higher Risk.
Liver Enzyme Levels. Evidence: 8/10. Source: PMID 35654975. Slightly Elevated.
HDL Cholesterol. Evidence: 7/10. Source: PMID 35213538. Typical Levels.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
This genotype is characterized by highly active fatty acid desaturase enzymes, which efficiently convert plant-derived fatty acids into long-chain polyunsaturated fatty acids like DHA [1]. While this ensures robust levels of essential fats, it also accelerates the production of arachidonic acid, a precursor to pro-inflammatory molecules. Consequently, large-scale genetic studies have linked this genotype to a higher risk of developing asthma [2] and nasal polyps [3]. Additionally, individuals with this genotype tend to have lower levels of protective HDL cholesterol [4] and higher baseline levels of the liver enzyme alanine aminotransferase [5]. This combination of factors suggests a more active inflammatory profile that may require careful dietary management of omega-3 and omega-6 ratios.
Highly efficient conversion of dietary fats; Increased risk of asthma and nasal polyps; Lower circulating HDL cholesterol.
Sample genotype: CC (Homozygous)
This genotype is associated with lower activity of the fatty acid desaturase enzymes, which reduces the conversion of dietary plant fats into longer-chain fatty acids [1]. While this means a lower baseline production of active omega-3 and omega-6 fats, it also significantly limits the generation of pro-inflammatory arachidonic acid. Consequently, individuals with this genotype enjoy a lower risk of developing asthma [2] and nasal polyps [3]. Furthermore, this genetic profile is linked to higher levels of protective HDL cholesterol [4] and healthier, lower levels of the liver enzyme ALT [5]. To compensate for the slower internal synthesis of long-chain fats, obtaining pre-formed EPA and DHA directly from marine sources like fish oil can be highly beneficial.
Slower conversion of plant-based fats; Lower risk of asthma and nasal polyps; Higher circulating HDL cholesterol.
Sample genotype: TC (Heterozygous)
This heterozygous genotype represents a biological middle ground, balancing fatty acid synthesis and inflammatory risks. Having one copy of the T allele provides moderate efficiency in converting plant-based fats into active long-chain polyunsaturated fatty acids [1]. However, this moderate activity still slightly elevates the production of inflammatory precursors compared to the C/C baseline. As a result, studies show a modest increase in the risk of respiratory conditions like asthma [2] and nasal polyps [3]. Circulating levels of HDL cholesterol and liver enzymes like ALT typically remain within the normal range but can be influenced by diet [4] [5]. Maintaining a balanced intake of dietary fats can help optimize this intermediate metabolic profile.
Moderate conversion of dietary fats; Slightly elevated risk of respiratory inflammation; Typical HDL cholesterol levels.
Variants with shared genetic architecture
rs174537 · MYRF Gene · Chr 11 · Cholesterol Levels
rs174533 · MYRF Gene · Chr 11 · Colorectal Cancer Risk
rs509360 · MYRF Gene · Chr 11 · Omega-3 Metabolism
Genetic Architectures of Childhood- and Adult-Onset Asthma Are Partly Distinct.
A loss-of-function variant in ALOX15 protects against nasal polyps and chronic rhinosinusitis.
Content updated August 2026.
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