What you carry at this position in your DNA and what research says about it.
Joint and Thyroid Health: 6/10 evidence, 30 publications.
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Sample genotype (not yours): C/C
Higher Risk of Joint Inflammation
Presence of two C alleles is linked to a slightly increased risk of rheumatoid arthritis and hypothyroidism. This is driven by a faster conversion of dietary fats into pro-inflammatory compounds.
What this genotype means: Faster conversion of fats to pro-inflammatory arachidonic acid; Slightly increased risk of rheumatoid arthritis; Slightly increased risk of hypothyroidism.
Sample genotype (not yours): C/T
Slightly Higher Risk of Joint Inflammation
A single C allele is associated with a moderate rate of fatty acid conversion and a slightly elevated risk of inflammatory conditions. Balancing dietary fats can help manage systemic inflammation.
What this genotype means: Moderate conversion of fats to pro-inflammatory arachidonic acid; Slightly increased risk of rheumatoid arthritis; Slightly increased risk of hypothyroidism.
Sample genotype (not yours): T/T
Typical Risk of Joint Inflammation
Two copies of the T allele are associated with slower fatty acid conversion and a typical risk of rheumatoid arthritis and hypothyroidism. This genotype tends to maintain lower levels of pro-inflammatory arachidonic acid.
What this genotype means: Slower conversion of fats to pro-inflammatory arachidonic acid; Typical risk of rheumatoid arthritis; Typical risk of hypothyroidism.
Gene function and biological role
Gene Function: The FADS2 gene encodes delta-6 desaturase, a key enzyme responsible for converting dietary fatty acids into long-chain polyunsaturated fatty acids [1]. This enzyme regulates the balance between omega-3 and omega-6 fatty acids, which are critical components of cell membranes and precursors to inflammatory signaling molecules [2]. By controlling the rate of fatty acid conversion, FADS2 directly influences systemic inflammation and immune system responses [3]. Variations in this gene can alter enzyme activity, shifting the body's lipid profile toward either pro-inflammatory or anti-inflammatory states [4]. Consequently, FADS2 is heavily studied in the context of cardiovascular health, cognitive development, and autoimmune diseases [5].
Variant Impact: The rs968567 variant is located in the regulatory region of the FADS2 gene, where it alters the binding of transcription factors like ELK1 [4]. This change directly impacts how actively the gene is transcribed, modifying the level of delta-6 desaturase enzyme produced in the body [3]. The major C allele is associated with more efficient conversion of fatty acid precursors into arachidonic acid, a key driver of inflammatory pathways [6]. Conversely, the minor T allele leads to higher levels of precursor fatty acids and lower levels of downstream inflammatory products [7]. This functional shift explains why the variant is linked to differences in autoimmune disease susceptibility and blood lipid compositions [8].
Key Insight: Dietary choices, particularly the intake of omega-3 and omega-6 fatty acids, interact directly with this variant to shape systemic inflammation levels.
Location: FADS2. Chromosome 11 · 11q12.2 · 61.8 Mb
Origin Story: The high frequency of the fast-converting C allele in most global populations is thought to have helped early human ancestors obtain sufficient long-chain fatty acids from plant-based diets, whereas the T allele became more common in regions with marine-rich diets.
Estimated prevalence by population
Global 80.1%; European 69.0%; African 93.6%; East Asian 99.7%; South Asian 89.1%; Americas 84.0%; Ashkenazi 79.0%; Finnish 81.0%; Middle Eastern 64.4%; Amish 68.2%.
Estimated CC genotype frequency.
Global 18.4%; European 28.1%; African 6.3%; East Asian 0.3%; South Asian 10.6%; Americas 15.3%; Ashkenazi 19.8%; Finnish 18.0%; Middle Eastern 31.7%; Amish 28.8%.
Estimated CT genotype frequency.
Global 1.5%; European 2.9%; African 0.1%; East Asian < 0.1%; South Asian 0.3%; Americas 0.7%; Ashkenazi 1.2%; Finnish 1.0%; Middle Eastern 3.9%; Amish 3.0%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Immunity & Inflammation
Autoimmune Diseases
Rheumatoid Arthritis. Evidence: 8/10. Source: PMID 24390342. Slightly Higher Risk.
Autoimmune Disease Risk. Evidence: 6/10. Source: PMID 34127860. Slightly Higher Risk.
Nutrition & Metabolism
Macronutrient Metabolism
Fatty Acid Conversion. Evidence: 6/10. Source: PMID 24816252. Fast Conversion.
Endocrine & Reproductive
Hormone Levels & Endocrine Regulation
Thyroid Function. Evidence: 6/10. Source: PMID 39067062. Slightly Higher Risk.
Showing effects for C/T genotype
Fatty Acid Conversion. Evidence: 6/10. Source: PMID 24816252. Moderate Conversion.
Showing effects for T/T genotype
Rheumatoid Arthritis. Evidence: 8/10. Source: PMID 24390342. Typical Risk.
Autoimmune Disease Risk. Evidence: 6/10. Source: PMID 34127860. Typical Risk.
Fatty Acid Conversion. Evidence: 6/10. Source: PMID 24816252. Slower Conversion.
Thyroid Function. Evidence: 6/10. Source: PMID 39067062. Typical Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Enzymatic activity of delta-6 desaturase is highly active in those carrying the C/C genotype, leading to rapid conversion of dietary fats into arachidonic acid [1]. While arachidonic acid is an essential fatty acid, high levels can be metabolized into pro-inflammatory eicosanoids that promote systemic inflammation [2]. Large-scale genetic studies have consistently linked this fast-converting genotype to an elevated risk of rheumatoid arthritis [3]. Additionally, the increased inflammatory state may contribute to a slightly higher susceptibility to other autoimmune conditions, such as hypothyroidism [4]. Managing dietary intake of omega-6 fatty acids, which are abundant in vegetable oils, while increasing anti-inflammatory omega-3s may help balance this genetic tendency.
Faster conversion of fats to pro-inflammatory arachidonic acid; Slightly increased risk of rheumatoid arthritis; Slightly increased risk of hypothyroidism.
Sample genotype: CT (Heterozygous)
A single copy of the C allele results in a moderate rate of delta-6 desaturase activity, balancing the conversion of precursor fats with downstream inflammatory markers [1]. This intermediate state leads to slightly higher levels of arachidonic acid compared to the T/T genotype, but lower than the C/C genotype [2]. Susceptibility to rheumatoid arthritis is slightly elevated, reflecting the modest increase in pro-inflammatory potential [3]. Similarly, there is a minor increase in the risk of developing hypothyroidism due to the shared inflammatory pathways [4]. Maintaining a healthy ratio of dietary omega-3 to omega-6 fatty acids is a practical way to support joint and thyroid health for this genotype.
Moderate conversion of fats to pro-inflammatory arachidonic acid; Slightly increased risk of rheumatoid arthritis; Slightly increased risk of hypothyroidism.
Sample genotype: TT (Homozygous)
Slower conversion of dietary fats characterizes the T/T genotype, resulting in lower levels of pro-inflammatory arachidonic acid and higher levels of precursor fatty acids like dihomo-linolenate [1]. This reduced inflammatory potential is associated with a lower, typical risk of developing rheumatoid arthritis [2]. Thyroid health is also favored, with a typical risk profile for hypothyroidism compared to carriers of the C allele [3]. Because the body converts plant-based omega-3s into active EPA and DHA more slowly, direct dietary sources of these marine fatty acids may be particularly beneficial [4]. Overall, this genotype provides a natural buffer against the systemic inflammation that drives several common autoimmune conditions.
Slower conversion of fats to pro-inflammatory arachidonic acid; Typical risk of rheumatoid arthritis; Typical risk of hypothyroidism.
Variants with shared genetic architecture
rs174570 · FADS2 Gene · Chr 11 · Fatty Acid Metabolism
rs174574 · FADS2 Gene · Chr 11 · Fatty Acid Metabolism
rs99780 · FADS2 Gene · Chr 11 · Omega-3 Metabolism
Genetic variation in lipid desaturases and its impact on the development of human disease.
An atlas of genetic influences on human blood metabolites.
Genetics of rheumatoid arthritis contributes to biology and drug discovery.
Uncovering the shared genetic components of thyroid disorders and reproductive health.
Content updated August 2026.
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