What you carry at this position in your DNA and what research says about it.
Gout Risk: 8/10 evidence, 4 publications.
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Sample genotype (not yours): G/G
Higher Risk of Elevated Uric Acid
This genotype is associated with higher levels of uric acid and triglycerides in the blood. These metabolic markers are linked to an increased likelihood of developing gout and cardiovascular issues.
What this genotype means: Elevated serum uric acid; Increased blood triglycerides; Lower circulating omega-3 fatty acids.
Sample genotype (not yours): A/A
Typical Risk of Elevated Uric Acid
This genotype is associated with lower levels of uric acid and triglycerides. This profile helps maintain a healthy metabolic balance and a lower risk of gout.
What this genotype means: Lower serum uric acid; Lower blood triglycerides; Higher circulating omega-3 fatty acids.
Sample genotype (not yours): G/A
Slightly Higher Risk of Elevated Uric Acid
Carrying one copy of the G allele is linked to slightly elevated levels of uric acid and triglycerides. This intermediate profile suggests a modest increase in the risk of gout and metabolic imbalances.
What this genotype means: Slightly elevated serum uric acid; Mildly increased blood triglycerides; Moderate circulating omega-3 fatty acids.
Gene function and biological role
Gene Function: FADS3 (fatty acid desaturase 3) is a member of the fatty acid desaturase gene family clustered on chromosome 11. While its sister genes FADS1 and FADS2 are well-known for metabolizing polyunsaturated fatty acids, the precise physiological role of FADS3 was long considered elusive. Recent research has identified FADS3 as a specialized desaturase enzyme that introduces double bonds into sphingoid bases, which are key building blocks of sphingolipids. This activity plays a critical role in regulating the human plasma sphingolipidome and maintaining lipid membrane structure. Additionally, FADS3 is involved in the synthesis of specific fatty acids and may help detoxify certain atypical, toxic lipid species.
Variant Impact: Located within the FADS3 gene on chromosome 11, the rs174455 variant is an intronic genetic change. This genetic variation is strongly associated with alterations in the ratio of different sphingolipids and fatty acids in human blood plasma. By influencing how the FADS3 enzyme is expressed or spliced, the variant alters the desaturation of lipid backbones. These downstream changes affect the systemic levels of circulating uric acid, triglycerides, and various complex lipid metabolites. Consequently, this single nucleotide polymorphism serves as a key genetic marker for individual metabolic profiles and lipid balance.
Key Insight: FADS3 was long considered an orphan desaturase with no known function, but recent studies revealed it specifically desaturates sphingolipids to regulate cell membranes and clear toxic lipid byproducts.
Location: FADS3. Chromosome 11 · 11q12.2 · 61.9 Mb
Estimated prevalence by population
Global 33.3%; European 12.8%; African 77.2%; East Asian 15.8%; South Asian 18.3%; Americas 36.9%; Ashkenazi 12.9%; Finnish 13.2%; Middle Eastern 20.8%; Amish 12.8%.
Estimated GG genotype frequency.
Global 39.5%; European 45.9%; African 21.3%; East Asian 47.9%; South Asian 49.0%; Americas 47.7%; Ashkenazi 46.1%; Finnish 46.2%; Middle Eastern 49.6%; Amish 45.9%.
Estimated GA genotype frequency.
Global 27.1%; European 41.3%; African 1.5%; East Asian 36.4%; South Asian 32.7%; Americas 15.4%; Ashkenazi 41.0%; Finnish 40.6%; Middle Eastern 29.6%; Amish 41.3%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Gout & Uric Acid
Uric Acid Levels. Evidence: 6/10. Source: PMID 31578528. Higher Levels.
Lipids & Cholesterol
Triglycerides. Evidence: 6/10. Source: PMID 34503513. Higher Levels.
Nutrition & Metabolism
Macronutrient Metabolism
Omega-3 Fatty Acids. Evidence: 6/10. Source: PMID 34503513. Typical Levels.
Blood Chemistry & Metabolites
Sphingolipid Levels. Evidence: 8/10. Source: PMID 36193934. Typical Levels.
Showing effects for A/A genotype
Uric Acid Levels. Evidence: 6/10. Source: PMID 31578528. Typical Levels.
Triglycerides. Evidence: 6/10. Source: PMID 34503513. Typical Levels.
Omega-3 Fatty Acids. Evidence: 6/10. Source: PMID 34503513. Higher Levels.
Sphingolipid Levels. Evidence: 8/10. Source: PMID 36193934. Higher Levels.
Showing effects for G/A genotype
Uric Acid Levels. Evidence: 6/10. Source: PMID 31578528. Slightly Higher.
Triglycerides. Evidence: 6/10. Source: PMID 34503513. Slightly Higher.
Omega-3 Fatty Acids. Evidence: 6/10. Source: PMID 34503513. Slightly Higher.
Sphingolipid Levels. Evidence: 8/10. Source: PMID 36193934. Slightly Higher.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Genetic studies show that carrying two copies of the G allele at this locus is associated with significantly higher levels of serum urate, also known as uric acid. Uric acid is a metabolic waste product that, when elevated, can crystallize in the joints and trigger the painful inflammatory condition known as gout. Additionally, this genotype is linked to increased levels of circulating triglycerides and certain diacylglycerols. These lipid alterations can influence overall cardiovascular health and metabolic efficiency. Interestingly, individuals with this genotype tend to have lower levels of specific beneficial fatty acids and cholesteryl esters, such as those containing omega-3 fatty acids. Managing dietary purines and monitoring lipid panels can be useful strategies for individuals with this genetic profile.
Elevated serum uric acid; Increased blood triglycerides; Lower circulating omega-3 fatty acids.
Sample genotype: AA (Homozygous)
Protection against elevated uric acid is strongest in those with the homozygous A/A genotype. By avoiding the urate-increasing effects of the G allele, individuals with this genotype have a lower risk of developing hyperuricemia and gout. This genetic profile is also linked to lower circulating levels of triglycerides, which supports cardiovascular wellness. Furthermore, the A/A genotype is associated with higher levels of several beneficial fatty acids and cholesteryl esters, including those bound to omega-3 fatty acids like EPA and DHA. These lipid patterns contribute to a highly favorable metabolic and cardiovascular profile. Overall, this genotype supports natural defenses against lipid imbalances and joint inflammation.
Lower serum uric acid; Lower blood triglycerides; Higher circulating omega-3 fatty acids.
Sample genotype: GA (Heterozygous)
Representing an intermediate metabolic profile, the heterozygous G/A genotype lies between the two homozygous forms. Research indicates that each copy of the G allele incrementally raises serum uric acid levels, placing carriers at a slightly higher risk for hyperuricemia and gout. This genotype is also associated with mild elevations in blood triglycerides and specific diacylglycerol lipids. At the same time, carriers show moderate levels of circulating fatty acids and cholesteryl esters compared to those with the G/G genotype. These subtle shifts in the plasma lipidome can influence long-term cardiovascular and metabolic health. Maintaining a balanced diet rich in healthy fats and low in high-purine foods can help support optimal metabolic function.
Slightly elevated serum uric acid; Mildly increased blood triglycerides; Moderate circulating omega-3 fatty acids.
Variants with shared genetic architecture
rs1000778 · FADS3 Gene · Chr 11 · Cardiovascular Lipid Levels
rs7115739 · FADS3 Gene · Chr 11 · Triglyceride and Lipid Levels
rs174448 · FADS3 Gene · Chr 11 · Omega-3 and Triglycerides
Content updated August 2026.
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