The Claim
Genetic variants in the SLC2A9 gene are associated with 1.7–5.3% of the variation in serum uric acid concentrations in European populations, and these variants are linked to reduced fractional excretion of uric acid and increased risk of gout, indicating a role for SLC2A9 in renal urate handling and gout susceptibility.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
Specific genetic differences in the SLC2A9 gene are associated with higher levels of uric acid in the blood, lower kidney excretion of uric acid, and a higher likelihood of developing gout in people of European ancestry.
See the scientific wording
Genetic variants in the SLC2A9 gene are associated with 1.7–5.3% of the variation in serum uric acid concentrations in European populations, and these same variants are linked to reduced fractional excretion of uric acid and increased risk of gout, suggesting a role for SLC2A9 in renal urate handling and gout susceptibility.
A protein in the kidney that pulls uric acid from the blood into the urine tubes works less well when certain genes are changed, so more uric acid stays in the blood, forms crystals in the joints, and causes gout.
What the research says
1 studyPeople with certain versions of the SLC2A9 gene have higher uric acid in their blood because their kidneys don’t flush it out well, and this makes them more likely to get gout — and the study proved this is true.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.