Expressive

rs11623662 - FUT8

Magnitude 2.2 · 1 study on file

Reported associations

  • A genome-wide association analysis reveals new pathogenic pathways in gout. - Nature genetics (2024) · Major TJ, Takei R, Matsuo H, Leask MP, Sumpter NA, Topless RK, Shirai Y, Wang W, Cadzow MJ, Phipps-Green AJ, Li Z, Ji A, Merriman ME, Morice E, Kelley EE, Wei WH, McCormick SPA, Bixley MJ, Reynolds RJ, Saag KG, Fadason T, Golovina E, O'Sullivan JM, Stamp LK, Dalbeth N, Abhishek A, Doherty M, Roddy E, Jacobsson LTH, Kapetanovic MC, Melander O, Andrés M, Pérez-Ruiz F, Torres RJ, Radstake T, Jansen TL, Janssen M, Joosten LAB, Liu R, Gaal OI, Crişan TO, Rednic S, Kurreeman F, Huizinga TWJ, Toes R, Lioté F, Richette P, Bardin T, Ea HK, Pascart T, McCarthy GM, Helbert L, Stibůrková B, Tausche AK, Uhlig T, Vitart V, Boutin TS, Hayward C, Riches PL, Ralston SH, Campbell A, MacDonald TM, Nakayama A, Takada T, Nakatochi M, Shimizu S, Kawamura Y, Toyoda Y, Nakaoka H, Yamamoto K, Matsuo K, Shinomiya N, Ichida K, Lee C, Bradbury LA, Brown MA, Robinson PC, Buchanan RRC, Hill CL, Lester S, Smith MD, Rischmueller M, Choi HK, Stahl EA, Miner JN, Solomon DH, Cui J, Giacomini KM, Brackman DJ, Jorgenson EM, Liu H, Susztak K, Shringarpure S, So A, Okada Y, Li C, Shi Y, Merriman TR · PubMed 39406924

    Gout is a chronic disease that is caused by an innate immune response to deposited monosodium urate crystals in the setting of hyperuricemia. Here, we provide insights into the molecular mechanism of the poorly understood inflammatory component of gout from a genome-wide association study (GWAS) of 2.6 million people, including 120,295 people with prevalent gout. We detected 377 loci and 410 genetically independent signals (149 previously unreported loci in urate and gout). An additional 65 loci with signals in urate (from a GWAS of 630,117 individuals) but not gout were identified. A prioritization scheme identified candidate genes in the inflammatory process of gout, including genes involved in epigenetic remodeling, cell osmolarity and regulation of NOD-like receptor protein 3 (NLRP3) i

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Lifestyle context

Concrete actions anchored to the cited research. We do not prescribe, we describe.

Diet

  • high alcohol consumption, especially beer Moderate

    Alcohol increases uric acid; T allele carriers have 3.1% elevated gout susceptibility per copy.

    limit to 0-1 drinks daily; minimize beer intake

  • high-purine foods (red meat, organ meats, anchovies) Moderate

    Dietary purines increase uric acid production; genetic predisposition amplifies this effect.

    limit red meat to 2-3 servings weekly; avoid organ meats and high-purine seafood

Discuss with your doctor

  • gout risk profile and prevention strategies Moderate

    Genetic predisposition to gout (p=3.00e-9) warrants personalized clinical assessment.

    discuss baseline risk, lifestyle interventions, and consideration of urate-lowering therapy if indicated

Lifestyle

  • adequate hydration Moderate

    Water supports uric acid solubility and renal clearance, reducing precipitation risk.

    aim for 2-3 liters daily; increase during exercise or heat exposure

  • body weight and BMI Moderate

    Obesity increases gout risk; genetic predisposition magnifies this relationship.

    maintain BMI 18.5-24.9; pursue gradual weight loss if overweight, avoid rapid loss

Screening

  • serum uric acid level Moderate

    rs11623662 T allele increases gout risk (OR 1.031); uric acid monitoring enables early detection.

    baseline measurement; annual screening or biannual if elevated (>6.8 mg/dL)