Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Cut Back on Sugary Drinks: Fructose is the dietary sugar that raises uric acid most directly, because the liver phosphorylates it fast enough to deplete ATP and leave purine breakdown products behind. A 2025 meta-analysis of 22 studies covering 235,790 people found sugar-sweetened beverage intake associated with hyperuricaemia (OR 1.33) and with gout (OR 1.21), and higher dietary fructose associated with gout at OR 1.66. Fruit juice showed a smaller association with hyperuricaemia (OR 1.15) and a gout association that was not statistically significant. Frontiers in Nutrition (PMC)
Rethink Beer and Spirits: In 47,150 men followed for 12 years, gout risk climbed with total alcohol intake, from a relative risk of 1.32 at 10 to 15 g a day up to 2.53 at 50 g or more. The association differed sharply by drink. Beer had the strongest independent effect at a relative risk of 1.49 per daily 12 oz serving, spirits 1.15 per drink, and wine 1.04 per 4 oz glass, which was not statistically significant. Beer's purine content is the usual explanation offered for the gap between beverages. The Lancet (PubMed)
Reduce Excess Body Weight: Mendelian randomisation, which uses inherited variants as a natural experiment, points to body weight acting on gout rather than merely travelling alongside it. Waist-to-hip ratio adjusted for BMI showed no such association, suggesting overall weight matters more than where fat is carried. Rheumatology (PMC)
Shift Protein Sources Toward Dairy: In the same cohort of 47,150 men, the highest fifth of meat intake carried a relative risk of gout of 1.41 and the highest fifth of seafood intake 1.51, compared with the lowest fifth. Dairy ran the other way, with a relative risk of 0.56. Purine-rich vegetables and total protein intake were not associated with increased risk, which undercuts the long-standing advice to avoid foods like beans, lentils, spinach and mushrooms. New England Journal of Medicine (PubMed)
Know the Limits of Diet: Diet takes most of the blame for gout, but it explains far less of the difference between people than is usually assumed. A meta-analysis of 16,760 adults tested 63 individual foods and whole dietary patterns against serum urate, and found that DASH, Mediterranean and healthy-eating scores each explained 0.3% or less of the variation, while common genome-wide genetic variation explained 23.9%. Fifteen individual foods, including beer, spirits, soft drinks and meat, did shift urate at the margin, so the changes above are still worth making. But persistent joint pain, swelling and repeated attacks are worth raising with a clinician rather than trying to solve through food alone. The BMJ (PMC)
How much of this is genetic?
Genetics explains 30% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Major TJ, Dalbeth N, Stahl EA, Merriman TR. An update on the genetics of hyperuricaemia and gout. Nat Rev Rheumatol. 2018.
Background and further reading
Gout is the most common form of inflammatory arthritis. It develops when persistently high levels of uric acid in the blood (hyperuricaemia) lead to the formation of needle-like monosodium urate crystals in and around joints. When these crystals trigger the immune system, they cause a gout flare: sudden, severe pain, swelling, redness, and warmth, classically at the base of the big toe, though the ankles, knees, wrists, and fingers can also be affected. Flares often begin at night and can last days to weeks. Over years, poorly controlled gout can cause visible urate deposits called tophi and joint damage. Gout affects an estimated 1-4% of adults in many Western populations and is more common in men and with increasing age.
Genetic Basis: The strongest genetic determinant of gout is inherited variation in the transporters that control how the kidneys and gut handle uric acid. The two largest-effect genes are SLC2A9 (which encodes the urate transporter GLUT9) and ABCG2; the common ABCG2 variant Q141K (rs2231142) reduces urate excretion and substantially raises gout risk. Additional urate-handling genes include SLC22A11 and SLC22A12 (URAT1). Serum urate itself is a highly heritable trait, with twin and family studies estimating heritability of roughly 40-70%, and large genome-wide association studies have identified hundreds of loci that influence urate levels. The clinical trait of gout is less heritable than urate concentration, because whether hyperuricaemia progresses to crystal formation and flares depends heavily on diet, body weight, kidney function, and other environmental factors.
Environmental Factors: Because urate is the end product of purine metabolism, diet and lifestyle strongly shape gout risk. Purine-rich foods (red meat, organ meats, and certain seafood), alcohol (especially beer and spirits), and sugar-sweetened beverages and other sources of fructose all raise serum urate and can precipitate flares. Obesity, high blood pressure, chronic kidney disease, and insulin resistance are strongly associated with gout, and some medications, notably thiazide and loop diuretics and low-dose aspirin, increase urate levels. Conversely, weight management, moderating alcohol and sugary drinks, staying well hydrated, and treating related metabolic conditions can lower urate and reduce the frequency of flares. Genetics sets the baseline tendency, but these modifiable factors substantially influence whether gout develops and how often it recurs.
The published research behind your score, and the variants it draws on.
21 published scores from 10 studies
The gout score combines 21 polygenic scores drawn from 10 published studies.
Ohta R (2024). A polygenic score method boosted by non-additive models. Nat Commun: 2k
Dalbeth N, Gosling AL, Gaffo A, Abhishek A Gout. The Lancet (2021)
These traits are influenced by some of the same genes and variants as this one
Content updated August 2026.
ReadYourDNA provides educational interpretation of DNA data you already have. It is not diagnostic, not a substitute for professional medical advice, diagnosis, or treatment, and is not intended to diagnose, treat, cure, or prevent any disease. Talk to a clinician before acting on any result.
Raw DNA Data Reports for 23andMe & AncestryDNA · About ReadYourDNA · FAQ · Methodology & Science · Pricing · Support and complaints · Legal & Contact · Health Traits · Pharmacogenomics · Carrier Status · Variant Explorer · The Human Karyotype · Privacy Policy · Terms of Service · Accessibility · Consumer Health Data Privacy · Your Privacy Choices · Editorial Standards · Your Data, Checkable · Sample Report · ReadYourDNA and Promethease compared · What is inside a 23andMe raw data file · What is inside an AncestryDNA raw data file · What a chatbot can and cannot do with your raw DNA file · Where a raw DNA file can still be uploaded in 2026
Written, maintained and operated by Martin Pechhacker, sole proprietor, Vienna, Austria. Trade register GISA 40064420. support@readyourdna.com