Shop details here are compiled from public online sources, so some may be out of date. Spot something wrong, or want to work with us? Get in touch.Read full disclaimer
Marikina Coffee Shop Directory
← Back to Coffee Studies & Investigations

Health & Longevity

Is Coffee Bad for Gout and Uric Acid? What the Long-Term Studies Found

Does coffee raise uric acid and trigger gout, or is it linked to lower uric acid levels?

Moderate evidence

September 15, 2026

Several good studies point the same way, but with real gaps, or the effect size is modest.

What the research found

  • In 45,869 men followed for 12 years, those drinking 4 to 5 cups a day had a 40% lower risk of developing gout, and those drinking 6 or more had a 59% lower risk, than non-drinkers.
  • In a nationally representative US sample of 14,758 adults, uric acid was 0.43 mg/dl lower in people drinking 6 or more cups a day than in non-drinkers.
  • Decaffeinated coffee showed a similar, weaker association, while tea and total caffeine did not, pointing to something in coffee other than caffeine.
  • Meta-analyses agree on a lower risk of gout, but disagree on whether coffee lowers uric acid itself, so that part is less settled.
  • All of this is observational research about developing gout, not about treating an attack, and nothing here replaces prescribed treatment.

Gout has a reputation as the disease of rich food and drink, and people who get it tend to receive long lists of things to avoid: organ meats, some seafood, beer, sugary drinks. Coffee often ends up on those lists by association, partly because it feels like an indulgence and partly because caffeine is chemically related to the purines that the body turns into uric acid. The research on coffee specifically tells a more surprising story, and it is one of the cleaner examples of popular assumption and published evidence pointing in opposite directions.

What uric acid and gout actually are

Uric acid is a waste product the body makes when it breaks down purines, compounds found in our own cells and in many foods. Normally it dissolves in the blood and leaves through the kidneys. When levels stay high, a state called hyperuricaemia, uric acid can form needle-like crystals in joints. The immune system's reaction to those crystals is a gout attack: sudden, intense pain and swelling, very often in the big toe. Not everyone with high uric acid develops gout, but high uric acid is the main underlying risk factor, which is why the two are usually studied together.

Caffeine is a methylxanthine, and its breakdown products are methylated forms of uric acid's chemical relatives. That resemblance is one reason people assumed coffee would push uric acid up. As it turns out, the body does not process those caffeine metabolites into the uric acid that causes gout, and the studies below measured what actually happens.

The men who were followed for twelve years

The landmark study is the analysis of the Health Professionals Follow-up Study by Choi, Willett and Curhan, published in Arthritis and Rheumatism in 2007[1]. They followed 45,869 men with no history of gout for 12 years, asking about coffee, decaf, tea and total caffeine every four years with validated questionnaires, and confirmed 757 new cases of gout using the American College of Rheumatology criteria.

Risk fell as coffee intake rose. Compared with men who drank no coffee, the adjusted relative risks were 0.97 for less than a cup a day, 0.92 for one to three cups, 0.60 for four to five cups, and 0.41 for six or more cups a day. In plain terms, the heaviest drinkers had about a 59% lower risk of developing gout during the study, and the trend across categories was statistically significant. Decaffeinated coffee showed an inverse association too: one to three cups a day had a relative risk of 0.67. Total caffeine from all sources and tea were not associated with gout risk at all.

The survey that measured uric acid directly

A second study by Choi and Curhan, also in 2007[2], looked not at gout itself but at the uric acid level in the blood, using 14,758 adults aged 20 and over from the US Third National Health and Nutrition Examination Survey, a nationally representative sample of men and women. Uric acid levels fell as coffee intake rose. After adjusting for age and sex, uric acid in people drinking four to five cups a day was 0.26 mg/dl lower than in non-drinkers, and in people drinking six or more cups it was 0.43 mg/dl lower. Those differences held after adjusting for other factors.

The same study found that the odds of hyperuricaemia were 43% lower in people drinking six or more cups a day than in non-drinkers, an odds ratio of 0.57. Decaffeinated coffee had a modest inverse association with uric acid. Tea did not, and neither did total caffeine from all beverages. The authors concluded that the inverse association with coffee appears to run through components of coffee other than caffeine.

The women's study, with 26 years of follow-up

Gout is more common in men, and one fair objection to the first study is that it only included men. The same research group answered it three years later. Choi and Curhan's analysis of the Nurses' Health Study, published in the American Journal of Clinical Nutrition in 2010[3], followed 89,433 women for 26 years, updating their coffee, decaf, tea and caffeine intake every two to four years, and confirmed 896 new cases of gout using the same American College of Rheumatology criteria.

The inverse association appeared again, and was, if anything, cleaner. The researchers measured coffee in millilitres, with 237 ml counted as one 8-ounce cup. Compared with women who drank no coffee, the adjusted relative risk was 0.97 for up to one cup a day, 0.78 for one to four cups, and 0.43 for four or more cups a day, a statistically significant trend. Decaf was also associated with lower risk, with a relative risk of 0.77 for a cup or more a day.

One detail differed from the men's study. In women, total caffeine from all sources was also inversely associated with gout: the highest fifth of caffeine intake had a relative risk of 0.52 compared with the lowest. That does not overturn the decaf finding, since decaf still showed an association, but it suggests caffeine may play some role in women that it did not appear to play in men. It is a reminder that the mechanism is genuinely unsettled rather than neatly solved.

Why decaf and tea matter so much here

The pattern across drinks is the most informative part of both studies. If caffeine were what lowered uric acid, then tea and total caffeine should show the effect, and decaf should not. The opposite happened: coffee and, more weakly, decaf showed it, while tea and caffeine did not. That points toward something specific to coffee.

The most discussed candidate is chlorogenic acid, a polyphenol present in coffee in large amounts and largely retained through decaffeination. Researchers have proposed that coffee compounds may affect insulin sensitivity, which in turn influences how efficiently the kidneys clear uric acid, since high insulin levels are associated with reduced uric acid excretion. Laboratory studies have also looked at whether coffee components inhibit xanthine oxidase, the enzyme that produces uric acid, which is the same target as the gout medicine allopurinol. These are plausible mechanisms under study, not proven explanations for the population findings.

What the meta-analyses say, and where they disagree

Pooled analyses agree on gout but not on uric acid. A systematic review by Zhang and colleagues in BMJ Open[4] combined 11 observational studies. For gout, the pooled adjusted relative risk comparing the highest with the lowest coffee intake was 0.43, a significant inverse association. For uric acid level itself, however, they found no significant difference between highest and lowest intake, and the pooled odds ratio for hyperuricaemia of 0.84 was also not significant. They concluded that the evidence was insufficient to confirm a lower risk of hyperuricaemia, and that coffee may be associated with a lower risk of gout.

A second meta-analysis by Park and colleagues in Seminars in Arthritis and Rheumatism[5], which included 9 studies and 175,310 people, came out more positive. It reported a significant lowering effect of coffee on uric acid, with a sex difference: women appeared to need more coffee, 4 to 6 cups a day, than men, 1 to 3 cups, to show lower levels. It also found that 1 cup a day or more was associated with a lower risk of gout.

The honest summary is that the gout finding is consistent, while the uric acid finding depends on which studies are pooled and how. That is not unusual. Uric acid is a single blood measurement that varies from day to day, while gout is a clinical event, and small studies of a noisy biomarker are exactly where meta-analyses tend to disagree.

A genetic study in an Asian population

Almost every study above was done in American or European populations, which matters for readers in the Philippines, where gout is common and diets differ. A 2022 study by Shirai and colleagues in ACR Open Rheumatology[6] is useful on two counts: it used Japanese genetic data, and it used Mendelian randomisation, a method that uses gene variants linked to drinking more or less coffee as a kind of natural experiment. Because those genes are handed out at conception, they are much less tangled up with lifestyle than a questionnaire answer is.

The researchers drew on genetic data on habitual coffee drinking from 152,634 people, uric acid levels from 121,745 people, and 3,053 gout cases compared with 4,554 controls. After removing gene variants that might affect gout through routes other than coffee, a statistical problem called pleiotropy, genetically predicted coffee consumption was still associated with lower gout risk, with an odds ratio of 0.75. When they adjusted for uric acid levels, the protective association remained, with an odds ratio of 0.50. Yet in analyses accounting for pleiotropy, coffee was not associated with uric acid levels in either the Japanese or European data.

That result fits neatly with the disagreement between the meta-analyses. It suggests that coffee may lower gout risk through some route other than simply lowering uric acid in the blood, perhaps by influencing inflammation or how crystals trigger an immune response. The authors also found that when they re-examined earlier European genetic datasets with the same care about heterogeneity, the protective result was not significant there, so the genetic evidence is promising rather than conclusive. Genetic studies carry their own assumptions, and this one should be read as supporting evidence, not proof.

How large are these effects, in real terms?

Relative risks like 0.41 or 0.43 sound dramatic, and it is easy to read them as coffee cutting gout by more than half. They need translating. A relative risk describes how the rate of new gout compared between groups during the study, not how much any one person's chances change. In the men's study, 757 cases arose among 45,869 men over 12 years, so gout was an uncommon event in that population to begin with. A large relative reduction of an uncommon event is a smaller absolute difference than the headline number suggests.

The heaviest-drinking categories are also where the numbers are least certain, because relatively few people drink six or more cups a day. That shows up in the wide confidence intervals around those estimates. The steady downward trend across categories is more convincing than any single figure, and it is the trend, repeated in men, in women, and in genetic data, that makes this association worth taking seriously.

The limits worth taking seriously

All of this is observational. It shows that people who drink more coffee develop gout less often, not that coffee prevents gout, and there are no long-term randomised trials of coffee for gout. Coffee drinkers may differ from non-drinkers in diet, weight, alcohol and medication use in ways that adjustment only partly captures. The men's cohort was made up of health professionals, mostly white and mostly well-educated, which limits how far its figures can be generalised.

It is also crucial to separate prevention from treatment. These studies are about who develops gout over years. They say nothing about what coffee does during an attack, or whether it can replace medicines such as allopurinol or febuxostat. The effect sizes, even where significant, are far smaller than what urate-lowering drugs achieve. Anyone with gout who has been prescribed medication should keep taking it.

Finally, the drink in these studies is coffee, mostly black or with milk. Sweetened drinks carry a separate concern, because fructose raises uric acid. A very sweet café drink or a sugary 3-in-1 sachet brings a known uric acid raiser along with the coffee, which could plausibly cancel whatever benefit the coffee is associated with.

What this means in practice

On current evidence, coffee does not deserve its place on gout avoidance lists. The largest prospective study in men found a strong, graded inverse association with gout; a nationally representative survey found lower uric acid in heavier coffee drinkers; and pooled analyses agree on lower gout risk even while they disagree about uric acid levels. The decaf and tea results suggest that caffeine is not the reason.

If you have gout or high uric acid, the practical reading is modest: moderate coffee does not appear to be a trigger worth cutting out on uric acid grounds, but it is not a treatment, and sugar and alcohol matter more. People with gout often have other conditions, including high blood pressure and kidney disease, that change how much caffeine is sensible, so it is worth reading our article on coffee and blood pressure and the one on coffee and kidney health alongside this one. Nothing here is medical advice.

Share this article

References (6)

Numbered in order of first mention. Links go to PubMed or the publisher, whichever reliably opens for a reader; the DOI is the durable form to quote.

  1. [1] Choi, H. K., Willett, W., & Curhan, G. (2007). Coffee consumption and risk of incident gout in men: a prospective study. Arthritis and Rheumatism, 56(6), 2049–2055. Read it ↗ doi:10.1002/art.22712

    Prospective cohort (Health Professionals Follow-up Study), 45,869 men followed for 12 years, 757 gout cases

  2. [2] Choi, H. K., & Curhan, G. (2007). Coffee, tea, and caffeine consumption and serum uric acid level: the third national health and nutrition examination survey. Arthritis and Rheumatism, 57(5), 816–821. Read it ↗ doi:10.1002/art.22762

    Cross-sectional analysis of 14,758 US adults in the Third National Health and Nutrition Examination Survey

  3. [3] Choi, H. K., & Curhan, G. (2010). Coffee consumption and risk of incident gout in women: the Nurses' Health Study. The American Journal of Clinical Nutrition, 92(4), 922–927. Read it ↗ doi:10.3945/ajcn.2010.29565

    Prospective cohort (Nurses' Health Study), 89,433 women followed for 26 years, 896 gout cases

  4. [4] Zhang, Y., Yang, T., Zeng, C., Wei, J., Li, H., Xiong, Y. L., et al. (2016). Is coffee consumption associated with a lower risk of hyperuricaemia or gout? A systematic review and meta-analysis. BMJ Open, 6(7), e009809. Read it ↗ doi:10.1136/bmjopen-2015-009809

    Systematic review and meta-analysis of 11 observational studies

  5. [5] Park, K. Y., Kim, H. J., Ahn, H. S., Kim, S. H., Park, E. J., Yim, S. Y., et al. (2016). Effects of coffee consumption on serum uric acid: systematic review and meta-analysis. Seminars in Arthritis and Rheumatism, 45(5), 580–586. Read it ↗ doi:10.1016/j.semarthrit.2016.01.003

    Systematic review and meta-analysis of 9 studies, 175,310 participants

  6. [6] Shirai, Y., Nakayama, A., Kawamura, Y., Toyoda, Y., Nakatochi, M., Shimizu, S., et al. (2022). Coffee Consumption Reduces Gout Risk Independently of Serum Uric Acid Levels: Mendelian Randomization Analyses Across Ancestry Populations. ACR Open Rheumatology, 4(6), 534–539. Read it ↗ doi:10.1002/acr2.11425

    Mendelian randomisation using Japanese genome-wide data (152,634 people for coffee intake), re-checked against European data

Related research

The practical guides

This is a summary of published research, not medical advice, and it cannot account for your own health, medication or circumstances. Talk to a doctor about those. If you think we have misread a study or a citation has moved, please tell us, see our disclaimer for how we handle sources and corrections. Interested in a partnership or collaboration? Get in touch.