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Gout & Hyperuricemia
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In one pass Gout is an acute inflammation that happens when there is so much uric acid in the blood that it comes out of solution as needle-shaped crystals in a joint.
Educational content, not medical advice — consult a clinician.
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Chapter 1
How uric acid triggers a flare
Gout is an acute inflammation that happens when there is so much uric acid in the blood that it comes out of solution as needle-shaped crystals in a joint. The crystals act like shards of glass, and the joint turns red, swollen and intensely painful. The most common first site is the base of the big toe. People often wake at night with it, cannot bear even the touch of a bedsheet, and then the attack slowly settles on its own over 3–10 days.
Most uric acid is made by the body itself as it breaks down old cells and DNA; only a smaller share comes from purines in food. Most of it leaves through the kidneys and the rest through the gut. Humans lack an enzyme that breaks uric acid down (uricase), so our blood levels run high to begin with. Plasma can hold only so much uric acid in solution, a physical ceiling, and above that line crystals can form. Before menopause, estrogen helps the kidneys excrete uric acid, which is why gout is more common in men and women catch up only after menopause.
A few situations need medical care immediately: a red, swollen, painful joint together with a high fever or chills, because a joint infection has to be ruled out; and a rash, fever or mouth ulcers in the first weeks after starting a urate-lowering drug.
Most uric acid is made by the body itself as it breaks down old cells and DNA; only a smaller share comes from purines in food. Most of it leaves through the kidneys and the rest through the gut. Humans lack an enzyme that breaks uric acid down (uricase), so our blood levels run high to begin with. Plasma can hold only so much uric acid in solution, a physical ceiling, and above that line crystals can form. Before menopause, estrogen helps the kidneys excrete uric acid, which is why gout is more common in men and women catch up only after menopause.
A few situations need medical care immediately: a red, swollen, painful joint together with a high fever or chills, because a joint infection has to be ruled out; and a rash, fever or mouth ulcers in the first weeks after starting a urate-lowering drug.
Numbers · The lab cut-offs and how gout is confirmed
Uric acid in plasma saturates at about 6.8 mg/dL; above that, crystals can form at any time. Clinicians generally treat 7 mg/dL for men and 6 mg/dL for women as the upper limits. It is a solubility line, not a health score where lower is always better, and most people with high uric acid never have a gout attack in their lives.In large US cohorts, the dietary factors most strongly linked to gout, and the most often overlooked, are sugary drinks, sweetened milk tea and fruit juice rather than seafood or red meat (the figures are in the chapter How sugary drinks raise uric acid). These are observed associations, but the pathway by which the liver turns fructose into uric acid makes them plausible. Gout also rarely comes alone: it tends to cluster with obesity, high blood pressure, fatty liver and type 2 diabetes, each raising the risk of the others.
For diagnosis, a single joint that suddenly turns red, hot, swollen and painful, plus a high blood uric acid, is usually enough for a doctor's clinical judgment. The definitive test is drawing fluid from the joint and seeing the needle-shaped urate crystals under a polarized-light microscope (the Dalbeth 2019 review). Blood uric acid sometimes dips during an attack, so one normal result does not rule out gout that is flaring right now.
Chapter 2
Which foods trigger it most
What to change first in a gout diet is not in the order most people expect: sugary drinks and alcohol come first, and seafood comes later.
In large US cohorts, men who drank two or more servings of sugary drinks a day had about 1.85 times the gout risk of men who almost never drank them (Choi 2008); the fifth of men eating the most seafood had about 1.51 times the risk (Choi 2004). These are observed associations, and because fructose takes a path through the liver that makes extra uric acid, the direction makes sense. For most people, swapping the daily milk tea for unsweetened tea or sparkling water is worth more than giving up seafood.
Alcohol comes second. Chinese readers need to know one thing first: the drink highest in purines is not beer but huangjiu, Chinese yellow rice wine (China's National Health Commission dietary guideline, 2024). People with gout are best off not drinking; for anyone in an acute attack, with poorly controlled gout on medication, or with chronic gouty arthritis, the guideline says no alcohol at all, not less.
In large US cohorts, men who drank two or more servings of sugary drinks a day had about 1.85 times the gout risk of men who almost never drank them (Choi 2008); the fifth of men eating the most seafood had about 1.51 times the risk (Choi 2004). These are observed associations, and because fructose takes a path through the liver that makes extra uric acid, the direction makes sense. For most people, swapping the daily milk tea for unsweetened tea or sparkling water is worth more than giving up seafood.
Alcohol comes second. Chinese readers need to know one thing first: the drink highest in purines is not beer but huangjiu, Chinese yellow rice wine (China's National Health Commission dietary guideline, 2024). People with gout are best off not drinking; for anyone in an acute attack, with poorly controlled gout on medication, or with chronic gouty arthritis, the guideline says no alcohol at all, not less.
Myth · Seafood, vegetables, tofu and vitamin C
Seafood, organ meats and red meat come later, but they do matter. In Choi 2004, a cohort of US men, the fifth eating the most meat had about 1.41 times the gout risk of those eating the least, and for seafood it was about 1.51 times (observed associations). Sardines, anchovies, oysters, shrimp and crab, and animal liver and kidney are highest in purines, with chicken, beef and pork in the middle; China's dietary guideline advises avoiding organ meats as far as possible.A few widely shared beliefs that do not hold up:
"High-purine vegetables are off limits": in the same cohort, eating more of the higher-purine vegetables such as spinach, broccoli and asparagus was not linked to a higher gout risk."Tofu and soy foods are off limits": soy has a little more purine than lean meat or fish, but the body makes poor use of purines from plants, and processing lowers them further, so China's dietary guideline says tofu and dried bean curd are fine in moderation."Fruit is all sugar, so you can't eat it": this lumps whole fruit together with fructose in liquid; the difference is in the chapter Whole fruit differs from sweet drinks.
Some things often called helpers, with evidence of mixed strength:
Cherries: Zhang 2012 was a case-crossover study (observational; people with gout compared the two days before an attack with ordinary two-day periods of their own). Two-day periods with cherries had a 35% lower risk of an attack ( 0.65; OR is the odds ratio).Coffee: in Choi 2007, a cohort of US men, those drinking 4 or more cups a day had about a 40% lower risk of gout (an observed association).Milk: in Choi 2004, men who ate more dairy had less gout (an observed association); in Dalbeth 2010, a small randomized crossover trial, blood uric acid dipped for a few hours after drinking milk.The American College of Rheumatology (ACR) 2020 gout guideline judged that the evidence on cherries and dairy comes mainly from observational studies and is of low or very low certainty, so it made no specific recommendation on them.Vitamin C: Choi 2009 followed US men for 20 years; those taking in more vitamin C had less gout, but supplements became significant only at 1000 mg a day, and the study did not measure blood uric acid. For people who already have gout, ACR 2020 conditionally recommends against adding vitamin C supplements: in two small randomized trials, the change in blood uric acid was clinically insignificant.
Drinking enough water every day, to help the kidneys clear uric acid, is not in dispute.
The last trap is weight loss: losing weight over the long run lowers uric acid, but losing it too fast (starving, very-low-calorie diets, keto) can make uric acid spike in the short term and set off an attack, so take it slowly.
Chapter 3
How sugary drinks raise uric acid
The most unexpected finding in gout diet research over the past twenty years is not "eat less seafood" but "drink less sugar water". The reason lies in how the liver handles fructose.
The sugar in sugary drinks (sucrose is glucose and fructose 50/50, and a common high-fructose corn syrup is 55% fructose) is absorbed fast when it arrives as a liquid, and nearly all the fructose goes first to the liver through the portal vein. Inside liver cells, the enzyme that takes it on is fructokinase (KHK). The route that breaks down glucose has a gate at the phosphofructokinase step, which slows things down when the cell has enough energy. Fructose, once KHK takes it on, bypasses that gate: however much arrives gets processed, burning through a large amount of , the cell's energy currency, all at once. ATP is broken down to AMP and then on through hypoxanthine and xanthine until it ends as uric acid.
In acute fructose-loading experiments, blood uric acid rises soon after drinking, by an amount that depends on the dose and the people tested. This pathway works the same way in everyone, regardless of age, sex, body size or how much they exercise.
The sugar in sugary drinks (sucrose is glucose and fructose 50/50, and a common high-fructose corn syrup is 55% fructose) is absorbed fast when it arrives as a liquid, and nearly all the fructose goes first to the liver through the portal vein. Inside liver cells, the enzyme that takes it on is fructokinase (KHK). The route that breaks down glucose has a gate at the phosphofructokinase step, which slows things down when the cell has enough energy. Fructose, once KHK takes it on, bypasses that gate: however much arrives gets processed, burning through a large amount of , the cell's energy currency, all at once. ATP is broken down to AMP and then on through hypoxanthine and xanthine until it ends as uric acid.
In acute fructose-loading experiments, blood uric acid rises soon after drinking, by an amount that depends on the dose and the people tested. This pathway works the same way in everyone, regardless of age, sex, body size or how much they exercise.
Evidence · The cohort studies on sugary drinks
Two long cohorts, one of men and one of womenChoi 2008 (a cohort of US male health professionals, 46,393 men, followed for 12 years): compared with under 1 serving a month, men drinking 1 serving of sugary drinks a day had about 1.45 times the gout risk, and 2 or more servings a day about 1.85 times (85% higher); the fifth with the highest total fructose intake had about 2.02 times the risk (102% higher). These results are after multivariable adjustment; diet soft drinks were not linked to gout.Choi 2010 (a cohort of US women nurses, 78,906 women, followed for 22 years): 1 serving of sugary soda a day meant about 1.74 times the risk (74% higher), and 2 or more about 2.39 times; orange juice at 1 serving a day meant about 1.41 times (41% higher). In absolute terms, gout is uncommon in women to begin with, so 1 soda a day added roughly 36 cases per 100,000 person-years, and the authors noted these drinks likely contribute only modestly to gout in women as a whole.Imamura 2015, a pooling many cohorts: sugary drinks and fruit juice were also linked to a higher risk of type 2 diabetes. That is a different disease, but, like gout, it reflects metabolism going wrong.
These are all observed associations, not randomized trials; but the link grows with the dose, and fructose has a mechanism that makes uric acid, so the direction is credible.
The three most common groups caught by it
Office workers who sit all day (the largest group). One or two milk teas, colas or sweetened coffee drinks a day add up, roughly, to 60–130 g of sugar, of which about 30–65 g is fructose; add takeout seafood, hot-pot red meat and beer at business dinners. A common trajectory: borderline blood uric acid (serum urate, SUA) at a check-up at 30, a first attack at 35, and the realization that "nobody ever told me". The best-value step is to swap the daily milk tea for unsweetened tea, an Americano or sparkling water; this single change pays off more than most small dietary tweaks.
Middle-aged and older people with metabolic syndrome (the largest group in clinics). High blood pressure, type 2 diabetes, abdominal obesity, metabolic dysfunction-associated steatotic liver disease () and high uric acid tend to cluster and push one another up. The mechanism runs both ways. When insulin is high, URAT1, the transporter in the proximal kidney tubule that takes uric acid back into the blood, reclaims more of it, so less is excreted. And in the Stanhope 2009 randomized trial, overweight and obese adults who drank fructose-sweetened drinks supplying 25% of their energy for 10 weeks gained visceral fat and lost insulin sensitivity (the group drinking glucose-sweetened drinks did not), which closes a vicious circle. Thiazide diuretics for blood pressure and some other long-term medicines also raise uric acid. What helps: control total sugar intake, bring the waist down by 5–10%, talk to your doctor about switching medicines, and start urate-lowering therapy when needed (see the chapter Urate-lowering therapy).
People who train hard (a small group that often thinks it is immune). "I work out every day, so a bit of milk tea is fine, right?" The answer is no. Long-term exercise is real protection: it improves insulin sensitivity and kidney blood flow, and lowers baseline uric acid by roughly 0.3–0.6 mg/dL. But that protection cannot block a large dose of liquid fructose. Muscle cells take up glucose through (a glucose transporter, the door that lets glucose in), and however well trained that ability is, it cannot do the liver's job of handling fructose (this is reasoning from the mechanism; the cohorts did not look at heavily trained people specifically). After training, lactate is up and you are dehydrated, so uric acid excretion is briefly impaired, and a large sugary drink at that moment gives a higher uric acid peak. A common trajectory: a man in his thirties who lifts, has 3–4 milk teas a week, adds sugar to his protein shakes and drinks beer at weekends, and around 35 feels sudden, severe pain in his big-toe joint. What to eat is on the page Fueling for people who train hard.
In practice · What to drink, and how to quit sweet drinks
First, how much to drink. China's dietary guideline says that where heart and kidney function are normal, you should drink 2000–3000 mL of water a day, aiming to keep urine output above 2000 mL. Uric acid leaves mainly through the kidneys, and too little urine is like narrowing the exit. Plain water comes first; lemon water, weak tea, unsweetened coffee and soda water are fine too; avoid large amounts of strong tea or strong coffee.⚠️ This does not apply to people with heart failure, chronic kidney disease (), or anyone on a fluid restriction: how much to drink must come from your own doctor.
From highest risk to lowest, for anyone
High risk (avoid, or strictly limit)
Sweetened milk tea, cola, Sprite and fruit-flavored soda: in the two cohorts above, from 1 serving a day, risk was about 45% higher in men and about 74% higher in women, and higher still with moreFruit juice (even 100% juice): the fiber is gone and the fructose is concentrated, so it comes close to a sugary drink; in the women's cohort, 1 glass of orange juice a day meant about 41% higher riskFull-sugar energy drinks: a lot of sugar, and the caffeine makes you pass more urine, so it is easy to end up short of water"Less sugar" and "half sugar" are not safety labels; a cup may still hold 40–60 g of sugar
Moderate (in moderation)
Alcohol: China's dietary guideline ranks huangjiu (yellow rice wine) highest in purines, then beer; baijiu is low in purines but high in alcohol, which makes lactate build up and holds back uric acid excretion. The familiar Western order, beer > spirits > red wine, is not wrong; its list simply has no huangjiu. People with gout are best off not drinking; for anyone in an acute attack, with poorly controlled gout on medication, or with chronic gouty arthritis, the guideline says no alcohol at allFull-sugar sports drinks: not needed for everyday hydrationFlavored milk drinks and sweetened yogurt drinks: watch the sugar
Recommended (drink freely)
Plain water: ≥ 2 L a day (2–3 L a day for people with gout whose heart and kidneys work normally), which helps excrete uric acid and also prevents uric-acid stonesUnsweetened tea (green, black, oolong, pu'er): almost no fructoseBlack coffee or an Americano: in the men's cohort of Choi 2007, those drinking ≥ 4 cups a day had about a 40% lower risk of gout (an observed association)Sparkling water with lemon: no sugar, still satisfying, and the best substitute for milk teaLow-fat milk and unsweetened soy milk (about 240–500 mL a day): people who ate more dairy had less gout (Choi 2004, observational); in the Dalbeth 2010 randomized crossover trial, blood uric acid in 16 healthy men fell by about 10% within 3 hours of a single high-protein skim-milk drinkUnsweetened coconut water: high in potassium and low in sugar, fine now and then
A few notes for everyone
Gout is no longer only an older man's disease. Some have set the rise of gout in Chinese men aged 30–40 beside the rise in sugary-drink consumption, and the two curves do overlap, but overlap on its own does not prove causeWomen before menopause are protected by estrogen, and their risk catches up fairly quickly afterwardsPeople with a family history, or who have had ≥ 1 attack already, need long-term management, not just a change of diet (see the chapter Urate-lowering therapy)Watch your lab results: routine check-ups after age 30 usually include blood uric acid and creatinine (standard in China; in the US you often have to ask), and the trend is what countsNot drinking sugar water is probably the easiest, best-value step for preventing gout
The practical psychology of quitting sweet drinks
You don't need to be perfect, and you don't need to take an oathHow often matters more than how much: 1 a week is far less than 1 a day, and an occasional treat does not undo the restGet substitutes ready first: keep unsweetened sparkling water and tea bags in the fridge and cupboard, or get a coffee machineChange your surroundings: route your commute around bubble-tea shops, keep sweet drinks out of the office pantry, and make "0 sugar" your default when ordering takeoutSocial settings: "I'm watching my diet at the moment" is a refusal everyone accepts, with no need to explainKeep a record: note how often you have sweet drinks for 1–2 weeks, then set a monthly target to cut down
The full story of how the liver handles fructose is in Fructose vs Glucose Metabolism; how alcohol holds back uric acid excretion is in Alcohol Metabolism.
In practice · Fueling for people who train hard
To keep gout risk down without holding back your training, what matters is the form of carbohydrate, not "sugar or no sugar".This page is for people who do regular strength training plus moderate-to-high-intensity cardio ≥ 4 times a week: a checklist you can follow. It is not written for people who sit most of the day, and it is not a push for anyone to start training.
60–90 minutes before training
Complex carbohydrate with some protein: oats with a banana, whole-grain bread with an egg, sweet potato with chicken breastAvoid: sugary drinks and large amounts of fructose (except for very long sessions that are about to start; see below)
During training
Under 60 minutes: water plus sugar-free electrolytes is enoughLong sessions over 90 minutes (running, cycling, a full match): absorption of a single glucose-type carbohydrate (glucose, maltodextrin) in the gut tops out at roughly 60–70 g an hour (Jeukendrup 2017, a review). If you need no more than that, maltodextrin plus glucose is enough and there is no need for high-fructose energy gels; to take in more, you have to add fructose, because it uses a different absorption route. For someone with gout, this is a trade-off between race-day performance and uric acid, and an occasional race is not the same as a daily milk teaHeavy sweating in the heat: add a sodium and potassium electrolyte powder, sugar-free or very low in sugar
30–60 minutes after training
20–40 g of good-quality protein: eggs, chicken breast, Greek yogurt, unsweetened wheyComplex carbohydrate: rice, sweet potato or oats, plus whole fruit (berries first; see the chapter Whole fruit differs from sweet drinks)Fluids and electrolytes (when you have sweated a lot)240–500 mL of low-fat milk: complete protein plus calcium; in the Dalbeth 2010 trial, blood uric acid dipped briefly after a single high-protein milk drink; for people who train, it may be the most underrated recovery drink, with more behind it than most expensive recovery drinksAvoid: downing a big milk tea, a sweetened protein shake, flavored whey or a full-sugar sports drink straight after training. Lactate is high and you are dehydrated, so uric acid excretion is briefly impaired, and a large dose of fructose makes it worse
Every day (training days and rest days)
Water ≥ 3 L a day (more on training days)Coffee: 2–4 cups a day are fine (in Choi 2007, men who drank more had less gout, an observed association)Cherries, blueberries and strawberries often, when in seasonProtein sources: mainly eggs, chicken breast, fish, soy foods and low-fat dairy, with organ meats and red meat in moderationProtein powder: choose sugar-free or low-sugar, and avoid flavored versions with 5–10 g of added sugar per serving
Weekends and social occasions
If you want milk tea: at most once a week, ideally on a rest day, with plenty of water, and not at the same meal as beer or seafoodBeer at social dinners: switch to unsweetened sparkling water with lemon, or soda water with a little whisky (spirits have fewer purines than beer, but they hold back uric acid excretion just the same)"Low sugar" is not a safety certificate: a 700 mL cup at "30% sugar" may still hold 30–45 g of sugar
Monitoring
Men over 30, women over 50, and people who train: blood uric acid and creatinine once a year (creatinine is used to estimate kidney filtration, )Family history, or an attack already: every 3–6 monthsReference lines: < 7 mg/dL for men and < 6 mg/dL for women; very active people sitting at the 6.5–7 borderline can watch and wait, but training more does not mean you can carry a higher uric acid
Summary for people who train
A 160 kg squat or 25 pull-ups is real protection, but it cannot block a big dose of liquid fructoseCutting sugary drinks to very little pays back far more than "adding 10 kg today"People who train are a minority of readers, and this page's advice does not apply to people who sit most of the day: their first job is to start moving, not to fine-tune training-day fueling
Chapter 4
Whole fruit differs from sweet drinks
One of the most common mistakes in gout diets goes: fructose causes gout, so fruit is off the table too.
The most consistent evidence is about fructose in liquid. Sugary drinks and juice are absorbed fast and deliver a large dose at once, hitting the liver all together; the fructose in whole fruit is wrapped in fiber, released slowly, and comes in smaller amounts, with an apple holding about 20 g of sugar. In cohort studies, sugary drinks and juice are linked to a higher gout risk again and again; the results for whole fruit are less consistent. In Choi 2008, a cohort of US men, fructose-rich fruits such as apples and oranges were also linked to a slightly higher risk, while China's National Health Commission dietary guideline (2024) finds no clear link between whole fruit and gout and recommends 200–350 g of fruit a day.
So the practical conclusion: stop the sugar in drinks first; keep eating whole fruit as usual, just not a lot at once.
The most consistent evidence is about fructose in liquid. Sugary drinks and juice are absorbed fast and deliver a large dose at once, hitting the liver all together; the fructose in whole fruit is wrapped in fiber, released slowly, and comes in smaller amounts, with an apple holding about 20 g of sugar. In cohort studies, sugary drinks and juice are linked to a higher gout risk again and again; the results for whole fruit are less consistent. In Choi 2008, a cohort of US men, fructose-rich fruits such as apples and oranges were also linked to a slightly higher risk, while China's National Health Commission dietary guideline (2024) finds no clear link between whole fruit and gout and recommends 200–350 g of fruit a day.
So the practical conclusion: stop the sugar in drinks first; keep eating whole fruit as usual, just not a lot at once.
Mechanism · Why a glass of juice is not an apple
A comparison on four fronts ( in the table is relative risk: 1.85 means about 1.85 times the risk of the comparison group)| Aspect | Sugary drinks, milk tea, juice | Whole fruit (eaten whole) |
|---|---|---|
| Absorption speed | Very fast (liquid, often on an empty stomach) | Slow (fiber slows stomach emptying) |
| Sugar in one go | Easily 50–100 g or more at once | 15–30 g at a time (1 apple is about 20 g) |
| What comes with it | Almost nothing but sugar | Fiber, polyphenols, vitamins, potassium |
| Short-term effect on blood uric acid | Rises soon after drinking in loading experiments | Predicted by the mechanism to be much smaller; not measured directly |
| Cohort studies | Men at ≥ 2 servings a day RR 1.85; women at 1 a day RR 1.74 | Inconsistent: apples and oranges were also linked in Choi 2008; the Chinese guideline finds no clear link |
Why the form changes the result
Soluble fiber (pectin) slows stomach emptying, so fructose enters the portal vein slowly.The liver is no longer hit by one large dose, so the KHK pathway is not pushed to its limit all at once.China's dietary guideline explains that the vitamin C, flavonoids, polyphenols, potassium and fiber in fruit together modify the effect of its fructose; how much each one contributes has not been measured separately.
Key evidence
Choi 2010 (US women) and Choi 2008 (US men): sugary drinks and fruit juice (orange juice in the women's cohort) were both linked to a higher gout risk.In the same Choi 2008 cohort, fructose-rich fruits such as apples and oranges were also linked to a higher risk (an observed association). So the safer statement is not "fruit is completely fine" but "the risk from fruit is far less clear than from sugary drinks, and its benefits are real".Zhang 2012 was a case-crossover study (observational; people with gout compared against themselves): two-day periods with cherries had a 35% lower risk of an attack ( 0.65), and cherry extract showed a similar link (OR 0.55).Muraki 2013 (three US cohorts, 187,382 people): those eating more whole fruit had a lower risk of type 2 diabetes, and those drinking more fruit juice had a higher one. The same split between fruit and juice shows up again in diabetes.China's National Health Commission dietary guideline (2024): limit sugary drinks, fresh-pressed juice, high-fructose corn syrup and candied fruit, while eating 200–350 g of fruit a day.
In practice · Which fruit is fine to eat
Eat freely (2–4 servings a day)Berries (blueberries, strawberries, cherries, blackberries): cherries have associative evidence from a case-crossover study, and the other berries are recommended on the same reasoningPears, bananas and citrus; apples and oranges are fine too, but they carry relatively more fructose, so don't eat a lot at onceKiwi, pineapple and dragon fruitThese fruits also supply the carbohydrate, potassium and antioxidants that training needs
In moderation (if uric acid is already high)
Grapes, mango, lychee, longan and watermelon (denser in fructose, so don't eat a lot at once)Dried fruit (raisins, dates, dried figs): drying concentrates the sugar, so keep portions smallLarge smoothies and milkshakes: blending breaks up the fiber, bringing them partway to juice
Avoid, or strictly limit
Fruit juice (even 100% juice): without its fiber it comes close to a sugary drink, and both Choi cohorts linked it to a higher gout riskCold-pressed and "detox" juices: the same as above; marketing language does not change the chemistryBig milkshakes and high-speed blended drinks: the fiber structure is badly broken down
Some common misunderstandings
"Bananas are too sugary to eat": wrong. A whole banana has little fructose, plus fiber and potassium, and is a good choice after training"An apple is just sugar": not quite. One apple has about 20 g of sugar, but its fiber and polyphenols slow absorption, so it is not the same as a can of cola"Fruit on an empty stomach harms the stomach": there is no evidence for this; eating fruit on an empty stomach does not harm a healthy person"Fruit at night makes you fat": weight depends mainly on total calories across the day, not on the clock"People with diabetes can't eat fruit": wrong. In the Muraki 2013 cohorts, people eating more whole fruit actually had a lower risk of type 2 diabetes (an observed association); juice is the problem
In practice · Fruit for people who train
A fruit strategy for people who trainWithin 30 minutes after training: a banana with eggs, or Greek yogurt, for fast glucose plus protein and potassiumEveryday snack: a handful of berries with a cup of unsweetened coffee or teaWhen a craving hits: instead of milk tea, have a piece of whole fruit and a glass of unsweetened sparkling water; you get the sweetness and avoid liquid fructoseIf you are worried: you can measure your blood uric acid once as a baseline, then again 60–90 minutes after eating fruit to see how you respond (most people will not see a clear rise); but a single test swings quite a bit on its own, so one or two results are only a rough guide
Fructose in drinks and fructose in fruit differ in form, not in how they feel. Swap milk tea and sweet sodas for apples, cherries and blueberries and you gain nutrition and fullness, with far less risk than the sweet drinks carried. Train hard, keep liquid sugar under control and eat whole fruit as usual, and you are a long way from gout.
The full story of how the liver handles fructose is in Fructose vs Glucose Metabolism.
Chapter 5
Urate-lowering therapy
Gout treatment runs on three tracks at once: settle the inflammation and pain during an attack, bring blood uric acid below target over the long term with urate-lowering drugs, and change lifestyle.
An acute attack: the earlier the better, ideally starting within 24 hours. Three kinds of drugs are used: nonsteroidal anti-inflammatory drugs (indomethacin, naproxen, diclofenac, at a full dose for 5–7 days); colchicine (0.5 mg a dose, 2–3 times a day, working best when started early); and corticosteroids (oral prednisone 30–40 mg for 5 days) for people who cannot take anti-inflammatories, have several joints affected, or have a severe attack.
⚠️ People with chronic kidney disease, or who take other medicines long term, should let their doctor choose which of these drugs to use and at what dose: a large share of colchicine leaves the body in urine, so it clears more slowly when the kidneys are weak, and taking it together with certain other drugs has caused fatal poisoning; nonsteroidal anti-inflammatory drugs can also make kidney function that is already impaired even worse.
Urate-lowering therapy (ULT) deals with blood uric acid over the long term. The American College of Rheumatology (ACR) 2020 guideline strongly recommends starting it in three situations: 2 or more attacks a year; any tophus (a lump of urate crystals); or joint damage from gout already visible on imaging.
An acute attack: the earlier the better, ideally starting within 24 hours. Three kinds of drugs are used: nonsteroidal anti-inflammatory drugs (indomethacin, naproxen, diclofenac, at a full dose for 5–7 days); colchicine (0.5 mg a dose, 2–3 times a day, working best when started early); and corticosteroids (oral prednisone 30–40 mg for 5 days) for people who cannot take anti-inflammatories, have several joints affected, or have a severe attack.
⚠️ People with chronic kidney disease, or who take other medicines long term, should let their doctor choose which of these drugs to use and at what dose: a large share of colchicine leaves the body in urine, so it clears more slowly when the kidneys are weak, and taking it together with certain other drugs has caused fatal poisoning; nonsteroidal anti-inflammatory drugs can also make kidney function that is already impaired even worse.
Urate-lowering therapy (ULT) deals with blood uric acid over the long term. The American College of Rheumatology (ACR) 2020 guideline strongly recommends starting it in three situations: 2 or more attacks a year; any tophus (a lump of urate crystals); or joint damage from gout already visible on imaging.
Clinical · Choosing urate-lowering drugs, and for how long
Other options for an attack: hard-to-treat attacks can be treated with interleukin-1 blockers (anakinra, canakinumab), which are expensive; a single large joint can also be treated with a steroid injection into the joint.Where ACR 2020 makes a conditional recommendation (decide case by case): a first attack together with moderate-to-severe chronic kidney disease ( stage ≥ 3), blood uric acid > 9 mg/dL, or urinary stones. For high uric acid without any attack, Chinese and US guidelines disagree; see the Hyperuricemia story.
Three kinds of urate-lowering drugs
Allopurinol: blocks xanthine oxidase (XO), the enzyme that makes uric acid, and is first-line. Start low, around 100 mg a day, and raise it step by step to 300–600 mg a day until the target is reached. It is cheap and has plenty of long-term data.⚠️ For people of Han Chinese, Korean or Thai descent (and African Americans), ACR 2020 conditionally recommends testing for the **HLA-B*5801** gene before prescribing. Carriers have more than 100 times the of Stevens-Johnson syndrome or toxic epidermal necrolysis (SJS/TEN, a severe and potentially fatal drug rash); as a rough estimate, screening about 250 people prevents 1 serious skin reaction. People who test positive switch to febuxostat or a uricosuric drug.Febuxostat: blocks XO selectively and is second-line, at 40–80 mg a day. The CARES trial (2018), in gout patients who already had cardiovascular disease, found more cardiovascular deaths with febuxostat than with allopurinol, and the FDA added a boxed warning; people at high cardiovascular risk should start with allopurinol.Uricosurics (probenecid, benzbromarone, lesinurad): second-line; they increase excretion by blocking URAT1, the transporter in the proximal kidney tubule that takes uric acid back. They are not suitable for chronic kidney disease or for people with uric-acid stones.
Target: blood uric acid < 6 mg/dL (< 360 µmol/L); for people with tophi it is often set at < 5 mg/dL.
A trap when starting: as blood uric acid falls quickly, crystals already in the joints partly dissolve and can actually set off an attack. To prevent this, take colchicine 0.5 mg once or twice a day for 3–6 months alongside the start of urate-lowering therapy. Don't stop the drug because of attacks early on; they are expected, not a sign that treatment has failed.
⚠️ If a rash, fever, or ulcers in the mouth or eyes appear in the first weeks on allopurinol or febuxostat, stop the drug and go to the emergency department immediately: this may be the severe drug rash described above, and it cannot be watched at home.
How long: most people need it long term, often for life, because gout is a chronic disease. A few people who have lost a lot of weight, changed their lifestyle a great deal and seen their tophi disappear can discuss reducing the dose with their doctor. Do not stop on your own; the risk of relapse is high.
Follow-up: check blood uric acid every 3 months and adjust the dose; once it is at target (< 6), with 1 year free of attacks and the tophi gone, treatment moves into a stable phase.
How this connects to other stories: how fructose raises uric acid is in Fructose vs Glucose Metabolism; how alcohol holds back uric acid excretion is in Alcohol Metabolism; uric-acid stones are in Kidney Stones; whether to treat high uric acid without symptoms is in Hyperuricemia.
References · 16
- Dalbeth, N., Choi, H. K., Joosten, L. A. B., Khanna, P. P., Matsuo, H., Perez-Ruiz, F., & Stamp, L. K. (2019). Gout. Nature Reviews Disease Primers, 5(1), 69. 10.1038/s41572-019-0115-y
- Choi, H. K., Willett, W., & Curhan, G. (2010). Fructose-rich beverages and risk of gout in women. JAMA, 304(20), 2270-2278. Nurses Health Study: 78,906 women with no gout at baseline followed 22 years (1984-2006), 778 confirmed incident cases by ACR survey criteria. Rising sugar-sweetened soda intake raised risk, and orange juice showed a comparable association. Versus under 1 serving a month: soda 1 serving/day RR 1.74, 2+ servings/day RR 2.39; orange juice 1.41 and 2.42. Top vs bottom fifth of fructose: RR 1.62. Absolute risk differences: 36 and 68 extra cases per 100,000 person-years for soda (1/day and 2+/day), 14 and 47 for orange juice, 28 for the top fructose fifth; diet soft drinks were not associated. The authors call the population contribution likely modest given the low incidence in women (abstract, PMID 21068145). 10.1001/jama.2010.1638
- Choi, H. K., & Curhan, G. (2008). Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ, 336(7639), 309-312. Health Professionals Follow-up Study: 46,393 men with no gout at baseline, 12 years of follow-up, 755 confirmed incident cases. Versus under one serving a month, 5-6 servings a week gave RR 1.29, one serving a day RR 1.45, and two or more servings a day RR 1.85. Top vs bottom fifth of fructose intake: RR 2.02. ⚠️ This is the MEN's cohort; the women's replication is choi-2010-jama-fructose-gout (JAMA, despite that id). 10.1136/bmj.39449.819271.BE
- Choi, H. K., Atkinson, K., Karlson, E. W., Willett, W., & Curhan, G. (2004). Purine-rich foods, dairy and protein intake, and the risk of gout in men. New England Journal of Medicine, 350(11), 1093-1103. Health Professionals Follow-up Study: 47,150 men with no gout at baseline, 12 years, 730 confirmed incident cases. Highest vs lowest fifth: meat RR 1.41 (1.07-1.86), seafood RR 1.51 (1.17-1.95), dairy RR 0.56 (0.42-0.74). Purine-rich vegetables and total protein intake were NOT associated with a higher risk (abstract, PMID 15014182). 10.1056/NEJMoa035700
- Zhang, Y., Neogi, T., Chen, C., Chaisson, C., Hunter, D. J., & Choi, H. K. (2012). Cherry consumption and decreased risk of recurrent gout attacks. Arthritis & Rheumatism, 64(12), 4004-4011. Case-crossover study (not a trial) of 633 people with gout followed online for 1 year, comparing the 2 days before each flare with 2-day control periods. Cherry intake: OR 0.65 (0.50-0.85), i.e. 35% lower flare risk; cherry extract: OR 0.55 (0.30-0.98); cherries plus allopurinol vs neither: OR 0.25 (0.15-0.42) (abstract, PMID 23023818). 10.1002/art.34677
- Choi, H. K., Gao, X., Curhan, G. (2009). Vitamin C Intake and the Risk of Gout in Men. Archives of Internal Medicine, 169(5), 502. A 20-year prospective cohort of 46,994 men with 1,317 incident gout cases. SERUM URATE IS NOT AN ENDPOINT here — the urate-lowering claim belongs elsewhere. Supplemental vitamin C was significant only from 1000 mg/day. 10.1001/archinternmed.2008.606
- General Office of the National Health Commission of China. (2024). Dietary guidelines for adults with hyperuricaemia and gout (2024 edition). Issued February 2024. Seven principles, of which the verified specifics are: at least 12 food varieties a day and 25 a week; organ meats such as liver, kidney and heart are generally higher in purine than ordinary meat and should be avoided as far as possible; egg white and milk are low in purine and can be eaten without concern; although soy is slightly higher in purine than lean meat or fish, purine in plant foods is poorly utilised by the body and processing lowers it further, so tofu and dried bean curd may be eaten in moderation; whole grains should be at least 30 percent of the staple portion and dietary fibre 25-30 g/day; at least 500 g of fresh vegetables daily with dark-coloured ones over half; milk protein promotes uric-acid excretion, so 300 mL or more of milk or equivalent dairy is encouraged daily; high-fructose items - sugary drinks, fresh-pressed juice, high-fructose corn syrup, preserved fruits - should be limited, but whole fruit shows no significant association with gout because its vitamin C, flavonoids, polyphenols, potassium and fibre modify the effect of its fructose, and 200-350 g of fruit a day is recommended; drink 2000-3000 mL of water daily where cardiac and renal function are normal, aiming to keep urine output above 2000 mL. On alcohol: purine content is HIGHEST IN HUANGJIU (Chinese yellow rice wine), followed by beer; baijiu is low in purine but high in alcohol, which drives lactate accumulation and suppresses uric-acid excretion. Patients in an acute gout attack, with poor drug control, or with chronic gouty arthritis should not drink at all. www.nhc.gov.cn/sps/c100088/202402/9ba512ba8e314a47a181db11d2fa188d/files/1743476135548_41457.pdf
- FitzGerald, J. D., Dalbeth, N., Mikuls, T., Brignardello-Petersen, R., Guyatt, G., Abeles, A. M., et al. (2020). 2020 American College of Rheumatology guideline for the management of gout. Arthritis Care & Research, 72(6), 744-760. Strongly recommends starting urate-lowering therapy (ULT) in patients with ≥ 2 flares/year, tophi, or radiographic damage; conditionally against initiating ULT for asymptomatic hyperuricemia. Treat-to-target SUA < 6 mg/dL. Strong indications are ≥ 1 subcutaneous tophus, radiographic damage attributable to gout, or ≥ 2 flares a year; after a FIRST flare ULT is conditionally recommended against, except that it is conditionally recommended when CKD stage ≥ 3, serum urate > 9 mg/dl, or urolithiasis is present (very low certainty). Start allopurinol at ≤ 100 mg/day, lower in CKD (strong). HLA-B*5801 testing before allopurinol is conditionally recommended for patients of Southeast Asian descent (e.g., Han Chinese, Korean, Thai) and African American patients, and conditionally recommended against for all others. Adding vitamin C is conditionally recommended against (low certainty): two small RCTs (n = 29 and n = 40) showed clinically insignificant serum urate changes. For cherries/cherry extract and dairy protein the evidence, mainly observational, was low or very low certainty, so the panel made NO recommendation either way. Limiting alcohol and purine intake (low certainty) and high-fructose corn syrup (very low), and weight loss if overweight (very low), are all conditional (full text, PMC10563586). 10.1002/acr.24180
- Choi, H. K., Willett, W., & Curhan, G. (2007). Coffee consumption and risk of incident gout in men: a prospective study. Arthritis & Rheumatism, 56(6), 2049-2055. 10.1002/art.22712
- Dalbeth, N., Wong, S., Gamble, G. D., Horne, A., Mason, B., Pool, B., et al. (2010). Acute effect of milk on serum urate concentrations: a randomised controlled crossover trial. Annals of the Rheumatic Diseases, 69(9), 1677-1682. 16 healthy men, each given a single dose (80 g protein) of each product - soy control and three skim-milk preparations - with blood drawn hourly for 3 h. Soy raised serum urate by about 10%; all milks lowered it by about 10% (p < 0.0001), and all products, soy included, raised fractional uric-acid excretion. A 3-hour acute effect in people without gout, not a long-term outcome (abstract, PMID 20472590). 10.1136/ard.2009.124230
- Stanhope, K. L., Schwarz, J. M., Keim, N. L., Griffen, S. C., Bremer, A. A., Graham, J. L., et al. (2009). Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation, 119(5), 1322-1334. Overweight/obese adults aged 40-72 drank glucose- or fructose-sweetened beverages supplying 25% of energy requirements for 10 weeks (39 enrolled, 7 did not complete). Weight gain was similar in both groups; visceral adipose volume rose only with fructose. Fructose raised hepatic de novo lipogenesis, 23-h postprandial triglycerides, fasting apoB, LDL, small dense and oxidized LDL, fasting glucose and insulin, and lowered insulin sensitivity; fasting triglycerides rose about 10% with GLUCOSE, not fructose. Neither the abstract nor the full text reports uric acid or urate (abstract, PMID 19381015; full text, jci.org). 10.1172/JCI37385
- Imamura, F., O'Connor, L., Ye, Z., Mursu, J., Hayashino, Y., Bhupathiraju, S. N., & Forouhi, N. G. (2015). Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction. BMJ, 351, h3576. 17 cohorts (38,253 cases; 10,126,754 person-years). Per serving a day: sugar-sweetened beverages +18% (+13% after adjusting for adiposity); artificially sweetened beverages +25% (+8%), with publication bias and residual confounding indicated; fruit juice +5% (non-significant) and +7% after adjustment. Population attributable fraction for SSB: 8.7% in the US, 3.6% in the UK (abstract, PMID 26199070). 10.1136/bmj.h3576
- Jeukendrup, A. E. (2017). Training the gut for athletes. Sports Medicine, 47(Suppl 1), 101-110. Names the two apical doors: SGLT1 for glucose/galactose saturates around 60-70 g/h of a single carbohydrate; fructose largely uses GLUT5. Adding fructose once SGLT1 is full raises exogenous oxidation; ingesting a single carbohydrate above that rate is linked with gastrointestinal problems. The paper proposes that repeated high carbohydrate intake during training might increase SGLT1 number or activity, then states the human evidence for that upregulation is limited. Do not read this record as a proven 'train the gut' protocol. 10.1007/s40279-017-0690-6
- Muraki, I., Imamura, F., Manson, J. E., Hu, F. B., Willett, W. C., van Dam, R. M., & Sun, Q. (2013). Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies. BMJ, 347, f5001. Across 187,382 participants in three cohorts, higher whole-fruit intake was associated with lower type 2 diabetes risk while higher fruit-juice intake was associated with higher risk; substituting whole fruit for juice was associated with lower risk. Abstract figures (NHS, NHS II, HPFS; 12,198 cases): per 3 servings a week, whole fruit HR 0.98; blueberries 0.74, grapes and raisins 0.88, apples and pears 0.93, bananas 0.95, cantaloupe 1.10; fruit juice 1.08 (1.05-1.11). Observational (abstract, PMID 23990623). 10.1136/bmj.f5001
- U.S. Food and Drug Administration. (2026, April). Colchicine tablets, for oral use (Macleods Pharmaceuticals) — full prescribing information. Contraindication: patients with renal or hepatic impairment should not be given colchicine together with P-gp or strong CYP3A4 inhibitors; in these patients, life-threatening and fatal colchicine toxicity has been reported with colchicine taken in therapeutic doses. Coadministration with P-gp and/or strong CYP3A4 inhibitors has resulted in life-threatening interactions and death. Dosage depends on age, renal function, hepatic function and coadministered drugs; colchicine clearance falls in renal impairment (40 to 65% of an oral 1 mg dose recovered unchanged in urine in healthy volunteers). dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=9111bbad-b020-44fb-b276-d7853e5acd2c
- U.S. Food and Drug Administration. (2025, July). Indomethacin capsules, for oral use (Glenmark Pharmaceuticals) — full prescribing information. Indicated among others for acute gouty arthritis. Boxed warning on serious cardiovascular thrombotic events and gastrointestinal bleeding. Renal toxicity: NSAIDs may precipitate overt renal decompensation, with the greatest risk in impaired renal function, dehydration, heart failure, liver dysfunction, diuretic or ACE-inhibitor/ARB use and the elderly; use should be avoided in advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function. dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=f7ed39e2-5431-4e47-935c-c7441d058f94