What Is the Best Diet for Gout?
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The Real Weight of Diet in Gout
The most frequently repeated advice about gout is: "Watch what you eat." This advice is not entirely wrong — but it places the center of gravity of the disease in the wrong place. How much of the blood uric acid level is attributable to diet has now been measured, and the result is surprising: all foods combined explain approximately 4% of the variation in uric acid, while genetics explains approximately 24%. This article explains what diet really changes, what it does not change, and what the main treatment is.
Points changed and added in this update:
- Spinach, mushrooms, cauliflower, peas, and legumes should not be restricted. In the study that followed 47,150 men for 12 years, purine-rich vegetables were found to have no association with gout risk (RR 0.96). In our previous article, this information was softened to "safe if consumed in moderation"; no restriction is needed at all.
- Vitamin C supplementation is not recommended. The American College of Rheumatology 2020 guideline explicitly does not recommend it; in a randomized study, its effect on uric acid was found to be clinically insignificant. Our previous article recommended vitamin C.
- The claim that "alkaline foods prevent crystallization" has no basis. Alkalinization of urine is an established treatment for uric acid kidney stones — not for gout in the joints.
- A medication review offers a greater return than diet and was entirely absent from the previous article: thiazide diuretics, low-dose aspirin, and certain medications significantly raise uric acid.
- An oncology section has been added: tumor lysis syndrome, rasburicase and G6PD deficiency, and the allopurinol–azathioprine interaction — the last of these is of vital importance.
What Is Gout? A Brief Reminder
Gout is an inflammatory joint disease caused when uric acid accumulating in the blood forms monosodium urate crystals in the joints. Uric acid is the breakdown product of purines, the building blocks of cells. Purines come from two sources:
| Source | Share |
|---|---|
| The body’s own cellular breakdown (endogenous) | The larger share |
| Purines consumed in food (exogenous) | The smaller share |
The main factor determining the blood uric acid level is not production, but renal excretion — and this excretion depends largely on genetically determined transporter proteins (particularly SLC2A9 and ABCG2). In most patients with gout, the problem is not "eating too many purines," but not excreting enough uric acid.
How Much Can Diet Change Uric Acid?
This question was answered by a study published in 2018 in BMJ that pooled 16,760 people from five large population cohorts. The study calculated how much of the variation in blood uric acid was explained by each factor:
What explains the variation in blood uric acid?
Percentage of variance explained (BMJ 2018, 16,760 people)
Genetics (heritability estimate)
23.9%
30 known gene variants
8.7%
All 63 foods combined
4.29%
DASH diet score
0.28%
Mediterranean diet score
0.06%
The authors’ conclusion: "In contrast to the genetic contribution, diet explains very little of the variation in uric acid levels in the general population."
In the same study, foods that raised uric acid were beer, spirits, wine, potatoes, chicken, soft drinks, and red meat; foods that lowered it were eggs, peanuts, skimmed milk, cheese, whole-grain bread, and non-citrus fruits.
So how much can we lower it through diet?
| Intervention | Reduction in uric acid |
|---|---|
| DASH diet (secondary analysis of a randomized study) | -0.25 mg/dL (95% CI -0.43 to -0.08). The effect is larger in those with a high baseline level. |
| Strict low-purine diet (<200 mg purines per day, 2 weeks) | -1.05 mg/dL (approximately 10.8%) |
| Stopping alcohol | -1.6 mg/dL — the largest individual dietary effect |
| Weight loss | A reduction in BMI of more than 5% lowers the likelihood of recurrent attacks by approximately 40% |
Now let us compare. The treatment target is to lower uric acid below 6 mg/dL. In a patient diagnosed with gout, the baseline value is often between 8-10 mg/dL — so the reduction needed is 2 to 4 mg/dL.
The best figure diet can offer is between 0.25 and 1 mg/dL. The American College of Rheumatology’s 2020 guideline puts it this way: "Dietary changes are likely to produce only small changes in serum urate levels." The British NICE guideline is even clearer: "There is insufficient evidence that any specific diet prevents attacks or lowers uric acid."
This does not mean that diet is unimportant. But it does mean this: in established gout, diet cannot replace medication. And not knowing this leads patients to think that "if I follow a stricter diet, I will not need medication" and delay effective treatment — which is the most common mistake in gout.
The best figure diet can offer is between 0.25 and 1 mg/dL. The American College of Rheumatology’s 2020 guideline puts it this way: "Dietary changes are likely to produce only small changes in serum urate levels." The British NICE guideline is even clearer: "There is insufficient evidence that any specific diet prevents attacks or lowers uric acid."
This does not mean that diet is unimportant. But it does mean this: in established gout, diet cannot replace medication. And not knowing this leads patients to think that "if I follow a stricter diet, I will not need medication" and delay effective treatment — which is the most common mistake in gout.
Dietary Changes That Actually Work
The effect of diet is limited — but not zero. The following changes are based on evidence and supported by guidelines. They are all conditional recommendations.
1. Alcohol — the single change offering the greatest return
Gout risk by type of alcohol
Relative risk for one serving per day (Choi et al., Lancet 2004; 47,150 men)
Beer (355 mL)
RR 1.49
Spirits (1 glass)
RR 1.15
Wine (120 mL)
RR 1.04
The result for wine was not statistically significant (95% CI 0.88-1.22). By total alcohol intake, however, the relationship is dose-dependent: at 50 g or more of alcohol per day, the risk rises 2.53-fold. The reason beer stands out is that, in addition to alcohol, it contains yeast-derived purines.
Is wine really harmless? It appears so in this single cohort; however, in patients already diagnosed with gout, another study reported that all types of alcohol increased attack risk. The honest statement is therefore: beer and spirits clearly carry a risk; the risk from wine is lower, but not zero; and in a patient experiencing attacks, distinguishing between types has little practical value.
2. Sugary drinks and fructose
| Consumption | Gout risk |
|---|---|
| 2 or more sugary soft drinks per day (compared with fewer than 1 per month) | RR 1.85 (1.08-3.16) |
| Fructose intake (highest fifth compared with the lowest) | RR 2.02 (1.49-2.75) |
| Diet (sugar-free) soft drinks | No association (p=0.99) |
| 2 or more glasses of orange juice per day | RR 1.81 (1.12-2.93) |
The mechanism is clear: fructose is rapidly phosphorylated in the liver, consumes the cell’s energy molecule ATP, and the resulting breakdown products directly increase uric acid production. This is the strongest causal chain related to diet.
Fruit juice and fruit are not the same. While orange juice was associated with risk in the study above, the 2018 study found whole non-citrus fruits to be associated with lower uric acid. Whole fruit provides fiber, water, and a feeling of fullness, naturally limiting the amount of fructose consumed. Fruit juice lacks these brakes. Practical rule: eat the fruit; do not drink its juice.
3. Weight loss
Excess weight both increases uric acid production and reduces renal excretion. A reduction in BMI of more than 5%lowers the likelihood of recurrent attacks by approximately 40%.
However, rapid weight loss triggers attacks rather than protecting against them. Prolonged fasting and crash diets cause tissue breakdown and ketone production; ketones compete with uric acid in the kidneys and inhibit its excretion. Weight should be lost, but gradually.
Another new warning: case series reported in 2026 indicate that semaglutide and tirzepatide and similar medications can temporarily raise uric acid and trigger attacks during rapid weight loss. Patients with gout using these medications should be careful in the first few months.
Another new warning: case series reported in 2026 indicate that semaglutide and tirzepatide and similar medications can temporarily raise uric acid and trigger attacks during rapid weight loss. Patients with gout using these medications should be careful in the first few months.
4. Meat and seafood: reduce them, do not ban them
| Food group | Gout risk (highest fifth vs lowest) |
|---|---|
| Red meat (total meat) | RR 1.41 (1.07-1.86) |
| Seafood | RR 1.51 (1.17-1.95) |
| Total protein intake | RR 1.07 — no association |
The last row is noteworthy: protein quantity itself does not pose a risk — what matters is the source of the protein. Organ meats (liver, kidneys, brain, tripe) are the foods highest in purines and should be restricted.
5. Low-fat dairy products — the only protective group
| Food | Gout risk |
|---|---|
| Low-fat dairy products | RR 0.58 (0.45-0.76) — 42% lower risk |
| Full-fat dairy products | RR 1.00 — no association |
Milk proteins (casein and lactalbumin) are thought to increase renal uric acid excretion. The protective signal is seen only with low-fat products.
What You No Longer Need to Restrict
1. Purine-rich VEGETABLES — no restriction is needed.
Spinach, asparagus, mushrooms, cauliflower, peas, lentils, chickpeas, and dried beans. These have been excluded from gout diets for decades. In the study that followed 47,150 men for 12 years and identified 730 new gout cases, the result for purine-rich vegetables was: RR 0.96 (0.74-1.24) — no association.
Why? Because plant purines have lower bioavailability than animal purines, and these foods also provide fiber, potassium, and vitamin C. Restricting these vegetables and legumes serves no purpose other than impoverishing the patient’s diet. In our previous article, this information was softened to "safe if consumed in moderation"; we are correcting that — no limit needs to be imposed either.
Spinach, asparagus, mushrooms, cauliflower, peas, lentils, chickpeas, and dried beans. These have been excluded from gout diets for decades. In the study that followed 47,150 men for 12 years and identified 730 new gout cases, the result for purine-rich vegetables was: RR 0.96 (0.74-1.24) — no association.
Why? Because plant purines have lower bioavailability than animal purines, and these foods also provide fiber, potassium, and vitamin C. Restricting these vegetables and legumes serves no purpose other than impoverishing the patient’s diet. In our previous article, this information was softened to "safe if consumed in moderation"; we are correcting that — no limit needs to be imposed either.
2. Vitamin C supplementation — not recommended.
In a randomized study involving forty patients with gout, 500 mg of vitamin C per day had a clinically insignificant effect on uric acid; when added to allopurinol, it provided no additional benefit. Even the study’s title says so: "Clinically insignificant effect of supplemental vitamin C on serum urate in patients with gout."
The American College of Rheumatology 2020 guideline conditionally recommends against adding vitamin C supplementation. Our previous article presented vitamin C-rich fruits as uric acid-lowering; fruit is healthy anyway, but vitamin C supplementation is not a treatment for gout.
In a randomized study involving forty patients with gout, 500 mg of vitamin C per day had a clinically insignificant effect on uric acid; when added to allopurinol, it provided no additional benefit. Even the study’s title says so: "Clinically insignificant effect of supplemental vitamin C on serum urate in patients with gout."
The American College of Rheumatology 2020 guideline conditionally recommends against adding vitamin C supplementation. Our previous article presented vitamin C-rich fruits as uric acid-lowering; fruit is healthy anyway, but vitamin C supplementation is not a treatment for gout.
3. "Alkaline foods" — this is a myth.
The pH of joint fluid cannot be meaningfully changed by the foods eaten. The claim that "alkaline foods prevent uric acid crystallization" has no scientific basis.
The source of the confusion is a real treatment, but it is for a different disease: in uric acid kidney stones, alkalinizing urine with potassium citrate (target urine pH approximately 6.5) dissolves stones and prevents new ones. This is an intervention involving urine, not joints — and is carried out with medication, not food.
The pH of joint fluid cannot be meaningfully changed by the foods eaten. The claim that "alkaline foods prevent uric acid crystallization" has no scientific basis.
The source of the confusion is a real treatment, but it is for a different disease: in uric acid kidney stones, alkalinizing urine with potassium citrate (target urine pH approximately 6.5) dissolves stones and prevents new ones. This is an intervention involving urine, not joints — and is carried out with medication, not food.
4. Drinking plenty of water — reasonable, but not proven.
The advice that "8-10 glasses of water per day prevent attacks" is common, but no randomized study has demonstrated this. Adequate fluid intake is a reasonable recommendation for kidney health and particularly for those with a history of uric acid stones; however, it should not be presented as a treatment that prevents attacks.
The advice that "8-10 glasses of water per day prevent attacks" is common, but no randomized study has demonstrated this. Adequate fluid intake is a reasonable recommendation for kidney health and particularly for those with a history of uric acid stones; however, it should not be presented as a treatment that prevents attacks.
5. Cherries — harmless, but not a treatment.
The idea that cherries reduce gout attacks comes from a 2012 study that followed 633 patients online: those who had consumed cherries in the previous two days had a 35% lower attack risk, and when taken together with allopurinol, a 75% lower risk. It looks impressive — but the study was not randomized, its data were based on patient self-reporting, and the accompanying editorial specifically emphasized that patients should not stop their standard treatment.
Randomized studies have not confirmed this signal. The American College of Rheumatology made no recommendation about cherries because of the low level of evidence — neither for nor against. Cherries are harmless to eat and are a healthy fruit; however, they do not replace medication.
The idea that cherries reduce gout attacks comes from a 2012 study that followed 633 patients online: those who had consumed cherries in the previous two days had a 35% lower attack risk, and when taken together with allopurinol, a 75% lower risk. It looks impressive — but the study was not randomized, its data were based on patient self-reporting, and the accompanying editorial specifically emphasized that patients should not stop their standard treatment.
Randomized studies have not confirmed this signal. The American College of Rheumatology made no recommendation about cherries because of the low level of evidence — neither for nor against. Cherries are harmless to eat and are a healthy fruit; however, they do not replace medication.
What Should Be Done Before Diet: Reviewing the Medication List
This section was entirely absent from our previous article — yet, in most patients, it offers a greater return than diet. Many commonly used medications significantly raise uric acid.
| Medication that RAISES uric acid | Approximate effect |
|---|---|
| Hydrochlorothiazide (blood pressure medication) | +0.3 to +0.76 mg/dL |
| Chlorthalidone | +0.7 mg/dL |
| Torsemide and other loop diuretics | +1.18 mg/dL |
| Low-dose aspirin (75 mg/day) | +%6,2 |
| Cyclosporine | +1.6 mg/dL |
| Tacrolimus | +1.5 mg/dL |
| Pyrazinamide (tuberculosis medication) | +4.6 mg/dL |
| Ethambutol (tuberculosis medication) | +3.2 mg/dL |
| Testosterone | +1.16 mg/dL |
| Atenolol / metoprolol | +0.5 / +0.3 mg/dL |
| Medication that LOWERS uric acid | Approximate effect |
|---|---|
| Losartan (blood pressure medication) | -0.16 to -1.05 mg/dL |
| Amlodipine | -1.0 to -1.1 mg/dL |
| Fenofibrate | -1.9 mg/dL |
| Atorvastatin | -0.52 mg/dL |
| SGLT2 inhibitors (empagliflozin, dapagliflozin) | -0.63 mg/dL (empagliflozin -0.77) |
Let us compare. A strict low-purine diet lowers uric acid by 1 mg/dL. In the same patient, switching a thiazide diuretic to losartan can provide a benefit of between 1 and 1.8 mg/dL — without requiring the patient to give anything up.
The American College of Rheumatology 2020 guideline formally recommends this: when possible, replace hydrochlorothiazide with another blood pressure medication and, as a blood pressure medication, prefer losartan. The first question for a patient newly diagnosed with gout should not be "what do you eat," but "which medications do you take."
The American College of Rheumatology 2020 guideline formally recommends this: when possible, replace hydrochlorothiazide with another blood pressure medication and, as a blood pressure medication, prefer losartan. The first question for a patient newly diagnosed with gout should not be "what do you eat," but "which medications do you take."
A new development: SGLT2 inhibitors. In a meta-analysis covering 51 randomized studies and 54,544 patients, these medications, used for diabetes and heart failure, lowered uric acid by an average of 0.54 mg/dL Observational studies show fewer gout events among people using these medications.
But caution: in the same meta-analysis, no statistically significant reduction in gout incidence was found (RR 0.96; p=0.75). In other words, these are not gout medications. The correct statement is: in a patient with both diabetes and gout, there is an additional reason to prefer an SGLT2 inhibitor. Guidelines have not yet been updated on this issue.
But caution: in the same meta-analysis, no statistically significant reduction in gout incidence was found (RR 0.96; p=0.75). In other words, these are not gout medications. The correct statement is: in a patient with both diabetes and gout, there is an additional reason to prefer an SGLT2 inhibitor. Guidelines have not yet been updated on this issue.
The Main Treatment: Uric Acid-Lowering Medications
Drug treatment for gout serves two separate goals: resolving the attack and permanently lowering uric acid. The two should not be confused.
Who should start urate-lowering therapy (ULT)?
| Condition | Strength of recommendation (ACR 2020) |
|---|---|
| The presence of a tophus (a urate deposit) under the skin | Strong recommendation |
| Gout-related joint damage on imaging | Strong recommendation |
| 2 or more attacks per year | Strong recommendation |
| More than one but infrequent attacks (fewer than 2 per year) | Conditional recommendation |
| First attack + stage 3 or higher kidney disease, or uric acid >9 mg/dL, or kidney stones | Conditional recommendation |
| A single uncomplicated attack | Conditionally not recommended |
| Asymptomatic high uric acid (no previous attacks) | Conditionally not recommended — preventing one attack over 3 years requires 24 people to be treated |
The fundamental principle of treatment: treat to target. The ACR 2020 guideline states this as a strong recommendation: the medication dose is increased until uric acid falls below 6 mg/dL, with blood levels monitored. A fixed dose or the approach that "it is enough if the patient has no complaints" is not recommended. In severe gout (tophi, frequent attacks), the European guideline sets the target below 5 mg/dL.
| Medication / practice | Information |
|---|---|
| Allopurinol | First-line, strong recommendation — including those with moderate-to-severe kidney failure. The starting dose should not exceed 100 mg per day (lower in kidney failure), and should then be increased gradually. |
| Febuxostat | For nonresponse or intolerance to allopurinol. Allopurinol is preferred in those with cardiovascular disease. |
| Attack prevention | When starting ULT, protection with colchicine, an NSAID, or a low-dose steroid is provided for at least 3-6 months (strong recommendation). Because crystals begin to dissolve when medication is started, attacks in the first few months may temporarily increase. |
| What is done during an attack? | Colchicine, an NSAID, or a steroid. Low-dose colchicine is superior to high-dose colchicine (strong recommendation): 1.2 mg, followed one hour later by 0.6 mg — a total of 1.8 mg. Diarrhea occurs in 76.9% with the high-dose regimen versus 23% with the low dose, with the same efficacy. |
| Is uric acid medication stopped during an attack? | No. The guideline even recommends starting medication during an attack. A patient already taking it should not stop. |
| Duration | Treatment continues indefinitely. |
Medication safety
Colchicine–antibiotic interaction — the most critical warning for Turkey. When colchicine is used with certain antibiotics such as clarithromycin or with cyclosporine, it causes potentially life-threatening and fatal interactions. The product information considers this combination contraindicated in patients with kidney or liver failure.
Clarithromycin is prescribed very widely in Turkey. A patient taking colchicine should mention this whenever an antibiotic is to be prescribed. Use with statins also increases the risk of muscle damage (rhabdomyolysis). In severe kidney failure, the dose is reduced to 0.3 mg per day.
Clarithromycin is prescribed very widely in Turkey. A patient taking colchicine should mention this whenever an antibiotic is to be prescribed. Use with statins also increases the risk of muscle damage (rhabdomyolysis). In severe kidney failure, the dose is reduced to 0.3 mg per day.
Febuxostat and cardiac risk — the story has reversed. Published in 2018, the CARES trial found higher cardiovascular mortality with febuxostat than with allopurinol (HR 1.34), and in 2019 the FDA added a boxed warning.
However, in 2020, 6,128 patients participated in the FAST trial, which did not confirm this finding: for the primary cardiovascular endpoint, febuxostat was noninferior, with HR 0.85 (0.70-1.03), and even all-cause mortality was lower (HR 0.75). Current practice, as recommended by NICE, is to prefer allopurinol in those with significant cardiovascular disease, while considering either medication an option in others.
However, in 2020, 6,128 patients participated in the FAST trial, which did not confirm this finding: for the primary cardiovascular endpoint, febuxostat was noninferior, with HR 0.85 (0.70-1.03), and even all-cause mortality was lower (HR 0.75). Current practice, as recommended by NICE, is to prefer allopurinol in those with significant cardiovascular disease, while considering either medication an option in others.
Allopurinol hypersensitivity syndrome and HLA-B*58:01. Allopurinol can cause rare but severe skin reactions (DRESS, Stevens-Johnson syndrome), and this risk is significantly higher in people carrying the HLA-B*58:01 gene (odds ratio approximately 118-fold). However, the frequency of this gene varies among populations: while it reaches 12.9% in Southeast Asia, it is 2.3% in populations of European ancestry.
The ACR 2020 guideline therefore recommends testing only in patients of Southeast Asian ancestry (Han Chinese, Korean, Thai) and African-American patients; it recommends against routine testing in all other ethnic groups — including Turkey. The proven way to reduce the risk is different: start at a low dose and increase slowly.
The ACR 2020 guideline therefore recommends testing only in patients of Southeast Asian ancestry (Han Chinese, Korean, Thai) and African-American patients; it recommends against routine testing in all other ethnic groups — including Turkey. The proven way to reduce the risk is different: start at a low dose and increase slowly.
Uric Acid in the Oncology Patient
High uric acid in patients with cancer has a different meaning than in patients with gout and is sometimes an emergency. This section was entirely absent from our previous article.
Tumor lysis syndrome (TLS) is the release of cellular contents into the bloodstream when many cancer cells break down simultaneously. Uric acid, potassium, and phosphate rise rapidly; calcium falls. The result may be kidney failure, arrhythmia, and seizures.
Laboratory diagnosis (Cairo-Bishop criteria) — between 3 days before and 7 days after chemotherapy, within 24 hours, at least two of the following:
Highest-risk situations: advanced Burkitt lymphoma; acute leukemias with a white blood cell count above 100,000; bulky diffuse large B-cell lymphoma; venetoclax treatment (especially in chronic lymphocytic leukemia), and CAR-T cell therapy.
Laboratory diagnosis (Cairo-Bishop criteria) — between 3 days before and 7 days after chemotherapy, within 24 hours, at least two of the following:
- Uric acid ≥8.0 mg/dL or a 25% increase from baseline
- Potassium ≥6.0 mEq/L or a 25% increase
- Phosphorus ≥4.5 mg/dL or a 25% increase
- Calcium ≤7.0 mg/dL or a 25% decrease
Highest-risk situations: advanced Burkitt lymphoma; acute leukemias with a white blood cell count above 100,000; bulky diffuse large B-cell lymphoma; venetoclax treatment (especially in chronic lymphocytic leukemia), and CAR-T cell therapy.
| Allopurinol | Rasburicase | |
|---|---|---|
| What it does | By blocking xanthine oxidase, it prevents new uric acid formation | Existing uric acid is enzymatically broken down and converted into allantoin |
| Does it lower existing uric acid? | No | Yes, rapidly |
| Dose | In adults, 100 mg/m² every 8 hours (maximum 800 mg/day); started 24-48 hours before chemotherapy | 0.2 mg/kg, a 30-minute infusion once daily for up to 5 days |
| Additional risk | Xanthine accumulation and xanthine nephropathy | See below |
Rasburicase — two warnings particularly important for Turkey.
1. Not used in G6PD deficiency. Rasburicase produces hydrogen peroxide while breaking down uric acid. In people deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD), this causes severe anemia (hemolysis) and methemoglobinemia. The medication’s boxed warning requires "screening for G6PD in high-risk individuals, such as patients of African or Mediterranean ancestry". Turkey — especially Southeastern Anatolia and the Mediterranean region — falls squarely within this definition. This is a step that must not be missed in Turkey.
2. The blood sample must be transported on ice. Rasburicase continues to break down uric acid inside the tube after the blood sample has been collected. If the sample is left at room temperature, the result comes out much lower than it really is, and the patient is mistakenly thought to have "improved." Correct practice is to collect the sample in a precooled heparinized tube, immediately place it in an ice-water bath, centrifuge it at 4°C, and analyze it within 4 hours.
1. Not used in G6PD deficiency. Rasburicase produces hydrogen peroxide while breaking down uric acid. In people deficient in the enzyme glucose-6-phosphate dehydrogenase (G6PD), this causes severe anemia (hemolysis) and methemoglobinemia. The medication’s boxed warning requires "screening for G6PD in high-risk individuals, such as patients of African or Mediterranean ancestry". Turkey — especially Southeastern Anatolia and the Mediterranean region — falls squarely within this definition. This is a step that must not be missed in Turkey.
2. The blood sample must be transported on ice. Rasburicase continues to break down uric acid inside the tube after the blood sample has been collected. If the sample is left at room temperature, the result comes out much lower than it really is, and the patient is mistakenly thought to have "improved." Correct practice is to collect the sample in a precooled heparinized tube, immediately place it in an ice-water bath, centrifuge it at 4°C, and analyze it within 4 hours.
A vital interaction: allopurinol + azathioprine or 6-mercaptopurine.
Azathioprine and 6-mercaptopurine are broken down in the body by the enzyme xanthine oxidase. Because allopurinol blocks this enzyme, when the two medications are used together, azathioprine accumulates in the body and causes severe bone marrow suppression (a decrease in white cells, platelets, and all blood cells). This condition is life-threatening.
Azathioprine and 6-mercaptopurine are broken down in the body by the enzyme xanthine oxidase. Because allopurinol blocks this enzyme, when the two medications are used together, azathioprine accumulates in the body and causes severe bone marrow suppression (a decrease in white cells, platelets, and all blood cells). This condition is life-threatening.
- With allopurinol: combined use should be avoided where possible. If essential, azathioprine is reduced to 25% of its normal dose (a 75% reduction), with a complete blood count during the first 3 months performed weekly, and monthly thereafter.
- With febuxostat: this combination is not recommended and no safe dose-reduction strategy has been defined. In other words, the solution of "let us lower the dose" for febuxostat does not apply.
"Does high uric acid increase my cancer risk?" This is a reasonable question from readers of an oncology website, and the honest answer is: evidence is inconsistent and full of confounding factors. Uric acid acts as an antioxidant at low concentrations and promotes inflammation at high concentrations. A 2025 review reports that uric acid supports tumor development in most cancers, but is protective in some cancers (soft tissue sarcoma, laryngeal cancer). Epidemiological studies contradict one another.
Gout and high uric acid also occur alongside obesity, alcohol use, kidney disease, and metabolic syndrome — all of which are independent cancer risks. What can be said today is this: there is no evidence that gout causes cancer, nor evidence that lowering uric acid protects against cancer. Uric acid medications are used for gout, not to prevent cancer.
Gout and high uric acid also occur alongside obesity, alcohol use, kidney disease, and metabolic syndrome — all of which are independent cancer risks. What can be said today is this: there is no evidence that gout causes cancer, nor evidence that lowering uric acid protects against cancer. Uric acid medications are used for gout, not to prevent cancer.
The Situation in Turkey
| Topic | Information |
|---|---|
| Gout prevalence | A population-based study in İzmir (2,835 adults) found 0.31% — low compared with Western countries. A more recent primary care study from Ankara exists, but its results could not be accessed. |
| Global trend | According to the global burden of disease analysis, gout cases are expected to increase by more than 70% by 2050. |
| Allopurinol | Ürikoliz 300 mg and generics are available |
| Febuxostat | Adenuric 80 and 120 mg are available |
| Colchicine | Available |
| Rasburicase | Fasturtec is the name under which it is available in Turkey |
| National guideline | A gout treatment guideline specific to Turkey could not be found; practice follows American and European guidelines |
Frequently Asked Questions
- If I follow a diet, will I not need medication?
- In established gout, you will most likely need it. The best reduction diet can provide is between 0.25 and 1 mg/dL, whereas reaching the target usually requires a 2-4 mg/dL reduction. Diet complements medication; it is not an alternative. This misconception is the most common reason for delayed gout treatment.
- Can I eat spinach, lentils, and mushrooms?
- Yes, no restriction is needed. In the study following 47,150 people, no association was found between purine-rich vegetables and gout. Plant purines do not behave like animal purines.
- Which foods should I actually reduce?
- In order: alcohol (especially beer), sugary drinks and fruit juice, organ meats, and excessive amounts of red meat and seafood. Most restrictions beyond these are unnecessary.
- Does a cherry regimen work?
- The evidence is weak. The positive signal from a single observational study was not confirmed in randomized studies, and guidelines make no recommendation about cherries. Cherries are harmless to eat; they do not replace medication.
- My uric acid is high, but I have never had an attack. Should I start medication?
- Generally, no. The guideline recommends against starting medication for asymptomatic high uric acid: preventing one attack over 3 years requires 24 people to be treated. However, the assessment differs if there are very high values, kidney stones, or kidney disease.
- Should I stop my uric acid medication during an attack?
- No. Do not stop medication you are taking. The guideline even recommends starting medication during an attack. The attack is also treated with colchicine, a painkiller, or cortisone.
- I started medication, but my attacks increased. Is it not working?
- Quite the opposite — this is expected. As uric acid falls, old crystals in the joints begin to dissolve, temporarily triggering inflammation. This is why medication is started with at least 3-6 months of preventive treatment (usually low-dose colchicine). Stopping medication during this period is the most common mistake.
- Does drinking plenty of water prevent attacks?
- No randomized study has demonstrated this. Adequate fluid intake is reasonable for general health and particularly for those with a history of kidney stones, but it should not be presented as a treatment that prevents attacks.
- I am receiving cancer treatment. Can I use gout medication?
- It can be used, but interactions must be checked. The most critical is the use of allopurinol or febuxostat with azathioprine/6-mercaptopurine; this combination can cause severe bone marrow suppression. Colchicine also interacts dangerously with some antibiotics. Tell your oncology team about all medications you use.
Glossary
- Uric acid
- The breakdown product of purines. Its solubility limit is approximately 6.8 mg/dL.
- Purine
- One of the building blocks of DNA and RNA. It becomes uric acid when broken down.
- Tophus
- A hard cluster of urate crystals accumulating under the skin. It is a strong reason for medication.
- Podagra
- A gout attack in the joint at the base of the big toe. The most typical initial site.
- ULT
- Urate-lowering therapy. Allopurinol and febuxostat are the main medications.
- Treat to target
- Increasing the medication dose until the blood level reaches the target (usually <6 mg/dL).
- Xanthine oxidase
- The enzyme that performs the final step in uric acid production. Allopurinol and febuxostat block it.
- Tumor lysis syndrome
- A rapid rise in uric acid, potassium, and phosphorus due to the simultaneous breakdown of cancer cells.
- G6PD deficiency
- An inherited enzyme deficiency that makes red blood cells susceptible to oxidative damage. Common in Mediterranean populations.
- RR / HR
- Relative risk / hazard ratio. 1.00 means no difference; if the confidence interval includes 1, the result is not significant.
DROZDOGAN Academy Commentary
Gout is one of the rheumatological diseases whose treatment is best understood but most poorly implemented. Below we share our own assessment of this paradox.
⚡ Why does this matter?
Because gout is one of the very few rheumatological diseases that can be completely cured. When uric acid is lowered enough and for long enough, crystals dissolve, attacks stop, and tophi disappear. Despite this, most patients with gout worldwide either receive no treatment or are treated at doses that fail to reach the target.One of the biggest reasons for this failure is framing the disease as a "dietary disease". When patients are told to "watch what you eat," two things happen: they blame themselves, and gain a reason to postpone effective treatment — "I will follow a stricter diet and will not need medication."
✅ What we know with confidence
First, the weight of diet has now been measured. A study published in 2018 showed that all foods combined explained only 4.29% of uric acid variation, while genetics explained 23.9%. This is the kind of evidence that settles the debate.Second, the mistaken restrictions are now known by name. For spinach, mushrooms, cauliflower, peas, and legumes, the risk ratio is 0.96 — meaning no association. These foods have been unnecessarily banned for decades, and the price is both a poorer diet and patients giving up entirely, saying, "they banned everything; I cannot follow this diet."
Third, treatment is clear. Treat to target (<6 mg/dL), allopurinol started at a low dose and titrated, and preventive treatment for the first 3-6 months. Applying these three measures brings gout under control.
⚠️ What should not be overstated
It would also be wrong to say that "diet is unimportant." Stopping alcohol alone provides 1.6 mg/dL of benefit, which is more than a strict low-purine diet. Weight loss reduces the likelihood of recurrent attacks by 40%. So the right message is not "diet is pointless," but "the part of diet that works is very narrow; the rest is an unnecessary burden".Enthusiasm for SGLT2 inhibitors is premature. These medications lower uric acid by 0.5-0.6 mg/dL, and observational studies show fewer gout events. However, a pooled analysis of randomized studies found no significant reduction in gout incidence (RR 0.96). These are not gout medications; in a patient with diabetes and gout, they are a reason for preference.
And some of the evidence is old. Most dietary data come from a single American male cohort that began in the 1980s. The finding that wine was "harmless" came from this cohort and has not been replicated in other data. Its direct applicability to Turkish dietary patterns is also limited.
🩺 Our position in practice
1. The first question should not be "what do you eat," but "which medications do you take." Switching a thiazide diuretic to losartan can provide 1-1.8 mg/dL of benefit without requiring patients to give anything up. This is more effective than the strictest diet, yet most patients are never asked about it.2. Reduce dietary advice to five points. Alcohol (especially beer), sugary drinks and fruit juice, organ meats, excessive red meat and seafood, and weight. Every ban beyond these serves only to reduce adherence. Long lists of forbidden foods make patients abandon the diet entirely.
3. Medication should not be delayed in established gout. For a patient with two or more attacks per year, tophi, or joint damage, the approach of "let us try diet first" is lost time.
4. Treatment should be guided by a target. "We started medication and the symptoms are gone" is not enough; the dose should be increased until the blood level falls below 6 mg/dL. Giving a fixed dose of allopurinol is the most common treatment error in gout.
5. The increase in attacks during the first few months should be explained to patients in advance. If it is not explained, patients stop the medication and cannot be persuaded to restart. This single-sentence explanation significantly improves treatment success.
6. Never overlook two points in oncology: before rasburicase, G6PD screening — Turkey falls squarely within the geography named in this medication’s boxed warning — and combining allopurinol/febuxostat with azathioprine. The latter is an easily preventable fatal interaction.
❓ Open questions
Do SGLT2 inhibitors really reduce gout attacks — will a randomized study be designed to test this? Almost all dietary data come from Western male cohorts; do the same associations hold across different food cultures? Will sufficiently large randomized studies be conducted for "promising but unproven" topics such as cherries and milk protein? And most practically: what system change is needed to increase the proportion of patients with gout who reach their target — because the problem is not a lack of knowledge, but failure to apply known treatment.Our brief verdict: Gout is not a "disease of overeating"; it is largely a genetically determined excretion problem. Diet is a small but real aid in this picture — through alcohol, sugary drinks, and weight. The main treatment is to lower uric acid to target and keep it there. The message to patients should not be "watch what you eat," but "this disease can be treated, but treatment involves medication and a target."
Transparency note. (1) Precise figures for how many mg/dL allopurinol and febuxostat lower uric acid were not given because they could not be verified from the primary source; the principle of titration to target was explained instead. (2) The effect of weight loss on uric acid per kilogram could not be verified; only the reduction in attack risk was given. (3) Cherries — numerical results from randomized studies could not be accessed. (4) Global gout prevalence — the exact case count and age-standardized rate could not be verified; only the 2050 projection was given. (5) The result of the current Turkish gout prevalence study in Ankara could not be accessed; the figure provided is from the 2014 study in İzmir. (6) SGK reimbursement conditions for gout medications in Turkey were not included because they could not be verified; medication prices were also omitted because sources contradicted one another. (7) The absolute incidence of allopurinol hypersensitivity syndrome and the frequency of the HLA-B*58:01 gene in the Turkish population could not be verified. (8) The interaction between allopurinol and capecitabine/5-FU is listed in drug databases but was not included because it could not be verified against current product information; patients taking these medications should nevertheless consult their oncologist. (9) The association between gout and cancer — pooled risk ratios from meta-analyses could not be accessed. (10) A gout guideline specific to Turkey could not be found; this does not mean that none exists.
This article is for information purposes and does not replace personal medical advice. Your physician should plan gout treatment by monitoring uric acid levels and assessing your coexisting conditions and medications. Do not start or stop any medication on your own.
References
- Major TJ, Topless RK, Dalbeth N, Merriman TR. Evaluation of the diet wide contribution to serum urate levels: meta-analysis of population based cohorts. BMJ 2018;363:k3951.
- FitzGerald JD, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care Res / Arthritis Rheumatol 2020.
- Richette P, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis 2017;76:29-42.
- National Institute for Health and Care Excellence. Gout: diagnosis and management. NICE guideline NG219, 2022.
- Choi HK, et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med 2004;350:1093-103.
- Choi HK, et al. Alcohol intake and risk of incident gout in men: a prospective study. Lancet 2004;363:1277-81.
- Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ 2008;336:309-12.
- Juraschek SP, et al. Effects of the DASH diet and sodium intake on serum uric acid. Arthritis Rheumatol.
- Stamp LK, et al. Clinically insignificant effect of supplemental vitamin C on serum urate in patients with gout: a pilot randomized controlled trial. Arthritis Rheum 2013;65:1636-42.
- Zhang Y, et al. Cherry consumption and decreased risk of recurrent gout attacks. Arthritis Rheum 2012;64:4004-11.
- Terkeltaub RA, et al. High versus low dosing of oral colchicine for early acute gout flare (AGREE). Arthritis Rheum 2010;62:1060-8.
- White WB, et al. Cardiovascular safety of febuxostat or allopurinol in patients with gout (CARES). N Engl J Med 2018;378:1200-10.
- Mackenzie IS, et al. Long-term cardiovascular safety of febuxostat compared with allopurinol in patients with gout (FAST): a multicentre, prospective, randomised, open-label, non-inferiority trial. Lancet 2020;396:1745-57.
- Lowering and raising serum urate levels: off-label effects of commonly used medications. Mayo Clin Proc 2022.
- SGLT2 inhibitors and serum urate: a meta-analysis of 51 randomized studies. Front Pharmacol 2025.
- Cairo MS, Bishop M. Tumour lysis syndrome: new therapeutic strategies and classification; and StatPearls, Tumor Lysis Syndrome.
- Elitek / Fasturtec (rasburicase) product information and boxed warnings; CPIC guideline, rasburicase and G6PD genotype.
- Medsafe New Zealand: azathioprine–allopurinol interaction; combined febuxostat and azathioprine/mercaptopurine use, September 2018.
- HLA-B*58:01 and allopurinol-related severe skin reactions: a living systematic review and meta-analysis. Sci Rep 2025.
- Birlik M, et al. The prevalence of gout in an urban area of İzmir, Turkey: a population-based epidemiological study. Int J Clin Pract 2014.
- Linking hyperuricemia to cancer: emerging evidence on risk and progression. Curr Oncol Rep 2025.
Sources
1. Gout diet: What's allowed, what's not, Mayoclinic, July 2020
2. Best Diet for Gout: What to Eat, What to Avoid, Healthline, September 2017
2. Best Diet for Gout: What to Eat, What to Avoid, Healthline, September 2017
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