Q&A

Quick, evidence-based answers to the most common gout questions — reviewed by our editorial team and grounded in the latest clinical guidelines from the American College of Rheumatology (ACR).

Understanding Gout

What is gout?

Gout is a form of inflammatory arthritis caused by the deposition of monosodium urate crystals in joints and soft tissues. It results from chronically elevated serum uric acid levels (hyperuricemia), typically above 6.8 mg/dL, which allows urate crystals to form and accumulate.

Is gout the same as high uric acid?

No. Hyperuricemia (high uric acid) is a necessary precondition for gout, but not everyone with elevated uric acid develops gout. Only about 20% of people with hyperuricemia will experience gout flares. Gout is the clinical disease — the inflammation, pain, and joint damage caused by urate crystal deposits.

Why does gout usually start in the big toe?

The first metatarsophalangeal joint (big toe) is the most common site for initial gout attacks for several reasons: it’s the coolest joint in the body (urate crystals precipitate more readily at lower temperatures), it bears significant mechanical stress during walking, and it has relatively poor blood circulation compared to larger joints.

Diagnosis & Testing

How is gout diagnosed?

The gold standard for gout diagnosis is joint fluid analysis — identifying monosodium urate crystals under polarized microscopy. In practice, many diagnoses are made clinically based on the characteristic presentation (sudden onset, severe pain, redness and swelling, often in the big toe), elevated serum uric acid, and response to anti-inflammatory treatment. Imaging (ultrasound or dual-energy CT) can also detect urate deposits.

What uric acid level is considered high?

A serum uric acid level above 6.8 mg/dL (403 µmol/L) is considered above the saturation point at which urate crystals can form. However, the ACR recommends a treatment target of below 6.0 mg/dL for patients on urate-lowering therapy, and below 5.0 mg/dL for those with tophi or frequent flares.

Can you have a gout attack with normal uric acid levels?

Yes. During an acute flare, serum uric acid can temporarily drop to normal levels as uric acid precipitates into crystals in the joint. This is why a single normal reading during a flare does not rule out gout. Uric acid should be rechecked 2-4 weeks after a flare resolves.

Treatment & Medication

What is the fastest way to stop a gout flare?

The ACR recommends three first-line options for acute gout flare treatment:

1. Colchicine (0.6 mg, 1-2 tabs at onset, then 1 tab 1 hour later) — most effective when started within 24 hours of symptom onset
2. NSAIDs (e.g., naproxen 500 mg twice daily, indomethacin 50 mg three times daily) — full anti-inflammatory doses
3. Corticosteroids (e.g., prednisone 30-40 mg daily, tapering over 10-14 days) — preferred when NSAIDs or colchicine are contraindicated

Should I take allopurinol during a gout flare?

If you’re already on allopurinol or another urate-lowering therapy (ULT), do not stop it during a flare. Stopping and restarting ULT causes uric acid levels to fluctuate, which can trigger more flares. If you’re not yet on ULT, the ACR recommends starting it after the current flare has resolved, while simultaneously beginning flare prophylaxis (colchicine or low-dose NSAIDs).

Why did my doctor prescribe colchicine daily?

Low-dose colchicine (0.6 mg once or twice daily) is prescribed as flare prophylaxis when starting or adjusting urate-lowering therapy. As uric acid levels drop and crystals dissolve, they can trigger inflammation. Prophylactic colchicine reduces flare frequency by about 70% during the first 3-6 months of ULT.

What if allopurinol isn’t working?

Many patients on allopurinol never reach the target uric acid level because their dose is never increased beyond 300 mg/day. The ACR recommends titrating allopurinol up to 800 mg/day as needed to reach serum urate below 6 mg/dL. If maximum-dose allopurinol fails, options include switching to febuxostat (Uloric) or adding a uricosuric agent like probenecid. For refractory cases, pegloticase (Krystexxa) may be considered.

Diet & Lifestyle

What foods trigger gout flares?

The foods most strongly associated with increased gout risk are:

• High-purine foods: organ meats (liver, kidney, sweetbreads), certain seafood (anchovies, sardines, herring, mussels, scallops)
• Alcohol: especially beer and liquor (wine in moderation is less problematic)
• Fructose-sweetened beverages: sugary sodas and fruit juices high in fructose corn syrup

Notably, purine-rich vegetables (like spinach, mushrooms, and lentils) do NOT increase gout risk and can be eaten freely.

Can I drink coffee if I have gout?

Yes — and it may actually help. Multiple large cohort studies have found that coffee consumption is associated with lower uric acid levels and reduced gout risk. The mechanism likely involves coffee’s effects on xanthine oxidase activity and insulin sensitivity. Both regular and decaf coffee show benefit, though regular coffee has a stronger effect.

Do cherries really help with gout?

There is promising evidence that cherries — particularly tart cherries — may reduce gout flare frequency. A 2012 study published in Arthritis & Rheumatology found that cherry extract supplementation reduced gout attack risk by about 35%. Cherries appear to work by lowering uric acid levels and reducing inflammation. However, cherries should complement (not replace) prescribed urate-lowering therapy.

How much water should I drink with gout?

Adequate hydration helps the kidneys excrete uric acid more efficiently. Most clinicians recommend at least 8-12 cups (2-3 liters) of fluid daily, with water as the primary source. This is especially important during a flare, during hot weather, and when starting urate-lowering therapy.

Is the keto diet good for gout?

It’s complicated. Short-term, very low-carb diets can temporarily raise uric acid levels (due to competition between ketones and uric acid for renal excretion). Long-term, weight loss and improved insulin sensitivity may actually reduce gout risk. If you have gout and are considering keto, talk to your doctor about monitoring uric acid levels closely during the transition period.

Related Conditions

Is gout related to kidney disease?

Yes, the relationship is bidirectional. Chronic hyperuricemia can cause urate crystal deposition in the kidneys, leading to kidney stones, urate nephropathy, and progressive kidney damage. Conversely, chronic kidney disease impairs uric acid excretion, making hyperuricemia worse. The ACR recommends kidney function testing for all gout patients and dose-adjusting allopurinol based on eGFR.

Does gout increase heart disease risk?

Yes. Gout is independently associated with increased cardiovascular risk, including coronary artery disease, heart failure, and atrial fibrillation. The chronic inflammation from urate crystal deposits contributes to endothelial dysfunction and atherosclerosis. Gout patients should have their cardiovascular risk factors (blood pressure, cholesterol, blood sugar) monitored and managed aggressively.

Can gout be cured?

Gout cannot be “cured” in the sense of a one-time treatment that eliminates it permanently. However, gout can be effectively controlled with urate-lowering therapy to the point where flares stop entirely, tophi dissolve, and crystal deposits clear. The ACR recommends indefinite continuation of ULT for most patients who meet treatment criteria, as discontinuation typically leads to recurrence within 6-12 months.