What Is Gout and Why Is It Becoming More Common?
Gout is a form of inflammatory arthritis caused by the deposition of monosodium urate crystals in joints and surrounding tissues. It is the most common inflammatory arthritis in men worldwide and one of the most painful acute arthritis presentations — patients frequently describe the pain as the worst of their life. More than 3% of US adults have gout, and its prevalence has risen sharply over the past three decades.
Gout prevalence is rising, driven by increasing consumption of purine-rich foods (red meat, organ meats, shellfish), alcohol (particularly beer), and fructose-sweetened beverages, combined with rising rates of hypertension, obesity, and metabolic syndrome — all of which independently increase uric acid levels.
Importantly, gout is both acutely treatable and chronically manageable — with appropriate treatment, flares can be prevented entirely. Yet many patients suffer recurrent attacks unnecessarily due to under-treatment and incomplete education about lifestyle management.
How Gout Develops
Uric acid is the end product of purine metabolism. Purines are found in body cells and in foods — particularly red meat, organ meats, shellfish, beer, and high-fructose corn syrup. In most people, uric acid dissolves in blood and is excreted through the kidneys. When uric acid levels exceed their solubility threshold in body fluids (typically above 6.8 mg/dL), it crystallises and deposits in cooler peripheral joints — particularly the big toe (first metatarsophalangeal joint), ankles, knees, and wrists.
The mechanism of pain: the immune system recognises urate crystals as foreign, triggering an intense inflammatory response mediated by the NLRP3 inflammasome and interleukin-1β. This produces the classic gout flare — severe pain, swelling, warmth, and redness in the affected joint, typically reaching maximum intensity within 12–24 hours.
Gout vs Osteoarthritis and Other Arthritis: Key Differences
Gout is easy to confuse with a flare of osteoarthritis or with rheumatoid arthritis, but the pattern is distinct:
- Onset: Gout attacks typically begin suddenly, often overnight or in the early morning hours
- Acuteness: Reaches peak intensity within hours; extremely severe pain is characteristic
- Pattern: Classically monoarticular (affecting one joint) and in the big toe (podagra); but any joint can be affected
- Temporal pattern: Acute attacks lasting days to weeks, followed by asymptomatic intervals — distinct from the persistent pain of osteoarthritis or RA
- Serum uric acid: Elevated (though can be normal during an acute attack)
- Confirmation: Joint fluid aspiration showing urate crystals is the gold standard; in typical presentations, clinical diagnosis is often made without aspiration
Acute Gout Treatment
NSAIDs
First-line for most acute gout attacks in appropriate patients. Indomethacin or naproxen at maximum doses for 5–7 days. Provides rapid anti-inflammatory relief. Contraindicated in kidney disease, peptic ulcer disease, and cardiovascular high-risk — all common in gout patients.
Colchicine
Highly effective and specifically targeted for gout. Low-dose colchicine (0.5 mg twice or three times daily) is now preferred over the older high-dose protocol (which caused significant GI toxicity). Most effective when started within 24 hours of flare onset.
Corticosteroids
Prednisolone (30–35 mg daily tapering over 5–7 days) is effective when NSAIDs and colchicine are contraindicated. Can also be injected directly into the affected joint for rapid relief.
During an acute flare, do not start urate-lowering therapy (allopurinol) — this can paradoxically worsen or prolong the flare by mobilising urate deposits.
Preventing Future Attacks: Urate-Lowering Therapy
Allopurinol is the cornerstone of long-term gout management. It inhibits xanthine oxidase, the enzyme that produces uric acid, reducing serum urate below the crystallisation threshold. Target: serum uric acid <6 mg/dL (below saturation point); <5 mg/dL for patients with tophi.
Starting dose: 50–100 mg daily, increasing slowly over months to achieve target. Most patients require 300 mg daily; some need 600–800 mg. Common mistake: stopping allopurinol after a flare — the flares that occur when starting allopurinol are part of the transition and not a reason to stop the medication.
Febuxostat is an alternative xanthine oxidase inhibitor for patients who cannot tolerate allopurinol. More expensive but effective.
Cover with low-dose colchicine (0.5 mg daily) for the first 3–6 months when starting allopurinol to prevent the mobilisation flares that commonly occur.
Dietary Management of Gout
Foods to reduce significantly
- Red meat and organ meats (liver, kidney, brain)
- Shellfish (shrimp, crab, mussels) and certain fish (sardines, anchovies, herring, mackerel)
- Beer and spirits (wine in moderation may be less problematic)
- High-fructose corn syrup and sweetened beverages
Protective foods
- Cherries and cherry juice: Convincing observational evidence showing regular cherry consumption reduces gout flare frequency by approximately 35%. Anthocyanins in cherries have direct urate-lowering and anti-inflammatory effects.
- Low-fat dairy: Milk, yogurt, and low-fat dairy consistently shown to reduce uric acid levels. Dairy proteins (casein, lactalbumin) promote renal urate excretion.
- Coffee: Regular coffee consumption is associated with lower uric acid levels in epidemiological studies.
- Vitamin C: 500–1,000 mg daily vitamin C modestly lowers serum urate.
Hydration
2–3 litres of water daily is strongly recommended — adequate hydration reduces urate crystallisation and supports renal excretion.
Frequently Asked Questions
Should I stop allopurinol if I get a gout flare while starting it?
No. Flares in the first weeks to months of allopurinol are a normal part of the transition as urate deposits mobilise, not a sign the drug isn’t working. Continue allopurinol and treat the flare separately with NSAIDs, colchicine, or steroids as advised by your doctor.
Can gout be cured by diet alone?
Diet helps but rarely resolves gout on its own for most patients with recurrent attacks. Purine and alcohol restriction typically lowers uric acid by a modest amount; most people who have had more than one flare need urate-lowering medication like allopurinol to reach target levels.
Is a normal uric acid level during a gout attack proof it isn’t gout?
No. Serum uric acid can be normal or even low during an acute flare because the attack itself changes how urate is handled. Diagnosis should not be ruled out on a single normal reading taken during a flare.
References
- Richette P, et al. (2017). 2016 updated EULAR evidence-based recommendations for the management of gout. Annals of the Rheumatic Diseases, 76(1), 29–42.
- Stamp LK, Chapman PT. (2019). Gout and its comorbidities: implications for therapy. Rheumatology, 52(1), 34–44.
- Zhang Y, et al. (2012). Cherry consumption and decreased risk of recurrent gout attacks. Arthritis and Rheumatism, 64(12), 4004–4011.
- Choi HK, et al. (2005). Intake of purine-rich foods, protein, and dairy products and relationship to serum uric acid levels. Arthritis and Rheumatism, 52(1), 283–289.
This article is for informational purposes and is not a substitute for medical advice. Last updated August 2026.
