Gout

Gout is caused by monosodium urate crystals in a joint, driven by serum urate. The consequences are attacks, then joint damage, then urate kidney stones, and the way to prevent all of them is to lower serum urate persistently.

Cherries have observational data and small studies suggesting reduced attack frequency, and a plausible mechanism through effects on xanthine oxidase and inflammation. The evidence is weak — observational, small, and subject to confounding by everything else a person who eats cherries does. It is not a way to lower urate.

Vitamin C modestly lowers serum urate in some studies; the effect is small and probably not clinically decisive at doses people take for that purpose.

What actually treats gout. An acute attack: an NSAID, colchicine, or a steroid, started early, decided by a clinician. Prevention of attacks: allopurinol or febuxostat, titrated to a serum urate target (commonly below 0.36 mmol/L / 6 mg/dL), with prophylaxis against attack during initiation. Diet: reducing alcohol (beer especially), sugar-sweetened drinks and fructose, purine-rich organ meats and shellfish, and losing weight — but diet alone rarely gets urate to target, and the framing of gout as a dietary disease has caused a lot of unnecessary guilt and a lot of untreated urate.

A useful warning. Do not start a urate-lowering drug during an acute attack without advice — it can prolong it. And a new drug start needs prophylactic cover, which is a clinical decision.

Topical NSAIDs and colchicine's toxicity. Topical NSAIDs are an option in some joints and have much less systemic exposure. Colchicine is effective and has a narrow margin: it causes severe diarrhoea at toxic doses, and it interacts badly with several drugs. Follow the prescribed dose exactly; do not "take a bit more".