[1] Gout occurs more commonly in those who regularly drink beer or sugar-sweetened beverages; eat foods that are high in purines such as liver, shellfish, or anchovies; or are overweight.

[1] This is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy, and changes in diet.

[5] Gout can present in several ways, although the most common is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint).

[16] Dietary causes account for about 12% of gout,[20] and include a strong association with the consumption of alcohol, sugar-sweetened beverages,[21] meat, and seafood.

[36] The rare genetic disorders familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch–Nyhan syndrome, are complicated by gout.

Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in nearly 75% of cases.

[10] Other conditions commonly complicated by gout include lead poisoning, kidney failure, hemolytic anemia, psoriasis, solid organ transplants, and myeloproliferative disorders such as polycythemia.

[42] Naked crystals may break out of walled-off tophi due to minor physical damage to the joint, medical or surgical stress, or rapid changes in uric acid levels.

[42] When they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages, which is initiated by the NLRP3 inflammasome protein complex.

[1] An evolutionary loss of urate oxidase (uricase), which breaks down uric acid, in humans and higher primates has made this condition common.

[17][43] Other triggers believed to be important in acute episodes of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration and extracellular matrix proteins.

[20] Rapid changes in uric acid may occur due to factors including trauma, surgery, chemotherapy and diuretics.

[16] The starting or increasing of urate-lowering medications can lead to an acute attack of gout with febuxostat of a particularly high risk.

[47] Gout may be diagnosed and treated without further investigations in someone with hyperuricemia and the classic acute arthritis of the base of the great toe (known as podagra).

[3] Eating dairy products, vitamin C-rich foods, coffee, and cherries may help prevent gout attacks, as does losing weight.

[62][63] A number of other medications may occasionally be considered to prevent further episodes of gout, including probenecid, febuxostat, benzbromarone, and colchicine.

[12][64][65] Long term medications are not recommended until a person has had two attacks of gout,[20] unless destructive joint changes, tophi, or urate nephropathy exist.

[5][12] While it has been recommended that urate-lowering measures should be increased until serum uric acid levels are below 300–360 μmol/L (5.0–6.0 mg/dL),[62][66] there is little evidence to support this practice over simply putting people on a standard dose of allopurinol.

[20] Long term therapy is safe and well-tolerated and can be used in people with renal impairment or urate stones, although hypersensitivity occurs in a small number of individuals.

[93] There is some evidence that COX-2 inhibitors may work as well as nonselective NSAIDs for acute gout attack with fewer side effects.

Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.

[107] Rates are high among Polynesians, but the disease is rare in aboriginal Australians, despite a higher mean uric acid serum concentration in the latter group.

A study based on the National Health Insurance Research Database (NHIRD) estimated that 4.92% of Taiwanese residents have gout in 2004.

These ancient manuscripts cite (now missing) Egyptian texts about gout that are claimed to have been written 1,000 years earlier and ascribed to Imhotep.

[111][116] Aulus Cornelius Celsus (30 AD) described the linkage with alcohol, later onset in women and associated kidney problems: Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra.

These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.

[118] In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning and its predilection for older males: Gouty patients are, generally, either old men or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery and the like exhausting passions.

About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle, or instep.

If it attacks the knees, it is called Gonagra; if the hands, Chiragra; if the elbow, Onagra; if the shoulder, Omagra; if the back or loins, Lumbago.

[111] In 1848, English physician Alfred Baring Garrod identified excess uric acid in the blood as the cause of gout.