Gout

Gout is a form of arthritis in which monosodium urate (MSU) crystals form in joints, causing pain, swelling, and redness in the affected area. These painful occurrences can be debilitating and tend to come on quickly; the big toe being the most commonly affected part of the body. The prevalence of gout varies depending on the population, with a worldwide prevalence around 1 to 4%.^[1]

Gout is characterized by “gout attacks” or “gout flares”, which involve periods of redness, swelling, and often intense pain in joints. In general, gout attacks will present with the following signs:

• Often occurs in one joint at a time
• Affected joint is swollen, red, and warm
• Frequently occurs at night or in the early morning
• Symptoms peak within 24 hours of onset and last around 3–14 days in the absence of medical treatment

Although symptoms are most common in the big toe, the knees, fingers, and ankles can also be affected.

Blood levels of uric acid levels will also usually be elevated in gout.

If gout is suspected, the primary diagnostic method is a joint fluid test, in which a sample of synovial fluid is taken from the affected joint and examined with a microscope for the presence of MSU crystals.

During a gout attack, a number of medications can help reduce inflammation, thereby improving pain and potentially reducing the duration of the attack. These include nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids.

Several medications can also be taken regularly to reduce uric acid levels, preventing future gout attacks. These medications act by reducing uric acid production (e.g., allopurinol) or increasing uric acid excretion (e.g., probenecid). Uric-acid lowering drugs can increase the risk of gout attacks initially, so they are often given with a medication called colchicine for the first 3–6 months to mitigate this risk.

Two dietary factors that may increase uric acid levels are purines (found in meat, particularly shellfish and organ meats, as well as legumes) and fructose (found in most sources of sugar). In general, limiting purines and fructose can lead to a reduction in uric acid levels, but this has not yet been shown to benefit people with active gout.

Some evidence suggests dairy products and salt (compared with low salt intake) may lower uric acid, but these have also not been shown to be beneficial in the context of gout.

Finally, weight loss can reduce uric acid levels, but more research is required to fully understand this relationship.

A few supplements have also been tested for their effect on uric acid levels. Vitamin C has been shown to lower uric acid, but most of the research looked at uric acid (often in response to exercise) among people who didn't have gout.

Tart cherry juice may lower uric acid levels in some people without gout, but it had no effect on uric acid levels or gout flares in a study of people with gout.^[2]

Gout is the result of MSU crystals forming in joints. The primary cause of MSU crystal formation is high levels of uric acid in the blood, either from a reduced ability to excrete uric acid or an increased production of uric acid. A variety of factors have been linked to a higher risk of gout, including heavy drinking, obesity, various dietary factors, certain medications, and kidney disease. Genetics can also contribute to higher uric acid levels and an increased risk of gout.