Gout is a form of inflammatory arthritis caused by a buildup of uric acid in the body. When uric acid levels get too high, sharp crystals form inside joints, triggering sudden and intense episodes of pain, swelling, and redness. It affects roughly 3.9% of adults in the United States and is one of the most common forms of arthritis worldwide, with men affected about twice as often as women.
How Gout Develops in Your Body
Your body produces uric acid as it breaks down purines, natural compounds found in your cells and in certain foods. Normally, uric acid dissolves in your blood, passes through your kidneys, and leaves your body in urine. But when your body makes too much uric acid or your kidneys don’t filter enough of it out, levels rise in the blood, a condition called hyperuricemia.
Crystal formation can begin once uric acid in the blood exceeds about 6.8 mg/dL. At that concentration, uric acid starts to crystallize into tiny, needle-shaped deposits called monosodium urate crystals. These crystals tend to settle in joints, where factors like temperature, pH, and fluid composition make crystallization more likely. The big toe joint is the most common site, but crystals can form in the ankles, knees, elbows, wrists, and fingers as well.
Once crystals deposit in a joint, your immune system treats them as foreign invaders. White blood cells swarm the area, releasing inflammatory chemicals that cause the redness, heat, swelling, and pain of a gout flare.
What a Gout Flare Feels Like
Gout flares tend to strike suddenly, often waking people up in the middle of the night. The affected joint becomes extremely tender. Even the weight of a bedsheet can feel unbearable. The skin over the joint typically turns red or purplish and feels warm to the touch. Many people describe the pain as the worst they’ve ever experienced in a joint.
Flares typically peak within the first 24 hours and then gradually improve over one to two weeks. Between flares, you may feel completely normal, with no joint symptoms at all. Early in the disease, flares may happen only once or twice a year. Without treatment, they tend to become more frequent and last longer over time.
Risk Factors
Several things raise your likelihood of developing gout. Obesity is a major one: excess weight promotes insulin resistance, which reduces the kidneys’ ability to clear uric acid from the blood. High blood pressure contributes through a similar mechanism, causing kidney changes that slow uric acid excretion.
Certain medications play a significant role. Diuretics, commonly prescribed for high blood pressure and heart failure, increase uric acid reabsorption in the kidneys. People taking diuretics have roughly 2.5 times the risk of developing gout compared to those not taking them. A family history of gout also increases your risk, as does being male and being over 65. Women’s risk rises after menopause, when the protective effect of estrogen on uric acid levels declines.
Foods and Drinks That Trigger Flares
Because uric acid comes from the breakdown of purines, what you eat and drink directly affects your uric acid levels. The highest-risk foods include:
- Organ meats like liver, kidney, and sweetbreads
- Certain seafood including anchovies, sardines, shellfish, and codfish
- Red meat such as beef, lamb, and pork (smaller portions help)
- Beer and distilled spirits, which both raise uric acid and are linked to more frequent attacks
- Foods with high-fructose corn syrup, found in many cereals, baked goods, and sweetened beverages
Cutting back on these foods won’t cure gout on its own, but dietary changes can meaningfully reduce how often flares occur, especially alongside medication.
How Gout Flares Are Treated
The goal during an active flare is to reduce inflammation and pain as quickly as possible. Three main types of medication are used as first-line options: anti-inflammatory painkillers (NSAIDs), a plant-derived anti-inflammatory called colchicine, and corticosteroids. Treatment works best when started at the very first sign of a flare. Waiting even a day or two makes the episode harder to control.
Your doctor will choose among these options based on your other health conditions. For instance, NSAIDs aren’t ideal for people with kidney problems or stomach ulcers, while corticosteroids may be a better fit for those situations. Most people feel significant relief within a few days of starting treatment.
Preventing Future Attacks
If you’re having repeated flares, long-term medication to lower uric acid becomes the central strategy. These medications work by blocking an enzyme called xanthine oxidase, which is responsible for the final step of uric acid production in your body. By slowing that enzyme down, less uric acid enters your bloodstream.
The treatment target is getting your uric acid level below 6 mg/dL. At that level, existing crystals gradually dissolve and new ones stop forming. This process takes time. It’s common to experience more flares during the first few months of treatment as crystals break up and irritate the joint lining. Your doctor will often prescribe a low-dose anti-inflammatory alongside the uric acid-lowering medication to prevent these early flares.
Reaching and maintaining target uric acid levels requires regular blood tests, especially in the first year. Many people need dose adjustments before finding the right level. The payoff is significant: with consistent treatment and lifestyle changes, gout is one of the most controllable forms of arthritis. Many people eventually become completely free of flares.
Complications of Untreated Gout
Left unchecked over years, gout can cause permanent damage. The most visible complication is the development of tophi, firm lumps of crystallized uric acid that form under the skin around joints, on the ears, or along tendons. Tophi are painless at first but can grow, erode bone, deform joints, and limit mobility.
Kidney damage is another serious risk. Uric acid crystals can deposit in the kidneys, forming urate kidney stones and causing direct tissue damage. Research shows that people with tophi lose kidney function significantly faster than gout patients without them, at a rate of roughly 4.8 points per year on kidney function tests compared to less than 1 point per year. Crystal deposits in the kidney’s filtering and collecting system can contribute to chronic kidney disease over time.
Gout also clusters with other metabolic conditions. People with gout are more likely to have obesity, diabetes, high blood pressure, and elevated cardiovascular risk. Managing uric acid levels appears to benefit some of these related conditions, though the connections are still being studied.
How Gout Is Diagnosed
Doctors diagnose gout based on a combination of symptoms, blood tests, and sometimes joint fluid analysis. A blood test showing uric acid above roughly 6.5 mg/dL supports the diagnosis, but it’s not definitive on its own. Some people have high uric acid without ever developing gout, and uric acid levels can actually drop during an acute flare, making a single blood draw misleading.
The gold standard is examining fluid drawn from the affected joint under a microscope. If needle-shaped urate crystals are visible, the diagnosis is confirmed. Imaging, including ultrasound and a specialized type of CT scan, can also detect crystal deposits in and around joints, which is particularly useful for people with atypical symptoms or when joint fluid can’t be obtained.