Gout is a type of inflammatory arthritis caused by the buildup of uric acid crystals in your joints. It’s the most common form of inflammatory arthritis, affecting roughly 8.3 million Americans, or about 3.9% of the U.S. population. The hallmark symptom is sudden, intense joint pain, most often in the big toe, that can wake you from sleep and make even the weight of a bedsheet feel unbearable.
How Uric Acid Turns Into Crystals
Your body produces uric acid as a natural byproduct of breaking down purines, 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. Problems start when uric acid levels rise too high. At normal body temperature and blood pH, excess uric acid combines with sodium to form a less-soluble salt called monosodium urate. When that salt reaches a tipping point in concentration, the molecules begin clustering together in your joint fluid.
Those clusters aggregate into tiny crystal nuclei, and once a nucleus reaches a critical size, it stabilizes and grows rapidly at its ends into needle-shaped crystals. This process, called nucleation, is the bottleneck. It can take years of elevated uric acid before crystals actually form, which is why many people have high uric acid for a long time before their first flare. Once those crystals are present in a joint, your immune system treats them as foreign invaders, triggering intense inflammation.
What Counts as High Uric Acid
Normal uric acid levels are typically below 6.8 mg/dL, though the threshold varies slightly by sex: above 6 mg/dL in women and above 7 mg/dL in men is generally considered elevated. Readings of 8 mg/dL or higher are diagnostic of hyperuricemia. Not everyone with high uric acid develops gout. Many people live with elevated levels and never form crystals or experience a flare. But the higher your levels climb and the longer they stay elevated, the greater your risk.
The Main Causes of Elevated Uric Acid
Gout comes down to a simple imbalance: your body either makes too much uric acid or doesn’t get rid of enough of it. Most people with gout fall into the second category. Their kidneys don’t excrete uric acid efficiently, so it accumulates in the blood over time. Several overlapping factors drive this imbalance.
Genetics
Your genes play a significant role in how your body handles uric acid. Large-scale genetic studies have identified several genes that directly regulate uric acid transport in the kidneys and gut. Two of the most important are SLC2A9 and ABCG2, both of which code for proteins that move uric acid out of the body. Variants in these genes are strongly linked to higher uric acid levels and increased gout risk. In one study of a Korean population, people with a specific ABCG2 variant had more than three times the odds of developing gout compared to those without it. If gout runs in your family, inherited differences in these transporter genes are a likely reason.
Diet
Purines occur naturally in your body, but they also come from food. When you eat high-purine foods, your body breaks them down into additional uric acid. The biggest dietary culprits include organ meats like liver, kidney, and sweetbreads, along with certain seafood: anchovies, sardines, shellfish, and codfish. Alcohol, especially beer, also raises uric acid both by increasing production and by impairing kidney excretion. Sugary drinks sweetened with fructose have a similar effect. None of these foods “cause” gout on their own, but in someone already prone to high uric acid, they can push levels past the crystallization threshold.
Kidney Function
Since your kidneys are responsible for clearing roughly two-thirds of the uric acid your body produces, anything that impairs kidney function raises your risk. Chronic kidney disease is one of the most common conditions found alongside gout. As kidney filtration declines, uric acid backs up in the blood. This is why gout becomes more common with age, as kidney efficiency naturally decreases over time.
Other Medical Conditions
Gout rarely exists in isolation. Hypertension, obesity, type 2 diabetes, and metabolic syndrome are all highly prevalent in people with gout. Interestingly, research using genetic analysis methods suggests the relationship often runs in one direction: these metabolic conditions drive uric acid levels up, rather than the other way around. Insulin resistance and excess body fat appear to directly impair uric acid excretion, meaning that reducing these risk factors could lower uric acid levels. Some experts consider hyperuricemia itself a marker of metabolic syndrome, even in people who haven’t had a gout flare.
Medications
Certain medications can raise uric acid as a side effect. Diuretics (water pills), commonly prescribed for high blood pressure and heart failure, are one of the most important drug-related causes of elevated uric acid. They increase uric acid reabsorption in the kidneys, reducing how much leaves the body. Low-dose aspirin has a similar, though milder, effect.
Who Gets Gout
Gout is far more common in men than women. About 5.9% of American men have gout compared to 2.0% of women. The gap narrows with age, particularly after menopause, when women lose the protective effect of estrogen on uric acid excretion. In men, risk starts climbing meaningfully after age 35 and continues rising. By age 65 and older, gout is at its most prevalent in both sexes, though men still outnumber women roughly four to one.
What a Gout Flare Feels Like
A gout attack typically strikes suddenly, often at night. The big toe is the classic target, but flares can hit the ankles, knees, elbows, wrists, or fingers. Pain is most severe within the first 4 to 12 hours. The affected joint becomes swollen, red, warm, and exquisitely tender. After the worst pain subsides, lingering discomfort can last from a few days to a few weeks. First flares tend to resolve faster. Later attacks often last longer and may involve multiple joints.
Without treatment to lower uric acid, flares tend to become more frequent over time. Crystals can also accumulate into visible lumps under the skin called tophi, and prolonged crystal deposits can cause permanent joint damage visible on X-rays.
How Gout Is Managed
Gout management has two distinct phases: stopping the immediate flare and preventing future ones.
For acute flares, anti-inflammatory medications are the first line of treatment. Your doctor will choose among options based on your other health conditions and medication tolerances. The goal is to reduce inflammation and pain as quickly as possible. Starting treatment at the first sign of a flare makes a significant difference in how severe it becomes.
Long-term prevention focuses on lowering uric acid below 6 mg/dL, the level at which existing crystals gradually dissolve and new ones stop forming. Urate-lowering therapy is strongly recommended if you’ve had two or more flares per year, have visible tophi, or show joint damage on imaging. Even after a single flare, treatment may be recommended if your uric acid is above 9 mg/dL, you have kidney disease, or you have a history of kidney stones. These medications are started at low doses and gradually increased, with uric acid levels checked along the way to hit the target. Most people continue this therapy indefinitely, since stopping it allows uric acid to rise again.
When starting urate-lowering therapy, you’ll also take a short course of anti-inflammatory medication for 3 to 6 months. This prevents the paradoxical flares that can occur as crystals begin dissolving, a common reason people mistakenly stop treatment. Lifestyle changes like reducing high-purine foods, limiting alcohol, staying hydrated, and maintaining a healthy weight support medication but rarely control gout on their own once flares have started.