Gout develops when uric acid builds up in your blood and forms sharp crystals inside a joint, triggering intense inflammation and pain. This doesn’t happen overnight. It’s typically the result of years of elevated uric acid levels, driven by a combination of genetics, diet, body composition, and how well your kidneys clear uric acid from your system. About 1 in 58 Americans now has gout, and the rate has climbed steadily since 1990.
How Uric Acid Builds Up
Everything starts with purines, chemical compounds your body produces naturally and that you also get from food. When purines break down, the end product is uric acid. Your liver handles most of this production, with a small contribution from the intestines. Roughly two-thirds of the uric acid in your body comes from your own cells turning over. The remaining third comes from what you eat and drink.
Your kidneys are responsible for removing about two-thirds of that uric acid through urine, while your intestines handle the rest. The kidneys filter uric acid through a complex process of absorption, secretion, and reabsorption. When any step in that process goes wrong, uric acid starts accumulating in the blood. This state, called hyperuricemia, is the precondition for gout. Most people who develop gout are “underexcretors,” meaning their kidneys simply aren’t clearing enough uric acid, rather than their bodies producing too much of it.
When Crystals Form in Joints
Having high uric acid doesn’t automatically mean you’ll get gout. But the higher your levels climb, the more dramatically your risk increases. In a large population study, people with uric acid levels under 6 mg/dL had only a 1.1% chance of developing gout over 15 years. At 10 mg/dL or above, that figure jumped to 49%. The risk at the highest levels was 64 times greater than at the lowest.
At a certain concentration, uric acid dissolved in your blood can no longer stay in solution, especially in cooler parts of the body like the joints of your feet and hands. It precipitates into needle-shaped monosodium urate crystals that deposit in the joint lining and surrounding tissue. Interestingly, the joint fluid of people who’ve had gout before appears to actively promote further crystal formation, which helps explain why gout tends to recur in the same joints.
Genetics Play a Larger Role Than Most People Realize
Your genes have a significant influence on how efficiently your kidneys handle uric acid. Two genes in particular stand out. One, called ABCG2, produces a protein that sits on the surface of kidney cells and actively pumps uric acid out into the urine. A common mutation in this gene cuts that pumping capacity roughly in half, and researchers estimate it accounts for at least 10% of all gout cases in white populations. Each copy of the risk variant increases your odds of gout by about 68%.
Another gene, SLC2A9, also regulates uric acid transport. Variants in both genes can leave you with chronically higher uric acid levels even if your diet and lifestyle are otherwise unremarkable. Gout runs in families for this reason. If a close relative has it, your own risk is meaningfully higher.
Who Gets Gout and When
Gout is far more common in men, with ratios ranging from 3:1 to 10:1 compared to women. The reason is largely hormonal. Estrogen helps the kidneys excrete uric acid more efficiently, which protects women during their reproductive years. After menopause, that protection fades. The incidence of gout in women rises from 0.6 per 1,000 person-years in those under 45 to 2.5 per 1,000 in women 75 and older. Women who use postmenopausal hormone therapy reduce their gout risk by about 18%, further supporting estrogen’s protective role.
Men typically develop gout between their 30s and 50s, while women rarely develop it before menopause.
How Body Weight and Metabolism Contribute
Excess body fat doesn’t just correlate with gout. It actively drives the process through several pathways. Fat tissue, particularly in the liver and abdomen, can produce uric acid on its own. Mature fat cells generate uric acid as a byproduct, which contributes to a cycle of low-grade inflammation and insulin resistance. Insulin resistance, in turn, makes the kidneys hold onto more uric acid rather than excreting it.
This is why gout clusters with other metabolic conditions like type 2 diabetes, high blood pressure, and fatty liver disease. The same underlying metabolic dysfunction that raises your blood sugar and blood pressure also raises your uric acid. Losing weight can meaningfully lower uric acid levels, but crash dieting or fasting can temporarily make things worse by producing ketones that compete with uric acid for excretion through the kidneys.
Foods and Drinks That Raise Uric Acid
Diet accounts for about one-third of the uric acid your body produces, so what you eat matters, even if it isn’t the whole picture. The highest-risk foods are organ meats like liver, kidney, and sweetbreads, which are exceptionally rich in purines. Red meat (beef, lamb, pork) and certain seafood, particularly anchovies, sardines, shellfish, and codfish, also contribute significantly.
Sugar deserves special attention. High-fructose corn syrup, found in soft drinks, many cereals, baked goods, and even some canned soups and salad dressings, raises uric acid through a different mechanism than purines. Fructose metabolism directly generates uric acid in the liver, making sweetened beverages one of the more potent dietary risk factors.
Among alcoholic drinks, beer is the worst offender. All beer, including light beer, contains a purine called guanosine that the body readily absorbs and converts to uric acid. One beer a day can raise uric acid levels by about 0.16 mg/dL, while six beers can push levels up by roughly 1 mg/dL. That may sound modest, but for someone already near the crystallization threshold, it can be the difference between a quiet joint and an agonizing flare. Spirits raise risk through a different route: the breakdown of ethanol produces lactic acid that competes with uric acid for elimination in the kidneys, essentially slowing uric acid clearance. Wine appears to carry less risk than beer or spirits, though it’s not entirely neutral.
Medications That Can Trigger Gout
Several common medications raise uric acid as a side effect. Diuretics, often prescribed for high blood pressure, are among the most frequent culprits. They work by increasing urine output, which concentrates the remaining fluid in your body and makes crystal formation more likely. Some types of diuretics also directly interfere with the kidneys’ ability to excrete uric acid. Low-dose aspirin has a similar effect, reducing uric acid clearance through the kidneys. If you’re already genetically predisposed to high uric acid, these medications can push you over the edge.
What Triggers an Actual Attack
Many people walk around with high uric acid for years without symptoms. An acute gout attack, the sudden onset of severe joint pain and swelling, often requires a trigger on top of the chronic buildup. Dehydration is one of the most common. When your body loses fluid through sweating, illness, or simply not drinking enough water, uric acid concentrations spike. This is why gout flares are more common in summer, when heat and humidity increase fluid loss.
Other triggers include sudden dietary excess (a night of heavy drinking and rich food), physical trauma to a joint, surgery, and illness. Acidic conditions in the body, such as those caused by diabetic ketoacidosis or heavy alcohol use, reduce the kidneys’ ability to secrete uric acid and can precipitate a flare. Even rapid weight loss can trigger an attack, as the breakdown of body tissue releases stored purines into the bloodstream all at once.
The crystals themselves don’t just sit passively in the joint. When your immune system detects them, it launches an inflammatory response as if fighting an infection, flooding the area with white blood cells. This is what causes the redness, heat, swelling, and extreme tenderness that make a gout attack so distinctive. The big toe is the classic location, but gout can strike the ankle, knee, wrist, or fingers.
The Slow Path From High Uric Acid to Gout
Gout doesn’t appear from nowhere. It follows a progression. First, uric acid levels rise gradually over years, often without any symptoms. Crystals begin depositing silently in joint tissue. Then, at some point, a trigger sets off the first acute attack. If uric acid levels stay elevated, attacks become more frequent and can start affecting multiple joints. Over time, without management, crystal deposits called tophi can form visible lumps under the skin and cause permanent joint damage.
The key insight is that gout is a cumulative disease. Every factor described above, genetics, kidney function, body weight, diet, alcohol, medications, contributes to the total uric acid load your body carries. For most people who develop gout, it isn’t one cause but several working together over many years.