The main cause of gout is a buildup of uric acid in the blood, a condition called hyperuricemia. When uric acid levels exceed roughly 6.8 mg/dL, the blood can no longer keep it dissolved, and it begins forming needle-shaped crystals that lodge in joints. In most cases, this buildup happens not because the body produces too much uric acid, but because the kidneys don’t flush enough of it out.
How Uric Acid Turns Into Crystals
Your body produces uric acid every day as it breaks down purines, compounds found naturally in your cells and in many foods. Normally, uric acid dissolves in the blood, passes through the kidneys, and leaves the body in urine. The system stays in balance.
When uric acid concentrations rise above 6.8 mg/dL, the blood becomes saturated and can no longer hold the uric acid in solution. At that point, uric acid molecules begin clustering with sodium and water into tiny, fibril-like structures too small to see. These microscopic clusters clump together into larger masses, and eventually transform into sharp, needle-like crystals. These crystals tend to settle in cooler parts of the body, especially the joints of the big toe, ankles, and knees, where lower temperatures make crystallization even easier.
Once crystals accumulate in a joint, the immune system treats them as foreign invaders. White blood cells flood the area, triggering intense inflammation. That’s what produces the sudden, severe pain, swelling, and redness of a gout attack, often striking in the middle of the night.
Why the Kidneys Are Usually the Problem
Uric acid levels can climb for two reasons: the body makes too much, or the kidneys excrete too little. Underexcretion accounts for the majority of cases. Only a minority of people with high uric acid are overproducers. For most, the kidneys simply don’t clear uric acid efficiently enough, allowing it to accumulate over months and years until crystals form.
Several factors can impair the kidneys’ ability to remove uric acid. Chronic kidney disease reduces filtering capacity directly. Dehydration concentrates uric acid in the blood and decreases urine output. Certain medications also interfere with the process. Some types of diuretics (water pills), commonly prescribed for high blood pressure or heart failure, make it harder for the kidneys to excrete urate. Low-dose aspirin has a similar effect. If you take these medications regularly, your uric acid levels may creep upward even if your diet hasn’t changed.
The Role of Diet and Fructose
While kidney excretion is the dominant factor, what you eat and drink influences how much uric acid your body generates in the first place. Foods high in purines, such as red meat, organ meats (liver, kidney), shellfish, and certain fish like sardines and anchovies, deliver raw material that the body converts into uric acid. Alcohol, especially beer, raises uric acid through multiple pathways: it contains purines, increases uric acid production, and simultaneously reduces kidney excretion.
Fructose deserves special attention. Unlike other sugars, fructose actively accelerates purine production in the liver. When the liver metabolizes fructose, it ramps up the enzymes responsible for building purines from scratch, then speeds up the breakdown of those purines into uric acid. This happens in a dose-dependent way: the more fructose consumed, the more uric acid produced. Sugary drinks sweetened with high-fructose corn syrup are a well-established gout trigger for this reason, and research published in Frontiers in Nutrition has mapped out how fructose drives this process at the molecular level. Even fruit juice in large quantities can contribute.
Who Gets Gout and Why It’s Increasing
Gout has become dramatically more common worldwide. Between 2000 and 2023, the global prevalence of hyperuricemia rose from 12.3% to 18.6% in men and from 6.7% to 11.2% in women. The total number of people with elevated uric acid roughly doubled in that period, climbing from around 352 million to over 800 million cases globally. Population growth and aging explain about half of this increase. The rest likely reflects changes in diet, rising obesity rates, and greater use of medications that affect uric acid levels.
Men develop gout far more often than women, partly because estrogen helps the kidneys excrete uric acid. After menopause, women’s risk rises significantly. Other factors that increase your likelihood include obesity (fat tissue produces more uric acid and reduces kidney excretion), a family history of gout, high blood pressure, diabetes, and metabolic syndrome. The geographic variation is striking: prevalence ranges from under 4% in parts of the Middle East and Central Asia to over 40% in Polynesia and Micronesia, where genetic factors and dietary patterns converge.
What Triggers an Actual Attack
Having high uric acid doesn’t guarantee a gout flare. Many people live with elevated levels for years without symptoms. An attack typically requires a triggering event that shifts conditions in favor of crystal formation or provokes the immune system to react to crystals already present. Common triggers include a heavy meal rich in purines, a night of drinking, sudden dehydration, physical trauma to a joint, or rapid weight loss. Even starting uric acid-lowering medication can paradoxically trigger an attack in the short term, because changing uric acid levels destabilizes existing crystal deposits.
The first attack usually hits a single joint, most often the base of the big toe. Pain escalates rapidly, often peaking within 12 to 24 hours. Without treatment, a flare typically resolves on its own within one to two weeks. But if uric acid levels remain elevated, attacks tend to come back more frequently, last longer, and eventually affect multiple joints. Over years, persistent crystal deposits can form visible lumps called tophi under the skin and cause permanent joint damage.
Lowering Uric Acid Is the Core Strategy
Since the root cause is excess uric acid, long-term management centers on bringing levels below 6 mg/dL, the point at which existing crystals gradually dissolve and new ones stop forming. For some people, dietary changes alone can make a meaningful difference: reducing red meat, shellfish, and alcohol intake, cutting back on sugary drinks, staying well hydrated, and maintaining a healthy weight. These steps typically lower uric acid by 1 to 2 mg/dL.
When lifestyle changes aren’t enough, medications that either block uric acid production or help the kidneys excrete more of it can bring levels into a safe range. Most people who start these medications need to stay on them indefinitely, because uric acid levels rebound once the medication stops. The good news is that with consistent treatment, gout is one of the few forms of arthritis that can be effectively controlled to the point where attacks stop entirely and crystal deposits disappear.