Uric acid is produced when your body breaks down compounds called purines, which are found in your cells and in many foods. Everyone has uric acid in their blood, but levels climb too high when your body either produces too much or can’t flush enough of it out through the kidneys. Normal levels range from 3.7 to 8.0 mg/dL in men and 2.7 to 6.1 mg/dL in women. When uric acid exceeds those thresholds, crystals can form in joints and kidneys, leading to gout and kidney stones.
How Your Body Makes Uric Acid
Purines are building blocks of DNA and RNA, present in every cell. When cells die or food is digested, purines get broken down in a two-step process. First, purines are converted into a substance called hypoxanthine, then into xanthine, and finally into uric acid. A single enzyme drives both of those last two steps. Most mammals have an additional enzyme that breaks uric acid down further into a more soluble compound, but humans lost that enzyme through evolution. That means uric acid is the end of the line for us: once it’s made, the only way to get rid of it is to excrete it.
About two-thirds of uric acid leaves the body through the kidneys, and the remaining third is eliminated through the gut. Anything that increases purine breakdown or slows kidney excretion will raise your levels.
High-Purine Foods
Diet is one of the most direct causes of elevated uric acid. Foods rich in purines deliver a raw supply of material that your body converts straight into uric acid. Organ meats are among the highest sources: chicken liver contains about 312 mg of purines per 100 grams, pork liver around 285 mg, and beef liver about 220 mg.
Certain seafood is also high. Anchovies clock in at roughly 273 mg per 100 g, mussels at 293 mg, and oysters at 185 mg. Even commonly eaten fish like salmon (177 mg), tuna (157 mg), and rainbow trout (181 mg) carry moderate to high amounts. Shellfish such as tiger prawns (192 mg) and squid (187 mg) are in a similar range. Dried fish products and concentrated broths are especially dense: dried bonito flakes contain about 493 mg per 100 g, and bonito-based soup stock can reach nearly 685 mg.
Lower-purine seafood options include cod (98 mg) and scallops (105 mg). Red meat and poultry, while not as extreme as organ meats, still contribute meaningful amounts when eaten in large portions.
Fructose and Sugary Drinks
Sugar-sweetened beverages are a major and often overlooked driver of high uric acid, and fructose is the reason. Unlike most sugars, fructose is processed in the liver through a pathway that rapidly consumes your cells’ energy currency, ATP. When ATP is depleted that quickly, its breakdown products flood into the purine degradation pathway and get converted into uric acid.
This happens fast. A single large sugary drink can cause a measurable spike in uric acid within minutes. High-fructose corn syrup, table sugar (which is half fructose), fruit juices, and sweetened sodas all trigger this effect. Whole fruit contains fructose too, but in much smaller concentrations and paired with fiber that slows absorption, so the impact is far smaller.
Alcohol’s Triple Effect
Alcohol raises uric acid through three separate mechanisms at once. First, when your liver processes ethanol, it accelerates the breakdown of purine compounds, generating more uric acid directly. Second, ethanol metabolism produces lactic acid, which competes with uric acid for excretion through the kidneys. While your kidneys are busy clearing lactic acid, uric acid backs up in the blood. Third, some alcoholic drinks are themselves high in purines, particularly beer, which contains purines from yeast and barley.
Beer tends to have the strongest effect on uric acid levels. Spirits have a moderate effect, and wine appears to have the least impact, though all alcohol contributes to some degree.
Kidney Excretion Problems
Your kidneys filter uric acid out of the blood, but they also reabsorb most of it back. Specialized transport proteins in the kidney’s filtering tubes control how much uric acid stays in the blood versus how much leaves in urine. Two of the most important are a reabsorption transporter called URAT1 and a glucose/fructose transporter called GLUT9, which together pull uric acid back into the bloodstream. A third protein, ABCG2, works in the opposite direction, pumping uric acid out for excretion.
When the balance tips toward too much reabsorption or too little secretion, uric acid accumulates. Chronic kidney disease, dehydration, and any condition that reduces blood flow to the kidneys can impair this process.
Genetics and Inherited Risk
Some people are genetically wired to retain more uric acid. Large-scale genetic studies have identified several genes that directly affect uric acid transport in the kidneys and gut. The most impactful is ABCG2, the gene that codes for the protein responsible for pumping uric acid out of cells. A common variation in this gene (found in people of both Asian and European descent) reduces its uric acid transport capacity by 53% compared to the normal version. Carrying that variant substantially raises your baseline uric acid and your risk of gout.
Variations in the SLC2A9 gene, which codes for the GLUT9 transporter, also play a significant role. When both gene variants are present together, the risk compounds. This helps explain why gout runs in families and why some people develop high uric acid despite a moderate diet.
Insulin Resistance and Metabolic Syndrome
Insulin resistance, the condition where cells stop responding normally to insulin, has a direct effect on uric acid. When insulin levels are chronically high, the kidneys reabsorb more uric acid and excrete less. High insulin increases the activity of URAT1 (the reabsorption transporter) and activates GLUT9, which pulls even more uric acid back into the blood. At the same time, insulin suppresses ABCG2, the transporter that pushes uric acid out.
This is one reason why high uric acid so often accompanies obesity, type 2 diabetes, and metabolic syndrome. Losing weight and improving insulin sensitivity can meaningfully lower uric acid levels, sometimes enough to prevent gout flares.
Medications That Raise Uric Acid
Several common medications interfere with the kidneys’ ability to clear uric acid. Thiazide diuretics, often prescribed for high blood pressure, increase uric acid reabsorption in the kidneys. Loop diuretics and spironolactone have similar effects. If you’ve been started on a blood pressure medication and your uric acid levels climbed afterward, the diuretic may be the cause.
Low-dose aspirin also appears to reduce uric acid excretion, likely by blocking one of the kidney’s secretion pathways. The effect is modest but relevant for people already near the upper limit of normal. Higher doses of aspirin actually have the opposite effect, lowering uric acid, but those doses are rarely used today.
Rapid Cell Turnover
Any condition that causes large numbers of cells to break down quickly will flood the body with purines, driving up uric acid. The most dramatic example is tumor lysis syndrome, which occurs when cancer treatment kills a large volume of tumor cells at once. The dying cells release their contents, including nucleic acids, into the bloodstream, and uric acid spikes rapidly. This is most common in aggressive blood cancers with large tumor burdens.
Less extreme but still significant: conditions like psoriasis and other diseases involving high cell turnover contribute to chronically elevated uric acid. Intense exercise, prolonged fasting, and crash diets can also temporarily raise levels by increasing tissue breakdown or producing compounds that compete with uric acid for kidney excretion.
Dehydration and Other Everyday Factors
Uric acid concentration in the blood rises whenever your fluid volume drops. Dehydration reduces blood flow to the kidneys and concentrates uric acid in a smaller volume of blood. Hot climates, intense physical activity, illness with fever, and simply not drinking enough water can all push levels up temporarily. Staying well hydrated is one of the simplest ways to keep uric acid in check.
Age and sex also play a role. Men tend to have higher uric acid levels than women throughout life. Women are partially protected by estrogen, which promotes uric acid excretion through the kidneys. After menopause, when estrogen levels drop, women’s uric acid levels rise and their gout risk begins to approach that of men.