Uric Acid

Uric acid is a naturally occurring waste product made when your body breaks down purines — chemicals that come from two main places:

1. Endogenous purines. Your own cells as they naturally turn over.

2. Exogenous purines. Foods and drinks you consume, especially red meat, organ meats, seafood, and certain beverages.

Uric acid is produced mainly in the liver, intestines, and the lining of blood vessels. Once produced, it dissolves into the bloodstream and is cleared primarily by the kidneys, which filter about 70% of uric acid into urine, while the remaining ~30% is removed through the intestines.

Your kidneys don’t simply “filter and dump” uric acid. They regulate it carefully using specialised transporter proteins in kidney tubules — such as URAT1, GLUT9, and ABCG2 — that control how much uric acid is reabsorbed back into the blood versus excreted into urine. In fact, the kidneys filter nearly all uric acid, then reabsorb ~88–92%, meaning only ~8–12% is ultimately excreted. This is one reason humans maintain higher uric acid levels than many other mammals; higher uric acid may have offered evolutionary advantages (including antioxidant effects and blood pressure regulation when salt was scarce). Typical reference ranges vary by lab, but are commonly around 3.4–7.0 mg/dL in men and 2.4–6.0 mg/dL in women.

Uric acid matters because it is not only a “waste marker” — it is strongly connected to inflammation, kidney function, cardiovascular risk, and metabolic health, and both high and extremely low levels can signal important underlying issues.

When uric acid production exceeds excretion, hyperuricaemia develops (often defined as >7.0 mg/dL in men or >6.0 mg/dL in women). The best-known consequence is gout, a highly painful inflammatory arthritis. In gout, excess uric acid forms needle-shaped crystals in and around joints. These crystals trigger a powerful immune response through activation of the NLRP3 inflammasome, increasing inflammatory signals such as interleukin-1β, which contributes to the classic gout flare: a joint that becomes red, swollen, hot, and intensely painful.

Beyond gout, elevated uric acid is strongly linked with metabolic syndrome — a cluster that includes abdominal obesity, insulin resistance, high blood pressure, high triglycerides, and low HDL cholesterol. The relationship appears bidirectional: insulin resistance can raise uric acid by reducing kidney excretion, while higher uric acid may worsen insulin resistance. This matters because metabolic syndrome amplifies risk for both type 2 diabetes and cardiovascular disease.

High uric acid is also associated with significant cardiovascular risk. Large-scale evidence (including meta-analytic data with over a million participants) shows hyperuricaemia is linked with increased risk of coronary heart disease, heart attack, and cardiovascular death, and that risk tends to rise further with each additional 1 mg/dL increase in uric acid. Proposed mechanisms include uric acid–driven inflammation, injury to the inner lining of blood vessels (endothelial dysfunction), increased oxidative stress, stimulation of smooth muscle growth in arteries, and activation of systems that raise blood pressure (including the renin–angiotensin system).

Kidney health is central to uric acid. Because the kidneys are the main route of uric acid removal, reduced kidney function can elevate uric acid. But elevated uric acid may also contribute to kidney injury: hyperuricaemia predicts the development and progression of chronic kidney disease (CKD) in many studies. High uric acid is also a well-established cause of kidney stones, which can cause severe pain and urinary obstruction and may worsen kidney health over time.

On the other end of the spectrum, hypouricaemia (abnormally low uric acid) is less common but can still be clinically relevant.

Dietary factors (foods and drinks)

Diet can shift uric acid significantly because purines are metabolised directly into uric acid. Higher intake of red meat and organ meats is consistently associated with higher uric acid and higher risk of hyperuricemia/gout. Seafood, especially certain fish and shellfish (e.g., anchovies, sardines, trout, tuna, shellfish), is also associated with higher risk.

Alcohol is a major driver — especially beer — because alcohol can increase uric acid production and reduce kidney excretion, and beer also contributes purines from yeast. Sweetened beverages are another key factor: drinks containing high-fructose corn syrup (such as regular soft drinks and sweetened drinks) can raise uric acid rapidly (within hours), because fructose metabolism accelerates purine breakdown.

Some foods and patterns are associated with lower uric acid or reduced gout risk. Low-fat dairy (milk, yoghurt, cheese) is consistently protective and may promote uric acid excretion. Vegetables (including higher-purine vegetables like spinach and asparagus) are generally not associated with increased gout risk and are often linked to lower hyperuriceamia risk. Coffee is associated with lower gout risk in observational data. Soy foods and nuts are also associated with lower hyperuricemia risk in dietary pattern research. A dietary index designed around maintaining normal urate has identified foods like blueberries, grapes, low-fat milk, and cheese as protective, while liquor, red meat, liver, artificially sweetened beverages, and tomato products were associated with higher uric acid in that index.

Lifestyle factors

Excess body weight, particularly visceral (abdominal) fat, is strongly associated with higher uric acid via increased insulin resistance, which reduces kidney uric acid excretion. Weight loss improves uric acid levels and lowers gout risk. Dehydration can concentrate uric acid and trigger gout attacks. Physical inactivity contributes to insulin resistance and higher uric acid; regular moderate exercise supports healthier levels, though intense exercise can temporarily raise uric acid due to increased cell turnover and purine release.

Related biomarkers and conditions

Uric acid often moves alongside markers of kidney function (since impaired filtration reduces excretion) and metabolic health (insulin resistance and diabetes-related patterns). Blood pressure and lipid patterns commonly cluster with hyperuricaemia. Certain medications can raise or lower uric acid by shifting kidney handling: for example, some diuretics reduce excretion and raise uric acid, while losartan and fenofibrate have uricosuric effects (promote excretion).

Micronutrients, genetics, and environment

Some micronutrients influence uric acid handling. Vitamin C at 500 mg daily has been associated with a modest reduction in uric acid (about 0.5 mg/dL) by promoting kidney excretion. Folic acid and zinc have shown uric acid–lowering effects in mechanistic work (including inhibition of xanthine oxidase — the enzyme that produces uric acid — and gut microbiome effects in experimental models). Genetics also matters: variation in urate transporters (URAT1, GLUT9, ABCG2) influences baseline levels and susceptibility to hyperuricaemia and gout.

If your results are high

If your uric acid is high (often >7.0 mg/dL in men or >6.0 mg/dL in women), this increases risk for gout, kidney stones, and cardiometabolic complications. Lifestyle and diet changes can reduce uric acid (often by ~1 mg/dL), but larger reductions may require medical management, so clinician input is recommended — especially if you have gout symptoms, kidney stone history, or CKD risk.

Diet:

• Focus on reducing major dietary drivers and emphasising protective foods.

• Limit red meat and avoid organ meats; reduce high-purine seafood (particularly shellfish and certain fish).

• Avoid beer and reduce alcohol overall, and avoid fructose-sweetened drinks (e.g., regular soft drinks and sweetened beverages).

• Build meals around protective patterns: include low-fat dairy (milk, yoghurt, cheese), plenty of vegetables (including spinach/asparagus), and consider foods associated with lower urate risk such as soy foods, nuts, and fruits highlighted in normo-urate dietary patterns (e.g., blueberries and grapes).

Lifestyle:

• Prioritise gradual weight loss if you have excess body weight, as this improves uric acid and lowers gout risk.

• Maintain regular moderate physical activity, and avoid dehydration; consistent hydration supports kidney excretion and may reduce flare risk.

• Be aware that very intense exercise can temporarily increase uric acid through higher cell turnover.

Supplements:

• Vitamin C 500 mg daily may modestly lower uric acid by increasing excretion.

• Folic acid and zinc have shown urate-lowering mechanisms in research contexts; supplementation decisions should be individualised and medically supervised.

If your results are low

If your uric acid is low, it can reflect underproduction (including rare genetic enzyme deficiencies) or overexcretion (kidney tubular disorders, certain medications, or metabolic conditions). Some studies suggest extremely low levels may be associated with adverse outcomes in a U-shaped pattern, though this remains debated.

Diet
Diet is not typically the main driver of clinically significant hypouriceamia compared with kidney handling and genetics; avoid overly restrictive patterns unless advised by your clinician.

Lifestyle
Because low uric acid can relate to kidney tubular handling, hydration and kidney-health context matter, but the most important step is targeted evaluation of the cause.

Supplements
Supplementation is not routinely indicated for low uric acid unless a specific deficiency or mechanism is identified clinically.

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