Uric acid is a waste product your body creates when it breaks down purines, compounds found in your cells and in many foods. It dissolves in your blood, travels to your kidneys, and leaves your body through urine. Most of the time this system runs smoothly, but when uric acid builds up too high, it can crystallize in joints and tissues, causing gout and other health problems.
How Your Body Makes Uric Acid
Purines are the building blocks of your DNA and RNA. Every cell in your body contains them, and you also take them in through food. When cells die and recycle their genetic material, or when you digest purine-rich foods, your body converts those purines through a chain of chemical steps that ends with uric acid.
The final step depends on a single enzyme that converts intermediate molecules (hypoxanthine, then xanthine) into uric acid. This enzyme is the bottleneck of the entire process, which is why medications that block it are so effective at lowering uric acid levels in people with gout.
Unlike most mammals, humans can’t break uric acid down any further. Most animals have an enzyme called uricase that converts uric acid into a more soluble compound that’s easy to excrete. Humans lost that enzyme millions of years ago through a genetic mutation. One prominent theory suggests this was actually advantageous: higher circulating uric acid gave our ancestors a stronger antioxidant defense, potentially extending lifespan and reducing cancer risk.
Uric Acid as an Antioxidant
Uric acid isn’t purely a waste product. In your bloodstream, it acts as one of the most powerful antioxidants your body has. It scavenges destructive molecules called free radicals, including singlet oxygen, peroxyl radicals, and hydroxyl radicals. It also protects red blood cell membranes from oxidative damage and neutralizes peroxynitrite, a particularly harmful compound, in the spaces between cells.
There’s a catch, though. Uric acid’s antioxidant powers only work in the watery environment of blood plasma. Inside cells, it can actually flip roles and act as a pro-oxidant, promoting the kind of damage it prevents outside cells. This “oxidant-antioxidant paradox” helps explain why both very low and very high levels of uric acid can be problematic.
Normal Blood Levels
Standard reference ranges for uric acid are 3.5 to 7.2 mg/dL for adult men and postmenopausal women, and 2.6 to 6.0 mg/dL for premenopausal women. The difference is largely hormonal: estrogen helps the kidneys excrete uric acid more efficiently, which is why levels tend to rise in women after menopause.
That said, some researchers argue the upper end of “normal” is too generous. A growing body of evidence suggests that keeping levels below 6.0 mg/dL better identifies truly healthy individuals, regardless of sex. The American College of Rheumatology uses this same threshold (below 6 mg/dL) as the treatment target for people with gout.
How Your Body Gets Rid of It
Your kidneys handle about 70% of uric acid removal, filtering it from the blood and sending it out through urine. The remaining 30% is eliminated through your intestines. That intestinal pathway becomes especially important if your kidneys aren’t working well, since it partially compensates for reduced kidney function.
Anything that impairs kidney function, from dehydration to chronic kidney disease, can slow uric acid clearance and allow levels to climb. This is one reason kidney problems and high uric acid so often go hand in hand.
What Happens When Levels Get Too High
The saturation point for uric acid in blood is 6.8 mg/dL. Above that concentration, uric acid can start forming needle-shaped crystals of monosodium urate. This condition is called hyperuricemia, and while it doesn’t always cause symptoms, it sets the stage for two major problems.
The first is gout. When urate crystals deposit in a joint, typically the big toe, they trigger an intense inflammatory reaction. The joint becomes red, swollen, and excruciatingly painful, often peaking within 12 to 24 hours. Repeated flares can eventually cause permanent joint damage visible on X-rays, and large deposits called tophi can form under the skin.
The second is kidney stones. Uric acid becomes less soluble in acidic urine, so people who produce concentrated, low-pH urine are especially prone to uric acid stones. These account for roughly 10% of all kidney stones and, unlike calcium stones, can sometimes be dissolved by making the urine more alkaline.
What Raises Uric Acid
Diet is one of the most controllable factors. Foods highest in purines include organ meats (liver, kidney, sweetbreads), certain seafood (anchovies, sardines, shellfish, codfish), and to a lesser degree some vegetables like asparagus, spinach, and green peas. Alcohol, particularly beer, is another well-known trigger because it both increases uric acid production and reduces kidney excretion.
Fructose deserves special mention. When your liver metabolizes fructose, it burns through energy reserves (ATP) so rapidly that the leftover molecular fragments get funneled into purine breakdown, generating uric acid as a byproduct. The enzyme that processes fructose has no built-in speed limit. It phosphorylates fructose as fast as it arrives, draining cellular energy stores and causing a cascade of purine degradation. Fructose also stimulates the creation of entirely new purines from scratch, compounding the effect. This is why sugary drinks and foods with high-fructose corn syrup are consistently linked to elevated uric acid and gout risk.
Beyond diet, other factors that raise uric acid include obesity, insulin resistance, diuretic medications, and any condition that increases cell turnover (such as psoriasis or certain cancers), since more cells breaking down means more purines being released.
When Levels Are Too Low
Very low uric acid is far less common but not without risk. In men, levels below 4 mg/dL have been associated with a 28% higher mortality risk in U.S. population data, with a particularly sharp increase in diabetes-related deaths. In women, levels as low as 3 mg/dL showed no significant increase in mortality risk, likely reflecting the naturally lower baseline in premenopausal women.
A rare genetic condition called familial hypouricemia causes chronically very low uric acid, generally below 2 mg/dL, due to mutations in kidney urate transporters. People with this condition are prone to exercise-induced acute kidney failure, though it isn’t associated with shortened lifespan overall. European guidelines for gout management advise against letting treatment push uric acid below 3 mg/dL for prolonged periods, acknowledging that some baseline level appears to be beneficial.
Managing High Uric Acid
For people without symptoms, dietary adjustments are typically the first approach: limiting high-purine foods, reducing fructose intake, staying well hydrated, and moderating alcohol. These changes alone can lower uric acid by about 1 mg/dL in many cases, which is meaningful but often not enough for someone already well above the threshold.
For people with gout, especially those with frequent flares, visible tophi, or joint damage on imaging, medication becomes important. The goal is to bring uric acid below 6 mg/dL and keep it there. This is a treat-to-target approach: levels are checked periodically and medication doses adjusted until the target is consistently met. Over time, maintaining that level allows existing crystals to slowly dissolve, reducing the frequency and severity of flares.