Uric acid: the gout number, and a metabolic one

Uric acid, or urate, is what the body makes when it breaks down purines, which come from its own cells and from food. Most of it leaves through the kidneys. In blood it is reported in mg/dL in the US or µmol/L elsewhere (1 mg/dL is about 59.5 µmol/L). At around 6.8 mg/dL, urate reaches the point where it can come out of solution and form crystals in joints, which is gout.

The ranges

Notice that the typical male reference range runs above the crystallisation point. A "normal" lab result can still be high enough for gout. The ACR target of under 6 mg/dL applies to people with gout on treatment; it is not a recommendation to treat a high uric acid without symptoms. Online claims that everyone should keep urate under 5 mg/dL for metabolic health are opinion.

What raises and lowers it

• Raises: alcohol (beer especially), sugary drinks and fructose, large amounts of red meat and some seafood, excess weight and insulin resistance, reduced kidney function, dehydration, diuretics and some other drugs, and male sex. MedlinePlus also lists excessive exercise.
• Lowers: urate-lowering drugs such as allopurinol and febuxostat, weight loss, reducing alcohol and sugary drinks, and some drugs prescribed for other reasons, such as losartan and SGLT2 inhibitors.

What it predicts

The classic data come from the Normative Aging Study, which followed 2,046 initially healthy men for 14.9 years (American Journal of Medicine, 1987). With urate of 9 mg/dL or more, the yearly rate of a first gout attack was 4.9%, and 22% had gout within five years. At 7.0 to 8.9 mg/dL the yearly rate was 0.5%, and under 7.0 it was 0.1%. Most people with high uric acid never get gout, which is part of why guidelines do not treat it without symptoms. In the same study there was no evidence that high urate damaged the kidneys.

Uric acid is also associated with high blood pressure, type 2 diabetes, kidney disease and heart disease in observational studies. Whether it causes them, rather than travelling with weight and insulin resistance, is still argued.

On GLP-1 drugs and weight loss

A post hoc analysis of SURMOUNT-1, published in Annals of the Rheumatic Diseases (2026), looked at 2,539 adults over 72 weeks. Serum uric acid fell by 0.69 mg/dL on tirzepatide 5 mg, 0.92 on 10 mg and 0.95 on 15 mg, against 0.18 on placebo, regardless of the starting level or BMI. A mediation analysis estimated that weight loss explained 72.7% of the fall. The trial was funded by Lilly, and a post hoc analysis does not test gout outcomes.

One practical point: rapid weight loss and dehydration can both raise uric acid in the short term, and changing urate levels in either direction can trigger flares in people who already have gout. Anyone with gout starting a GLP-1 should tell the prescriber.

How to test

• Fast if you can, and avoid alcohol and a large meat or seafood meal the day before.
• Be hydrated, and note diuretics or recent illness.
• During a gout flare, uric acid can read normal or low. A result taken two weeks or more after the flare settles is more representative.
• Read it with eGFR, since the kidneys clear most of it.

Tracking it in Peptide AI

In Peptide AI, uric acid sits in the metabolic panel. The app reads it from a lab PDF or manual entry, scores the panel from 0 to 100 alongside an overall grade, flags values that warrant prompt physician consultation, and plots each result against your dose timeline. Log the draw date, whether you fasted, and anything unusual in the days before, such as illness, a hard session or a dose step, so the next result is compared like with like. Bloodwork tracking shows the series next to the dose log, weight and side effects, and the panels page lists every marker the app groups. More markers are in the bloodwork guides.