By Dr. Asnat Raziel, bariatric surgeon specializing in obesity treatment, metabolic health and healthy longevity; Director of the Multidisciplinary Center for Obesity Treatment, Assia Medical, Assuta Ramat HaChayal, Tel Aviv
Gout, uric acid and diet: not a disease of kings, but a metabolic problem
High uric acid is much more than the “disease of kings” of old, and a gout and uric acid diet is only part of the story. Simply put, uric acid is a natural breakdown product of purines. Purines are substances found in our bodies and in many foods. Normally, uric acid dissolves in the blood and leaves through the kidneys into the urine. But when the body makes too much, or when the kidneys don’t clear it well, blood levels rise.
At high concentrations, uric acid forms tiny needle-like crystals. These crystals settle in the joints, the kidneys and other tissues. The result is severe pain, inflammation and sometimes cumulative damage.
The normal range varies between laboratories. Usually it is up to about 7 mg/dL in men and up to about 6 mg/dL in women. However, above about 6.8 mg/dL the blood is saturated, and the acid begins to crystallize.
The attack that strikes in the middle of the night
The best-known form is gout. Typically, it is a sudden attack of severe pain in a joint, often at the base of the big toe. But it also appears in the ankle, knee, wrist or elbow.
The joint turns red, swollen and hot. Sometimes even the touch of a bedsheet is unbearable. Without treatment, the attacks come back more and more often and involve more joints. Over the years, chronic joint damage develops, along with lumps of crystals in the tissues called tophi.
Not just joint pain
Excess uric acid is not limited to gout. It raises the risk of kidney stones and can harm kidney function. In addition, studies have linked it to high blood pressure, obesity, type 2 diabetes, fatty liver disease and metabolic syndrome. That is why hyperuricemia (a high level of uric acid in the blood) is now considered part of the overall metabolic picture. It also ties into the connection between the heart, the kidneys and metabolism.
Why does uric acid get too high?
In most cases, the problem is not overproduction. Rather, the kidneys become less able to excrete the acid. Several factors raise the risk:
- Obesity and excess belly fat.
- Insulin resistance and diabetes.
- High blood pressure and chronic kidney disease.
- Diuretics and low-dose aspirin.
- Alcohol, especially beer.
- Sweetened drinks high in fructose.
There is also a significant genetic tendency that affects how the kidneys excrete uric acid.
A gout and uric acid diet that can change the picture
Diet is not the only factor, but it certainly matters. A large study of about 47,000 men found that eating a lot of meat and seafood was linked to a higher risk of gout. In addition, fructose-sweetened drinks raised the risk in the same population.
It is worth cutting back on:
- Large amounts of red meat, and organ meats such as liver and kidneys.
- Sausages and processed meats.
- Sardines, anchovies, herring, mackerel and seafood.
- Beer and alcoholic drinks.
- Soft drinks and juices high in fructose.
On the other hand, it is a good idea to eat more of these:
- Vegetables of all kinds, and fruit in moderation.
- Legumes, whole grains, nuts and almonds.
- Olive oil.
- Low-fat dairy products, which studies have linked to a lower risk of gout.
- Enough water, depending on your health. Water dilutes the urine and helps the body excrete the acid.
What about purine-rich vegetables in a gout and uric acid diet?
For years, doctors told people with gout to avoid asparagus, spinach, cauliflower, mushrooms and legumes. However, that same large study found that plant purines did not raise the risk of gout. So there is no need to drop them from your menu. On the contrary, they are part of a healthy diet rich in fiber, vitamins and antioxidants.
Uric acid and obesity: weight, diet and gout
Excess weight is one of the most important risk factors. Fat tissue increases uric acid production and impairs its clearance. In addition, insulin resistance reduces how much the kidneys excrete. Improving insulin sensitivity through diet helps here too.
Gradual weight loss usually lowers uric acid levels and the risk of attacks. On the other hand, extreme diets, prolonged fasting and very rapid weight loss can temporarily raise uric acid and trigger an attack. That is why I recommend treating obesity without extreme diets.
Obesity medications may help, too
The new data are encouraging. An analysis of the SURMOUNT-1 trial, published in 2025, included 2,539 adults with obesity or overweight. They received tirzepatide, the active ingredient in Mounjaro, or placebo for 72 weeks. At the 15 mg dose, uric acid fell by an average of 0.95 mg/dL, compared with 0.18 on placebo. According to the researchers, weight loss explained 72.7% of the change.
For semaglutide, the picture is more modest. In a follow-up study of oral semaglutide in 236 people with diabetes, levels fell by 0.2 mg/dL after 12 months. In those who started above 6, the drop reached 0.8 mg/dL. Even so, these drugs are not approved to treat gout, and they do not replace a uric acid-lowering medication.
When is medication needed?
Not everyone with high uric acid needs medication. According to the American College of Rheumatology guidelines, treatment starts when there are two or more attacks a year, tophi, or joint damage on X-ray. After a first attack, doctors consider treatment mainly when there is advanced chronic kidney disease, a level above 9 mg/dL or kidney stones.
The first-line drug is allopurinol, which blocks the production of uric acid. The guidelines recommend it for people with kidney disease too, starting at a low dose that is raised gradually. Another option is febuxostat, which works in a similar way. However, the FDA added a warning about an increased risk of death from heart disease to its label. For that reason, doctors mostly reserve it for people who cannot take allopurinol.
When treatment begins, patients also receive preventive anti-inflammatory treatment, such as low-dose colchicine, for at least three to six months. Here is why: the drop in uric acid can actually trigger temporary attacks until the crystals dissolve. The target is a level below 6 mg/dL. For patients with severe disease, the European guidelines recommend going even lower, below 5 mg/dL.
The bottom line on gout, uric acid and diet: you can prevent the next attack
Gout is one of the few diseases in which we can almost completely prevent repeat attacks. The way to do it is a combination of the right medication, gradual weight loss, physical activity, enough fluids and a Mediterranean diet. The key message: treating the pain during an attack is not enough. You need to treat the root of the problem, high uric acid, and in doing so protect your joints, your kidneys and your whole metabolic health.
This article provides general information and is not a substitute for personal medical advice.
References
2020 American College of Rheumatology Guideline for the Management of Gout
2016 updated EULAR evidence-based recommendations for the management of gout
Purine-rich foods, dairy and protein intake, and the risk of gout in men
Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study
FDA adds Boxed Warning for increased risk of death with gout medicine Uloric (febuxostat)
The SURMOUNT-1 analysis was conducted with researchers from Eli Lilly, the maker of tirzepatide.
