Why Uric Acid Deserves More Attention

Uric acid is best known for causing gout, a painful inflammation of the joints that often starts in the big toe when crystals form in the joints. But gout is only the final chapter. Long before that, uric acid can quietly disrupt your metabolism and increase your risk for serious health problems.

Your body produces uric acid when it breaks down purines, which are natural compounds found in many foods and also released during normal cell turnover. Under healthy conditions, your kidneys filter uric acid and excrete it through your urine. But if you're producing too much or clearing too little, uric acid builds up in your blood.

Unlike most mammals, humans lack an enzyme called uricase, which helps break uric acid down into a more easily excreted form. This evolutionary quirk may have once helped our ancestors store fat and survive periods of famine. But today, it just makes us more vulnerable to chronic diseases.

Elevated uric acid levels can affect several systems at once. It raises blood pressure by reducing nitric oxide, which your blood vessels need to relax. It promotes insulin resistance by increasing oxidative stress. It drives fat into the liver and makes it harder to burn. It weakens your mitochondria, so you burn less energy and tire more easily.

The good news is that you can lower uric acid and in many cases, you'll see improvements quickly once you make the right changes. Let's walk through six strategies that help you do that.

Strategy 1: Cut Fructose to Lower Uric Acid at the Source

Fructose is a simple sugar found naturally in fruit and added to a lot of processed foods in the form of high-fructose corn syrup. What makes it uniquely problematic is how your body processes it. Unlike glucose, which is used by nearly every cell and tightly regulated by insulin, fructose bypasses that regulation is handled almost entirely by your liver.

When you consume a lot of fructose, your liver cells rapidly burn through ATP (adenosine triphosphate), the energy currency of your cells. That energy drop triggers a rise in AMP (adenosine monophosphate), which your body quickly converts into uric acid using an enzyme called xanthine oxidase. So fructose directly stimulates uric acid production.

It also promotes fat production in your liver, a process called de novo lipogenesis. This contributes to non-alcoholic fatty liver disease (NAFLD) and worsens insulin resistance.

Common sources of excess fructose:

• Soda and soft drinks
• Sweetened teas and energy drinks
• Fruit juice (especially if sweetened)
• Table sugar (which is half fructose, half glucose)
• High-fructose corn syrup (common in processed foods, sauces, cereals)

When it comes to fruit, context matters. Whole fruits are generally fine in moderation because the fiber and antioxidants slow sugar absorption. But juicing or drying strips away those natural brakes, concentrating fructose and delivering it to your liver rapidly. In that form, it becomes metabolically similar to drinking soda.

Strategy 2: Cut Back on Animal-Based Purines to Reduce Uric Acid Load

While fructose ramps up uric acid production by disrupting liver energy metabolism, purine-rich foods drive it up by providing the raw materials your body converts into uric acid.

Purines are metabolized into uric acid through an enzyme called xanthine oxidase, the same enzyme involved in fructose metabolism. Unlike fructose, which boosts uric acid indirectly by depleting cellular energy stores, purines directly increase uric acid through biochemical breakdown. Consuming more purines means your liver must work harder to convert them. This becomes especially problematic if your body already struggles to eliminate uric acid due to insulin resistance, kidney dysfunction, or systemic inflammation, causing accelerated buildup.

Notably, animal-based purines typically raise uric acid more significantly than plant-based purines. This distinction may stem from their quicker absorption rates and the presence of fats and pro-inflammatory substances in animal products, which can amplify metabolic stress. Plant-based purines, conversely, tend to be buffered by fiber, antioxidants, and slower digestion, thus moderating their impact on uric acid levels.

High-purine foods to limit or avoid include:

• Organ meats (e.g., liver, kidney, sweetbreads)
• Certain seafood (e.g., sardines, anchovies, mussels, herring)
• Meat broths, gravies, consommés
• Red meat, especially when consumed frequently or in large portions

Lower-impact protein options include:

• Legumes (beans, lentils, peas
• Soy-based proteins (tofu, tempeh)
• Vegetables (spinach, mushrooms, asparagus)

Complete avoidance of purines is not possible. However, shifting towards plant-based proteins can reduce your uric acid levels by 10-15% and simultaneously improve insulin sensitivity, benefiting overall metabolic health.

Strategy 3: Stay Well Hydrated to Support Uric Acid Excretion

Water plays a central role in how your body clears uric acid. Your kidneys filter uric acid from your blood and excrete it through your urine. When you are even mildly dehydrated, that filtration slows down. The urine becomes more concentrated, which reduces uric acid clearance and increases the risk of crystal formation in your joints and kidneys.

Staying well hydrated helps in two important ways. It increases the volume and flow of urine, allowing your kidneys to excrete uric acid more efficiently. It also keeps your urine less acidic and less saturated, making it harder for uric acid crystals to form.

Hydration becomes especially important after high-sodium meals. Sodium raises blood osmolarity, which triggers the release of vasopressin, an antidiuretic hormone that tells your kidneys to retain water. This leads to reduced urine output and a higher concentration of uric acid. High sodium can also activate aldose reductase, an enzyme that converts glucose into fructose inside your body. That internal fructose is then metabolized in the liver and adds to your uric acid burden.

Tips for hydration:

• Drink 2 to 3 liters of fluid per day, adjusted for body size, activity, and climate
• Use electrolyte-balanced fluids during intense exercise or heavy sweating, but avoid sugary sports drinks
• Use urine color as a guide; pale yellow is ideal, dark yellow suggests dehydration
• Have water before and during meals that are high in sodium or protein

Hydration alone won't fix high uric acid, but it prevents the conditions that allow crystals to form and supports nearly every other uric acid-lowering strategy by enhancing kidney function.

Strategy 4: Control Blood Sugar to Prevent Internal Fructose Production

Insulin resistance also reduces the kidneys' ability to excrete uric acid. Instead of eliminating it, the kidneys reabsorb more, increasing both production and retention and compounding the metabolic burden.

Common dietary culprits include:

• White bread, white rice, and instant oats
• Potatoes, chips, crackers, and processed snack foods
• Sugary breakfast cereals and baked goods
• Ultra-processed foods with added starches and sugars

Swap these for low-glycemic, whole-food alternatives. This helps steady your blood sugar, reduce insulin spikes, and cut back internal fructose. Over time, it improves metabolism, supports fat loss, and lowers uric acid naturally.

Strategy 5: Lose Body Fat and Build Muscle to Normalize Uric Acid

Excess body fat contributes to elevated uric acid levels by increasing its production and reducing its excretion. This occurs mainly due to the influence of fat tissue on insulin resistance. Fortunately, even modest weight loss can significantly reduce uric acid. As you lose weight, insulin sensitivity improves and inflammation decreases, helping your kidneys eliminate uric acid more efficiently.

To achieve these benefits, a gradual weight loss of 1-2 pounds per week is recommended, primarily through a combination of calorie control and regular physical activity. That said, rapid weight loss, crash dieting, or very-low-carbohydrate ketogenic diets should be avoided, as they can temporarily raise uric acid levels due to increased ketone production and purine turnover from muscle breakdown.

Strategy 6: Use Medications When Lifestyle Alone Isn't Enough

Sometimes diet and exercise aren't enough. If uric acid stays elevated, or if you've had gout, kidney stones, or signs of metabolic dysfunction, medication may be necessary. The goal is to either reduce uric acid production or increase its excretion, depending on the cause.

The most common medications are xanthine oxidase inhibitors (XOIs). These block the enzyme that turns purines into uric acid.

• Allopurinol is the most widely used. Treatment usually starts at 100 mg per day and is gradually increased until uric acid drops below 6 mg/dL, or 5 mg/dL in more severe cases. It's effective, inexpensive, and generally well tolerated. But it carries a rare risk of allopurinol hypersensitivity syndrome, a potentially fatal reaction. This risk is higher in people with the HLA-B*58:01 gene variant, which is more common in individuals of Asian and African ancestry. Genetic testing is recommended in high-risk groups.
• Febuxostat is another option. It may lower uric acid more effectively in some people. Unlike allopurinol, which is cleared by the kidneys, febuxostat is metabolized by the liver, so it may be safer for people with kidney problems. However, it carries a black box warning due to a possible increase in cardiovascular mortality seen in some trials. It's usually reserved for those who can't tolerate or don't respond to allopurinol.

If the main issue is underexcretion, medications that increase uric acid clearance can help. These are called uricosurics. They work by blocking uric acid reabsorption in the kidneys.

• Probenecid is the primary uricosuric available in the United States. It increases uric acid excretion but is less effective in people with reduced kidney function. It can also raise the risk of kidney stones if fluid intake is low. It can be combined with an xanthine oxidase inhibitor when monotherapy isn't enough.

Additionally, several other medications used for other conditions also have uric acid-lowering effects and may be useful in patients with overlapping cardiometabolic issues. For example, Losartan, a blood pressure drug, has mild uricosuric effects, and fenofibrate, used to lower triglycerides, can modestly reduce uric acid levels.

Medication should be considered when uric acid remains above 6.8 mg/dL, the point where crystals start to form. It's also worth considering if levels are over 6.0 mg/dL and you have insulin resistance, fatty liver, high blood pressure, or declining kidney function.