When you think of heart disease, your mind probably goes to cholesterol, blood pressure, and blood sugar. But there’s another key marker, that’s often ignored—and it could be silently contributing to inflammation, high blood pressure, insulin resistance, and cardiovascular risk.

That marker? Uric acid.

What is uric acid?

Uric acid is a byproduct of purine metabolism—purines are found in our cells and in certain foods like red meat, seafood, and alcohol (especially beer). Normally, uric acid is filtered by the kidneys and excreted in urine. But when levels climb too high, that’s when the trouble starts.
Although most people associate uric acid with gout, growing evidence links it to cardiometabolic dysfunction even in people without joint symptoms (1), (2).

Why uric acid matters for your heart and your metabolism

Uric acid is now considered a metabolic signal—a biomarker that reflects how well your body is managing energy, blood sugar, and inflammation.

Here’s why it matters:

• High uric acid = metabolic red flag. Elevated levels are associated with insulin resistance, increased triglycerides, and visceral adiposity—even when glucose appears normal (3).
• It reflects mitochondrial strain. Uric acid increases when mitochondria are overwhelmed by excess sugar, especially fructose, which is metabolized in the liver and rapidly generates uric acid (4).
• It’s linked to systemic inflammation independent of gout.  Uric acid activates one of the body’s internal ‘alarm systems’ (the NLRP3 inflammasome*) triggering low-grade, widespread inflammation (2), and contributing to the development atherosclerosis (5).
  * If you’ve worked with me, you may have heard this analogy before: NLRP3 is like a built-in smoke detector—once it’s triggered, it sets off an immune response that can quietly fuel chronic disease over time.

Bottom line: healthy uric acid levels are a marker of metabolic health and efficiency.

Elevated uric acid is associated with:

• Increased blood pressure – It suppresses nitric oxide, reducing vascular flexibility and increasing systemic resistance (1).

• Endothelial dysfunction*– High levels behave as a pro-oxidant inside blood vessels, damaging the delicate inner lining and impairing how they function (6).
  *As I often explain to clients, think of your blood vessels like plumbing—when the lining gets damaged, it’s like rust building up in your pipes. They lose their flexibility and protective coating, making it easier for trouble (like plaque or clots) to take hold and harder for your heart to stay healthy.

• Progression of atherosclerosis – Uric acid contributes to foam cell formation and plaque instability (7).

• Insulin resistance – Multiple studies show a bidirectional relationship between uric acid and impaired glucose metabolism (8).  Click to read my previous post about insulin resistance.

• Kidney strain – Elevated levels can damage renal microvasculature and impair uric acid clearance, creating a vicious cycle (2). 

What’s an optimal range of uric acid?

Most labs consider up to 7.0 mg/dL as “normal.” But from a functional medicine, and more proactive heart health perspective, lower levels are considered safer for long-term cardiovascular and metabolic health:

• < 5.5 mg/dL for women
• < 6.0 mg/dL for men
• < 5.0 mg/dL for anyone with insulin resistance, prediabetes, or high blood pressure (1), (3).

Why it may not have been tested for you to-date…

Uric acid isn’t included in standard lipid panels or annual physicals unless you’ve had gout. But from a functional perspective, it’s a low-cost, high-value marker—one that can highlight metabolic dysfunction before it shows up in traditional labs.

Five practical steps you can take today:

1. Request serum uric acid on your next round of labs
2. Eliminate high-fructose corn syrup, especially in processed foods and soft drinks
3. Limit alcohol, especially beer
4. Focus on fiber-rich, polyphenol-packed foods (e.g., berries, greens, legumes)
5. Prioritize sleep, daily movement, and blood sugar balance to support healthy metabolism

Uric acid might be a small molecule, but it speaks volumes. If you're serious about being proactive about your heart health—minimizing your need for medication, and maximizing your vitality—it warrants attention!

Want help interpreting your labs and creating a plan that actually moves the needle?  Book one of my complimentary 30-minute proactive heart health strategy sessions and let’s talk. 

References:

1. Feig DI, Kang D-H, Johnson RJ. (2008). Uric acid and cardiovascular risk. N Engl J Med, 359:1811–1821.
2. Johnson RJ, Nakagawa T, Jalal D, Sánchez-Lozada LG, Kang D-H, Ritz E. (2013). Uric acid and chronic kidney disease: which is chasing which? Nephrol Dial Transplant, 28(9):2221–2228.
3. Kanbay M et al. (2016). Uric acid in metabolic syndrome: From an innocent bystander to a central player. Eur J Intern Med, 29:3–8.
4. Lanaspa MA et al. (2012). Uric acid induces hepatic steatosis by generation of mitochondrial oxidative stress: potential role in fructose-dependent and -independent fatty liver. J Biol Chem, 287(48):40732–44.
5.  Yu, W., Cheng, J-D. (2020).  Uric Acid and Cardiovascular Disease: An Update From Molecular Mechanism to Clinical Perspective.  Frontiers in Pharmacology, 11, https://doi.org/10.3389/fphar.2020.582680
6. Sautin YY, Johnson RJ. (2008). Uric acid: the oxidant–antioxidant paradox. Nucleosides Nucleotides Nucleic Acids, 27(6–7):608–619.
7. Baldwin W et al. (2021). Hyperuricemia as a mediator of endothelial dysfunction and atherosclerosis: Pathophysiological mechanisms and clinical implications. Med Hypotheses, 146:110429.
8. Kodama S et al. (2009). Association between serum uric acid and development of type 2 diabetes. Diabetes Care, 32(9):1737–1742.