You may already know that elevated uric acid levels cause gout. Uric acid has proven emerging roles in various diseases such as gout, renal dysfunction, hypertension, hyperlipidemia, diabetes and obesity. Serum uric acid is more closely related to early-phase mechanisms in the development of type 2 diabetes mellitus than late-phase mechanisms, because uric acid concentration rises prior to diagnosis of diabetes and then declines with diabetes duration. In addition, serum UA, a by-product of oxidation of purines that is filtered by glomeruli in the kidney and reabsorbed by the proximal tubule, may promote insulin resistance by inhibiting endothelial cell function.
Uric acid has antioxidant capacities extracellularly and can be responsible for 2/3 of the total plasma antioxidant capacity, where it chelates metals and scavenges oxygen radicals. However, intracellularly, it has pro-inflammatory and pro-oxidant activity.
It has been shown that uric acid is a circulating marker for oxidative damage in conditions like ischemic liver, atherosclerosis, diabetes, and chronic heart failure.
But did you know uric acid can serve as a marker for fructose toxicity?
Fructose, when over-consumed, is very taxing to your body’s metabolic processes. One of the by-products of fructose metabolism is uric acid, so when you consume too much sugar—particularly concentrated fructose—your uric acid levels may rise. Fructose turns you into a uric acid factory! Elevated uric acid is thought to explain much of the damage fructose causes in your body.
The safest range for uric acid is between 3 and 5 mg/dl, and there appears to be a steady relationship between uric acid levels and blood pressure and cardiovascular risk, even down to the range of 3 to 4 mg/dl. This is a noninvasive and cost-effective method to diagnose and monitor metabolic syndrome and its components.