Uric acid is a double edged sword. It is a waste product of purine and nucelic acid metabolism. It is also an antioxidant. When it is elevated, it is implicated as a causative factor in cardiovascular disease, diabetes type 2 and metabolic syndrome. Chronically elevated levels of uric acid is also a primary factor in gout, in which uric acid crystals precipitate in the tissues. Over 3/4ths of patients with heart disease and elevated triglycerides will present with high levels of uric acid.
High levels of uric acid are one of the key factors associated with cardiovascular disease and metabolic syndrome.
An article I wrote months ago, indicated the evidence that elevated uric acid may be due in large part to excess mycotoxins, which are fungal metabolites. This was first purported 20 years ago by the former head of the World Health Organization, A.V. Constantini, MD who contends that high uric acid is fungal in origin, and not metabolic in origin.
There is also a large body of evidence which reveals that high levels of uric acid can be generated through the consumption of fructose. Fructose is fruit sugar, and it is also present in fructose that is highly refined to create high fructose corn syrup (HFCS).
Nitric oxide (NO) is a vasodilator. NO is synthesized from the amino acid L-arginine. Nitric oxide allows the outer lining (endothelium) of blood vessels to relax their musculature. NO is thus one of the most powerful regulatory molecules of the cardiovascular system. When uric acid reacts with nitric oxide, the production of nitric acid will be depleted.
This does not bode well for patients suffering from gout and metabolic syndrome. A loss of NO can be a direct cause of vasoconstriction and hypertension, typically patterns which emerge among patients with CVD.
Reducing Uric Acid
High levels of uric acid is a symptom and reflects dysregulation. Many clinicians believe that serum uric acid levels greater than 5 mg/dL is considered elevated. Elevated uric acid levels are somewhat of a conundrum. For some individuals, purine-rich foods like organ meats, red meats and sardines can cause an elevation in uric acid. Although this is not the case for all people.
Recent studies certainly indicate the relationship between fructose and elevated uric acid.
What is apparent is that there are no “one size fits all” approaches for reducing uric acid. I would argue that elevated uric acid is the ‘tip of the iceberg’, which may be reflective of a number of de-regulatory processes in the body.
One may hypothesize that cutting out HFCS and excessive fructose is a viable solution. And while this may be necessary for some individuals, what is needed is a more individualized therapy, one that is holistic in nature, and takes into account the entire person and their biochemical needs, rather than attempting to lower a number on a test.