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Why Uric Acid is an important marker for your clients’ health

There are a number of myths and misconceptions about Uric Acid, and the important role it plays in your clients’ health picture. From how Uric Acid is produced to its relationship with sugar and the conditions associated with this marker, this blog post will support you in understanding why Uric Acid is an important element of your clients’ health.

“What does Uric Acid tell me about my clients’ health?”

There are a few things we would like you to keep in mind when you see UA levels above or below the optimal range on your FDX report.

Increased UA levels can be associated with the following [15], [5], [6], [7], [8]:


Rheumatoid arthritis

Kidney stones

Intestinal hyperpermeability (IP)

Cu toxicity (*check these markers: Cu serum/RBC, ceruloplasmin)

Iron overload, hemochromatosis (*check serum Fe, Ferritin levels)

Low estrogen (*estrogen plays a role in metabolizing UA)

*Keep in mind when working with female clients [6]:

Postmenopausal women: higher levels of UA are linked with lower E2 levels.

Premenopausal women: each mg/dl increase in UA is associated with a 139% elevation in the odds of anovulation.

Decreased UA levels can be associated with the following [15]:

Insufficient Molybdenum levels (*urine/hair analysis is suggested)

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A key myth about Uric Acid that needs busting

Before we dive into the resaerch behind Uric Acid and the role it plays in the body, there’s a key misconception that needs addressing. It is common to think that Uric Acid (UA) is mainly produced from the exogenous purine pool, which is supplied by the intake of animal proteins. Hence, when doctors see elevated serum UA, they often recommend a low purine diet, which essentially means staying away from meat, organ meats, shellfish, and bone broths. Some may also recommend limiting alcohol intake. But it’s not that simple.

It turns out, you might consume a very tiny amount of animal products, and barely drink any alcoholic beverages, and still have enough circulating purines to raise UA levels in your blood. So, how does that happen?

Firstly, let’s look at the journey of Uric Acid in the body.

How is Uric Acid created?

Uric Acid is a final product of the metabolic breakdown of purine nucleotides (adenine and guanine). [1] Synthesis of UA happens mainly in the liver via de novo and the salvage pathways. In addition, some of it can be produced by other tissues that contain enzyme xanthine oxidase, such as the intestines, the muscles, kidneys, and the vascular endothelium. [12] The purine nucleotides break down, which involves deamination, dephosphorylation, phosphorylation, and oxidation reactions, yields its final product, xanthine. Xanthine gets further oxidized by xanthine oxidase (which requires a trace mineral Molybdenum), to uric acid, which gets metabolized by the kidneys and excreted predominantly in the urine. [1], [13]

Purines, like cholesterol, have exogenous and endogenous sources. In other words, our bodies themselves produce purines from live and dying cells, when degrading their nucleic acids (adenine and guanine) into UA. [2] In fact, roughly two-thirds of the total UA pool is generated endogenously. [13] Purine and pyrimidine nucleotides can be endogenously produced by de novo synthesis via the pentose phosphate pathway. But what is even more interesting, is that the main driver of high UA levels, in both, animals and humans, is fructose. [4]

The relationship between fructose and Uric Acid

There is evidence to suggest a correlation between increased fructose consumption in the form of HFCS, table sugar (fructose + glucose), and sugar-sweetened beverages, over the past century (and recent decades in particular), and the rise of hyperuricemia among large populations. [14] One recent meta-analysis of prospective cohort studies based on large groups of people, confirmed the link between fructose intake and an increased risk of gout development, driven by hyperuricemia. [3] At this point, multiple studies demonstrated a clear correlation between increased serum UA levels and sugar consumption. [14]

As we know, fructose is mainly metabolized in the liver, unlike another monosaccharide glucose. When fructose gets phosphorylated by the liver enzyme ketohexokinase, the intracellular levels of phosphate and ATP drop, which triggers the hypoxanthine-xanthine pathway produce UA. The latter results in increased levels of circulating UA. [2], [3]

Image 1: Uric acid synthesis: salvage pathway and de novo synthesis. 1
Source: https://link.springer.com/article/10.1007/s11892-020-01313-z

Hyperuricemia, inflammation, and chronic diseases

Increased levels of circulatory UA trigger an inflammatory response in “endothelial cells, kidney and vascular muscle fibers, and pancreas islets of Langerhans.” [2] So, UA can impair endothelial and vascular function when its concentration rises. [14] According to Richard Johnson, M.D, the world’s leading expert on fructose, high serum UA can be a major contributing factor to such chronic illnesses as kidney disease, metabolic syndrome, diabetes, and hypertension. [4] In his work, he also mentions that even though conventionally, UA levels below 416 umol/L can be considered “normal” by many physicians, a sufficient amount of evidence suggests that serum UA levels above 327 umol/L should be perceived as a “red flag” when seen in blood test results. Other experts in the field (P. Attia MD, and Dr R Lustig) go even further and suggest that a healthy level of serum UA should not exceed 297.5 umol/L.

It has been shown that chronic hyperuricemia and gout represent potential risk factors for both cardiovascular and neurological diseases. [3], [1] Keep in mind, that the monosodium urate crystals that lead to gout formation, can start forming at serum UA levels level of 404.5 umol/L. The risk of developing hypertension can go up 2-fold with an increase in UA concentrations [3]. The main mechanism behind the UA ability to contribute to both gout and cardiovascular risk development is increased inflammation. [1]

Image 2. Uric acid induced inflammatory response
Source: https://www.sciencedirect.com/science/article/pii/B9780124116023000354

A recent randomised study done over the period of two consecutive years, on 30 overweight adolescent males demonstrated that just by replacing sugar-sweetened beverages with low-fat milk, systolic blood pressure and UA levels can be significantly reduced. [14] That same study mentioned a “strong linear association” between serum UA concentrations and systolic blood pressure in children. Children with METs and NAFLD experienced reduction in diastolic and systolic blood pressure, respectively, when fructose consumption was reduced. [14]

Hyper- and Hypouricemia

As humans, we are predisposed to certain abnormalities in urate metabolism, which can result in either hyper- or hypouricemia. [10] A total body urate pool accounts for approximately 1200mg, and a typical urinary urate excretion ranges between 250 to 750mg per day (~ 70% of the daily UA production). [13] On a daily basis, a healthy male produces approximately 700mg of UA, of which 500mg is excreted into urine, and the rest (200mg) into the intestine, which is then excreted through feces. Any imbalance here results in hyper- or hypouricemia. Hyperuricemia, most of the time (~90% of cases) is a result of UA underexcretion from the kidneys, while renal hypouricemia is typically caused by renal UA overexcretion. [11] So, when it comes to the mechanism behind the urate imbalance, hyperuricemia can be classified into overproduction and underexcretion, while hypouricemia is classified into underproduction and overexcretion of UA. Such abnormalities can be then identified as primary/secondary, genetic/non-genetic. [10] For instance, in some people renal hypouricemia can be caused by loss-of-function mutations in the SLC22A12 gene encoding URAT1, or mutations in SLC2A9 (GLUT9). [11]

There are also such factors as certain drugs, estrogen and androgen imbalance, salicylate levels and even niacin intake that can impact levels of UA in the blood. For instance, salicylates have a “biphasic effect” on serum UA levels, depending on their dosage. In smaller doses, salicylates can raise serum UA, while an increased dosage will lead to a drop in serum UA concentration. [11],[13] Nicotinic acid, that is commonly used in dyslipidemia treatment, tends to increase UA levels in the blood, when administered at therapeutic doses of 1,500mg/day and higher. [13]

A breakdown of the factors that can affect serum UA levels in humans:

Overproduction of UA can be caused by the following [10], [12]:

PRPP synthetase superactivity (error of purine metabolism)

HPRT deficiency (error of purine metabolism)


alcohol ingestion

Cell breakdown/turnover: lymphoproliferative diseases, myeloproliferative disease, polycythemia vera, Paget disease, psoriasis, tumor lysis, hemolysis, rhabdomyolysis, overexercising. [12]


Underexcretion of UA can be caused by the following [10], [13]:

renal insufficiency

excessive use of diuretics (loop diuretics and thiazide-type diuretics)


Underproduction of UA can be caused by the following [10], [11]:

xanthine dehydrogenase/ xanthine oxidase deficiency

purine nucleoside deficiency

certain drugs (allopurinol)

Acute/chronic kidney disease, acidosis (lactic acidosis, ketoacidosis), hypovolemia, medication/toxins (diuretic, niacin, pyrazinamide, ethambutol, cyclosporin, beryllium, salicylates, lead, alcohol), sarcoidosis, hyperparathyroidism, hypothyroidism, Bartter syndrome, Down syndrome. [12]


Overexcretion of urine (and UA with it) can be caused by the following [10],[11]:

familial renal hypouricemia

Fanconi’s syndrome


certain uricosuric drugs (benzbromarone and probenecid)

Drugs that increase serum AU levels. [13]
Drugs that lower serum AU levels. [13]

Hyperuricemia in adults is defined as follows [9]:

serum UA levels >416 umol/l (>7 mg/dl) in men

serum UA levels >357 umol/l (>6 mg/dl) in women


Hypouricemia in adults is defined as follows [11]:

serum UA levels <150 umol/l (<2.5 mg/dl) in men

serum UA levels <124  umol/l (<2.1 mg/dl) in women

Serum UA levels are provided on the metabolic panel of your client’s FDX report. They look like this:

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