Recommended URIC acid's pandemics role

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Notes on Gary Taube's Case Against Sugar, Uric acid section


Uric acid:  Taubes Notes, journal articles summation

An estimated 6% of men and 2% of women have gout (p 238).  The association of gout with meat based upon the conversion of an amino acid to purine lack merit.  For one thing the eating of meat increases the secretion of uric acid, and secondly vegetarians get gout, and switching to a vegetarian diet has at most modest effect upon gout, moreover gout was placed in the late 40s at 7% in India a nation of mostly vegetarians (239).   [Incongruously, this association with meat is still upheld by experts (obvious KOLs) who won’t embrace its cause, fructose].  Gout is associated with CVD, and in 1951 Harvard researches established that men who suffer heart attacks are  4 times more likely to be hyperuricemic (p 140).  In the 1960 gout was linked to insulin resistance.  The evidence for the role of fructose is two-fold:  One is that were a significant amount of sugar is added to the diet gout follows—“historians refer to this as the ‘gout wave’.”  Second is that “fructose increases serum levels of uric acid” (p 241)    Fructose accelerates the breakdown of ATP, which” increases the formation of uric acid…  Alcohol raises uric acid through the same mechanism…. The effect of fructose  on ATP also works to stimulate the synthesis of purines and the metabolism of fructose leads to the production of lactic acid, which reduces the excretion of uric acid by the kidney and thereby raises uric acid concentrations indirectly p 242)    

Nearly all of life science the simple answer is wrong.  Uric acid is considered a powerful antioxidant; however, it also functions chemically in other way beside the formation of crystals that through abrasion cause joint inflammation (gout episodes).  Often considered an antioxidant, biochemical and in vitro data indicate that non-crystalline, soluble uric acid also can react to form radicals, increase lipid oxidation, and induce various pro-oxidant effects in vascular cells. In vitro and in vivo findings suggest that uric acid may contribute to endothelial dysfunction by inducing anti-proliferative effects on endothelium and impairing nitric oxide production. Pro-inflammatory and proliferative effects of soluble uric acid have been described on vascular smooth muscle cells (VSMCs), and in animal models of mild hyperuricemia, hypertension develops in association with intra-renal vascular disease.”Seminars in Nephrology   Volume 25, Issue 1, January 2005, pgs 39-42, “Prolonged hyperuricemia is associated with the development of hypertension, renal arteriolosclerosis, glomerulosclerosis, and tubulointerstitial injury.” Supra 19-24.  We recently reported that uric acid reduces levels of endothelial nitric oxide (NO), a key mediator of insulin action. NO increases blood flow to skeletal muscle and enhances glucose uptake. Animals deficient in endothelial NO develop insulin resistance and other features of the metabolic syndrome. As such, we propose that the epidemic of the metabolic syndrome is due in part to fructose-induced hyperuricemia that reduces endothelial NO levels and induces insulin resistance” AT 2005.  The role of fructose through urea acid is clear in an assortment of ways causal through endothelial dysfunction the conditions associated with the western diet.




Urea serves an important role in the metabolism of nitrogen-containing compounds by animals and is the main nitrogen-containing substance in the urine of mammals. It is a colorless, odorless solid, highly soluble in water, and practically non-toxic (LD50 is 15 g/kg for rats). Dissolved in water, it is neither acidic nor alkaline. The body uses it in many processes, most notably nitrogen excretion. The liver forms it by combining two ammonia molecules (NH3) with a carbon dioxide(CO2) molecule in the urea cycle. Urea is widely used in fertilizers as a source of nitrogen and is an important raw material for the chemical industry.

Structural formula of urea                                  Harnsäure Ketoform.svg

      UREA                                 URIC ACID  (a hydrogen is lost from a nitrogen on position 3 or 9)


The blood urea nitrogen (BUN) test is a measure of the amount of nitrogen in the blood that comes from urea. It is used as a marker of renal function, though it is inferior to other markers such as creatinine because blood urea levels are influenced by other factors such as diet and dehydration.[14]


Uric acid is a heterocyclic compound of carbonnitrogenoxygen, and hydrogen with the formulaC5H4N4O3. It forms ions and salts known as urates and acid urates, such as ammonium acid urate. Uric acid is a product of the metabolic breakdown of purine nucleotides, and it is a normal component of urineHigh blood concentrations of uric acid can lead to gout and are associated with other medical conditions including diabetes and the formation of ammonium acid urate kidney stones.

In humans and higher primates, uric acid (actually hydrogen urate ion) is the final oxidation (breakdown) product of purine metabolism and is excreted in urine. In most other mammals, the enzyme uricase further oxidizes uric acid to allantoin.[12] The loss of uricase in higher primates parallels the similar loss of the ability to synthesize ascorbic acid, leading to the suggestion that urate may partially substitute for ascorbate in such species.[13] Both uric acid and ascorbic acid are strong reducing agents (electron donors) and potent antioxidants. In humans, over half the antioxidant capacity of blood plasma comes from hydrogen urate ion.[14]

The normal concentration range of uric acid (or hydrogen urate ion) in human blood is 25 to 80 mg/L for men and 15 to 60 mg/L for women[15] (but see below for slightly different values). An individual can have serum values as high as 96 mg/L and not have gout.[16] In humans, about 70% of daily uric acid disposal occurs via the kidneys, and in 5–25% of humans, impaired renal (kidney) excretion leads to hyperuricemia.[17] Normal excretion of uric acid in the urine is 250 to 750 mg per day (concentration of 250 to 750 mg/L if one litre of urine is produced per day — higher than the solubility of uric acid because it is in the form of dissolved acid urates). 

 Wikipedia 2018

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What I write if reflects what I believe. I am not advising you to violate what your doctor recommends.