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A novel way to view taurine is as another potential buffer for sulfate renewal in times of acute deficiency.
synthesis of cholesterol sulfate by an atheroma counterproductive while leading to system-wide deficiencies in cholesterol and sulfate.
Down syndrome (trisomy 21) provides another interesting example. Down syndrome is associated with a low risk of atherosclero- sis44,45 combined with premature susceptibility to heart failure46 and Alzheimer’s disease.47 A key enzyme present on chromosome 21 is Cu/Zn superoxide dismutase (SOD), which is 50 percent overexpressed in association with Down syn- drome.48 SOD dismutates superoxide to hydrogen peroxide, thus reducing the bioavailability of superoxide for the oxidation of reduced sulfur sources (such as homocysteine thiolactone and cysteinylglycine derived from glutathione)31 to form sulfate. Down syndrome patients are sus- ceptible to Alzheimer’s at least twenty to thirty years earlier than one would normally expect, and dementia is clinically detected in association with Down syndrome at least three times more frequently than in individuals without trisomy 21.49 It is probable that sulfate deficiency plays a significant role in the Alzheimer’s brain, as evidenced by the severe deficiency in sulfatide, the only sulfonated lipid, observed in association with Alzheimer’s disease.50
Statin drugs likely represent another path- way to heart failure. Many have argued that statin drugs produce pleiotropic effects (so-called beneficial effects that are not the drugs’ main or intended action) through an anti-inflammatory effect,51-53 and, further, that other treatments aimed at reducing inflammatory signaling might be effective treatments.54 I predict that both statin therapy and these other treatments instead will lead to heart failure. Statins disrupt G-protein coupled receptor signaling via their suppression of the synthesis of geranylgeranyl pyrophos- phate, leading to defective protein prenylation (lipid modification),55 which explains their in- duction of arterial calcification.56 It is plausible
that statin drugs promote heart failure through impairment of cholesterol sulfate synthesis in the atheroma, both by reducing the bioavailability of LDL to the atheroma and by interfering with the inflammatory response.
Not surprisingly, low cholesterol is consis- tently associated with poor survival statistics in heart failure.57-59 Total cholesterol levels under two hundred milligrams per deciliter increase the risk of dying from heart failure by up to three- fold.57,58 One group of researchers provocatively asks: “Could elevated total cholesterol, which is so firmly established to be deleterious for the development of coronary heart disease and coronary heart disease mortality, actually turn out to be good for patients with chronic [heart failure]?”59
THE ROLE OF TAURINE
Taurine plays a critical though as yet poorly
understood role in cardiovascular disease. Tau- rine is the only sulfonated amino acid. The highest concentrations of taurine are found in the heart, where taurine represents 50 percent of the free amino acid pool,60 with large con- centrations also stored in the brain and liver. Although some bacteria can utilize taurine as a fuel source,61 it has long been maintained that mammalian cells cannot metabolize taurine.62 However, preoperative infusion of taurine de- creases reperfusion injury following coronary bypass surgery,63 and in rat studies, taurine supplementation has improved heart function following a heart attack.64
Blood platelets also retain taurine. Studies on dogs, cats and humans have demonstrated a direct linear relationship between plasma taurine levels and platelet taurine levels.65,66 Platelets from taurine-deficient cats and humans are more sensitive to clotting stimuli.66 Studies in dogs have shown that ischemia (heart attack) induced a 47 percent loss of taurine in the heart’s left
WHY THE ATHEROMATA ARE CONCENTRATED IN CORONARY ARTERIES
The heart is arguably the most important organ in the body, and it needs a constant supply of cholesterol and sulfate in order to stay healthy and maintain its blood supply. Cholesterol is actively recruited into the arteries rather than the veins, because it can then be released as cholesterol sulfate once sulfate becomes available, which will then immediately enter the coronary capillaries to supply this critical nutrient to the heart's vascular supply.
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Wise Traditions
SUMMER 2017