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ventricle and a 26 percent loss in both atria.67,68 Human white blood cells produce an enzyme called myeloperoxidase (MPO) during ischemia and reperfusion injury.69 Elevated MPO is an es- tablished risk factor for cardiovascular mortality following artery grafts.70 MPO often serves as a potent bacteriocidal weapon,71 potentially link- ing it to the infectious theory of heart disease.35,72 Hypochlorite, produced in response to MPO, avidlyoxidizesmanysulfhydryl-dependentpro- teins, leading to platelet activation and causing white blood cells to attach to the walls of blood vessels. It has been proposed that taurine protects from these damaging effects by reacting with and neutralizing hypochlorite to form taurine chlo- ramine,73 a much more reactive compound than taurine. As we have seen, taurine is released from the heart during ischemia and would be readily available in the serum because it is not taken up by the platelets.74 However, taurine chloramine activates complement,75 which in turn promotes an inflammatory response, providing oxidizing agents that could in theory promote the oxidation
of sulfur in taurine chloramine.
Thus, a novel way to view taurine is as
another potential buffer for sulfate renewal in times of acute deficiency. Assuming that sulfate insufficiency is an important factor in heart dis-
ease, one should ask whether taurine chloramine can become a substrate for sulfate synthesis. Taurine chloramine already contains sulfur at an oxidation state of +5, so it only needs to oxidize the sulfur from +5 to +6 to produce sulfate. (A positive oxidation state shows the total number of electrons that have been removed from an element to get to its present state.)
Notwithstanding the claim that taurine is not easily broken down by mammalian cells, 25 percent of the traced sulfur in supplemental taurine turns up in the urine as sulfate.62 One hypothesis is that the gut bacteria metabolize the taurine to sulfate. Moreover, because taurine chloramine is more reactive, perhaps it can be metabolized to yield free sulfate, with microbial infective agents playing a facilitative role. If so, this would justify both cardiac storage of taurine as a back-up source of sulfate during times of severe deficiency as well as the presence of microbes in cardiovascular lesions,35,72 lending further credibility to the infectious theory of heart disease.
Taurine’s protection during ischemia and re- perfusion occurs through an as yet undetermined mechanism.76 There is a severe loss of taurine from the heart during ischemia that can lead to heart failure if the taurine is not replenished. A
One hypothesis
is that the gut bacteria metabolize the taurine to sulfate.
SOURCE OF SULFUR Garlic
Alpha-lipoic acid
Chondroitin sulfate
Glucosamine sulfate
TABLE 1: SULFUR AND CARDIOPROTECTION COMMENTS
Offers an excellent source of sulfane sulfur and has been consistently recognized as a healthy supplement.4,89
Confers cardioprotective benefits90 that may derive from its ability to increase sulfane sulfur levels and rhodanese activity in the heart, liver and kidney.91
Reduces levels of inflammatory markers such as interleukin 1-beta.92 Reduces levels of inflammatory markers such as interleukin 1-beta.92
AP39 (synthetic chemical)Shown in rat studies to supply hydrogen sulfide gas to mitochondria and protect them from
Vanadyl sulfate N-acetylcysteine
Magnesium sulfate
DNA oxidation damage,5 potentially representing a promising future prevention and treatment option in humans.
Provides cardioprotective benefits93 that may be due to its ability to supply sulfate, as its sulfate anion dissociates rapidly in solution.
Has shown significant benefit during acute myocardial infarction through multiple effects, in- cluding reduction in oxidative stress, more rapid reperfusion, better left ventricular preservation and function, and reduced infarct size.94
Achieved a 24 percent relative reduction in all-cause mortality and a 25 percent relative reduc- tion in left ventricular failure in the treatment group during a placebo-controlled experiment on magnesium sulfate supplementation during acute myocardial infarction,95 with the possibility that the sulfate rather than the magnesium was the critical beneficial factor.
SUMMER 2017
Wise Traditions
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