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plays a significant role in inducing the export of cholesterol from the macrophages into AI-HDL, but it also induces enrichment of sulfate in the HSPGs.29 This implies that it escorts cholesterol sulfate rather than cholesterol in its unsulfated form out of the cell. This idea is also supported by the fact that cholesterol sulfate, unlike cho- lesterol, is water-soluble, and therefore readily crosses the cytoplasmic gap between the endo- thelial reticulum and the plasma membrane. Both homocysteine30 and gamma-glutamyltransferase (GGT)31,32 are risk factors for heart disease, and both can be explained because they provide substrate for sulfate synthesis when the normal sun-catalyzed sulfate synthesis mechanisms are not working. GGT breaks glutathione down into cysteinylglycine and glutamate, and cysteine from cysteinylglycine can be oxidized to form sulfate.33
Atheromata (plural of atheroma) harbor various pathogenic microbial species, the most significant of which is probably Chlamydia pneumoniae.34,35 The strong association between chronic C. pneumoniae infection and athero- sclerosis has prompted some researchers to identify it as the pathogen implied in a chronic infection theory of heart disease. While many proponents of this hypothesis enthusiastically have embraced the concept of antibiotic treat- ment specific to C. pneumoniae, clinical trials have been disappointing.36
C. pneumoniae are dormant except when internalized into host cells. Within these cells, they produce a unique form of heparan sulfate, using a set of enzymes that are not found in any other known bacterial species.37 I hypoth-
esize that C. pneumoniae play a special role in enhancing the supply of heparan sulfate to an atheroma, and they may well be able to do so in the absence of functional CYP enzymes.
MULTIPLE PATHWAYS TO HEART FAILURE
Deaths from heart attack have steadily decreased in the industrialized world over the past few decades,38,39 but we are simultaneously experiencing an increasing health care burden in an emerging epidemic of heart failure.40 In fact, heart failure is the single most frequent cause of hospitalization for those over sixty-five years old, affecting five million Americans as of 2010.41 I maintain that heart failure is a direct sequela to insufficient supply of cholesterol and sulfate to the heart. Since an atheroma plays a significant role in supplying these nutrients, it can be anticipated that factors that interfere with the healthy function of the atheroma will lead, over time, to heart failure.
Other pathways to heart failure furnish addi- tional observations. For example, Chagas disease is an infectious disease endemic to regions of South America caused by the Tryptanosoma cruzi pathogen.42,43 Patients who recover are susceptible to premature death by heart failure many decades later. These individuals suffer from frequent small heart attacks but are remark- ably free of atherosclerosis.43 The explanation for this unique profile follows logically from the fact that T. cruzi produces an antigenic molecule that closely mimics cholesterol sulfate.42 As a result, Chaga disease patients develop antibod- ies to cholesterol sulfate. This would render the
Total cholesterol levels under two hundred milligrams per deciliter increase
risk of dying from heart failure by up to three-fold.
PATHOLOGY OR THERAPY?
SUPEROXIDE/INFLAMMATION: Inflammation is necessary to trigger the cascade response that ultimately restores sulfate supplies to the vasculature through oxidation of sulfur-containing molecules like cysteine, homocysteine, hydrogen sulfide gas and taurine.
ATHEROMA: The atheromata in the artery wall supplying the heart actively recruit cholesterol and fats so that they can be ready to produce cholesterol sulfate once sulfate becomes available, and replenish the heart's supply of this critical nutrient.
CLOSTRIDIA PNEUMONIAE: This microbe infects the artery wall where it can perform an important service, providing heparan sulfate to the heart.
HEART ATTACK: The complex cascade that takes place during a heart attack appears to be aimed at producing sulfate by oxidizing taurine molecules that are stored in the highest concentration in the heart and released during a heart attack.
SUMMER 2017
Wise Traditions
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