Page 17 - Summer 2017 Journal

To answer these questions, I propose a uni- fying theory for the etiology of cardiovascular disease. The theory involves cholesterol sulfate, a molecule that circulates in the bloodstream and performs a variety of important regulatory functions. I believe that the cause of heart disease is an inadequate supply of cholesterol sulfate to the heart. When there are pathologies that impair the normal conditions for making cholesterol sulfate, an atheroma develops as an alternative means of supplying the heart with vital cho- lesterol sulfate. When neither the normal nor back-up mechanisms are able to make adequate cholesterol sulfate, the outcome is heart failure, a much worse prognosis than atherosclerosis.
A number of diverse observations involving various forms of sulfur support the hypothesis that impaired sulfur supply to the vasculature is the key factor in cardiovascular disease. For example, early studies on primates showed that a high-fat, high-cholesterol diet fed to monkeys (not a normal diet for them!) could induce athero- sclerosis, but that simultaneous supplementation with sulfur-containing nutrients was protective.1 Similarly, experiments on rats showed that
a diet supplemented with excess cholesterol, cholic acid (a bile acid) and vitamin D2 could induce aortic lesions expressing calcification and plaque formation, but it was possible to prevent such lesions completely through simultaneous supplementation with chondroitin sulfate (a modified sugar molecule containing oxidized sulfur).2
As another example, children with disorders in the metabolism of cysteine (a sulfur-contain- ing amino acid) develop atherosclerosis-like arterial damage at an early age.3 Interestingly, the consumption of garlic—a rich source of sulfane sulfur—is inversely correlated with the progression of cardiovascular disease.4 Finally and remarkably, synthetic hydrogen sulfide do- nors (molecules that release therapeutic hydrogen sulfide) can protect mitochondria in endothelial cells (the thin layer of cells that line the interior of blood vessels) from oxidative damage.5
CHOLESTEROL SULFATE SYNTHESIS Normally, keratinocytes (the predominant cells found in the epidermis), red blood cells (RBCs) and platelets produce cholesterol sulfate
When there are pathologies that impair the normal conditions
for making cholesterol sulfate, an atheroma develops as
an alternative means of supplying the heart with vital cholesterol sulfate.
ARTICLE SUMMARY
• Impaired sulfate supply to the heart is a key factor in cardiovascular disease.
• Red blood cells, platelets and cells in the skin synthesize cholesterol sulfate catalyzed by sunlight.
• Cholesterol sulfate, unlike cholesterol, is water soluble, so it can travel freely in the blood rather than packaged
up inside an LDL particle.
• Glyphosate, the active ingredient in the pervasive herbicide Roundup, disrupts sulfate synthesis in the skin and disrupts bile flow from the liver, leading to a systemic deficiency in cholesterol sulfate.
• Sulfate provides negative charge in the blood vessel wall and for the red blood cells and platelets, promoting flow.
• Sulfate also maintains the structured water that lines the vessel walls and presents a slick, frictionless surface to the
red blood cells.
• The atheroma actively recruits cholesterol to be ready to produce cholesterol sulfate when sulfate becomes available.
• Inflammation, while damaging to surrounding tissues, performs a useful service by promoting an oxidative environment necessary to make sulfate.
• A heart attack is a well-choreographed sequence of events aimed to restore sulfate supplies by oxidizing taurine, which is stored in large amounts in the heart.
• Statin drugs, by reducing the supply of cholesterol sulfate to the heart, will lead to heart failure down the road, a worse prognosis than cardiovascular disease.
SUMMER 2017
Wise Traditions
17