Page 20 - Summer 2017 Journal

I hypothesize 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.
laries is to maintain a thick layer of gelled water coating the inner surface. This structuring effect on water is due to the “kosmotropic” properties of sulfate,25 which provides a near-frictionless surface contact with the red blood cells10 that is further enhanced by the negative charge in both the glycocalyx and the red blood cell membrane.
As the red blood cells drop off cholesterol sulfate in the capillaries, they also lose their negative charge, which means that the venous end has a lower pH than the arterial end. An increase in carbon dioxide content on the venous side enhances this effect, as is immediately following cardiac arrest, when carbon dioxide accumulates in the veins and the voltage difference between arteries and veins sharply increases.26 Thus, an electrical gradient also propels the negatively charged red blood cells through the capillaries. Capillary resistance is the dominant factor in high blood pressure, which we can therefore expect to correlate with an impoverishment in cholesterol sulfate in red blood cell membranes and heparan sulfate in the capillary walls. Both increased friction at the walls and decreased force from the electromagnetic field impede movement of red blood cells through the capillaries.
The glycocalyx is constantly shed and rebuilt in a dynamic process that is promoted by inflam- matory agents.27 Complement and endotoxin (from bacteria) both induce glycocalyx shedding through a G-protein coupled receptor response. Such matrix remodeling is especially active during ischemia and reperfusion (the two criti- cal stages of a heart attack). Membrane-bound
matrix metalloproteinases (MMPs) can detach fragments of the glycocalyx from the artery wall, which can then be redistributed to other parts of the vasculature (such as the capillaries) as reinforcements. Thus, it is highly conceivable that the glycocalyx in atherosclerotic regions is a source of raw materials needed to maintain the health of the heparan sulfate proteoglycans (HSPGs) in the capillary glycocalyx.
As an alternative means of supplying cholesterol sulfate to the heart, an atheroma is uniquely suited to cholesterol sulfate’s manu- facture by platelets. The sulfate is supplied by breaking down homocysteine thiolactone, a precursor that is ready to become sulfate under the right circumstances; the lipid stores in the macrophages supply the cholesterol; the red blood cells supply adenosine triphosphate (ATP) to energize the reaction; and the inflam- matory response provides superoxide needed to oxidize the sulfur atom in homocysteine.10 HDL-cholesterol plays a critical role, because platelets will take up cholesterol only from AI-HDL (the “good” variant of HDL), and they will increase their production of cholesterol sulfate three-hundred-fold in the presence of 3’-phosphoadenosine-5’-phosphosulfate (PAPS), a source of transferrable sulfate produced by sulfation of ATP.28 (Note that when ATP is in short supply, this will affect the ability to uti- lize any sulfate that is synthesized, resulting in blood with overly high viscosity due to sulfate's property of gelling the blood.)
The lipoprotein apolipoprotein E (ApoE)
FIGURE 3: Red blood cells are propelled through the capillary due to the electromagnetic force created by the voltage difference between the artery and the vein. Negative charge in the glycocalyx (due to sulfates) repels red blood cells (also negatively charged) and prevents them from sticking to the wall. Gelled water lining the capillary forms a slick frictionless surface to support low resistance.
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Wise Traditions SUMMER 2017