FROM: AA OXIDOPATHY web article
Our story so far--Stress Proteins that protect other proteins in time of stress are themselves vulnerable to toxins. Check out this timeline. Then be sure to get some "Cholesteril" which is PANTETHINE, a form of B-5 that forms Master Coenzyme A that wipes out the deadly toxin in Candida, ACETALDEHYDE...And it lowers cholesterol! Take Vitamin E for antioxidant protection of "chaperone" Stress Proteins/SP's and to protect the heart and blood vessels. And take Caprylic Acid or Undecylenic Acid or Silver Colloid water to keep Candida levels down. Blessings! Drs. Ali & Ali write:

SPs—protein molecules in composition—are predictably vulnerable to oxidant stress. (The chaperons themselves need chaperoning!) When oxidatively denatured by accelerated oxidative injury, SPs are mutated and assume the destructive capacity of foreign antigens, thus triggering autoimmune injury.421

Four other aspects of chronic fungemia are pertinent to our discussion of the role of fungemia to the pathogenesis of IHD:

1. Close molecular homology between human SPs (molecular weight 70,000) and SPs of fungal and bacterial origin.406,422 Specifically, SPs of Candida albicans show an over 50% homology with human SPs.423 This, of course, creates a serious potential for clinical autoimmune injury caused by chronic Candida overload. Indeed, the ability of the T cells of patients infected with Histoplasma and malaria organisms to respond to peptides of human SPs has been documented.424

2. Ability of some Candida-derived SPs to block the production of plasminogen activator, and so diminish the fibrinolytic capacity of the plasma. One action of such Sps would be to oppose the unclotting side of the CUE equation and promote atherogenesis.425

3. Ability of some fungal SPs to block certain steroid synthetic pathways.426-428 Through such actions, fungal SPs may be expected to play a broad array of adverse roles in homeostasis of cellular membrane receptors and plasma components, damaging the ecology of circulating blood and triggering autoimmune responses.

4. There are sporadic reports of physicians treating IHD with griseofulvin and other antifungal agents.429 Higher blood levels of folic acid are associated with a lower incidence of IHD.430 It seems probable that at least some of the cardioprotective effects of griseofulvin and folic acid may be attributed to their antifungal properties. More importantly, many of the commonly used cholesterol-lowering drugs belong to the class of statin drugs with well-established, albeit very limited, cardioprotective actions.431-436 It seems likely that some, if not most, of the rather limited benefits of the statin group of lipid-lowering drugs are due to their ability to reduce the total mycotoxin burden and prevent or ameliorate oxidative coagulopathy and AA oxidopathy.

In summary, we hold that the high frequency and extent of fungemia in patients with active IHD and those with risk factors and the observed ability of fungal buds and mycelia to cause congealing of plasma (and so setting in motion oxidative coagulopathy) are strong reasons for attributing a pathogenetic role to fungal (and bacterial) toxins in atherogenesis. We return to this subject in Part II of this communication when we discuss inflammatory, infectious, and autoimmune theories of IHD.