“Chelation therapy is extremely benefitial for all forms of artherosclerotic cardiovascular disease including angina pectoris and coronary artery disease, intermittent claudication and gangrene in artherosclerotic cardiovascular disease of the legs and feet, and strokes and transient ischemic attacks in atherosclerotic cardiovascular disease of the neck and brain arteries.”
– Dr. Schahter
Earlier versions of this paper were published elsewhere over the years, and have periodically been updated as newer information comes to light. A thorough search of the literature in 2012 reveals nothing to contradict earlier versions. Newer information and updated references have been added.
Cranton EM, Frackelton JP: Free radical pathology in age-associated diseases: Treatment with EDTA chelation, nutrition and antioxidants.
– Journal of Holistic Medicine 1984;6(1):6-37. [Copyright © 1984 Elmer M. Cranton, updated 2012]
ABSTRACT: The widely accepted Free-Radical Theory of Aging has given us a coherent and unifying scientific explanation for the many diverse benefits resulting from disodium EDTA chelation therapy. The Free Radical Theory will be discussed foremost in this paper. The emerging Cell-Senescence Model of Aging, however, combined with concepts of apoptosis (programmed cell death), adding to the free radical explanation, and gives us a broader scientific rationale for EDTA chelation. A recent discovery shows compromised and ischemic cells take up toxic levels of otherwise essential and nutritional metallic elements. Reports that infective microorganisms are shielded against bodily defenses by biofilms, bound in place by metallic cations, provide another mechanism of action. Any proposed mechanism must explain why full benefit takes several months to occur and why improvement continues long after therapy is completed. Benefits can be explained, at least in part, by rebalancing of metallic cations between cells and organs, reactivating metalloenzymes dependent on ions for function, and by removal of metals reaching toxic intracellular levels, or that act as catalysts of free radical proliferation.