EDTA Chelation Therapy: A NEW THEORETICAL MECHANISM OF ACTION

A NEW THEORETICAL MECHANISM OF ACTION
OF EDTA CHELATION THERAPY

By Elmer M. Cranton, M.D.

Copyright © 2005 Elmer M. Cranton, M.D.

We still do not know for certain how EDTA chelation therapy benefits atherosclerosis and other age-related diseases. We only know that it binds to metallic ions in the body. EDTA rapidly removes ionic metals via urinary excretion, and in the process it redistributes many metals within in the body. We have many theories attempting to explain how EDTA reverses symptoms, improves cardiovascular function, enhances quality of life, and improves blood flow, but we still do not know the most important mechanism(s) of action.

A recent study by Frustaci and associates in Italy showed that nutritional trace elements accumulate to potentially toxic levels in diseased myocardium.¹ Marked increases in intracellular concentrations of myocardial trace and toxic elements were measured by neutron activation analysis in separate groups of patients with ischemia, valvular disease and idiopathic cardiomyopathy. The nutritional elements, iron, zinc, chromium and cobalt increased from three- to seven-fold in compromised myocardium.

In patients with advanced valvular disease and idiopathic cardiomyopathy, intracellular metals increased to a similar extent as in those with ischemic coronary artery disease.

TABLE I

Mean Myocardial Trace and Toxic Element Concentrations, Measured by Neutron Activation Analysis (ng/gm)
Metallic Element	Normal Healthy Controls	Mild Valvular Disease, No Compromise	Ischemic Myocardium with Coronary Artery Disease		Compromised Myocardium with Valvular Disease		Idiopathic Dilated Cardio-myopathy
Metallic Element	ng/gm	ng/gm	ng/gm	Ratio of Increase*	ng/gm	Ratio of Increase*	Ratio of Increase*
Zn	7,500	9,000	21,000	2.8	16,000	2.1	17
Cr	100	177	720	7.2	630	6.3	23
Co	15	20	89	5.9	100	6.6	5.7
Fe	34,000	39,000	148,000	4.3	130,200	3.8	4.7
Sb	1.1	1.5	6.5	5.9	6.0	5.4	12,000
Hg	6	8	23	3.8	30	5.0	22,000

Adapted from Frustaci A, et al. J Am Coll Cardiol. 1999 May;33(6):1578-83,p1581.
*Ratios are computed relative to levels measured in normal, healthy, control subjects.

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In another study, copper and zinc accumulations in the brain are implicated in Alzheimer’s syndrome. Alzheimer's researchers at the Massachusetts General Hospital have reported that buildup of copper and zinc in the brain causes the type of protein deposits that are a hallmark of Alzheimer's disease.² Using mice bred to develop a form of Alzheimer's, they found that a metal chelator, clioquinol, neutralized those metals and reduced by half the neurofibrillatory tangles and abnormal accumulations of beta-amyloid. Unfortunately, clioquinol is much too toxic for use in humans.

Beta-amyloid protein in the brain was found to trap copper. The bound copper catalyzed the release of hydrogen peroxide, causing further neurological damage. Accumulations of zinc in the brain acted to create a vicious cycle of increasing beta-amyloid and trapping more copper, leading to progressively more cell damage.

Nutritional trace elements have a very narrow margin between physiologic and toxic levels. As shown in Table I above, zinc rises to potentially toxic levels in the diseased heart. Chromium and cobalt accumulate even more. It seems likely that other nutritional elements not yet measured may accumulate to a similar extent. Iron accumulates to toxic levels and also acts as a catalyst to greatly speed the production of damaging free oxygen radicals.

We must now carefully consider this recent evidence indicating that EDTA benefits patients, at least in part, by removing abnormal accumulation of essential nutritional trace elements from diseased organs and arterial walls.

EDTA in the body remains extracellular, and can only remove intracellular accumulations of metallic ions by first binding and removing elements outside of cells. That process establishes a strong concentration gradient, which then acts to draw unwanted intracellular metals out through cell walls. Only then can they be chelated. That is one reason why EDTA is administered slowly, over several hours. Diffusion outward is a relatively passive process and occurs much more slowly than the subsequent binding by EDTA. That may also be the reason why no data have been published showing improved blood flow using oral EDTA. Absorption of oral EDTA is minimal and plasma concentrations are far lower, resulting in a much weaker intracellular to extracellular concentration gradient.

Based on recent findings, it now seems possible that an important mechanism of action of EDTA chelation therapy is to restore safe and desirable levels of essential nutritional metallic elements within cells. A spectrum of such metals has been shown to accumulate to toxic levels in both diseased and stressed cells. Urinary excretion of metallic toxins and free radical catalysts might be only a secondary benefit.

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REFERENCES

1. Frustaci A, Magnavita N, Chimenti C, Caldarulo M, Sabbioni E, Pietra R, Cellini C, Possati GF, Maseri A. Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction. J Am Coll Cardiol. 1999 May;33(6):1578-83.

2. Cherny RA, Atwood CS, Xilinas ME, Gray DN, Jones WD, McLean CA, Barnham KJ, Volitakis I, Fraser FW, Kim Y, Huang X, Goldstein LE, Moir RD, Lim JT, Beyreuther K, Zheng H, Tanzi RE, Masters CL, Bush AI. Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice. Neuron. 2001 Jun;30(3):665-76.