| Main Menu   | Home  |  About Us  |  What's New | FAQSite Search   | Contact Us   |  Books  | Privacy Policy | 

A NEW THEORETICAL MECHANISM OF ACTION OF EDTA CHELATION THERAPY

By 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 bound ionic metals via urinary excretion, and in the process it also 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 elements were measured by neutron activation analysis in separate groups of patients with ischemia, valvular heart disease and idiopathic cardiomyopathy. The nutritional elements, iron, zinc, chromium and cobalt increased from three- to seven-fold in compromised myocardium. Metallic elements become toxic at increased levels of that magnitude.

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

Trace elements increase toxic in heart

Antimony and mercury also elevated to quite high levels. With no know exposure to antimony or mercury, technical is a possibility. If these findings are confirmed, this study is extremely important and should have priority for further investigation.

In another study, copper and zinc accumulations in the brain were implicated in Alzheimer’s syndrome. Alzheimer's researchers at the Massachusetts General Hospital reported that buildup of copper and zinc in the brain causes the same type of protein deposits that are a hallmark of Alzheimer's syndrome.2 Using a strain of mice especially bred to develop a form of Alzheimer's, they found that a metal chelator, clioquinol, neutralized those metals and reduced by half the formation of  neurofibrillatory tangles and  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. This 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, trapping more copper, leading then 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 might accumulate to a similar extent. Iron accumulates to toxic levels and also acts as a catalyst to  speed the production of damaging free oxygen radicals.

We must carefully consider this recent evidence indicating that EDTA benefits patients, at least in part, by removing abnormal accumulations 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 concentration gradient, which draws 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 slow, and resulting plasma concentrations are much lower than achieved by the intravenous route, resulting in a much weaker intracellular to extracellular concentration gradient.

Based on recent findings, it now appears that an important mechanism of action of EDTA chelation therapy is to restore safe and desirable levels of essential nutritional metallic elements in compromised cells. Urinary excretion of metallic toxins and free radical catalysts might be only a secondary benefit.

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.

Copyright © 2012 Elmer M. Cranton, M.D., all rights reserved

Last modified: