Elmer M. Cranton, M.D.
We still do not know the most important mechanisms by which EDTA chelation therapy benefits symptoms of
atherosclerosis and arterial blockage. We do know of many different
actions of EDTA within the body, but we do not know which of those actions are most
beneficial. It is quite possible that an unknown and still unsuspected
action is primarily responsible for the observed improvement.
Human nature is such that people seem to require an explanation for their observations and experiences before believing that they are real. For that reason, as well as an intellectual attempt to understand the science involved, we put forth a number of theories that might explain how EDTA chelation therapy benefits symptoms of arterial disease.
EDTA is not metabolized in the body. It is very rapidly excreted through the kidneys unchanged, other than being binding metallic elements. Various metal ions are loosely bound (chelated) by EDTA using valence electrical charges, some much more ti than others. One principal action we can be sure of is that EDTA reversibly binds to positively charged polyvalent metal ions in solution. We do not know which metals are most important for clinical benefits.
We have proposed a number of elegant theories about neutralizing free radical catalysts, parathormone stimulation, calcium removal, reduction of cross linkages, rearranging metals in the body, removal of unwanted metals, improving blood vessel elasticity, dissolving biofilms, and improving flow of blood via blood cell theology. But we must, in all humility, admit that these are still only theoretical explanations for observed benefits.
EDTA-metal complexes might act as catalysts in the body, following which EDTA could be dissociated and excreted in association with another metal of little significance. Activity of ferric-EDTA complexes with hydrogen peroxide in the Fenton reaction is one such example. The removal of metals from the body as a whole might be of minor importance in producing cardiovascular benefits.
It is also possible that EDTA acts to restore physiologic concentrations of nutritional metals that were recently shown to accumulate in diseased organs. EDTA can act to remove essential trace elements from areas of excess, redistributing them in a physiologic balance throughout the body. Current research points in that direction.
Metallic trace elements are all toxic in excess. Metallic elements have a narrow margin between physiologic and toxic concentrations. A mere three- to four-fold increase could be quite toxic to metabolism. That is certainly what happens with calcium.
When myocardial cells become compromised by coronary artery ischemia or advanced valvular disease, essential nutritional metals accumulate intracellular to toxic levels, compared with myocardial cells from healthy control subjects. As examples, intracellular cobalt and chromium increase 600%; iron increases 400%; and zinc increases 280% (JACC 1999;33(6):1578-1583).
An example is the accumulation of calcium deposits that can be visualized with ultra-fast CT scans (EBCT) of coronary arteries in patients. This raises interesting questions about optimal amounts and timing of trace element supplementation during a course of chelation therapy.
The binding action of EDTA is much greater to many nutritional elements than it is to toxic metals. Increase in urinary excretion of nutritional elements following disodium EDTA infusion, relative to baseline excretion: Manganese 126 times baseline; zinc 62 times baseline; iron 56 times baseline; cobalt 12 times baseline; and calcium 10 times baseline.
Increase in urinary excretion of common toxic metals following EDTA infusion, relative to baseline excretion: Lead 8 times baseline; cadmium 5 times baseline; nickel 5 times baseline; aluminum 3 times baseline; arsenic 1.3 times baseline; and mercury no significant increase.
The above data do not support the theory that heavy metal detoxification is primarily responsible for EDTA chelation benefits. An alternative theory might be that instead of total body detoxification, EDTA acts to reduce excess levels of intracellular trace elements located in specific diseased tissues. Active transport of a spectrum of metals into and out of cells might be normalized by restoration of intracellular energy metabolism and integrity of cell membranes. EDTA remains outside of cells. Slower infusions of EDTA will allow more time for equilibration and for trace metal rebalancing to occur across intact cell membranes.
The concentration of calcium ions outside of cells is 10,000 times greater than within cells. This creates an enormous diffusion gradient across cell membranes, requiring intact membrane integrity and well-functioning metabolic pumps—both of which are compromised by ischemia and inflammation. Disodium EDTA acts on calcium, while calcium EDTA would have no efffect.
William J. Walsh, PhD, senior scientist and treace element specialist at the Pfeiffer Treatment Center has stated that the . . . “greatest mischief is usually caused by nutrients that are stored in excessive amounts, rather than those at depleted levels.” Dr. Walsh described marked imbalances of nutritional trace elements in a range of disorders, including learning disabilities, attention deficit disorder, autism, depression, bipolar disorders, criminal behavior, and schizophrenia. Anecdotal reports of benefit from EDTA chelation therapy in such conditions could be explained by redistribution and normalization of nutritional metal distribution.
All metallic nutrients have the potential to become toxic when they accumulate locally within cells, even if they are deficient elsewhere in the body. It seems unrealistic to limit our focus to a few toxic metals, merely because that was once the principal use of chelation therapy.
In the final analysis, these are all theories theories. We still do not know for certain the principal mechanism of how EDTA improves atherosclerosis. Whatever mechanism is proposed, it must explain the consistently observed delay of several months for full benefit.
EDTA chelation therapy remains fertile ground for future research.
Copyright © 2012 Elmer M. Cranton, M.D., all rights reserved