EDTA Chelation Therapy Retains Some Mysteries

EDTA Chelation Therapy Retains Some Mysteries

Elmer M. Cranton, M.D.

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

        We really don't know how EDTA chelation therapy benefits symptoms of atherosclerosis and arterial blockage. We do know a number of different actions of EDTA within the body, but we do not know which actions are most beneficial. It is quite possible that an unknown and still unsuspected activity is primarily responsible for the observed improvement in blood flow and symptoms.

        Human nature is such that people often require an explanation for 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 excreted through the kidneys unchanged. Various metal ions are loosely bound to EDTA by valence electrical charges, some much more so 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, removal of toxic metals, improving blood vessel elasticity and blood cell rheology, etc. But we must, in all humility, admit that these are still only theoretical explanations for the many reported 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 are known 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 if they accumulate intracellularly. Nutritional elements have a narrow margin between physiologic and toxic concentrations in cells. A mere three- to four-fold intracellular 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 intracellularly to potentially toxic levels, when 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).

         Increases of that magnitude can occur even in poorly nourished patients, who would otherwise benefit from supplementation. An example is the accumulation of calcium deposits that can be visualized with ultra-fast CT scans (EBCT) in patients with osteoporosis and overall calcium deficiency. 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 with a number of essential nutritional elements than it is with the more familiar toxic metals. The following data is from Chapter 37, Table 20, A Textbook on EDTA Chelation Therapy:

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 <1.3 times baseline.

        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 diseased tissues. Active transport of a spectrum of metals into and out of cells could thus be normalized by restoration of intracellular energy metabolism and integrity of cell membranes. When infused, EDTA remains outside of cells. Slower infusions of EDTA will allow more time for equilibration and for trace metal rebalancing to occur.

        The concentration of calcium ions outside of cells is 10,000 times greater than intracellular levels. 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 could not be expected to produce this benefit.

        William J. Walsh, PhD, senior scientist 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 excess nutritional metals. 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 all remain just theories. We still do not know how or why EDTA improves symptoms of arterial disease. Whatever mechanism is proposed, it must explain the consistent delay of several months for optimal benefit. The remaining mysteries of EDTA chelation mechanisms provide fertile ground for future research.

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