Lacking adequate scientific foundation for claims made and with inherent risks and limitations, EDTA is being used by practitioners and sold to consumers without adequate understanding of these risks and limitations.
1) Despite claims to the contrary, EDTA does not effectively chelate mercury; The molecular affinity of mercury for EDTA is several orders of magnitude less than the affinity of mercury for the sulfhydryl groups to which mercury is bound in the body. Therefore, EDTA is not suitable for persons with amalgam (silver) fillings or any other form of mercury exposure. Leading authorities in the field of metal toxicity including Dr. David Quigg, Scientific Director of Doctors Data, Inc. point out that while EDTA has some chemical affinity for mercury, it is not nearly enough to overcome the powerful affinity of mercury for sulfhydryl groups in bodily tissues required for effective chelation. Furthermore, no form of EDTA (oral, rectal or IV) avoids the risk of forming a neurotoxic complex with mercury reported by Duhr, et al*. This is particularly relevant for young, old, or very ill persons who may have some degree of impairment of blood-brain barrier function. See Duhr* and Stoiber**.
2) "I am confident that EDTA does NOT cross the blood brain barrier, nor does it go intracellularly."
Garry F. Gordon, MD,DO,MD(H)/ Gordon Research Institute
Greenberg's Note: This is a critical point admitted by a long time advocate of EDTA chelation. A study in the British Journal of Industrial Medicine shows that past 7 days of exposure EDTA is significantly less effective in mobilizing lead from the body, why? Because this heavy metal is now intracellular. So the question is, of what benefit is EDTA on persons that have had constant exposure to lead over a period of years? The answer is simple ... quite limited past 7 days after the exposure.
3) "EDTA (ethylene diamine tetraacetic acid) is an effective and widely studied chelating agent. It cannot chelate mercury, however, DMSA and DMPS, the chemicals which work intravenously to chelate mercury, are not approved by the FDA. "
Maile Pouls, Ph.D. Director of Research/ Extreme Health
Greenberg's Note: DMSA the active compound in Succimer/Chemet is approved by the FDA and has been since the early 1990's for detoxification of lead in children. Special thanks to David Quig PhD/ Doctors Data Inc. for bringing this to my attention.
4) Chemistry Professor Boyd Haley (cirrculum vitae) released a short paper titled Concepts for Safe Human Body Mercury Removal. It suggests that natural vitamins and supplements should be used first, rather than automatically turning to the usual drugs – EDTA, DMSA or DMPS. “The drugs do not effectively enter the cells or cross the brain blood barrier as do natural compounds,” he says. “It is my opinion they (the drugs) should be used only after the use of natural compounds has failed. Using the adage ‘do no harm,’ I think supplementing the body’s metabolic system that is active and needed for the natural removal of mercury is the best approach.” DAMS Newsletter
5) EDTA promotes excretion of lead, cadmium and arsenic through the kidneys, which is not our divinely designed route of excretion for these metals (the gastro-intestinial tract is). Excretion of lead by use of EDTA burdens renal functions, with a real danger of kidney failure (renal tubular necrosis). Chelation products that promote excretion of heavy metals through the gastro-intestinial tract are inherently much safer, particularly where appropriate biochemical (cracked cell chlorella as cation exchange) and antioxidant support is provided and reabsorption of heavy metals is prevented.
6) No form of EDTA protects the body from oxidative stress or replenishes depleted glutathione and anti-oxidant levels. EDTA in its function as a chelator, mobilizes lead, cadmium and arsenic and can redistribute these mobilized metals in the body. It's like stirring up the soup pot and letting it all settle back down to wherever it may. This can lead to adverse side effects, particularly in a person whose glutathione and anti-oxidant levels are depleted.
7) There is important evidence that lowering of toxic metal levels can promote cardiovascular health by reducing pathogenetic effects of heavy metals on endothelial cells, particularly with respect to phospholipase D activation, beta adrenergic hypersensitivity and mitochondrial dysfunction. Mercury and lead are strongly implicated in cardiovascular disease and undoubtedly, other heavy metals are as well. Currently the NIH is performing a study on the possible benefits of EDTA for cardiovascular disease. It has been going on since 2003 and is slated to end in 2008, with no results or conclusions available. However, it is difficult to see how results of this study can be conclusive because of issues related to patient selection (lack of efficacy for mercury and other metals) and the multifaceted nature of cardiovascular disease (diabetes, gout, hypertension, elevated homocysteine, hypothyroidism, etc). Furthermore, since the NIH study involves IV chelation, it is unlikely that the results will be directly applicable to oral EDTA chelation. http://nccam.nih.gov/chelation/chelationstudy.htm http://nccam.nih.gov/news/2002/chelation/q-and-a.htm#fourteen Just in, an article found in the July '08 issue of "New Scientist Magazine". Critics of the NIH funded study on chelation raise questions and ask to end the study.
Read full article
9) EDTA (Suppository Forms) Check their studies closely, when they say "It's been clinically proven" they mean it has been clinically proven to be absorbed, this claim and additionally the safety aspects is hotly debated by IV chelation expert Dr. Elmer Cranton, see what Dr. Cranton has to say, here. An EDTA suppository is still EDTA, a narrow spectrum chelator, it still causes essential mineral depletion and it still promotes excretion through the kidneys. There is a reference to a pre-pilot study, if you look closely it's a study of one, yes that's correct, one person.
10) EDTA is known to enhance the excretion of essential minerals such as zinc, iron, manganese, copper and cobalt leading to significant depletion, metabolic dysfunction and even more serious health ramifications.
11) EDTA is a narrow spectrum chelator, working very well for lead and to a lesser degree for cadmium and arsenic. There are however 13 other metals that can negatively affect your health, including mercury, bismuth, tin, aluminum, nickel, antimony, silver, beryllium, platinum, thallium, thorium, titanium, tungsten and uranium. EDTA does not chelate these metals well. Because these metals contaminate the environment and our bodies and because multiple metals markedly lower the toxic threshhold for the body, narrow spectrum chelators will provide limited benefits.
12) EDTA unquestionably is beneficial for acute and chronic lead poisoning. However, its current uncritical use for individuals with chronic mercury and/or multiple metal exposures is unlikely to produce significant, let alone optimal benefits. Furthermore, without adequate testing for multiple metals and appropriate monitoring for kidney function and trace mineral depletion, its use can entail significant risks.
EDTA even for acute lead poisoning is only proven beneficial if administered IV within 7 days of the acute lead exposure ... after that it is of limited benefit.
See Study in PDF
13) Heavy exposure to multiple toxic metals usually leads to glutathione depletion with multiple serious ramifications. These include immune dysfunction leading to manifold chronic infections, inability to detoxify metals and chemicals (impaired phase 2 detoxification) leading to multiple chemicle sensitivities, inability to protect the body against oxidative stress, mitochondrial dysfunction leading to a host of other health issues and the inability to convert thyroxine to T3 with resultant functional hypothyroidism, often weight gain and significant slowing of metabolism and detoxification mechanisms. The use of EDTA (a narrow spectrum chelator) by itself is unable to address these issues.
14) EDTA is a known and documented chelator of lead with an affinity to bind to arsenic and cadmium. As stated above EDTA DOES NOT permeate the cell wall so it is ineffective in removing metal ions that are within the cell, the same metal ions that cause glutathione depletion and mitochondrial dysfunction.
A Final Thought:
"I hope you will take the time to investigate the products you may have been considering including my own formulations of Chelorex®. Compare the ingredients, the amounts, the effectiveness, the science behind the ingredients, and the cost. You'll find that Chelorex® provides ingredients for both chelation/mobilization of 16 heavy metals, addresses the problems of redistribution and reabsorption of toxic metals, deals with the critical issue of glutathione depletion and its widespread and profound influence on multiple physiological functions. Chelorex® also avoids the significant risks of kidney damage and essential trace mineral depletion inherent in the use of synthetic chelators, protects against oxidative stress, crosses the blood-brain barrier and addresses the problem of mitochondrial dysfunction; and it accomplishes this in a cost effective manner. Chelation is not a race it is best performed in a slow, methodical, safe and effective manner."
ABSTRACT: "We have found that EDTA and EGTA complexes of Hg2+, which conventional wisdom has assumed are biologically inert, are potentially injurious to the neuronal cytoskeleton. Tubulin, a majorprotein component of the neuronal cytoskeleton, is the target of multiple toxicants, including many heavy metal ions. Among the mercurials, inorganic mercuric ion (Hg2+) is one of the most potent inhibitors of microtubule polymerization both in vivo and in vitro. In contrast to other heavy metals, the capacity of Hg2+ to inhibit microtubule polymerization or disrupt formed microtubules cannot be prevented by the addition of EDTA and EGTA, both of which bind Hg2+ with very high affinity. To the contrary, theaddition of these two chelating agents potentiates Hg2+ inhibition of tubulin polymerization. Results herein show that HgEDTA and HgEGTA inhibit tubulin polymerization by disrupting the interaction of GTP with the E-site of brain beta-tubulin, an obligatory step in the polymerization of tubulin.
Both HgEDTA and HgEGTA, but not free Hg2+, prevented binding of [32P]8N3GTP, a photoaffinity nucleotide analog of GTP, to the E-site and displaced bound [32P]8N3GTP at low micromolar concentrations. This complete inhibition of photoinsertion into the E-site occurred in a concentration- and time-dependent fashion and was specific for Hg2+ complexes of EDTA and EGTA, among the chelating agents tested. Given the ubiquity of Hg2+ in the environment and the widespread use of EDTA in foodstuffs and medicine, these mercury complexes may pose a potentially serious threat to human health and play a role in diseases of the neuronal cytoskeleton."
**Thomas Stoiber (a), Daniela Bonacker (b), Konrad Bohm (a), Hermann M. Bolt (b), Ricarda Thier (c), Gisela H. Degen (b), Eberhard Unger (a): (a) Institut fur Molekulare Biotechnologie, Beutenbergstr. 11, Jena D-07745, Germany (b) Institut furArbeitphysiologie an der Universitat Dortmund, Ardeystr. 67 Dortmund D-44139, Gemany (c) School of Biomedical Sciences, University of Queensland, St. Lucia, Qld 4072, Australia. Disturbed micotubule function and induction of micronuclei by chelate complexes of mercury(II). Mutation Research 563 (2004) 97-106
ABSTRACT: Interactions od mercury (II) with the microtubule network of cells may lead to genotoxicity. Complexation of mercury(II) with EDTA is currently being discussed for its employment in detoxification processes of polluted sites.This prompted us to re-evaluate the effects of such complexing agents on certain aspects of mercury toxicity, by examining the influences of mercury(II) complexes on tubulin assembly and kinesin-driven motility of microtubules. The genotoxic effects were studied using the micronucleus assay in V79 Chinese hamster fibroblasts.
Mercury(II) complexes with EDTA and related chelators interfered dose-dependently with tubulin assembly and microtubule motility invitro. Theno-effect-concentration for assembly inhibition was 1 ΩM of complexed Hg(II), and for inhibition of motility it was 0.05 ΩM, respectively. These findings are supported on the genotoxicity level by the results of the micronucleus assay, with micronuclei being induced dose-dependently starting at concentrations of about 0.05 ΩM of complexed Hg(II). Generally, the no-effect concentrations for complexed mercury(II) found in the cell-free systems and in cellular assays (including the micronucleus test) were identical with or similar to results for mercury tested in the absence of chelators. This indicates that mercury(II) has a much higher affinity to sulfhydryls of cytoskeletal proteins than to this type of complexing agents. Therefore, the suitability of EDTA and related compounds for remediation of environmental mercury contamination or for other detoxification purposes involving mercury has to be questioned.