Did you know:
- That EDTA (oral, Iv or suppository) forms a neuro-toxic complex with Mercury?
- That EDTA does not effectively mobilize Mercury?
- That EDTA is about 5% adsorbable in oral form?
- That EDTA does not cross the "Blood Brain Barrier"?
- That EDTA is NOT SAFE if you have Mercury Amalgams in place?
- That EDTA alone will not prevent reabsorption of mobilized metals?
Alan Greenberg, M.D.'s 15 Reasons Why Chelorex® is Your Best Choice for Removing Toxic Heavy Metals ... the Way Nature Intended:
(1) EDTA does not effectively chelate mercury; therefore EDTA is not suitable for persons with amalgam (silver) fillings or any other form of mercury exposure. 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.**
(2)Heavy metals deplete glutathione levels, markedly increase oxidative stress, impair chemical detoxification mechanisms and adversly affect thyroid function. Chelorex® contains no synthetic chelating agents, therefore, causes no adverse reactions in chemically sensitive people (up to 40% of persons receiving synthetic chelators may have moderate to severe adverse responses.
(3) Chelorex® contains natural components including glutathione precursors, reduce oxidative stress, preserve mitochondrial function and help to enhances thyroid function.
(4) Chelorex® helps to raise metallothionein levels which also enhances toxic metal excretion.
(5) Chelorex® has Selenium, Zinc and Magnesium reduce effects of heavy metals and protect against trace mineral depletion. Selenium is particularly important since it is an essential cofactor for most glutathione-related enzymes.
(6) Chelorex® provides safe, gentle and effective mobilization of toxic metals by enhancing the natural mechanisms for excretion through the biliary tract. while avoiding the toxic overload associated with synthetic chelators. Faster is not safer.
(7) Chelorex® has multiple potent antioxidants protect against free radical damage.
(8) Chelorex® shows marked enhancement of GI excretion of toxic metals (1280% at 14 days) with protection against reabsorption of toxic metals from GI tract.
(9) Kidney function is protected because unlike EDTA, DMSA and DMPS, Chelorex's® primary route of excretion is intestinal.
(10) Chelorex® has been shown to be effective in our clinical testing for reduction of the entire spectrum of toxic metals: bismuth, cadmium, tin, lead, mercury, aluminum, nickel, antimony, arsenic, silver, beryllium, platinum, thallium, thorium, titanium, tungsten and uranium. This is important because the presence of multiple toxic metals significantly lowers the toxic threshold for each metal. No other chelation product has a broader spectrum.
(11) Chelorex® is the most cost effective of all chelators. Oral chelation with Chelorex is less than 1/10th the cost of IV chelation.
(12) Chelorex® is the only natural oral chelating formula with significant (4+ Years/400+ Subjects) testing results indicating efficacy in reducing heavy metals.
(13) Chelorex® can safely be taken daily and therefore can be used for long-term protection for persons with sustained environmental exposure to heavy metals.
(14) Chelorex® contains both water-soluble agents and lipid soluble agents, capable of penetrating the blood-brain barrier and the cell membrane so that CNS and intracellular metals can be mobilized.
(15) Chelorex® can lower mercury levels safely in persons with amalgam fillings. Chelorex® can be used before, during and after amalgam replacement
*Duhr EF, Pendergrass JC, Slevin JT & Haley BE. HgEDTA complex inhibits GTP interactions with the E-site of brain beta-tubulin. Toxicol Appl Pharmacol 122(2):273-280(1993)
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 ?M of complexed Hg(II), and for inhibition of motility it was 0.05 ?M, 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 ?M 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.