October 3, 1997
Dr. Terry Chappell
President ACAM
Bluffton, Ohio
Dear Terry,
Thank you for your FAX of 10/1/97. I appreciate the time and thought that went into your response.
In your FAX you stated that in the stack of documents you reviewed on oral EDTA there was very little evidence that it impacts vascular disease improves clotting, or reduces iron or heavy metal stores already in the body. You admit that such actions could result in reduced free radicals. I am supplying you with articles that clearly document the strong binding capacity of EDTA to copper and iron (Exhibit 1). This is cited as the primary reason that 90 million pounds of this substance are utilized annually, much of it as a food additive.
I am also sending a reference from the Annals of Internal Medicine, Vol. 47, 1957, "Editorial: Chelation," (Exhibit 2) which states on pagelO37 the well known ascending order of some of the metals of biological interest that are chelated by EDTA. Furthermore, this article states that there are reports showing an effect of EDTA prolonging prothrombin time, citing Am J Olin Path 24: 39, 1954; and J Lab & Olin Med 42: 550, 1953; and furthermore I enclose A Comparative Study of the Use of Ferric Chelate in Iron Deficiency Anemia," C.F. Herridge, British Medical Journal, V.2, P.140, July 19, 1958 (Exhibit 1). This last article reports that lowering of the prothrombin activity was found in half of the group, though it was not thought to be of clinical importance at that time.
I personally believe that generally the anti-clotting effect is far more subtle, and probably more of a synergistic influence with other anti-clotting, anti-platelet substances such as garlic, ginkgo, polysaccharides, EPA.
I am also supplying you with 6 references regarding the benefits from oral EDTA, all documenting a lowering of cholesterol. There is one article showing an increase in cholesterol levels but this was only in RATS. (Exhibit 3.) I think the preponderance of favorable evidence regarding cholesterol lowering in humans from ingestion of oral EDTA is clear.
Although the evidence regarding removal of copper was limited to 3 out of 6 cases in Wilson's Disease and although oral EDTA was not always beneficial in iron overload, the evidence that oral EDTA inhibits the absorption of iron and copper seems overwhelming. Even that beneficial and probably life-extending activity may not be as
Important as the potential for continuous, economical, and convenient presence of EDTA in body fluids binding copper and iron so tightly that they are largely unavailable for biological activities including catalyzing free radical reactions.
I am enclosing 11 abstracts and 17 portions of published articles regarding the influence EDTA has on iron bioavailability (Exhibit 1), including:
- "The effect of various ligands on the absorption, distribution and excretion of iron following oral administration." W. Forth, et al. Arch Exptl Pathol Pharmakol. 252(3); pp242-57 (1965) (Ger.) In the presence of EDTA, diminished iron retention to be due to a marked increase in excretion. Furthermore, EDTA-bound iron is poorly utilized by the erythropoietic system.
- "Food iron absorption in man; the effect of EDTA on absorption of dietary non-heme iron." Amer J of Clin Nut 1976:29(6);pp614-620. This study reports a decrease of absorption of non-heme iron of 72% when EDTA is present at a 2:1 molar ration.
- "Effect of orally administered EDTA on iron absorption in man." P.S. Davis et al, Australis Ann Med 16(1);70-4. 1967. EDTA significantly reduces iron absorption when present in a ration of 10:1 or more.
- "The Enhancement of Iron Excretion in Iron-Storage Diseases." W.G. Figueroa. Metal-Binding in Medicine, MJ Seven, M.D, ed, J.B. Lippincot, Ch 17 (1960). This study claims that oral EDTA does not increase output of iron in the urine.
- "The Effect of the Prolonged Intake of EDTA on the Utilization of Calcium & Iron by the Rat." BA Larsen, Can J Biochem Physiol. Vol E8 (1960) pp813-817. This author states that EDTA ingestion causes less iron to be absorbed, and more of what is absorbed to be excreted.
- "Effect of pH and chelating agents on iron binding by dietary fiber: implications for iron availability." MJ Leigh, Am J Clinical Nutrition, 38: Aug 1983, pp202-213. This article states that all iron research must take into account the level of ascorbic acid. The key end result may be assumed to be due to the great stability of the iron/EDTA complex at all pH levels.
- "A comparison of the effect of Fe-3 Specific EDTA on urinary iron excretion in a patient with hemochromatosis." F Gilbert McMahon, Journal of Lab and Clinical Med, p600, October 1956. This reports a two-fold increase in urinary iron excretion from intravenous administration. yle='font-family: Arial'>"Design of chelates for the therapeutic objectives." Martin Rubin, Fed Proc 20(Supp 10; Pt 2): pp149-157. Sept 1961, states that EDTA is able to hold iron in the presence of even a specific iron-binding protein (siderophilin) of the plasma. Dr. Rubin states that iron, presented to the cell in the form of an EDTA chelate, is unavailable for incorporation into hemoglobin. This strongly suggests that it is not available to catalyze free radical pathology!
I believe that your concern that oral EDTA might chelate out normal minerals through the GI tract has been more than adequately answered by the 21 abstracts and/or portions of published articles I am submitting that show in fact oral EDTA appears to treat malabsorption problems, and that EDTA is apparently absorbed as the complexes of several minerals (Exhibit 2). In fact, there are two rat studies (Exhibit 2) that indicate increased deposition of calcium and phosphorus in the bones following oral EDTA administration. (See Abstracts No. CA55:5762e, Vozar; CA54:25290h, Vozar, both included.) EDTA has been able to virtually substitute for zinc in zinc-deficient animals, and has been shown to enhance the absorption of heparin, Vitamin B12 and increase the blood levels of antibiotics in chickens by 100%. Special salts of iron EDTA are being considered for world wide application because of these well documented studies on EDTA, which is commonly used as a feed additive for animals and thus has been studied extensively.
I agree with you that the effective doses of EDTA in products out to be at least 500mg, preferably 800mg or more. Researchers calculate the average human Is already ingesting 15 to 50mg in their standard diet.
Your comment that "There is evidence that lead workers taking oral EDTA can reduce the amount absorbed into the body" clearly indicates that ACAM failed to provide you with any of the 88 abstracts and portions of 27 published articles that I am supplying to you at this time (Exhibit 4), which is but a fraction of what Mr. Scharffenberg has collected. These references come from mainstream medicine, and have documented without exception an increase of excretion of lead with oral EDTA of from 3 to 30 times. Virtually every one of these articles describes significant lead lowering benefits from the oral ingestion of EDTA.
There may be relative contraindications to the use of oral EDTA in the case of an acutely lead-poisoned person unless the intestinal tract is emptied with something like an enema, as per the review article" Lead Poisoning, Review of the Literature and Report on 45 Cases." RK Byers, Children’s Hosp, Boston, Harvard med School, Pediatrics 23:585-603 March 1959. It apparently enhances lead absorption from the gut so it would seem rather obvious that good medicine requires that, whenever possible, you first remove patients from all know sources of lead for maximum effectiveness.
The issue regarding the absorption of lead from the intestinal tract has been studied in some depth. "Effects of calcium sodium ethylenediamine-tetra-acetate on the kinetics of distribution and excretion of lead in the rat," N Castellino and S Aloj, Brit J Indust Med, 1965, 22:172, reviewed this issue and concluded that oral administration of calcium EDTA caused a great increase of urinary lead excretion without modifying its intestinal absorption. They reported that approximately 18% of orally ingested lead was absorbed by rats whether they were treated with EDTA or not.
The main problem that led to the loss of favor or oral EDTA around 1960 was the AMA’s strong concern regarding the potential for abuse by industrial physicians who would use the tablets instead of improving the working conditions. Now that it is well documented that all of us provably have adverse health effects because of the levels found in everyone today, and since there is no safe level and these adverse effects have been documented at every measurable level, the widespread employment of nontoxic and inexpensive therapies for removing lead must take on greater importance. Oral EDTA must be evaluated versus penicillamine and DMSA, both of which are far more expensive and clearly more toxic.
Since the dangers of low level lead toxicity are supposedly known by all ACAM members, then they should also know how to facilitate removal of lead with the use of natural therapies including Vitamin C, garlic, zinc, and calcium. Oral EDTA is a vitally important additional method of increasing lead removal from the body. These natural adjunctive de-leading therapies provide significant protection to patients, because, for example, by aggressively administering zinc, any potential for zinc deficiency associated with oral EDTA therapy is entirely avoided. These recommendations, therefore, should help to mitigate any of the criticisms ever leveled at oral EDTA, such as the fear of mutagenesis if zinc is allowed to become deficient. Just as we chose to point out where the early researchers with intravenous EDTA had erred, and we were able to overcome their errors successfully through such cautions as mineral replacement.
I have indicated to you that if ACAM chooses to persist in pretending that there is inadequate documentation regarding the benefits from the oral ingestion of EDTA after you have reviewed the extensive materials I am supplying you here, after it was in the PDR for 20 years, approved years ago by FDA for lead poisoning, and has been used widely throughout the world, that I will find it necessary to resign.
I believe there is legitimate confusion in regarding the therapeutic potential or oral EDTA in vascular disease, which I can agree is not yet solidly established; however, it would seem likely that if we look at stability constants, EDTA certainly prevents excess iron absorption and, depending on other factors such as pH, etc., it is really chelating iron out of the body as the literature indicates. The published stability constants clearly indicate that oral EDTA would decrease the circulating levels of free iron and copper because they are bound to EDTA and not therefore biologically available to catalyze free radical reactions. While these actions may be considered by some to be theoretical, the removal of lead from the oral ingestion of EDTA cannot be considered as anything other than established FACT!
In order for ACAM to again meet our ethical responsibilities to the public and to our members, I believe that they need to openly state that oral EDTA effectively lowers lead levels in humans. Members may want to review the literature for themselves to learn why it is so commonly added to our food, and what researches believe is its mechanism of action in preserving foods. Once this is understood it will become clear that, since it is extremely cheap and safe when taking adequate mineral replacement, the benefit-risk ration of including it with other known metal chelators/anti-platelet substances such as garlic makes total sense.
Further, I believe it is unethical and irresponsible to fail to advise our physician members about the effectiveness of oral EDTA with a clear statement form the academy, or at lease from our scientific committee. Without that action, I fear that many members will continue to tell patients that oral EDTA supplements are a waste of time, thereby dangerously misinforming patients since all studies clearly show the dangers of gradually accumulating levels of toxic metals such as lead and cadmium in tissues, especially in the brain (particularly the pituitary gland) with aging, and oral EDTA clearly can help to prevent and possibly even reverse this problem.
You may recall that ACAM gave medical researcher Richard Scharffenberg a very short time, (less than 3 months!) and an entirely inadequate budget to begin to research the oral EDTA issue. ACAM’s decision not to permit him to complete the task did not endear the academy to Mr. Scharffenberg; but as I have remained friends with him I still get some updates. Presently, an outside party has commissioned Scharffenberg to do the job that I asked ACAM to pursue. Since his work product belongs to someone else, I am not able to supply ACAM with more than a fraction of what has been located by Mr. Scharffenberg. ACAM can certainly get all of these published articles from someone else, and I again urge ACAM to get its own complete file on EDTA.
I fear our EDTA "war" is not over, even when we settle with the FTC. For example, the Federal Health Office in Germany published the article "Implications of Heavy Metal Toxicity Related to EDTA Exposure" (HH Dieter, Toxicological and Environmental Chemistry, Vol 27, pp 91-95, 1990.) (Exhibit 5) This article sounded the alarm that EDTA is building up in all surface waters at an alarming rate. And although there is extensive documentation regarding its usefulness and safety, there is new research regarding nephrotoxicity form accumulated cadmium after chronic low-level exposure of an EDTA/cadmium complex that forms in surface water and potentially may accumulate in renal tubular cells. The German health office has published more on this subject, emphasizing their concerns in subsequent medical literature.
I am sending you an article regarding cadmium toxicity documenting that this theoretical danger can be avoided when the dose of EDTA is higher than the amount of cadmium. (See "Effects of Chelation Agents on Oral Uptake and Renal Deposition and Excretion of Cadmium," Brigitta Engstrom, National Institute of Environmental Medicine, Stockholm, Environmental Health Perspectives, Vol 54, pp 219-232, 1984.) (Exhibit 6) The Engstrom article clearly shows increased body elimination and decreased acute toxicity. Note: It is only very low intakes of EDTA in combination with cadmium that produce this theoretical risk.
I believe that the current FTC problem would be better handled if ACAM really had a well organized, complete file of the world’s chelation literature; meaning you get every reference from every reference, and you even get things translated as needed. Also please remember, Martin Rubin still has in his possession scientific information regarding EDTA from ACAM that is not available anywhere else.
I am giving you some references from my slide outline, which have shown around the world (Exhibit 7). I can’t understand how anyone questioning the effectiveness of oral EDTA in lead toxicity that then fully reviews these references can deny this useful application of oral EDTA to the public. I see such denial as no different from mainstream physicians who, because of their vested self-interest, choose to dismiss anything we publish regarding EDTA and vascular disease.
I have copied all of one article just to give you some flavor of the type of references contained in all of them. (Morgan, South Med J, Vol 68, No. 8) (See Reference Nos. 10, 12, 13, Brit J Ind Med and Arch of Indust Health.) all of these references need to be obtained in order to do a comprehensive search of the literature.
I am sending you seven articles regarding the influence of various diseases on the absorption of EDTA (Exhibit 8). The proven increased intestinal absorption of chromium EDTA with various diseases makes the oral route all the more effective in sicker patients who are PROVEN to absorb a higher percentage of EDTA (probably up to the 18% level published elsewhere).
For years, a common method of taking 3gm of oral calcium EDTA was in grapefruit juice. Current interest in the drug interaction with grapefruit juice is that there was some hidden benefit from this approach to oral EDTA administration.
Ward Dean, MD, has been actively studying oral EDTA and wrote about it in the August and September, 1997, issues of Nutrition News (Exhibit 9) In April, 1997, I gave an interview to Life Enhancement News where I stated that the mechanism of action of oral EDTA will NEVER replace intravenous EDTA; it merely complements it. Additionally, I am enclosing a copy of my article "Oral chelation with EDTA," from 1986 issue of the Journal of Holistic Medicine, Vol 8, Nos. 1&2 (Exhibit 10).
The incomplete copies of oral EDTA-related literature described herein that I am sending you under separate cover represent a mere fraction of the resource references that I have, which is small portion of the more than 400 articles regarding oral EDTA that Richard Scharffenberg has gone on to collect.
With my own extensive clinical experience as Medical Director of the largest alternative medicine clinic in California, and as Medical Director of Mineralab where I routinely dealt with an international clientele and saw first hand the effectiveness of oral EDTA combined with other natural chelators such as garlic in heavy metal cases, supported by the VOLUME of papers I have reviewed regarding its effectiveness in lead toxicity, it is clear to me that it is urgent for ACAM to set aside any political and economic fears it may have and provide this important information to its members.
If ACAM decides to inform their membership that there is such substantial evidence that the benefit-risk ratio of using oral calcium disodium EDTA in cases of low level lead exposure is virtually beyond question, I believe our member physicians will be motivated to further study the entire issue of oral calcium EDTA. There are so many other potential benefits of which they need to become aware.
For instance, it appears that by binding free copper and iron there may be significant improvement with some of the newer markers of free-radical damage, such as provided by Genox Labs in Baltimore (Exhibit 11, from Richard Cutler, PhD, who did 18 years research with the National Institute on Aging and is a recognized expert on aging; who in his introduction to the use of his tests clearly advocates the use of food additives that bind copper and/or iron).
If ACAM members are denied this kind of information because some members fear a loss of revenue, it would increase their revenue because their patients live longer, so they keep coming back.
I have sent you many articles regarding the use of EDTA in Food (Exhibit 12), and how it not only enhances the uptake of several essential nutrients from Vitamin B12, heparin and essential minerals, but also has a synergistic effect with certain nutrients such as polysaccharides (which I have studied intensively since I worked with Lester Morrison, MD, who spent more than $10 Million developing a synergistic formula based initially on tracheal cartilage rings, later going into other sources of polysaccharides, which he documented, would reverse arteriosclerosis and protect from myocardial infarction, etc.) When we added EDTA to his formula, the effective dose required to prevent blood clotting in the standard Chandler loop test employed in his research was substantially reduced. My knowledge of this research, combined with the incredibly low mortality rate I experienced in my practice has made me extremely low mortality rate I experience in my practice, has made me extremely optimistic regarding the benefits of what I consider to be a total oral chelation approach, which finally involved the use of more than 70 different synergistically combined nutrients (AMNI-OC PAK). Morrison’s formula alone showed a better than 70% reduction in second heart attach rate. (Morrison, Lester M, MD, and Schjeide, O Arne, PhD. Coronary Heart Disease and the Mucopolysaccharides (Glyco-saminoglycans). (1974) Charles c. Thomas, Publisher. 2600 South First Street, Springfield, Illinois 62717. ISBN 0-398-02903-2. Morrison, Lester M, MD and Schjeide, Ole A, PhD. Arteriosclerosis: Prevention, Treatment and Regression. (1984) Charles C. Thomas, Publisher. 2600 South First Street, Springfield, Illinois 62717. ISBN 0-398-04919-X. Morrison, Lester M, MD with Nugent, Nancy. Dr. Morrison’s Heart-Saver Program. (1982) St. Martin’s Press, 175 Fifth Avenue, New York, NY 10010. ISBN 0-312-21481-2.)
It seems unlikely to me that, since EDTA has been documented to be an effective food preservative that prevents oxidative damage to food by free metals and has FDA approval to be added to our diet at levels of 25-800mg, that ACAM could effectively argue that its physician members should be fully informed regarding every potential use of this molecule that our organization has championed all these years.
Interestingly, since we became aware of the negative articles in the literature regarding the use of EDTA for vascular disease, we were ale to overcome these objections through our careful review of all the relevant literature. There are strong similarities to the story regarding the effectiveness of oral EDTA in heavy metal toxicity.
In the final analysis, there are so many publications supporting the effectiveness of oral EDTA alone in treating lead toxicity, that for ACAM not to support this is WORSE than mainstream medicine ignoring our claims of effectiveness with intravenous chelation, because supposedly our members believe they are experts in the use of EDTA.
It is unfortunate that ACAM has ignored my advice to have ALL published articles at its fingertips as well as someone who knows the subject inside and out so we can better defend it, our organization and its members, when we predictably are attacked.
If our academy believes that ETDA is nontoxic enough to inject intravenously into our patients, then they must believe that is virtually nontoxic. The fact that it prevents the copper catalyzed oxidation of Vitamin C should make ACAM interested in seeing that all of our patients get this remarkably inexpensive compound included in our oral supplement programs. (See HL Mammoth et al, Annals, NY Acad of Sci, V88, 1960.) Exhibit 12)
Included in the literature I am sending you is documentation (seven articles, Exhibit 8) that the sicker the patient, the more likely the leaky bowel sill supply even greater absorption of the oral EDTA. The proven ability of EDTA to chelate with metals such as copper and iron so they are completely inactivated and cannot react as metal ions, holds some interesting prospects for future life extension research; leading experts in aging research continue to believe that these metals catalyze free radicals, to our great detriment.
In any event, without proven harm, it is baffling how ACAM can fail to support something that lowers the levels of toxic metals while enhancing the uptake of essential nutrients, while CLEARLY enhancing Vitamin C antioxidant properties.
In 1959, F. Bersworth and Martin Rubin got a patent for the prophylactic use of CaEDTA, to be blended with food products, to PREVENT metal poisoning. Today, with our food supply so challenged, this idea appears quite rational. We know that EDTA protects against many toxic metals including nickel, cadmium (as long as dose is high enough), vanadium (which some research links to diabetes), cobalt, iron, and copper overload. EDTA has also been shown to help lower the body burden of internally deposited fission products (SS Atomic Energy Commission). In fact, a rat study showed significant protection against the toxicity of cisplatin.
I have included substantial documentation (15 articles, Exhibit 13) regarding long term safety which, after careful review, cannot be considered a significant issue. (See "The Metabolism of EDTA, Food and Cosmetic Toxicology." British Industrial Biological Research, "Safety evaluation studies of calcium EDTA." Bernard L. Oser et al, Food and Drug Research Labs. Toxicol Appl Pharmacol. 5:2142-162, 1963. Also Toxicological Profile, Current Use, and Regulatory Issues on EDTA compounds for assessing use of Sodium Iron EDTA for food fortification; Paul Whittaker et al, Center for food safety, FDA, Washington DC Regulatory Toxicology and Pharmacology 18:419-427 (1993).
The complex issue regarding iron balance is covered in Fd Cosmet Toxicol. Vol 2, pp 741-750. Pergamon Press (1964) which shows that iron absorption is apparently only decreased when positive iron balance exists.
It is interesting that many experts in anti-aging are convinced that lowering levels of iron in our bodies should increase life span; and the studies have included show that oral EDTA prevents absorption or iron (UNLESS you are deficient).
It is also interesting that although ACAM is well aware of how I feel about oral EDTA, I am never invited to address the membership to let them make up their own minds. I have never even been invited to sit on a Hot Seat Panel!
With the documentation I am supplying you herewith, I insist that it is unprofessional conduct for any ACAM physician who is supposed to know all about the adverse health effects associated with increased levels of lead, to tell ANYONE that taking a garlic/EDTA is like throwing money down the drain, or any words to that effect. Any statement that would cause a patient to stop taking a garlic/EDTA chelation product in this day and age of known virtually universal heavy metal toxicity affecting the health of very one of us, has to constitute unprofessional conduct. I sincerely believe such statements are doing irreparable harm if the patient listens and stops receiving the protection.
Even if the physician chooses not to believe in the effectiveness of EDTA, refusal to accept the extensively documented benefits of garlic, not only as a heavy metal chelators, but also for its documented protection against organic toxins including food dyes, etc, and its know anti-platelet and anti-cancer and cholesterol-lowering activities, would seem to be a wanton disregard of their patient’s best interests.
I am sending you just a few pages from Scharffenberg’s printout of more than 400 references as Exhibit No. 14. This should make it clear how inadequate ACAM’s submission to you of oral EDTA articles was.
Exhibit 15 discusses benefits from EDTA in epilepsy, prophyria, and psoriasis. There are many additional and interesting references like this that ACAM members should finally have information about.
Thank you for your attention in reviewing this lengthy document. I know that you will personally see that this request is honored. Thank you, again, for your FAX explaining that the issue regarding oral EDTA may be beginning to adversely affect my professional standing.
Sincerely,
Garry F. Gordon, MD,DO,MD(H)



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