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What Is Atherosclerosis?
Atherosclerosis (ath-er-o-skler-O-sis) is a disease in which plaque (plak) builds up inside your arteries. Arteries are blood vessels that carry oxygen-rich blood to your heart and other parts of your body.
Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrows your arteries, limiting the flow of oxygen-rich blood to your organs and other parts of your body. This can lead to serious problems, including heart attack, stroke, or even death.
Coronary heart disease (CHD) occurs if plaque builds up in the coronary arteries. These arteries supply oxygen-rich blood to your heart.
Plaque narrows the coronary arteries and reduces blood flow to your heart muscle. It also makes it more likely that blood clots will form in your arteries. Blood clots can partially or completely block blood flow.
When blood flow to your heart muscle is reduced or blocked, it can lead to angina(chest pain) and a heart attack. CHD also is called coronary artery disease or heart disease. It’s the leading cause of death for both men and women in the United States.
Plaque also can form in the heart’s smallest arteries. When this happens, it’s calledcoronary microvascular disease (MVD). In coronary MVD, plaque doesn’t always cause blockages in the arteries as it does in CHD.
Carotid Artery Disease
Carotid (ka-ROT-id) artery disease occurs if plaque builds up in the arteries on each side of your neck. These arteries supply oxygen-rich blood to your brain. When blood flow to your brain is reduced or blocked, it can lead to a stroke.
Peripheral Arterial Disease
Peripheral arterial disease (P.A.D.) occurs if plaque builds up in the major arteries that supply oxygen-rich blood to your legs, arms, and pelvis.
When blood flow to these parts of your body is reduced or blocked, it can lead to numbness, pain, and, sometimes, dangerous infections.
The cause of atherosclerosis isn’t known. However, certain traits, conditions, or habits may raise your risk for the disease. These conditions are known as risk factors.
You can control some risk factors, such as lack of physical activity, smoking, and an unhealthy diet. Others you can’t control, such as age and a family history of heart disease.
Some people who have atherosclerosis have no signs or symptoms. They may not be diagnosed until after a heart attack or stroke.
The main treatment for atherosclerosis is lifestyle changes. You also may need medicines and medical procedures. These treatments, along with ongoing medical care, can help you live a healthier life.
Better treatments have reduced the number of deaths from atherosclerosis-related diseases. These treatments also have improved the quality of life for people who have these diseases. However, atherosclerosis remains a common health problem.
You may be able to prevent or delay atherosclerosis and the diseases it can cause. Making lifestyle changes and getting ongoing care can help you avoid the problems of atherosclerosis and live a long, healthy life.
ORAL EDTA — The Family Friend
The Solution For Heart Disease by Karl Loren
The Food and Drug Administration has approved the synthetic amino acid, ethylene diamine tetraacetic acid (EDTA), as a pharmaceutical agent for the treatment of lead and other heavy metal poisoning or exposure. In older literature, the FDA also approved intravenous EDTA treatment as “possibly effective in occlusive vascular disorders … arrhythmias and atrioventricular induction defects … and in the treatment of pathologic conditions to which calcium tissue deposits or hypercalcemia may contribute other than those listed above.”‘ These “possibly effective” indications were removed from FDA-approved literature in the late 1970′s for reasons known only to the FDA. Fortunately, physicians are not limited solely to FDA-approved indications and may prescribe approved drugs for whatever “unapproved” conditions they find them to be effective. Consequently, since EDTA is approved for the treatment of heavy metal poisoning (especially lead), many physicians continue to use pharmaceutical EDTA with great benefit in many diseases and conditions other than the officially approved uses. There are two medical associations whose physician members are trained in the administration of EDTA for the treatment and prevention of atherosclerosis and other chronic degenerative diseases. These organizations are the American College for Advancement in Medicine (800-532-3688) and the Great Lakes Association of Clinical Medicine(800-286-6013). Members of these organizations and their patients find that EDTA chelation therapy is highly effective as an alternative or addition to more traditional/widely accepted approaches such as angioplasty or bypass surgery.
Beneficial Uses of Oral EDTA In Cardiovascular Disease
In addition to the controversial but widespread recognition of EDTA’s intravenous benefits, is its less well-known clinical uses when administered orally. Early clinical studies with EDTA reported loss of fat in rats, reduction of cholesterol in rabbits, and reduced blood pressure in humans. Consequently, a study of the effects of oral EDTA on patients with atherosclerosis and/or hypertension was conducted on 10 patients. Four of these patients had hypertension, four had angina pectoris, one had peripheral vascular disease (intermittent claudication), and one was recovering from a heart attack. All were treated with 1 gm of oral EDTA daily for 3 months. Seven of the ten patients experienced significant reductions in their cholesterol levels, and blood pressure was reduced in all ten. The most marked change occurred in the patient with intermittent claudication, whose cholesterol dropped from 278 mg per 100 ml to 128! This patient also reported improved exercise tolerance, and the researchers found improved pulsations in the extremities. The four patients with angina pectoris also A reported improvement.
In another series of 20 patients who suffered from hypercholesterolemia, hypertension, angina or peripheral vascular disease, one gram of EDTA was administered orally every day for 3 months. During that short time, elevated cholesterol levels in nine of the patients dropped to within the normal range. No adverse results were experienced by any of the patients. Angina attacks were reduced in frequency and severity in five individuals. One person who previously had suffered a heart attack and experienced several angina attacks daily thereafter, obtained complete relief.
In another study, two patients with extremely elevated cholesterol were treated with oral EDTA. One patient took EDTA in progressively increasing doses ranging from 500 mg to 4 gm daily for one year, and the other took 1,000 mg daily for three years. Although the first patient suffered a heart attack after three years of therapy, she recovered uneventfully, and had reduced angina pains and improved sense of well-being with continued use of EDTA. The second patient – in addition to hypercholesterolemia had a condition known as xanthomatosis (yellowish papules in the skin, related to elevated blood lipids). She not only experienced dramatic reductions in her cholesterol levels with oral EDTA treatment, but her skin lesions completely resolved. Other laboratory studies (including kidney and liver function) remained normal throughout the study for both patients. This is further confirmation of the safety of oral EDTA, considering that doses as high as 4 gm daily were consumed.
Further support of the anti-atherosclerotic effects of oral EDTA are provided by Italian researchers who found that two grams of oral EDTA daily were effective in reducing blood cholesterol. Scientists at Wayne State University quantified reversal in atherosclerotic plaque in rabbits that were treated with daily subcutaneous EDTA injections.
EDTA’s Multiple Uses as a Food Additive
In addition to its remarkable pharmaceutical uses, the FDA has also approved EDTA as a food additive that is generally recognized as safe (GRAS). EDTA’s array of biochemical properties make it extremely valuable as a food additive. It has the ability to:(1) bind with many metals;(2)act synergistically with other antioxidants to stabilize fats and oils;(3)prevent discoloration of potato products; (4)stabilize vitamins;(5)prevent discoloration of fish and shellfish;(6)prevent flavor changes in milk;(7)inhibit the thickening of stored condensed milk;(8)enhance the foaming properties of reconstituted skim milk;(9)prevent color changes of scrambled eggs prepared from egg powder; (10)preserve canned legumes;(11)prevent gushing in beer;(12)promote flavor retention and delay loss of carbonation in soft drinks; (13)prevent oxidation of meat products; and(14)prevent discoloration of canned fruits and vegetables. In fact, EDTA’s use in foods is so widespread that its presence in bloody evidence even created questions during the O.J. Simpson trial as to its source-i.e., from food or from blood previously drawn as evidence-since EDTA is also used as an anticoagulant in blood used for laboratory studies.
Normal Artery – Fatty Streak – Fibrous Plaque – Complicated Plaque
Absorption of EDTA
In 1954, Dr. Harry Foreman and his colleagues performed a landmark study to deter- mine how much orally administered EDTA the body absorbs. The scientists found that the body absorbs a maximum of 5 per cent of orally consumed EDTA and that it can take up to three days for the EDTA to be totally excreted. If someone consumed nutritional supplements that contained 800 mg of EDTA (used as a stabilizer of the ingredients in the supplement), then we can assume from Dr. Foreman’s research that about 40mg will be absorbed each day and that 1,200 mg will be absorbed each month. That equates to almost the same amount of EDTA administered in one intravenous chelation treatment using the low-dose optimum protocol of Drs. Born and Geurkink that was described in last month’s article. Consequently, those unable to obtain intravenous chelation therapy due to financial , occupational, geographical or other restraints, or who wish to undergo a less- intensive preventive approach may be able to obtain many of the same benefits of intravenous chelation therapy by consuming food-additive EDTA that is used as a stabilizer in food supplements.
Because of concern that long-term use of EDTA might result in depletion of certain elements, Drs. Ira Manville and Robin Moser recommended that a potent vitamin and mineral formula (such as Personal Radical Shield TM or MultiMin TM) be administered during treatment with EDTA.”(This should be taken with meals and not with the EDTA formula.) Dr. Garry Gordon agrees and also recommends that because EDTA binds to nutritional as well as to unwanted metallic elements, it is most effective when taken on an empty stomach” (I hr before or 2-3 hours after a meal.)
1. Calcium disodium edetate and disodium edetate. Federal Register, Volume 35, No. 8, Tuesday, January 13,1970,585-587,
2. Perry, H. Mitchell, Schroeder, Henry A. Depression of cholesterol levels in human plasma following ethylenediamine tetraacetate and hydralazine. J Chronic Diseases, 1955, 2: 5, 520-532.
3. Schroeder, Henry A. A practical method for the reduction of plasma cholesterol in man. J Chronic Diseases, 1956, 4: 461-468.
4. Perry, Jr., and Camel, G., Some effects of CaNa2EDTA on plasma cholesterol and urinary zinc in man, in: Metal Binding in Medicine, by Marvin J. Seven and L. Audrey Johnson (eds), 1960,J.B. Lippincott Company, Philadelphia, 209-215.
5. Mariani, B., Bisetti, A., and Romeo, V. Blood-cholesterol-lowering action of the sodium salt of calcium ethylene diamino tetraacetic acid. Gazz Intem Med e Chir, 1957. 62: 1812-1823.
6. Wartman, A., Lampe, T.L., McCann, D.S., and Boyle, A.J. Plaque reversal with MGEDTA in experimental atherosclerosis:Elastin and collagen metabolism. J Atherosclerosis Res, 1967, 7:331-341.
7. Aamoth, H.L., and Butt, F.J. Maintaining food quality with chelating agents. Annals New York Academy of Sciences, 1960,526-531.
8. Furia, T. EDTA in Foods-A Technical Review. Food Technology, 1964, 18: 12, 1874-1882.
9. Foreman, H., Trujillo, T. The metabolism of C14 labeled ethylene diamino tetraacetic acid in human beings. J Lab Clin Med, 1954, 43: 566- 571.
10. Born, G.R., and Geurkink, T.L. Improved peripheral vascular function with low dose intravenous ethylene diamine tetraacetic acid (EDTA). Townsend Letter for Doctors. July, 1994, #132, 722-726.
1 1. Manville, I., and Moser, R. Recent developments in the care of workers exposed to lead. AMA Arch Indust Health, 1955, 12:528-538.
12. Gordon, G. Oral Chelation with EDTA. J Holistic Medicine,
198618: 1 & 2, 79-80,
EDTA Chelation: A Misunderstood Therapy for Atherosclerosis and other Chronic Diseases
By using nutritional therapy and lifestyle modifications, many of these risk factors can be reduced or eliminated. However, despite their best efforts, some people may still develop coronary artery disease, carotid artery disease or other vascular illness. These conditions may be manifested by chest pain with exertion (angina); (2) memory loss or temporary disorientation or sensory loss due to reduced blood flow to the brain, (transient ischemic attacks temporary or pain in the calves after walking relatively short distances which is relieved by rest (intermittent claudication).
EDTA Chelation: A Misunderstood Therapy for Atherosclerosis and other Chronic Diseases
The two leading causes of death for men and women over the age of 50 are heart attacks and strokes. Atherosclerosis, or “hardening of the arteries,” is usually involved in the pathogenesis of these conditions. A significant focus of nutritional therapy is to reduce various risk factors that predispose an individual to atherosclerosis. These risk factors include: (1) a high ratio of total cholesterol to high density lipoproteins; (2) elevated blood levels of homocysteine, fibrinogen, lipoprotein a, glucose, or insulin; (3) family history; (4) cigarette smoking; (5) obesity; and (6) sedentary lifestyle. By using nutritional therapy and lifestyle modifications, many of these risk factors can be reduced or eliminated. However, despite their best efforts, some people may still develop coronary artery disease, carotid artery disease, or other vascular illness. These conditions may be manifested by: (1) chest pain with exertion (angina); (2) memory loss or temporary disorientation or sensory loss due to reduced blood flow to the brain, (transient ischemic attacks temporary “mini-strokes”); or (3) pain in the calves after walking relatively short distances which is relieved by rest (intermittent claudication). All of these symptoms or conditions, which should be evaluated by a physician, are worrisome indicators that there may be significant arterial narrowing in the affected portions, as well as elsewhere in the body.
The problem with the “mainstream” approach to vascular disease is that, for the most part, it’s like putting a band-aid on a major traumatic injury. Certainly, surgeons can bypass a few “blockages” with a vein graft or prosthesis, or literally smash arteries open with a balloon angioplasty, but these approaches appear primitive and crude when one realizes that atherosclerosis is not a localized injury; it is a systemic disease. This disease is present not only in the coronary or carotid arteries, but also in the brain, lungs, kidneys, and legs. (Fig. 1) Furthermore, the blockages not only occlude the larger vessels that can be seen and manipulated by surgeons and cardiologists, but the smaller vessels as well. And it is in the capillaries of the micro-circulation where the oxygen exchange to the tissues takes place. Clearly, the optimum treatment for atherosclerosis would be a biological approach which removes plaque and restores blood flow throughout the entire arterial system and which treats the micro as well as the macro vessels. But is there such a biological approach that really works?
Common sites of Atherosclerotic lesions; brain, lungs, aorta,abdominal aorta, kidneys & extremities
EDTA Chelation Therapy
Chelation therapy is a controversial therapy that is administered by approximately 2,000 to 3,000 physicians in the U.S. It consists of the intravenous infusion of a solution containing ethylene diamine tetraacetic acid (EDTA), a synthetic amino acid, as well as vitamins, minerals, and other substances. The one- to three-hour treatments (depending on the dose) are administered to a patient who sits comfortably in an easy chair, reading, talking, watching TV or even sleeping. The treatments are administered as often as several times per week to as infrequently as one every other month, depending on the degree of illness and the patient’s length of previous treatment. Usually a course of twenty to thirty treatments are adequate to reverse significant blockages, whereupon the patient is put on a less frequent maintenance regimen.
Proponents of EDTA chelation therapy of which I am one believe that it is highly beneficial in the prevention and treatment of atherosclerosis as well as other chronic degenerative diseases. On the other hand, its detractors (most of the mainstream medical establishment) claim that it is worthless at best and may even constitute medical fraud.
History of EDTA Chelation Therapy
EDTA was synthesized in Germany in 1935, and first patented in the U.S. in 1941. Its first uses were in industry as a chelating agent, as an anticoagulant for clinical laboratory use, and as a treatment for lead poisoning. In 1955, Dr. Norman Clarke, then Director of Research of Providence Hospital in Detroit, Michigan, reported on his use of intravenous EDTA to dissolve what he referred to as “metastatic calcium”; (i.e., calcium that has been deposited where it was not wanted, as in arteries [atherosclerosis], joints [arthritis], kidneys [kidney stones], and the bony ossicular system in the ears [otosclerosis]), with generally favorable results. Since then, hundreds of papers have been published on the effects of chelation therapy in a variety of chronic diseases, with the vast majority reporting favorable results. The numbers of papers on EDTA chelation therapy are too numerous to cite here. However, many can be found in the books and papers that are referenced at the end of this article.
I believe the most extensive confirmation of the beneficial cardiovascular effects of EDTA chelation therapy have been two massive “meta-analyses” of both published and unpublished studies.1,2 These papers evaluated the results of over 24,000 chelation patients, in which 88% demonstrated clinical improvement. Typical of these studies was that of Hancke and Flytlie3 which described improvements in 80-91% of a series of 470 patients with coronary artery disease. The report included 92 patients who were referred for surgical intervention, but of whom only 10 ultimately required surgery either during or after their chelation therapy. The authors estimated that EDTA chelation therapy not only resulted in an improvement in overall cardiovascular health, but saved over $3 million in insurance money as well!3
Perhaps one of the reasons for the controversy surrounding EDTA is that even its strongest proponents can’t seem to agree on the mechanism by which it works. The first, and probably most widely held belief, is that the benefits are due to EDTA’s ability to bind with ionic calcium in the blood. This temporarily lowers the blood calcium level, which stimulates the parathyroid gland to release parathyroid hormone (PTH). PTH in turn stimulates osteoclastic and osteoblastic activity of the bone, mobilizing calcium from unwanted parts of the body (i.e., arteries, joints, etc). This mechanism is described in detail in Dr. Garry Gordon’s, The Chelation Answer.4
However, in another popular “bible” about chelation, Bypassing Bypass, Dr. Elmer Cranton dismisses the “calcium-chelation misconception.” He believes that removal of toxic heavy metals and normalization of mineral metabolism are secondary mechanisms and proposes that the benefits of chelation are due primarily to its free radical-fighting effects.5
Dr. Johan Bjorksten, father of the “cross-linkage theory of aging,” believes that the benefits of EDTA are due to its ability to dissolve inter- and intra-molecular cross-linkages.6
Kindness and Frackelton reported several years ago that EDTA has a profound effect on thrombin-induced platelet aggregation. Platelet aggregation is an essential step in the formation of a blood clot. Intra-arterial blood clots are a major cause of heart attacks and strokes, especially when the vessel has been narrowed by atherosclerotic plaque. Kindness and Frackelton demonstrated that this physiological anti-clotting property of EDTA is superior to that of aspirin, without the dangers inherent in aspirin therapy.7
I believe that one of the least-touted but most significant mechanisms of EDTA may be that of its ability to “resuscitate mitochondria.” Mitochondria are the “power plants” of every cell in the body. (Fig. 2) It is within the mitochondria that the process of oxidative phosphorylation takes place, which generates energy-producing ATP without which life could not exist. Loss of mitochondrial function has long been considered to be one of the primary causes of the aging process.8,9,10 Recently, the role of impaired mitochondrial function in the pathogenesis of many diseases has been increasingly recognized.11,12,13 EDTA was recognized as early as the 1950′s to have the ability to stabilize mitochondria.14 Hunter and colleagues suggested that this effect of EDTA was likely to be due to its combining with the mitochondrial membrane rather than its chelating with metal ions.15 Gallagher’s studies tended to confirm their belief.14
Mechanisms aside, the one issue that all chelating physicians overwhelmingly agree on is the tremendous benefits that can be obtained in a variety of degenerative, age-related conditions, using this safe, non-invasive, relatively inexpensive therapy.
Are there any Adverse Effects of Chelation Therapy?
The most serious potential adverse effect of EDTA chelation is nephrotoxicity (kidney damage). This is dependent on the dose, the rate of infusion, the patient’s kidney function, and the patient’s body burden of toxic heavy metals. Kidney damage was not uncommon in the early days of chelation therapy, when doses of EDTA in the range of 5-10 grams per day were used, and treatments were administered as often as 5 days per week. Kidney damage can be easily prevented, however, by carefully adjusting the frequency, dose and rate in which the EDTA is administered. In addition, I have found that judicious administration of EDTA over prolonged periods (three to six months and longer) actually improves kidney function.
Other potential adverse effects include hypocalcemia (excessively low blood levels of calcium) due to EDTA’s binding excessively with calcium in the blood; hypoglycemia (low blood sugar), believed to be due to accompanying hypocalcemia; and phlebitis (inflammation of the vein) usually due to improperly prepared solutions. Rarely reported side effects include chills and fever following infusion, exacerbation of congestive heart failure due to fluid overload, fatigue (usually due to hypoglycemia or hypocalcemia), seizures, arrythmias, or rash. Although these have been reported occasionally by others, I have never observed any of these rare side effects despite having administered thousands of IV EDTA treatments.
The risk of incurring any of the above adverse effects has further been greatly reduced by the recent finding of Drs. Grant Born and Tammy Geurkink16 that even greater benefit can be obtained by most patients who are treated with only 1.5 grams of EDTA per treatment, rather than with the standard dose of three grams. These physicians randomly divided 30 patients into two groups, each of which consisted of eight males and seven females. One group was treated with “high dose” EDTA (3 grams), and the other was treated with “low dose” (1.5 grams). All patients’ vascular status was determined using a non-invasive, hand-held Doppler ultrasound instrument which measured blood flow in the lower extremities. After 20 EDTA treatments, every patient in the high dose group improved significantly. Strikingly, every patient in the low dose group also improved, and this group had an even greater degree of overall improvement! Consequently, I now use only the low dose EDTA in all of my patients, and I believe the benefits that my patients have experienced parallel those of Drs. Born and Geurkink. So, not only are the benefits of EDTA apparently increased with the low dose therapy, but the minimal risks of adverse side effects are even further reduced.
Alpha-lipoic Highly recommended source of nutrients and supplements. vitamins antioxidants supplements
How did we qualify them ?
1. Chappell, L.T., and Stahl, J.P. The correlation between EDTA Chelation therapy and improvement in cardiovascular function: A Meta-Analysis. J Adv Med, 1993, 6: 3, 139-160.
2. Chappell, L.T., Stahl, J.P., and Evans, R. EDTA Chelation treatment for vascular disease: A Meta-Analysis using unpublished data. J Adv Med, 1994, 7: 3, 131-142.
3. Hancke, C. and Flytlie, K., Benefits of EDTA Chelation Therapy in Arteriosclerosis: A retrospective study of 470 patients. J Advancement in Medicine, 1993., 6: 3, 161-171.
4. Walker, Morton, and Gordon, Gary. The Chelation Answer. M. Evans and Company, New York, 1982.
5. Cranton, Elmer. Bypassing Bypass (2d Ed). Medex Publishers, Trout Dale, VA 24378-0044, 1992.
6. Bjorksten, Johan. The crosslinkage theory of aging as a predictive indicator, in: A Textbook on EDTA Chelation Therapy, 1989, by Elmer M.Cranton (ed). Available from: American College for Advancement in Medicine, Laguna Niguel, CA, 1989.
7. Kindness, G., and Frackelton, J.P. Effect of EDTA on platelet aggregation in human blood. J Adv Med, 1989, 2: 4, 519-530.
8. Harman, D. The biologic clock: The mitochondria? J Am Geriatr Soc, 1972, 20: 145-147.
9. Miquel, J., Economos, A.C., Fleming, J., and Johnson, J.E. Mitochondrial role in cell aging. Exp Gerontol, 1980, 15: 575-591.
10. Miquel, J. An update on the mitochondrial-DNA mutation hypothesis of cell aging. Mutation Research, 1992, 275: 209-216.
11. Wallace, D.C. Mitochondrial genetics: a paradigm for aging and degenerative diseases?Science, 1992, 256:1063-1064.
12. Shoffner, J.M. and Wallace, D.C. Oxidative phosphorylation diseases and mitochondrial DNA mutations: diagnosis and treatment, Ann Rev. Nutr, 1994, 14: 535-568.
13. Flier, J.S. and Underhill, L.H. Mitochondria, DNA and disease, New England J of Medicine, 1995, 233:638-644.
14. Gallagher, C.H. Aging of mitochondria. Nature, 1960, 187: 732, 566-568.
15. Hunter, F.E., Malison, R., Bridgers, W.F., Schutz, B., and Atchison, A. J Biol Chem, 1959, 234: 693.
16. Born, G.R., and Geurkink, T.L. Improved peripheral vascular function with low dose intravenous ethylene diamine tetraacetic acid (EDTA). Townsend Letter for Doctors. July, 1994, # 132, 722-726.
What’s the Fuss Over Chelation? by Jonathan Collin, M.D.
(previously published in the Seattle Post Intelligencer)
For those of you who may be confused by the ongoing controversy over chelation therapy, let me give you a few pointers. Chelation chemistry is a well recognized field of study, having broad application in research, industry, and in medicine. Chelation therapy, as a specific treatment for hardening of the arteries, is disputed, and this is where the controversy comes in.
What does chelation mean? It basically is defined as a chemical reaction involving a protein structure binding a metal element. When the protein and metal join, the bond, known as ligand, forms one of the most stable structures in nature. Your blood hemoglobin is a chelate formed by the bonding of iron to the blood protein. In plants, chlorophyll represents a chelation of magnesium to plant protein. Anytime a chemist wishes to control metalsin solution, he will use a chelating agent to remove the metal element.
Waiting for “proof”
One particular chelating agent, EDTA, has the remarkable ability to bind a wide range of metals. Unlike hemoglobin which normally only accepts iron, and chlorophyll which only accepts magnesium, EDTA will bind with calcium or magnesium or iron or lead or even plutonium. The ability of EDTA to bond with calcium makes it very useful in medical technology. A blood specimen will not clot if EDTA is in the specimen container. The binding of EDTA to lead offers the very best medical therapy for lead poisoning. EDTA has a high affinity for radioactive substances, giving it high marks for treatment in radiation poisoning. So what is the chelation therapy controversy?
A growing number of physicians in the state of Washington, throughout the United States, and internationally, particularly in the Federal Republic of Germany, the Netherlands and Brazil, are using EDTA to treat atherosclerosis, circulatory conditions caused by hardening of the arteries. While EDTA is a perfectly legitimate therapy for lead poisoning, it is considered unproven as a treatment for atherosclerosis.
Although drug manufacturers published statements touting the role EDTA had in treating circulatory conditions in the past, the FDA forced the companies to remove these comments from their labeling. The American Medical Association, the National Institutes of Health, the American Heart Association, Medicare, and the U.S. Public Health Service feel that EDTA’s use for these disorders is investigational and has not yet been proven. Yet, the number of doctors who are using EDTA to improve blood flow to the heart’s coronary vessels is increasing yearly.
For years, only a very small contingent of doctors used EDTA in this manner. Fewer than 10 formed a group, the American Academy of Medical Preventics, in 1974. Now, 600 physicians have become seriously involved in chelation therapy, and consider it unequivocally a validated treatment. Although statistics on this are difficult to compile, the Academy estimates 500,000 Americans have received in excess of five million chelation treatments between 1974 and 1989. Most of these individuals demonstrated improved post-chelation circulation studies without manifesting significant side-effects. It stretches the imagination to consider this treatment investigational.
Instead of launching new experimentation and tabulating new data, medical spokesmen of the AMA, the American Heart Association, and the NIH were asked their opinion of EDTA chelation therapy. No reputable scientific study is ever made on the basis of opinion. The articles appearing in the Public Health Service report, disputing the validity of EDTA chelation, were not based on careful scientific research. Instead, anecdotal reports of self-acclaimed chelation critics professed the inadequacy and toxicity of chelation.
If EDTA is truly ineffective and harmful, why aren’t there good scientific data available to confirm these allegations?
One reason might be that the medical community is afraid to touch this hot potato with a 10-foot pole. Nobody having a credible academic standing wants to get his name tainted with a controversial therapy.
I say that chelation does work. When Norman E. Clarke, M.D., Charles N. Clarke, M.D., and Robert E. Mosher, Ph.D. described how angina pectoris was successfully treated by EDTA in 1956, they conducted careful scientific work. They had no ulterior motives; there were no hidden vested interests. Their report was based on the simplest of scientific methods; they just observed changes in patients receiving the treatment. Cardiologists Meltzer, Ural and Kitchell confirmed their findings. Carlos Lamar, M.D., further corroborated the results.
Recently, 20 papers have been published in the peer-review literature affirming the efficacy of EDTA in atherosclerosis. The original findings have never been reliably challenged. A specialist board, the American Board of Chelation Therapy, has been organized and is establishing the diplomate requirements for a new specialty in EDTA chelation therapy. EDTA chelation therapy is an appropriate, scientific therapy. Until responsible medical authorities conduct legitimate scientific research, disparaging reviews of EDTA should be disallowed. Parties interested in learning more about chelation are directed to books now widely available on the topic, and must seek the medical attention of private practitioners willing to administer the treatment.
Reprinted from the Port Townsend Health Letter—Winter 1990