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?

Fig.1 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

Mechanisms

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

Fig. 2 Structure of a Mitochondrion

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.

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References

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.