Steve Parcell, ND
EDTA chelation therapy is approved by the Food and Drug Administration (FDA) as a treatment for lead and heavy metal poisoning. About one million people in the United States are treated with EDTA chelation therapy every year. Chelation therapy is a medical treatment that improves cellular function by removing toxic metals (such as lead and arsenic) and abnormally elevated tissue levels of nutritional minerals (such as cobalt and iron). EDTA is best administered intravenously (through a vein).
EDTA is the abbreviation for the chemical compound ethylenediaminetetraacetic acid invented in the 1940s by Gerold Schwarzenbach. Interest in chelation was high during World War II as a treatment for arsenic poisoning after being exposed to poison gas. Researchers then learned that EDTA removed other toxic metals (metallic ions) as well. During the cold war interest in EDTA stemmed from its ability to detoxify radioactive isotopes. A metallic ion is the scientific name for metals in their charged unbound state. They can be negatively or positively charged. Common ions include iron (Fe2+), zinc (Zn2+), Magnesium(Mg2+), Calcium( Ca2+), lead(Pb2+), copper(Cu3+) and mercury (Hg2+).
In the 1950s the medical use of EDTA began to pick up speed after a group of workers in a Michigan battery factory were successfully treated with for lead poisoning with EDTA. Next the US Navy adopted EDTA as a treatment for sailors exposed to lead while painting ships and other naval property.
EDTA was first used to treat heart disease in the 1950s by Norman E. Clark, MD a prominent cardiologist at Providence Hospital in Detroit. He thought that because EDTA binds calcium EDTA might reverse coronary artery disease. Dr. Clarke had success using EDTA and was first to propose that EDTA had a primary effect on restoring cellular function through its ability to bind metallic ions.
Every study on EDTA chelation has been positive despite what you might have heard. I’ll discuss this later on. After Dr. Clarke’s finding clinical research continued on humans which showed improved exercise tolerance, increased walking distance, improved mental functioning and better circulation to the extremities.
In 1964 the distinguished Alfred Soffer, MD of Northwestern University Medical School and former director of cardiopulmonary laboratory of Rochester New York published a book called Chelation Therapy. In this book he stated “atherosclerotic patients suffering with leg pain from occlusive peripheral vascular disease appeared to benefit from repeated administration of EDTA, especially those patients with diabetes.” Millions of EDTA infusions have been given in the last 40 years with very few negative side effects.
At least 20 books have been authored on the subject of chelation (pronounced key-lay-shun) therapy. The majority of these books were written by respected medical doctors. Using chelation therapy for the treatment of heart disease is still considered to be an experimental treatment. EDTA chelation therapy is FDA approved for toxic metal poisoning.
Chelation literally means “to chemically bind to.” Chelation therapy is used to remove toxic metals such as lead and arsenic, or minerals such as iron and calcium from the blood. Chelation can be administered either orally or intraveneously. Chelation has many effects on the body. The net effect is a reversal of many age-related changes. Chelation is one of the most profound anti-aging treatments available becasue toxic metals accelerate aging. In conventional medicine, chelation is used to rid the body of excess or toxic metals such as lead or calcium (as in hypercalcemia). EDTA is FDA approved for heavy metal poisoning, digitalis toxicity and elevated blood calcium levels. A person who has lead poisoning may be given chelation therapy in order to remove excess lead from the body before it can cause damage. EDTA (ethylene diamine tetra-acetic acid), a synthetic amino acid that is delivered intravenously. EDTA was first used in the 1940s for the treatment of heavy metal poisoning. EDTA chelation removes minerals from the blood such as lead, iron, copper and calcium and is approved by the U.S. Food and Drug Administration (FDA) for use in treating lead poisoning and toxicity from other heavy metals. Although it is not approved by the FDA to treat heart disease, some physicians and alternative medicine practitioners use EDTA chelation as a way to treat this disorder. It may be effective because it reduces oxidative stress, is anticoagulant (decreases clotting), lowers serum calcium and lowers blood pressure.
Does EDTA chelation therapy have side effects?
When used as approved by the FDA for treatment of heavy metal poisoning, EDTA has a low occurrence of side effects. The most common side effect is a burning sensation experienced at the site where the EDTA is delivered into the veins. Rare side effects can include fever, hypotension (a sudden drop in blood pressure), hypocalcemia (abnormally low calcium levels in the blood), headache, nausea, vomiting and bone marrow depression (meaning that blood cell counts fall). Injury to the kidneys has been reported with EDTA chelation therapy, but it is rare. Other serious side effects can occur if EDTA is not administered by a trained health professional.
Does EDTA chelation therapy reverse atherosclerosis?
In some cases it may help but this depends on many factors. The efficacy and mechanism of action is still being studied. We have noticed that it is most effective when elevated levels of heavy metals are present. Several theories have been proposed for the mechanism of action. One theory suggests that EDTA chelation might work by directly removing calcium found in fatty plaques that block the arteries, causing the plaques to break up. Another is that the process of chelation may stimulate the release of a hormone that in turn causes calcium to be removed from the plaques or causes a lowering of cholesterol levels. A third theory is that EDTA chelation therapy may work by reducing the damaging effects of oxygen ions (oxidative stress) on the walls of the blood vessels. Reducing oxidative stress could reduce inflammation in the arteries and improve blood vessel function. Since EDTA is also an anticoagulant it may work by preventing the collection of platelets which can lead to formation of blood clots on the walls of blood vessels. In addition, intravenous treatments often include high dose magnesium and vitamins which have their own beneficial effects. Magnesium, in particular, is an effective treatment for high blood pressure, coronary spasm and congestive heart failure. Magnesium reduces inflammation, endothelial dysfunction, oxidative stress and platelet aggregability. Magnesium also acts as a mild calcium blocker and as a vasodilator. Chelation therapy may actually work because of the sum of all the biochemical and physiologic effects that is has.
Is There Evidence That EDTA Chelation Therapy Reverses Coronary Artery Disease (CAD)?
The bulk of the evidence supporting the use of EDTA chelation therapy is in the form of case reports and case series, published in peer review journals but lacking the numbers of patients we typically like to see. Many patients who have undergone chelation therapy have improvement in CAD symptoms such as chest pain. Chelation may also be able to lower plaque in the arteries as measured by EBCT heart scans, though this finding has not been published. In addition, there are approximately 12 published studies and 5 randomized controlled clinical trials regarding the use of EDTA chelation for CAD. Although each descriptive study did report a reduction in angina, they were uncontrolled clinical observations or retrospective data, typically with a small number of participants. Of the five clinical trials in which patients were randomly selected to receive chelation therapy or a placebo, three trials involved so few people that only a dramatic improvement could have been detected. The fourth study was never published in final form, so its conclusions are uncertain. Finally, the fifth study reported that EDTA chelation was associated with an improvement in ability to exercise, but it had only 10 participants. There is currently a large study underway and we hope that it will demonstrate a clear positive outcome. In the most recent study (the TACT Trial) published in 2013 patients who received chelation had less heart attacks than patients who did not receive chelation.
Can chelation therapy be used to prevent restenosis in patients following percutaneous transluminal coronary angioplasty (PTCA)?
Recently a multicenter, retrospective study was completed on 220 patients with known vascular disease treated from 1992- 2001 with I.V. EDTA and followed for three years. This study demonstrated that in those patients who received chelation, fewer cardiac events occurred and less procedures were needed than the untreated group. Of the patients who received chelation only 4% needed repeat angioplasties and none required coronary artery bypass surgery (CABG). In the untreated group 22.3 % needed repeat angioplasties and 11.8 % needed CABG.
How frequently is EDTA chelation therapy used?
It is estimated by the American College for Advancement in Medicine, a professional association that supports the use of chelation therapy, that more than 800,000 visits for chelation therapy were made in the United States in 1997 alone. Since the 1950s millions of EDTA infusions have been administered. Typically, 30 to 40 initial IV infusions are given and then the patient is re-evaluated for maintenance therapy.
What is the cost of chelation therapy?
This will depend on the frequency of treatment and dose of EDTA. Typically it costs between $2,000 and $3,000 for an effective course of treatment over one year.
Why is chelation therapy not more widely accepted?
The answers are as follows:
We are still waiting for more studies with larger numbers of patients. Because of this, chelation therapy (for cardiovascular disease) is not taught in hospitals or medical schools. The patent ran out on EDTA many years ago so there is no financial incentive for drug companies to do the studies. This is why the current study is being paid for by the National Institutes of Health (US government funded). It is an inexpensive treatment as compared to interventions such as coronary bypass surgery and angioplasty. It doesn’t completely replaces these procedures but if more people underwent chelation therapy it could lead to less of these procedures being performed. Doctors that perform these procedures would lose money as a result.
Why are toxic metals bad?
Heavy metals accumulate over time in humans and animals. This is called “bioaccumulation” and can be especially dangerous to human health. Toxic metals enter the human body mainly through inhalation and ingestion. Ingestion is the main route of exposure to these elements in human population. Vegetables take up metals by absorbing them from contaminated soils, as well as from deposits on different parts of the vegetables exposed to the air from polluted environments.
It has been reported that nearly half of the mean ingestion of lead, cadmium and mercury through food is due to plant origin (fruit, vegetables and cereals). Moreover, some population groups seem to be more exposed, especially vegetarians, since they absorb more frequently ‘tolerable daily doses’. Chronic low-level intakes of heavy metals have damaging effects on human beings and other animals, since there is no good mechanism for their elimination. Metals such as lead, mercury, cadmium and copper are cumulative poisons.
The heavy metals cadmium, lead and mercury are common air pollutants, as a result of various industrial activities. Although the atmospheric levels are low, they contribute to the deposition and build-up in soils. Cadmium exposures are associated with kidney and bone damage. Cadmium has also been identified as a potential human carcinogen, causing lung cancer. Lead exposures have developmental and neurobehavioural effects on fetuses, infants and children, and elevate blood pressure in adults. Mercury is also toxic but the main concern is associated with methylmercury, that accumulate in the food chain, i.e. in predatory fish in lakes and seas, as these are the main routes of human exposure.
Toxic metals all share two fundamental destructive mechanisms: inhibition of enzyme activity, inhibition of normal cellular function, neurotoxicity and initiation of oxidative stress. Toxic metals exposure also ages you faster and can cause cancer. EDTA binds to these metals and neutralizes them. Patients often ask me how they got heavy metals.
How does chelation therapy work?
There a numerous ways in which chelation may work. The effects on humans may be a sum of all the mechanisms of action or just one – we still do not know for sure just why chelation is so helpful in atherosclerosis. The following is a list of all the mechanism by which EDTA chelation may work:
- EDTA chelation improves the elasticity of arteries by reducing the number of cross linkages in the connective tissue and elastic tissue comprising arterial walls. Cross linking accelerates aging is what causes skin to wrinkle, sag and loose its youthful elasticity. In the artery cross linking causes stiffness. EDTA decreases the cross linkages in the arterial wall allowing it to expand and contract as it was designed to do. As arteries become less stiff improved circulation and lower blood pressure is a result.
- Chelation therapy can also reduce the non metallic cross linkages that occur between molecules such as sulfur to sulfur cross linkages. One of the metals EDTA removes in aluminum. Aluminum can cause cross linkages between collagen and elastic tissue, making soft tissue and arteries more rigid and speeding the aging process. This makes arteries more elastic or flexible, returning them to a more youthful state. Another benefit of this is a lower blood pressure.
- EDTA chelation therapy is a potent antioxidant. This is the most important action of EDTA.
- During the short time that EDTA circulates in the body it temporarily lowers blood calcium. This signals the parathyroid gland to step up production of parathyroid hormone to help bring calcium levels back up. This may be how EDTA chelation increases bone density
- EDTA help balance prostaglandin production. Prostaglandins are important hormones that control inflammation, clotting and blood vessel tone. The two most important protaglandins for blood vessel health are thromboxane and prostacyclin. Prostacyclin reduces platelet “stickiness” and thromboxane causes platelets to stick together and also promotes arterial spasm. EDTA restores the normal production of prostacyclin. Prostacyclin helps prevent arterial spasm, blood clots, counters plaque formation, reduces platelet stickiness and improves blood flow. Fatty acid oxidation (lipid peroxidation) inhibits prostacyclin production. EDTA is able to reduce oxidation of fats in cell membranes by chelating out the metallic ions that cause lipid peroxidation. Measuring and reducing lipid peroxidation is a big deal in anti-aging medicine. EDTA inhibits oxidation of lipids in the cell membrane and restores optimal platelet function.
- EDTA acts as an anticoagulant through its beneficial effect on platelets.
- EDTA lowers blood calcium levels and helps normalize calcium metabolism by stimulating uptake of calcium in bones. Evidence demonstrates the chelation therapy may help improve bone density.
The way I describe chelation to patients is this: You are getting an intravenous antioxidant that removes toxic metals and
1: KITCHELL JR, PALMON F Jr, AYTAN N, MELTZER LE.
The treatment of coronary artery disease with disodium EDTA. A reappraisal.
Am J Cardiol. 1963 Apr;11:501-6. No abstract available.
PMID: 14033183 [PubMed – indexed for MEDLINE]
2: CLARKE NE Sr, CLARKE NE Jr, MOSHER RE.
Treatment of occlusive vascular disease with disodium ethylene diamine
tetraacetic acid (EDTA).
Am J Med Sci. 1960 Jun;239:732-44. No abstract available.
PMID: 13810513 [PubMed – indexed for MEDLINE]
3: RITTER J, MARTI-FECED C.
[Trials and results of the treatment of patients with manganese poisoning and of
the prevention of manganese poisoning by EDTA calcium or calcitetracemate
Arch Mal Prof. 1960 Mar;21:115-30. French. No abstract available.
PMID: 14437623 [PubMed – indexed for MEDLINE]
4: ARONOV DM.
[1ST EXPERIENCE WITH THE TREATMENT OF ATHEROSCLEROSIS PATIENTS WITH CALCINOSIS OF
THE ARTERIES WITH TRILON B (DISODIUM SALT OF EDTA).]
Klin Med (Mosk). 1963 May;41:19-23. Russian. No abstract available.
PMID: 14058480 [PubMed – indexed for MEDLINE]
5: MELTZER LE, KITCHELL JR, PALMON F Jr.
The long term use, side effects, and toxicity of disodium ethylenediamine
tetraacetic acid (EDTA).
Am J Med Sci. 1961 Jul;242:11-7. No abstract available.
PMID: 13769308 [PubMed – indexed for MEDLINE]
6: RUKAVINA JG, ORKIN M, LYNCH FW.
The effect of an intravenous chelating agent, edathamil disodium (Na 2-EDTA), in
3 cases of sarcoidosis.
J Invest Dermatol. 1958 Nov;31(5):259-62. No abstract available.
PMID: 13598931 [PubMed – indexed for MEDLINE]
7: BOYLE AJ, JASPER JJ, MCCORMICK H, KOSAI M, MCCANN D, GOODWIN J, CLARKE NE,
Studies in human and induced atherosclerosis employing ethylenediaminetetraacetic
Bull Schweiz Akad Med Wiss. 1957 Apr;13(1-4):408-25. No abstract available.
PMID: 13436989 [PubMed – OLDMEDLINE]
8: Chappell LT.
Should EDTA chelation therapy be used instead of long-term clopidogrel plus
aspirin to treat patients at risk from drug-eluting stents?
Altern Med Rev. 2007 Jun;12(2):152-8. Review.
PMID: 17604460 [PubMed – indexed for MEDLINE]
9: Seely DM, Wu P, Mills EJ.
EDTA chelation therapy for cardiovascular disease: a systematic review.
BMC Cardiovasc Disord. 2005 Nov 1;5:32. Review.
PMID: 16262904 [PubMed – indexed for MEDLINE]
10: Mellau LS, Jørgensen RJ.
Does EDTA-infusion affect calcium homeostatis leading to increased resistance to
Acta Vet Scand Suppl. 2003;97:29-34. Review.
PMID: 14621393 [PubMed – indexed for MEDLINE]
11: Foglieni C, Fulgenzi A, Ticozzi P, Pellegatta F, Sciorati C, Belloni D,
Ferrero E, Ferrero ME.
Protective effect of EDTA preadministration on renal ischemia.
BMC Nephrol. 2006 Mar 15;7:5.
PMID: 16536881 [PubMed – indexed for MEDLINE]
12: TEICHMANN W.
[CASE REPORT ON THE TREATMENT OF LEAD POISONING WITH THE CHELATING AGENT NA
2-EDTA IN SMALL DOSES.]
Z Gesamte Inn Med. 1963 Jul 1;18:597-9. German. No abstract available.
PMID: 14047064 [PubMed – OLDMEDLINE]
13: GERGER T, MOESCHLIN S.
[Therapeutically usable nontoxic dose of calcium disodium ethylenediamine
Praxis. 1959 Jun 4;48(23):545-8. German. No abstract available.
PMID: 13667772 [PubMed – indexed for MEDLINE]
14: SOFFER A, TORIBARA T.
Changes in serum and spinal fluid calcium effected by disodium
J Lab Clin Med. 1961 Oct;58:542-7. No abstract available.
PMID: 13914781 [PubMed – indexed for MEDLINE]
15: van Rij AM, Solomon C, Packer SG, Hopkins WG.
Chelation therapy for intermittent claudication. A double-blind, randomized,
Circulation. 1994 Sep;90(3):1194-9.
PMID: 8087928 [PubMed – indexed for MEDLINE]
16: Guldager B, Jelnes R, Jørgensen SJ, Nielsen JS, Klaerke A, Mogensen K, Larsen
KE, Reimer E, Holm J, Ottesen S.
EDTA treatment of intermittent claudication–a double-blind, placebo-controlled
J Intern Med. 1992 Mar;231(3):261-7.
PMID: 1556523 [PubMed – indexed for MEDLINE]
17: Sloth-Nielsen J, Guldager B, Mouritzen C, Lund EB, Egeblad M, Nørregaard O,
Jørgensen SJ, Jelnes R.
Arteriographic findings in EDTA chelation therapy on peripheral arteriosclerosis.
Am J Surg. 1991 Aug;162(2):122-5.
PMID: 1907432 [PubMed – indexed for MEDLINE]
18: Knudtson ML, Wyse DG, Galbraith PD, Brant R, Hildebrand K, Paterson D,
Richardson D, Burkart C, Burgess E; Program to Assess Alternative Treatment
Strategies to Achieve Cardiac Health (PATCH) Investigators.
Chelation therapy for ischemic heart disease: a randomized controlled trial.
JAMA. 2002 Jan 23-30;287(4):481-6.
PMID: 11798370 [PubMed – indexed for MEDLINE]
19: Villarruz MV, Dans A, Tan F.
Chelation therapy for atherosclerotic cardiovascular disease.
Cochrane Database Syst Rev. 2002;(4):CD002785. Review.
PMID: 12519577 [PubMed – indexed for MEDLINE]
20: Guldager B, Jørgensen PJ, Grandjean P.
Metal excretion and magnesium retention in patients with intermittent
claudication treated with intravenous disodium EDTA.
Clin Chem. 1996 Dec;42(12):1938-42.
PMID: 8969629 [PubMed – indexed for MEDLINE]
 The oxidation of fats in cell membranes is called “lipid peroxidation” by scientists and is one of the main ways in which cells age.