EDTA Chelation

An essential part of regaining your health, staying healthy and getting ready for stem cell therapy is chelation! To understand why this is true a little background is needed:

There are two general types of poisons that affect our bodies – heavy metals and chemicals. Heavy metals include lead, mercury, cadmium, etc. which react with oxygen, glucose, etc. to produce free radicals which damage tissues where the metals are embedded in the body.

Metals such as copper, zinc, iron, etc. are usually a part of the structures of proteins in living organisms. If these metals are released into tissues, they react with oxygen and form free radicals. Heavy metals such as lead and mercury sabotage the body’s free radical mop up system which basically keeps them from forming molecules with unpaired electrons. These free radical electrons then can react with other molecules and form a chain reaction of destruction. The result is that your tissue “spoils” or becomes “rancid”. These “rancid” membranes are a major part of aging and disease. One of the biggest challenges in reversing aging and chronic disease processes is to actually reverse this “rancidity” of diseased tissues. Chelation removes the basic cause behind the formation of “rancid” membranes by removing the free metals that bring about  the formation of “rancid” oxidized cell membranes.

EDTA chelation is endorsed for the treatment of atherosclerotic vascular disease by the American College for Advancement in Medicine (ACAM), comprising of 750 licensed physicians. Its proponents claim that EDTA consistently improves blood flow and relieves symptoms associated with atherosclerosis in over 80% of the patients treated. In early studies, it was observed that patients being treated for acute lead intoxication with EDTA and who had cardiovascular disease showed improved stress tolerance and less chest pain with physical exertion. In 1956 Norman Clarke published an article in the American Journal of Medical Science on the successful treatment of patients with severe angina pectoris through the use of EDTA.

In 1988, Drs. Olszewer and Carter reported on the treatment of 2870 patients with EDTA chelation therapy. Over 93% of the patients who suffered from narrowed coronary arteries showed good to excellent improvement. 97% of those with narrowed leg arteries showed improvement and 60% of patients with narrowed brain arteries showed increased circulation from EDTA chelation.

More than one million patients have received over twenty million infusions to-date. No significant adverse effects have been reported when the ACAM protocol has been followed. Early reports of renal injury and more recent adverse effects resulted from excessive doses being given (greater than 50 mg/Kg/day), from infusions that were too fast (less than three hours), and from failing to replace calcium, magnesium and other nutrients that are recommended in the ACAM protocol.

Click Here to Read More!

The benefits of EDTA chelation are proposed to include:

  • Binds with calcium ions in arterial walls and plaque. With a decrease in the extracellular quantities of calcium, the arterial wall becomes more compliant, less rigid and more elastic. This results in a greater delivery of blood to each of the body’s organs in instances in which the arterial compliance had been previously compromised.
  • Binds with extracellular calcium (outside the cell) which induces calcium withdrawal from inside injured artery wall cells. With the removal of calcium, the cell is better able to resume normal energy production, waste removal and  functioning.
  • Binds with heavy metals such as lead, mercury, cadmium, aluminum, uranium, etc. These metals block enzyme activity and their removal helps restore enzyme functions within the arterial walls.
  • Binds to iron and copper ions, transition metals that promote free radical reactions. By removing these metal ions, EDTA chelation slows or stops free radical damage. This includes reductions in lipid peroxidation and oxidized cholesterol.
  • EDTA has an “anti-sticky” effect on blood platelets. Lipid peroxides and free radicals inhibit the synthesis of prostacyclin. Reducing these influences helps to normalize the balance between prostacyclin levels and thromboxane, and reduce the risk of “sticky” platelets and blood clots that can block an artery.
  • EDTA has a membrane fluidizing effect on erythrocytes, making them more flexible and better able to maneuver through small capillaries. This results in improved tissue oxygenation.
  • EDTA uncouples disulfide and mineral cross-links, enabling greater flexibility in connective tissue.
  • EDTA may inhibit NF kappa B which plays a pivotal role in programmed cell death.
  • EDTA’s chelation of zinc and copper may reverse the cortical deposition of amyloid beta involved in Alzheimer’s disease.

In summary, arteries become hardened and non-elastic as atherosclerosis develops. EDTA chelation therapy “softens” these hardened arteries by reducing the collagen and elastin cross linkages by removing the metals that are generating the cross-linking free radicals.

The claimed and reported results of these effects from chelation include:

  • Improved circulation
  • Reduction of liver produced cholesterol
  • Lowered insulin requirements in diabetics
  • Reduced high blood pressure
  • Normalization of cardiac arrhythmia’s
  • Relief from leg muscle cramps
  • Normalized weight
  • Improved psychological and emotional status
  • Enhanced sensory performance
  • Fewer excessive heart contractions
  • Lessened varicose vein pigmentation
  • Lightened age spots
  • Fewer arthritic aches and pains
  • Less reliance on pain medication
  • Hair loss stopped and reversed
  • Reversal of impotence
  • Alzheimer symptoms ameliorated or reversed
  • Reduced need for diuretics
  • Cold extremities warmed
  • Chronic fatigue syndrome overcome
  • Memory and concentration improved
  • Cataract vision loss restored
  • Skin, hair, nail improvement

Contraindications include:

  • Renal Failure
  • Malignant Disease
  • Congestive Heart Failure
  • History of parathyroid disease or surgery and/or hypokalemia
  • Tuberculosis
  • Pregnancy
  • History of severe bleeding from previous injury, surgery or dental extractions
  • Medications: Coumadin, Ticlid, Plavix.

The Protocol for Mixing EDTA bottles is as follows.
In Sterile Water add the following:

  • EDTA – up to 20 ml (3 grams)
  • Sodium Bicarbonate, 50 mEq/50 ml – 20 ml
  • Vitamin C, 6 ml, 500 mg/ml, 3.0 gm.
  • Mg Chloride, 2 grams – 10 cc
  • Heparin, 0.25 ml, 10,000 u.ml = 5000 units
  • Folic Acid, 0.25 ml, 10 mg/ml = 2.5 mg
  • Pyridoxine, 1 ml, 100 mg/ml = 100 mg
  • Hydroxycobalamin, 1 ml, 1000 mcg/ml – 1000 mcg
  • B-Complex – 100, 1 ml
  • Lidocaine HCL, for IV infusion, 2%, 20 mg/ml – 5 ml = 100 mg

Let’s look at each of these components more closely:

  • EDTA – reduces collagen and elastin cross linking
  • Sodium Bicarbonate – helps balance the pH
  • Vitamin C

* precursor of collagen; increases the healing rates of wounds
* improves immune function
* moderate amounts can reduce vascular thrombosis
* an antioxidant, reduces oxidative stress
* improves physical endurance
* inhibits LDL cholesterol
* lowers blood concentrations of lead
* improves endothelial function (blood vessel wall cells)

  •   Magnesium

* Involved in over 300 enzyme systems
* Required for protein and carbohydrate metabolism
* Involved in nerve and muscle electrical potentials and transmitting impulses across
* Intravenous administration can be helpful for atrial tachycardia, ventricular fibrillation and tachycardia
* Can reduce angina attacks in patients with coronary artery disease
* Can decrease LDL and total cholesterol and increase HDL
* Plays a role in blood pressure regulation

  • Heparin

* enhances circulating lipoprotein lipase activity
* has antioxidant effects
* prevents endothelial injury and dysfunction
* enhances protective activity of vascular nitric oxide
* inhibits harmful endothelin effects
* inhibits chronic inflammatory damaging actions
* inhibits vascular smooth muscle cell proliferation and migration
* inhibits angiotensin-converting enzyme and thus blocked harmful effects of an overactive rennin-angiotensin system
* negates the effects of advanced glycation end products (AGE) and their receptor (RAGE).

  •  Folic Acid

* Promotes metabolism of homocysteine, reducing hyperhomocysteinemia (which injures blood vessel walls) when given with vitamin B12 and pyridoxine. Hyperhomocysteinemia is a risk factor for coronary, cerebral and peripheral atherosclerosis, thromboembolism, deep vein thrombosis, myocardial infarction and ischemic stroke.
* Important in the methylation of DNA, promotes genetic stability (reduces chromosome breaks and risk of cancer)

  •   Pyridoxine (Vitamin B6)

* Required for metabolism of methionine and trans-sulfuration of homocysteine, reducing hyperhomocysteinemia (which injures blood vessel walls) when given with vitamin B12 and folic acid.
* Required for amino acid, carbohydrate and lipid metabolism
* Required for serotonin, norepinephrine and dopamine metabolism
* Required for metabolism of polyunsaturated fatty acids and phospholipids
* Required for the synthesis of the heme in hemoglobin
* Has some antioxidant and free radical scavenging capacity

  •  Hydroxycobalamin (Vitamin B12)

* Promotes metabolism of homocysteine, reducing hyperhomocysteinemia (which injures blood vessel walls) when given with folic acid and pyridoxine.
* Required for nucleoprotein and myelin synthesis
* Required for cell methylation and reproduction
* Maintains sulfhydryl groups in reduced form required by enzymes for protein synthesis and carbohydrate and fat metabolism
* Required for folate metabolism
* Reduces risk of depression, memory loss, and muscle weakness

  •   B-Complex

* Consists of thiamine, riboflavin, niacin/niacinamide, pantothenic acid, pyridoxine, vitamin B12, folic acid, choline, APBA and inositol. The B vitamins work best as a group and assist the function of pyridoxine, folic acid and vitamin B12.

  • Lidocaine

* helps reduce the local pain of infusion

Chelation is gaining acceptance in conventional medicine as an adjunct treatment for Alzheimer’s Disease. By removing unbound iron, copper, aluminum, zinc, etc. in the brain, which generate free radicals and contribute to the development of collagen and elastin cross linking by free radicals (as advanced glycation end products), chelation assists in blocking the factors that contribute to diabetes, atherosclerosis, neurodegenerative diseases including Alzheimer’s, and aging.

In addition the NIH conducted a multicenter medical trial with EDTA chelation for atherosclerosis. Previous studies were flawed in that the ACAM protocol was not followed. There is also the need for the drip to be sufficiently slow and for the patient’s blood to be checked through the week to insure that essential minerals are maintained within the normal range.

When this study was completed, the results were summarized as follows:

“A $30 million National Institutes of Health-funded trial to assess the safety and efficacy of EDTA chelation therapy in 1708 post-myocardial infarction (MI) patients was completed in 2014.  The trial demonstrated a significant (P=0.035) 18% reduction in a combined primary endpoint of death, MI, stroke, coronary revascularization or hospitalization of angina.  In diabetic patients the benefit was more impressive, with a 41% relative reduction in risk (P=0.0002) and a 43% reduction in total mortality (P=0.011).  Safety data were also favorable.  A reduction of oxidative stress by chelation of toxic metals has been proposed as a possible mechanism of action.”

  1. Aronov, D.M.: “First experience with the treatment of atherosclerosis patients with calcinosis of the arteries with trilon-B (disodium salt of EDTA). KLIN MED (Russ Moscow), 1963; 41: 19-23.
  2. Bates, G.W., C. Billups, P. Saltman. “The kinetics and mechanism of iron (III) exchange between chelates and transferrin. II. The presentation and removal with ethylenediaminetetraacetate.” J BIOL CHEM, 1967; 242: 2816.
    Bjorksten, J: “Possibilities and limitations of chelation as a means for life extension.” REJUVENATION, 1980; 8: 67-72.
  3. Blumer, W. “Leaded gasoline – a cause of cancer.” ENVIRONMENTAL INTERNATIONAL, 1980; 3: 465-71.
  4. Boyle, A.J., J.J.Casper, H. McCormick et al.: “Studies in human and induced atherosclerosis employing EDTA.” BULL SCHWEIZ AKAD MED WISS, 1957; 13: 408 (Swiss, Basel).
  5. Boyle, A.J., N.E. Clarke, R.E. Mosher, D.S. McCann: “Chelation therapy in circulatory and sclerosing diseases.” FED PROC 1961; 20(3): (Part II Suppl 10): 243-57.
  6. Brecher, A. “BYE-BYE BYPASS: THE TRUTH ABOUT CHELATION THERAPY. Troup, Texas, Health Savers Press, 1989.
    Brucknerova, O. J. Tulacek. “Chelates in the treatment of occlusive arteriosclerosis.” VNITRNI LEK, 1972; 18: 729.
  7. Casdorph, H.R.: “EDTA chelation therapy, efficacy in arteriosclerotic heart disease.” J HOLISTIC MED, 1981; 3(1): 53-59.
  8. Casdorph, H.R., C.H. Farr: “EDTA chelation therapy III: Treatment of peripheral arterial occlusion, an alternative to amputation.” J HOLSTIC MED, 1983; 5(1): 3-15.
  9. Cashion,, W.R. Jr.: “What about chelation?” TEXAS MEDICINE, 1984; 80:6.
    Castellino, N. S. Aloj. “Effects of calcium sodium ethylenediaminetetra-acetate on the kinetics of the distribution and excretion of lead in the rat. BRIT J INDUS MED, 1965; 22: 172.
    Chappell, L.T., J.P. Stahl. “The correlation between EDTA chelation therapy and improvement in cardiovascular function: a meta-analysis.” J ADV MED, 1993; 6: 139.
  11. Chappell, L.T.: “EDTA chelation therapy should be more commonly used in the treatment of vascular disease.” ALTERNATIVE THERAPIES HEALTH MED, 1995; 1: 53.
  12. Chappell, L.T., R. Miranda, M.Rubin, J.O. Carter, J. Trowbridge. “Chelation therapy (Letter).” CIRCULATION, 1995; 92: 1350.
    “Chelation Therapy (Diagnostic and therapeutic technology assessment).” JAMA, 1983; 250: 672.
  13. “Chelation Therapy.” Resolution: 66 (I-84). AMA House of Delegates., 1984.
    “Chelation Therapy – An informal summary.” Department of Health & Human Services. National Institutes of Health. National Heart, Lung, and Blood Institute. Bethesda, Maryland, June 1992.
  14. “Chelation Therapy: A second look.” THE HARVARD MEDICAL SCHOOL HEALTH LETTER, 1984; IX: 1.
  15. Chen, I.W., H.M., Park, L.R. King, G.K. Bahr, R.E. Goldsmith: “Radioimmunoassay of parathyroid hormone: peripheral plasma immunoreactive parathyroid hormone response to ethylenediaminetetraacetate.” J NUCL MED, 1974; 15: 763.
  16. Christensen, K. and D. Theilade: “EDTA chelation therapy: an ethical problem.” MEDICAL HYPOTHESES, 1999; 53(1): 69-70.
  17. Clark, N.E., C.N., Clarke, R.E. Mosher: “The in vivo disolution of metastatic calcium: An approach to atherosclerosis.” AM J MED SCI, 1955; 229: 142-49.
  18. Clark, N.E., C.N. Clarke, R.E. Mosher: “Treatment of angina pectoris with disodium ethylene diamine tetraacetic acid.” AM J MED SCI, 1956; 232: 654-66.
  19. Clark, N.E.: “Atherosclerosis, occlusive vascular disease and EDTA.” AM J CARDIOL, 1960; 6: 233-36.
  20. Conti, C.R.: “Chelation therapy for atherosclerosis: one man’s view.” CLIN CARDIOL, 1995; 18: 545.
  21. Cranton, E.M.: “Kidney effects of ethylene diamine tetraacetic acid (EDTA): A Literature Review.” J HOLISTIC MED, 1982; 4: 152.
  22. Cranton, E.M., J.P. Frackelton: “Free radical pathology in age-associated diseases: treatment with EDTA chelation, nutrition and antioxidants.” J HOLISTIC MED, 1984; 6:6.
  23. Cranton, E.M. “The current status of EDTA chelation therapy.” J HOLISTIC MED, 1985; 7:3.
    Cranton, E.M. “Protocol of the American College of Advancement in Medicine for the safe and effective administration of EDTA chelation therapy.” J ADV MED, 1989; 2:269.
  24. Cranton, E.M. “A Textbook on EDTA chelation therapy.” J ADV MED, 1989; 2: 1-416.
  25. Cranton, E.M. and A. Brecher: “BYPASSING BYPASS: THE NEW TECHNIQUE OF CHELATION THERAPY.” New York, Stein and Day, 1990.
    Cranton, E.M. and J.P. Franckelton. “Negative Danish study of EDTA chelation biased (Letter).” TOWNSEND LETTER FOR DOCTORS, 1992; July, 604-605.
    Craven, P.C. and H.F. Morrelli. “Chelation Therapy.” WESTERN J MED, 1975; 122: 277.
  26. Curran, C.L.: “Metal chelating agents and hepaticcholesterol synthesis.” PROC SOC EXPER BIOL & MED, 1955; 88: 101.
    Deucher, D.P.: “EDTA chelation therapy: an antioxidant strategy.” J ADV MED, 1988; 1: 182.
  27. Doolan, P.D., S.L. Schwartz, J.R. Hayes, J.C. Mullen, N.B. Cummings: “An evaluation of the nephrotoxicity of ethylenediaminetetraacetate and diethylenetriaminepentaacetate in the rat.” TOXICOL APPL PHARMACOL, 1967; 10: 481-500.
  28. FDA, “Calcium disodium edetate and disodium edetate. Drugs for human use; durg efficac study implementation.” Department of Health, Education and Welfare, Fod and Drug Administration, Federal Registrar, 1970, 35 F.R., 437.
  29. Friedel, W., F.H. Schulz, L. Schoder: “Therapy of atherosclerosis through mucopolysaccarides and EDTA (ethylene diamine tetraacetic acid).” (German), DEUTSCH GESUNDH, 1965; 20: 1566-70.
  30. Godfrey, M.E., R. Agnihotri, A. Strauss. “Chelation and arteriosclerosis.” NZ MED J, 1988; 101(838): 21.
  31. Godfrey, M.E. “EDTA chelation as a treatment of arteriosclerosis.” NZ MED J, 1990; 93: 199.
  32. Godfrey, M.E., J.P. Frackleton, L.T. Chappell.: “Chelation therapy for intermittent claudication (Letter).” NZ MED J, 1994; 107: 495.
  33. Gordon, G.B., R.B. Vance: “EDTA chelation therapy for atherosclerosis: History and mechanisms of action.” OSTEOPATHIC ANNALS, 1976; 4: 38-62.
  34. Gordon, G. F. “Chelation Therapy: History and Mechanisms of Action, an Update.” CLINICAL PRACTICE OF ALTERNATIVE MEDICINE, in press.
    Gotto, A.M. Jr. “Chelation therapy in 1984.” TEXAS MEDICINE, 1984; 80: 36.
  35. Gould, R.G. “Metals and chelating agents in relation to atherosclerosis.” FED PROC, 1961; 20(Suppl 10): 252.
  36. Grier, M.T. and D.G. Meyers. “So much writing, so little science: A review of 37 years of literature on edetate sodium chelation therapy.” ANN PHARMACOTHER, 1993; 27: 1504.
  37. Guldager, B. R. Jelnes, S.J. Jorgenson, et al. “EDTA treatment of intermittent claudication – a double-blind placebo-controlled study.” J INTERN MED, 1992; 231: 261.
  38. Gutteridge, J.M.C. “Ferrous-salt promoted damage to deoxyribose and benzoate, the increased effectiveness of hydroxyl-radical scavengers in the presence of EDTA.” BIOCHEM J, 1987; 243: 709.
  39. Halstead, B.W.: THE SCIENTIFIC BASIS OF EDTA CHELATION THERAPY. Golden Quill Publishers, Box 1278, Colton, CA 92324, 1979.
  40. Hancke, C. and K. Flytlie. “Benefits of EDTA chelation therapy on arteriosclerosis.” J ADV MED, 1993; 6: 161.
  41. Hardy,H.L. “Clinical experience with the use of calcium disodium ethylenediaminestetraacetate in the therapy of lead poisoning.” FED PROC, 1961; 20 (Suppl 10): 252.
  42. Hay, D.R. “Chelation therapy.” NZ MED J, 1988; 101(841): 122.
  43. Hay, D.R. “Chelation therapy.” NZ MED J, 1988; 101(845): 246.
    Jonas, W.B.: “Meta-analysis of EDTA chelation: math that doesn’t matter.” J ADV MED, 1994; 7: 109.
  44. Jonas W.B. “Effectiveness of EDTA chelation therapy.” CIRCULATION, 1995; 5: 1352.
  45. Jones, R.J. “Chelation therapy (Letter).” JAMA, 1983; 250: 672.
  46. Julian, J.J.: PASS OR BYPASS? CHELATION EXTENDS LIFE. Wellness Press, Hollywood, 1981. Kaman, R.L., C.J. Rudolph, E.W. McDonagh, F.M. Walker. “Effect of EDTA chelation therapy on aortic calcium in rabbits on atherogenic diets: quantitative and histochemical studies.” J ADV MED, 1990; 3:13.
  47. Kitchell, J.R., L.E. Meltzer, M.J. Seven:”Potential uses of chelation methods in the treatment of cardiovascular diseases.” PROG CARDIOVASCULAR DIS, 1961; 3: 338-49.
  48. Kitchell, J.R., F. Palmon, N. Aytan, L.E. Meltzer: “The treatment of coronary artery disease with disodium EDTA, a reappraisal.” AM J CARDIOL, 1963; 11: 501-6.
  49. Kozlov, V.A. and V.M. Novikova: “Calcium ion-dependent immunosuppressive effect of ethylenediaminetetraacetic acid (EDTA).” EPIDEMIOL IMMUNOBIOL, 1978; 1: 69.
  50. Lamar, C.P. “Chelation therapy for occlusive arteriosclerosis in diabetic patients.” ANGIOLOGY, 1964; 15: 379-94.
  51. Lamb, D.J. and D.S. Leake. “The effect of EDTA on the oxidation of low density lipoprotein.” ATHEROSCLEROSIS: 1992; 94: 35.
  52. Liberman, U.A. U. Barzel, A. De Vries, H. Ellis.: “Myositis ossificans traumatica with unusual course. Effect of EDTA on calcium, phosphorus and manganese excretion.” AM J MED SCI, 1967; 254:35.
  53. Lonsdale, D. “EDTA chelation Therapy (Letter). AM J SURG, 1993; 166: 316.
    Lyons, R.D.: “Chelation: miracle cure or false hope?” MED J AUST, 1985; 142: 519.
  54. Magee, H.R.: “Chelation therapy for atherosclerosis (Letter).” MED J AUST, 1985; 143: 127.
  55. Magee, R.: “Chelation therapy for atherosclerosis .” MED J AUST, 1985; 142: 514.
  56. Marcelle, R. and J. Lecomte. “On the cardiovascular activities of the sodium salt of ethylenediaminetetraacetic acid.” CR SOC BIOL, 1959, 153: 1483.
  57. Margolis, S.: “Chelation therapy is ineffective for the treatment of peripheral vascular disease.” ALTERNATIVE THERAPIES HEALTH MED, 1995; 1: 53.
  58. Mayan, H., O. Salomon, R. Pauzner, et al.: “EDTA-induced pseudothrombocytopenia.” SOUTH MED J, 1992; 85: 213.
  59. McDonaugh, E.W., C.J. Rudolph, E. Cheraskin: “The influence of EDTA salts plus multi-vitamin-trace mineral therapy upon total serum cholesterol/high-density lipoprotein cholesterol.” MEDICAL HYPOTHESIS, 1982; 9: 643-46.
  60. McDonaugh, E.W., C.J. Rudolph, E. Cheraskin: “The effect of intravenous disodium ethylenediaminetetraacetic acid (EDTA) upon blood cholesterol in a private practice environment.” JOURNAL OF THE INTERNATIONAL ACADEMY OF PREVENTIVE MEDICINE, 1982; 7: 5-12.
  61. McDonaugh, E.W., C.J. Rudolph, E. Cheraskin: “The effect of EDTA chelation therapy plus supportive multivitamin-trace mineral supplementation upon renal function: A study in serum creatinine.” J HOLISTIC MED, 1982, 4: 146-51.
  62. McDonaugh, E.W., C.J. Rudolph, E. Cheraskin: “The effect of EDTA chelation therapy plus supportive multivitamin-trace mineral supplementation upon renal function: A study in blood urea nitrogen (BUN), J HOLISTIC MED, 1983; 5(2): 871-879.
  63. Meltzer, L.E., M.E. Ural, J.R. Kitchell; “The treatment of coronary artery disease with disodium EDTA.” in Seven, M.J. and L.A. Johnson (eds): METAL BINDING IN MEDICINE, J.B. Lippincott, Co., Philadelphia, 1960, pp. 132-36.
    Meltzer, L.E., F.J. Palmon, J.R. Kitchell. “Hypoglycemia induced by disodium ethylenediamine tetra-acetic acid.” LANCET, 1961: 2: 637.
  64. Meltzer, L.D.,J.R.Kitchell, F.J. Palmon: “The long term use, side effects, and toxicity of disodium ethylenediamine tetraacetic acid (EDTA).” AM J MED SCI, 1961: 242:11.
  65. Montgomery, M.R. “Advances in medical fraud: chelation therapy replaces Laetrile.” J FLORDIA MED ASSOC, 1986; 73: 681.
  66. Nakano, J., B. Cole, T. Ishii. “Effects of disodium EDTA on the cardiovascular responses to prostaglandin E1.” EXPERIENTIA, 1968; 24: 808.
  67. Oliver, L.D., R. Mehta, H.E. Saries.: “Acute renal failure following administration of ethylenediamine-tetraacetic acid (EDTA).” TEX MED, 1984; 80:40.
  68. Olszewer, E. and J.P. Carter: “EDTA Chelation therapy: a retrospective study of 2,870 patients.” J ADV MED, 1989, 27: 197.
  69. Olszewer, E. and J.P. Carter. “EDTA chelation therapy in chronic degenerative disease.” MED MYPOTHESES, 1988; 27(1): 41.
  70. Olszewer, E., F.C. Sabbag, J.P. Carter: “A pilot double blind study of sodium-magnesium EDTA in peripheral vascular disease.” J NATL MED ASSN; 82(3): 174-177.
  71. Olwin, J.H., J.L. Koppel: “Reduction of elevated plasma lipid levels in atherosclerosis following EDTA chelation therapy.” PROC SOC EXP BIOL MED, 1968; 128: 1137-1139.
  72. Ontka, J.A.: “Physical and chemical changes in isolated chylomicrons: prevention by EDTA.” J LIPID RES, 1970, 11: 367.
  73. Oser, B.L., M. Oser, H.C. Spencer: “Safety evaluation studies of calcium EDTA.” OXICOL APPL PHARMACOL, 1963; 5: 142.
  74. Parfitt,AM:”Study of parathyroid function in man by EDTA”J CLIN ENDOC,1969; 29:569.
  75. Patterson, R.: “Chelation therapy and Uncle John.” CMAJ, 1989; 140(7): 829.
    Pavek, K. J. Drinal, F.V. Selecky. “Circulatory effects of disodium edetate in digoxin-induced ventricular tachycardia.” CARDIOLOGIA, 1967; 50: 297.
  76. Payne, B.A., R.V. Pierre. “Pseudothrombocytopenia: A laboratory artifact with potentially serious consequences.” MAYO CLINIC PROC, 1984; 59: 123.
  77. Peng, C.F., J.J. Kane, M.L. Murphy, and K.D. Straub.: “Abnormal mitochondrial oxidative phosphorylation of ischemic myocardium reversed by Ca2+-chelating agents.” J MOLECULAR CELL CARDIOL, 1977; 9: 897.
  78. Pentel, P., C. Jorgensen, J. Somerville: “Chelation therapy for the treatment of atherosclerosis, an appraisal.” MINN MED, 1984; Feb. 101.
  79. Perry, H.M., H.A. Schroeder: “Depression of cholesterol levels in human plasma following ethylenediamine tetraacetate and hydralazine.” J CHRON DIS, 1955; 2: 520.
  80. Perry, H.M. and H.A. Schroeder: “Lesions resembling vitamin B complex deficiency and urinary loss of zinc producted by ehtylenediamine tetraacetate.” AM J MED, 1957, 22: 168.
  81. Peterson, G.R.: “Adverse effects of chelation therapy (Letter).” JAMA, 1983; 250: 2926.
    Platts-Mills A.: “EDTA chelation therapy.” NZ MED J, 1988; 101(849): 465.
    Price, J.M.: “Some effects of chelating agents on tryptophan metabolism in man.” FED PROC, 1961; 20 (Suppl 10): 223.
  82. Rathmann, K.L. and L.K. Golightly: “Chelation therapy of atherosclerosis.” DRUG INTELL CLIN PHARM, 1984; 18: 1000.
  83. Riordan, H.D., E. Cheraskin, M.Kirks, et al. “Another look at renal function and the EDTA treatment process.” J ORTHO MED, 1987; 2: 185.
  84. Riordan, H.D., E. Cheraskin, M.Kirks, et al. “Electrocardiographic changes associated with EDTA chelation therapy.” J ADV MED, 1988; 1: 191.
  85. Riordan, H.D., E. Cheraskin, M.Kirks, et al. “EDTA chelation/hypertension study: clinical patterns as judged by the Cornell Medical Index Questionnaire.” J ORTHOMOLECULAR MED, 1989; 4: 91.
  86. Rubin, M. S. Gignac, S.P. Bessman, E. Belknap. “Enhancement of lead excretion in humans with EDTA.” SCIENCE, 1953; 117: 659.
  87. Rudolph, C.J., E.W. McDonagh, R.K. Barber: “The effect of EDTA chelation on serum iron.” J ADV MED, 1991; 4: 39.
  88. Rudolph, C.J., E.W. McDonagh, R.K. Barber: “A non-surgical approach to obstructive carotid stenosis using EDTA chelation.” J ADV MED, 1991; 4: 157.
  89. Schroeder, H.A., H.M. Perry, Jr: “Antihypertensive effects of metal binding agents.” J LAB CLIN MED, 1955; 46: 416.
  90. Schroeder, H.A.: “A practical method for the reduction of plasma cholesterol in man.” J CHRON DIS, 1956; 4: 461.
  91. Scott, P.J.: “Chelation therapy for degenerative vascular disease.” N Z MED J, 1982; 95: 538.
  92. Schnert, K.W., A.F. Claque, E. Cheraskin: “The improvement in renal function following EDTA chelation and multivitamin trace mineral therapy: A study in creatinine clearance.” MED HYPOTHESES, 1984; 15: 301.
  93. Silverglade, A.: “Chelation clinics.” CHEST, 1985; 87: 274.
  94. Sloth-Nielsen, J., B. Guldager, C. Mouritzen, et al. “Arteriographic findings in EDTA chelation therapy on peripheral arteriosclerosis.” AM J SURG, 1991; 162: 122.
  95. Soffer, A.: CHELATION THERAPY. Charles C. Thomas, Springfield, IL, 1964.
    Soffer, A.: “Chelation Therapy for arteriosclerosis.” JAMA, 1975; 233: 1206.
  96. Soffer, A.: “Chelation clinics, an abuse of the physician’s freedom of choice.” CHEST, 1984; 86: 157.
  97. Spence, J.D.: “Chelation therapy for intermittent claudication.” ACP JOURNAL CLUB, 1992; July/Aug., pg. 8.
  98. Stevens, F.S.: “The effect of chelating agents on collagen interfibrillar matrix interactions in connective tissue.” BIOCHIM BIOPHYS ACTA, 1967; 140: 522.
    Stevenson, J.G. and T.R. Covington: “Chelation therapy in atherosclerosis.” ANN INTERN MED, 1982; 97: 789.
  99. Surawicz, B., M.G. MacDonald, V.Kaljot et al. “Treatment of cardiac arrhythmias with salts of ethylenediamine tetraacetic acid (EDTA).” AM HEART J, 1959; 58: 493.
  100. Surawicz, B.: “Use of the chelating agent, EDTA, in digitalis intoxication and cardiac arrhythmias.” PROG CARDIOVASC DIS, 1960; 2: 432.
  101. Swenerton, H. and L.S. Hurley: “Teratongenic effecs of a chelating agent and their prevention by zinc.” SCIENCE, 1971; 173: 62.
  102. Teisinger, J.: “Biochemical responses to provocative chelation by edetate disodium calcium.” ARCH ENVIRON HEALTH, 1971; 23: 280.
  103. Thompson, L.J. “Chelation Therapy.” N Z MED J, 1990; 103: 326.
  105. Van der Schaar, P.: “Exercise tolerance in chelation therapy.” J ADV MED, 1989; 2: 563.
  106. Van Rij, A.M., C. Solomon, S.G.K. Packer, et al: “Chelation therapy for intermittent claudication. A double-blind, randomized, controlled trial.” CIRCULATION, 1994; 90: 1194
  107. Van Rij, A.M., C. Solomon, S.G.K. Packer, et al: “(Chelation Therapy) Response (Letter)”, CIRCULATION, 1995; 5: 1350. Van Rij, A.M., C. Solomon, S.G.K. Packer, et al: “(Effectiveness of EDTA chelation therapy) Response (Letter).” CIRCULATION, 1995; 5: 1352.
  108. Vohra, F. and F.H. Kratzer. “Influence of various chelating agents on the availability of zinc.” J NUTRITION, 1964; 82: 249-56.
  109. Walker, F.: “The effects of EDTA chelation therapy on plague calcium and mineral metabolism in atherosclerotic rabbits.” Physiology (Dissertation Abstracts International), 1980, 41, No. 04.
    Walker, M.: THE MIRACLE HEALING POWER OF CHELATION THERAPY. Canfield, Ohio, Fischer Publishing, 1984.
  111. Walker, M.: THE CHELATION WAY: THE COMPLETE BOOK OF CHELATION THERAPY. Avery Publishing, Garden City Park, NY, 1990.
    Wartman, A., T.L. Lampe, D.S. McCann, A.J. Boyle: “Plaque reversal with MgEDTA in experimental atherosclerosis: Elastin and collagen metabolism” J ATHEROS RES, 1967; 7: 331.
  112. Wilder, L.W., L.R. DeJode, S.W. Milstein, et al. “Mobilization of atherosclerotic plaque calcium with EDTA utilizing the isolation-perfusion principle.” SURGERY, 1962, 52: 793.
  113. Williams, D.R., B.W. Halstead: “Chelating agents in medicine.” J TOXICOL CLIN TOXICOL, 1983; 19(10): 1081-115.
  114. Windsor, E. and G.E. Cronheim. “Gastro-Intestinal Absorption of Heparin and Synthetic Heparinoids.” NATURE, 1961: 190 (4772): 263-4.
  115. Wirebaugh, S.R. and D.R. Geraets.: “Apparent failure of edetic acid chelation therapy for the treatment of coronary atherosclerosis.” DICP ANN PHARM, 1990, 24:22.
  116. Wissler, R.W., D. Vesselinovitch: “Regression of atherosclerosis in experimental animals and man.” MOD CONCEPTS CARDIOVAS DIS, 1977; 46: 28.
  117. Wynn, J.E., B. Riet, T. van, J.F. Borzelleca: “The toxicity and pharmacodynamics of EGTA: Oral administration to rats and comparisons with EDTA.” TOXICOL APPL PHARMACOL, 1970, 16: 807.
  118. Yang, W.C.: “Stimulatory effect of EDTA on cardiac mitochondrial respiration.” BIOCHEM BIOPHYS RES COMMUN, 1960; 2: 22.
  119. Avila MD, Escolar E, Lamas GA.  Chelation therapy after the trial to assess chelation therapy: results of a unique trial.  Curr Opin Cardiol 2014; 29(5):481-8.