1930. Franz Munz, in attempting to decrease Nazi Germany’s reliance on foreign imports, developed EDTA (ethylene-
1930. Frederick Bersworth synthesized EDTA at Clark University in Worcester, Mass. Using a different production technique, he was able to obtain his own US patent in 1945.
1947. EDTA was approved by the FDA as a safe food additive. Medical experimentation began that year with unsuccessful attempts to treat breast cancer and kidney stones.
1950 Mark Rubin at Georgetown University demonstrated that EDTA would chelate plasma calcium.
1951. MgEDTA (the same form used in modern day chelation treatments) was used experimentally to chelate calcium and the released magnesium was found to lower blood pressure.
1952. CaEDTA began being used to treat lead poisoning. Practitioners reported dramatic improvement in elderly lead toxic patients with coexisting atherosclerotic cardiovascular disease. Multiple researchers also reported resolution of angina and arrhythmia due to digitalis toxicity.
1956. (Am J Med Sci 232:654-
1957. A. J. Boyle demonstrated the reversal of atherosclerosis in man using EDTA.
1960. (Am J Card 6:233-
subsequent paper about the same 3000 patients he stated “We find in all cases of angina [that] the patient [has] no need for vasodilators (medicines used to dilate arteries ) after about the fifth infusion… and that ninety percent of these problems in the lower extremities make significant gains including regaining the ability to walk long distances comfortably, freedom from claudication (painful cramps due to blocked arteries ), and evidence of improved distal circulation.”
1961. (Am J Med Sci 242:51-
be used without danger over prolonged periods.”
1963. (Am J Card 11:501-
1964. (Angiology 15:379-
1968. (Proc Soc Exp Biol Med 128(1):1137-
1969. (International Congress of Angiology in Prague) Langhof et al reported that EDTA treatments in 12 patients with atherosclerosis gave good results after 6-
1969. Abbott’s patent on EDTA ran out and there was no further commercial support of research in the US.
1972. Nikitina and Abramova (Czechoslovakia) reported on 25 patients with CAD, 8 with cerebrovascular disease (CVD involves arteries to the brain), and 7 with PVD all of whom had significant improvement. Their conclusion was that EDTA is the treatment of choice for atherosclerotic disease of arteries.
1976. Tamburino (IRCS Med Sci Libr Compendium 4:362) Reported that “Osteoporosis …is reversed by EDTA, which initiates deposition of new bone matrix” due to induction of PTH and concomitant increase in osteoblastic/osteoclastic activity in bones.
1977. (J Mol Chem Cardiol 9:897-
Comment: This improves energy production in the heart muscles during angina or a heart attack and can protect the heart from damage.
1980. (Environmental International 3:465-
59 (1.7%) treated patients died from cancer compared to 30 of 172 (17.6%) untreated patients.
1983. (J Holistic Med 5(1):3-
1985. Schettler et al at the Univ. of Heidelberg in Germany performed a double blind placebo controlled study comparing EDTA to a platelet inhibitor called Fludilat. The study was sponsored by the manufacturer of Fludilat. The EDTA treated group showed a 250% increase in average walking distance compared to 64% for Fludilat. The EDTA patients continued to improve 30 days after
treatment stopped while the Fludilat group all reverted to their pretreatment levels. This study was never published.
1986. The US FDA granted an IND to study EDTA chelation in the treatment of claudicatory peripheral vascular disease. Unfortunately when the Persian Gulf War developed the medical personnel doing the study were transferred and funding was stopped. Thirty patients had completed the blinded study but even those results have not been reported from Walter Reed Hospital where the study was being performed.
1988. (Medical Hypoth 27:41-
improvement in 8% of treated patients with PVD and claudication; and marked improvement in 24% and good improvement in 30% of patients with degenerative cerebral diseases. Overall nearly 90% of the patients showed good to excellent improvement as measured by walking distance, EKG and Doppler changes.
1988. (J Adv Med 1(4):182-
1989. (J Adv Med 2(4):553-
1989. (J Adv Med 2(4):563-
1989. (J Adv Med 2(1,2) Rudolph and McDonagh studied 117 lower extremities in 77 elderly patients with documented occlusive PVD. After an average of 26 treatments ankle/brachial Doppler measurements demonstrated significant improvements in arterial blood flow.
1990. (J Nat Med Assoc 82(3):173-
1990. (J Adv Med 3(1):5-
1991. (Am J Surg 162:122-
1991. (J Adv Med 4:39-
1991. (J Adv Med 4(3):157-
1992. (J Adv Med 5(3):189-
1993. (J Adv Med 6(3):139-
1993. (J Adv Med 6(3):161-
1994. (J Adv Med 7:131-
1994. (N Z Med J 109:83) Andre M van Rij et al reported on 32 patients, 15 of which received 20 chelation treatments with all the vitamins and minerals that are part of the ACAM protocol. The other 17 patients received identical infusions missing only the EDTA. All patients had severe multi-
1994. Presentation at the American Chemical Society: M Rubin et al presented evidence of EDTA decalcification of coronary arteries documented by ultrafast CT scan.
1994. (J Adv Med 4(7):203-
1995 (Surgery and Surgeons 61(2):58-
1996. (Townsend Letter for Physicians 157/58:92-
1997. (J of Integrative Med 1(1):113-
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