Introduction

The patient is a 56-year-old male first seen at The Center in August 1997. His main complaints were easy bruising, low back pain, rapidly progressing coronary artery disease and “cold feet.” The history revealed that he was a self-employed carpenter, a college graduate, and was married with one son and daughter. Both parents died of heart related problems: the father at 72 years of age and the mother at 77 years. He has two brothers, 51 and 49 years of age: both are in good health. In 1990, he had an aortic heart valve replaced with a St. Jude’s valve. In 1995, he required coronary angioplasty. In 1996, due to progressive heart disease, he had triple bypass surgery. Following the bypass surgery, he had two mild strokes, one in December of 1996 and the second one in February of 1997. His medications included coumadin 10 mg daily with 7.5 mg on alternate days and aspirin, 81 mg daily. While completing some of his evaluation papers at The Center, he complained of chest pain.

He said that at the time of his visit to The Center, his illness had cost his insurance companies between $120,000 to $150,000 as well as $5,000 to $10,000 of his own money. When asked how he would know if the treatment received at The Center worked, he stated “that his feet would be warm.” In the winter, they were cold no matter how warmly he dressed. This presented a problem, since much of his work was outdoors as a carpenter.

Due to the possibility of vascular/circulation problems (“cold feet”, angina), a thermogram was performed. This showed poor circulation in his lower legs, especially in his left leg. The usual comprehensive physical, psychological and laboratory evaluations were also performed. A chemistry profile, CBC, and urinalysis were essentially normal. His serum cholesterol was 201 mg/dL, HDL was 52 mg/dL, and LDL 129 mg/dL. The lipoprotein(a) was 46.4 mg/ dL (normal < 30 mg/dL). His urine vitamin C was “0”, his buffy coat and plasma vitamin C was normal. The urine pyrrole was elevated and RBC fatty acids showed an imbalance in the omega 6, omega 3, and saturated fatty acids. Vitamin A and E as well as the B vitamins were normal. A diagnostic chelation with a pre and post evaluation of 24-hour urine for toxic and essential minerals showed a slight body burden of aluminum and lead. Thyroid function was normal.

The patient agreed to a series of 30 I.V. EDTA chelation treatments to be given over a thirty week period. He was also started on Cardiorite® (two to four tablets a day) and Zinc Boost (with B6) one dropper-full in juice or water each day. After completing the chelation treatments, he stated “I don’t have any angina pain any more. I actually feel good.” His legs no longer felt cold and “he is looking forward to winter and being outside.” A repeat thermogram showed improved circulation to both of his legs. A repeat chemistry profile, serum creatinine and urinalysis were normal. His cholesterol was 167 mg/dL.

Comments and Discussion:

Two of the authors (JAJ and HDR) had previously reported the improvement of essential hypertension in a 51-year old male after EDTA chelation therapy.¹ Ethylene diamine tetraacetic acid (EDTA) chelation for lead poisoning is a treatment accepted by the traditional medical community. EDTA treatment for atherosclerosis, heart disease, stroke, arthritis, etc., has not yet been accepted by the traditional medical community. The main criticisms are the lack of data from double blind, placebo controlled studies, and that treatments are risky and/or useless. Dr. Garry F. Gordon, a cofounder of the American College of Advancement in Medicine (ACAM), stated that his organization has over 7,000 articles about the medical use of EDTA, and estimates that there are about 10,000 articles published in various journals on EDTA.² “EDTA chelation therapy is a form of treatment aimed at reducing calcium deposits, removing the heavy metals that inhibit enzyme systems, controlling lipid peroxidation, and reducing platelet stickiness in the clinical management of atherosclerosis and related disorders.” EDTA can be administered either orally or intravenously. Following oral administration, 80 to 95 percent of the dose appears in the feces within 24 hours. After I.V. administration, 95 percent of the dose appears in the urine by 24 hours, and less than 0.5 percent remains in the body after 48 hours. EDTA is not metabolized and is excreted almost unchanged in the urine. Urine pH and alterations in urine flow rate do not affect overall excretion rate of EDTA.³ The management of atherosclerosis by EDTA is said to work under the hypothesis that metastatic calcium deposits are in equilibrium with blood calcium. By effectively lowering the calcium concentration present in the blood, metastatic calcium is mobilized in order to maintain this equilibrium.³ When this free calcium is removed from the arteries by chelation therapy, the arteries become flexible again, allowing them to carry more blood each time the heart pumps. This causes less resistance to blood flow and tends to lower the blood pressure.

Chelation gives the additional benefit of removing lead, cadmium, mercury, and aluminum, which are protoplasmic poisons. In the many years The Center has used chelation therapy, not one patient has suffered any type of kidney dysfunction.⁴ We found just the opposite in a study conducted at The Center: it was found that kidney function either stayed the same as before or improved as a result of the chelation therapy. The chelation treatment solution used at The Center is as follows:

Sterile water 500 mL EDTA* 3.0 g Vitamin C 15 g Vitamin B6 1.0 mL Magnesium chloride 4.0 mL 2% Procaine 2.0 mL Heparin 1000 units

*(KeylateR, Key Co., Kirkwood, MO, 63122)

Additional information regarding the protocol may be obtained from one of the authors (MS).

References

1. Jackson JA, Riordan HD: Improvement of essential hypertension after EDTA infusion treatment. J Orthomol Med, 1992; 7; 1: 16.

2. Oral chelation for improved heart function. Life Enhancement Newsletter, 1997; 4: 32.

3. Craven PC, Morrelli HF: Chelation therapy (Medical Information). West J Med, 1975, 122: 277-278.

4. Health Hunter Newsletter, Editor Richard Lewis, 1999; 12; 6: 1-5.