The concept of chelation therapy as a way to remove heavy and toxic metal is well established as a standard medical procedure for over 50 years. The use of IV chelation therapy for cardiovascular disease and arthrosclerosis (made popular by a book titled Bypassing Bypass) has met with extensive resistance from mainstream medicine. There is little doubt that it works well, especially for those with end stage peripheral vascular disease needing amputation.
EDTA is the agent of choice in chelation therapy. The course of IV chelation usually takes place over 10-12 weeks, at the frequency of 3 times a week. Each session takes about 2-3 hours, infusing 1.8 grams to 3 grams of EDTA-sodium.
Dr. Abraham, one of the world’s authority on chelation, developed a new, less expansive, and more convenient way to administer chelation – oral chelation.
The traditional amount of IV EDTA administration is 3 grams per IV session. Many in the fore-front of chelation therapy are advocating a lower dose of 1800 mg of EDTA to achieve the similar effect. Taking 1800 mg of oral chelation for 20 days ( 300 mg x6 tablets) daily at 5% intestinal absorption rate will deliver to the body the same amount of EDTA as in one IV session of 1800 mg . In other words, the amount of oral EDTA based on 1800 a day is equivalent to one IV treatment every 3 weeks.
Before embarking on oral chelation treatment, accurate determination of the degree of minerals and toxic element presence should be carried out. Since serum levels are not accurate, it is best to perform a pack red blood cell intracellular element analysis. Hair mineral analysis is another method to measured the amount of mineral present in the body, though the result reflects historical data, standardized reference standard is not readily available, and interpretation can vary from laboratory to laboratory.
Alternatively, a 24 hour, 6 hour, or spot urine pre and post-provocation study using oral chelation agent such as EDTA-Mg K2 or DMPS is a good way to yield a qualitative and quantitative analysis of the amount of mineral and toxic metal load in the body prior to starting of chelation treatment to remove toxic metal. Such test can be repeated 3 months after treatment to determine the degree of toxic metal removal.
It is important to note that anyone on chelation treatment must be supplemented with a high potency anti-oxidant and mineral formula with adequate protection against chromium deficiency. Up to 400 mcg of chromium polynicotinate is needed for the healthy , and up to 800 mcg for those with diabetes because chromium is easily bounded to EDTA and excreted out of the body.
Here is Dr. Abraham’s Abstract on Oral Chelation:
By Guy E. Abraham, M.D. FACN
It is estimated that over 400,000 individuals have undergone intravenous (IV) EDTA chelation therapy since its inception some 50 years ago (1). The usual dosage per session is 3 grams of the disodium salt. Magnesium is added to the IV fluid for its known biological effects. Since only a few milligrams of lead and other toxic metals are excreted in the urine in response to IV EDTA, the use of 3 grams of EDTA seems excessive.
Based on studies performed with radioactive EDTA in young adult male subjects, oral EDTA is poorly absorbed by the intestinal tract, with an estimated bioavailability of less than 5 percent (2). However, one must keep in mind the fact that detoxification of heavy metals by EDTA occurs also in the gastrointestinal tract by blocking re-absorption of these metals after secretion by the liver in the bile which is then excreted in the intestinal tract. The intestinal route of detoxification of toxic metals by EDTA is as important as their renal excretion. The binding affinity of EDTA for heavy metals is high enough to prevent their intestinal re-absorption, after EDTA chelation of these metals in the intestinal tract.
The first study on oral EDTA in human subjects was published in 1953, some 50 years ago (3). Seven patients with increased levels of blood and urine lead levels were treated with Ca EDTA both orally and intravenously. The urinary excretion of lead was 10 to 40 times above baseline following IV EDTA, whereas it was 5 to 10 times higher with oral EDTA. The blood lead levels and red blood cell abnormalities improved in patients receiving IV and oral EDTA. Considering the fact that IV EDTA is at least 20 times more bioavailable than the oral route, enteral EDTA compares favorably to the IV route.
The second study of oral Ca EDTA disodium was published in 1954, using a daily dose of 2 grams for 7 days (4). In the symptomatic patients with lead intoxication, the symptoms improved remarkably following oral EDTA and the blood profile returned to normal. No disturbance of serum electrolytes was observed.
In 1956, a third publication reported the results of a study using a daily oral dose of 4 grams of Ca EDTA disodium in 14 patients with industrial lead poisoning (5). There was a marked increase in urine lead excretion, from 5 to 35 times baseline levels. There was a marked increase in fecal lead excretion also, above the estimated oral intake of lead. By the second and third day, most patients experienced very considerable improvements in their subjective symptoms, a feeling of general well being replacing the fatigue, weakness and loss of appetite. Based on their calculations, the authors concluded that this approach increases both urine and fecal lead levels, and most likely resulted in the removal of lead from bones. Several other studies (6-8), confirmed the effectiveness of oral EDTA.
The question then is: Why are we using relatively large doses of EDTA intravenously for detoxification of toxic metals, when the oral route worked very well, is non invasive and does not require constant visits to medical clinics which disrupt daily routine? At four hours per session and three sessions per week, this represents a loss of 12 hours per week. The ideal form of oral EDTA would be the di-potassium salt of the magnesium chelate, since these two very important intracellular minerals would be dissociated in the intestinal tract and available for absorption. The affinity of EDTA for magnesium is very low, resulting in exchange of magnesium for toxic metals in the intestinal tract. This is the approach of choice and preliminary data so far suggest that with the exception of chromium, red cell levels of trace elements do not decrease following 3 months of oral Mg EDTA K2 at a daily dosage of 1.8 gm In some subjects, there is a slight drop in red cell chromium, which is correctable with chromium supplementation. The red cell levels of mercury, lead and cadmium decreased Significantly following 3 months on oral EDTA. There is so far no side effects except urinary urgency in some subjects during the first hour after ingestion.
Oral route for EDTA chelation therapy using the di-potassium salt of EDTA magnesium chelate, based on the above rationale should be considered.
This approach is practical, noninvasive, and based on preliminary data, effective. More studies are needed however in order to fully validate this approach.
1. Elmer Cranton, M.D., Bypassing Bypass The New Technique of Chelation Therapy. 2nd Edition, Hampton Roads Publishing Co. 1997. Pg 35.
2. Foreman, EI., and Trujillo, T. T.: The Metabolism of C14 Labedled Ethylenediaminetetraacetic Acid in Human Beings, J. Lab. & Clin. Med. 43:566-571 (April) 1954.
3. Sidbury, J. B., Jr.: Bynum, J. C.; and Fetz, L. L.: Effect of Chelating Agent on Urinary Lead Excretion: Comparison of Oral and Intravenous Administration, Proc. Soc. Exper. Biol. & Med. 82:226, 1953.
4. Cotter, L. H.: Treatment of Lead Poisoning by Chelation, J.A.M.A.155:906-908 (July 3) 1954.
5. Shiels, D. O.; Thomas, D. L. G.; and Kearley, E.: Treatment of Lead Poisoning by Edathamil Calcium Disodium, A.M.A. Arch. Indust. Health 13:489-498 (May) 1956.
6. Pagnotto, L.D.; Elkins, H. B.: and Bayka, I.: Oral Administration of Edathamil Calcium Disodium (Calcium Disodium Versenate), A.M.A. Arch. Indust. Health 17:29-33 (Jan.) 1958.
7. Bell, R. F.; Gilliland, J. C.: Boland, J. R.; and Sullivan, B. R.: Effect of Oral Edathamil Calcium Disodium on Urinary and Fecal Lead Excretion, A.M.A. Arch. Indust. Health 13:366-371. (April) 1956.
8. Manville, I. A., and Moser, R.: Recent Developments in the Care of Workers Exposed to Lead, A.M.A. Arch. Indust. Health 12:528-538 (Nov.) 1955.