History of Chelation Therapy

The use of chelation therapy employing the synthetic amino acid EDTA (Ethylene Diamine Tetracetic Acid) can be described in detail at various other web sites including that of the American College for Advancement in Medicine  (www.acam.org).  I offer this brief introduction to this alternative or off label or beyond the package insert use of EDTA in  degenerative diseases but the real purpose of our web site is to share with both professionals and lay individuals our 30 plus years of clinical outcomes that we have published on the benefits of this therapy.  Additionally, we would like to offer some scientific evidence that this therapy, whose benefits are considered controversial in traditional medical circles, has a definitive use in disorders of the cardiovascular system.


Chelation therapy with EDTA is a therapy that we, as demonstrated in our published papers, have used (see papers 5, 14, 23, 24, 27 & 30 in published paper section of web site) successfully in treating the calcific disorders of mankind, namely atherosclerotic vascular diseases (and certain types of arthritis ( paper 29 in published paper section of web site). Image 1


Chelating agents have long been a part of standard therapeutic regimes in medicine (1).  Chelation therapy with EDTA is the therapy of choice for removing certain heavy metals, especially lead, from the body (2).  See Image 2


As with many medical stories, its use for these conditions was accidentally discovered in the 1950s in Michigan when Dr. Norman Clarke treated individuals with lead poisoning with EDTA.  He reported that those patients with coronary heart disease noticed an improvement in their cardiac symptoms as well as relief from their lead toxicity (3). From this discovery, the modern era of chelation therapy began.


The term chelation comes from the Greek word chele which means claw.  See Images 3 & 4.


Chemically, the chelating agent is C or claw shaped and attacks a positively charged metal and surrounds it making it inactive and eventually removes it from the body.  A chemical ball and stick  diagram of a chelating agent attacking a metal ion is pictured below. See Image 5.


There are many theories as to how this treatment is medically useful to the patient with calcified blocked arteries (see papers 5, 14, 23, 24, 27, & 30) in the published papers section).  The reader must realize what a theory is and that is an assumption or guess based on limited knowledge or information (4).  Originally it was theorized that EDTA simply wandered merrily down the artery (as depicted below) picking up calcium and dissolving plaque but that probably does not happen, that simply anyway.  See Image 6.


Two current theories exist as to how EDTA actually improves the circulation as we have previously demonstrated.  The first is what I call the Parathyroid Theory.  The parathyroid glands are four in number and are located in the neck behind the thyroid gland.  The function of parathyroid hormone is to maintain or control calcium levels in the blood.  It does so by breaking down calcium deposits in the body (5).  When EDTA is infused into the blood stream, it lowers the serum calcium which causes the parathyroid hormone (PTH) to be released in large quantities (6).  The PTH may theoretically be aiding in the plaque dissolution from the arteriosclerotic deposits but the explanation of our results has not been proved at the molecular level, hence it just a theory at this point.  See Image 7.

The Second theory is the Free Radical Theory (7).  A free radical is a highly charged molecule that contains an unpaired election (note: in most stable atoms, electrons are paired).  This free radical is very energetic and wreaks havoc on the tissues.  See Image 8.


It is a generally held premise that these free radicals are formed naturally (by the leakage of the electron transport system in a cellular metabolic machinery) and unnaturally by the intake of oxidized or heated fatty foods (8).  Once formed, these free radicals continue to form because metal ions such as iron and copper catalyze their formation and propagation (7).  The hydroxy free radical then attacks the unsaturated fatty acid in the membrane that surrounds the cell and can destroy the cell (9).  See Image 9.


  This can result in cell death and degeneration and may be a precursors to atherosclerotic vascular disease.  The way chelation appears to intervene is by reducing free iron and copper.  The overwhelming free radical generation can then be stopped, minimized or slowed down to a point that our tissue antioxidants can keep up with the problem (7).


In addition, it must not be forgotten that EDTA removes heavy metals such as lead and cadmium, both of which can contribute to hypertension which can contribute to heart disease (10,11).


With regards to the side effects of this therapy, the only real criticism that has persisted is that this therapy affects the kidneys negatively.  In the next section (i.e. Published papers) we have addressed that very issue and will report that not only is EDTA not nephrotoxic when used properly (according to ACAM protocol [12]), but it may actually improve kidney function (13).


   All of the above theories sound plausible but as I originally stated they are only theories to help explain our results.  The real purpose of this web site is to show the clinical results from our combined 50+ years of experience with this therapy.  To view these results, go to the published papers section of this web site.


References:

1.     Physicians desk reference, 49th ed, 1995, pages 879,1380,1438,1519.

2.     Conn RB:  Current diagnosis 1991; 409-11.

3.     Clark NE, Clarke NE Jr, Mosher R: Treatment of occlusive vascular disease with disodium ethylenediaminetetracetic acid (EDTA). Am J Med Sci 1960; 239:732-44.

4.     Soukhanov AH, Sr Ed.: Webster’s II New Riverside University Dictionary.  Riverside Publishing Co 1984; 1200.

5.     Shepard RS:  Human Physiology. JB Lippincott, pub 1971; 389.

6.     Rozema T., unpublished communication from lecture at International chelation conference in Prague. 

7.     Cranton EM, Frackleton J: Free radical pathology in age associated diseases: Treatment with EDTA chelation, nutrition and anti-oxidants. J Holistic Med 1984; 6:6-37.

8.     Demopoulos HB: Control of free radicals in biological systems. Fed Proc 1973; 32: 1903-8.

9.     Halstead BW: The scientific basis for EDTA chelation therapy. California: Golden Quill 1979.

10.     Bautman V, Landy E, Maesaka JK, Wedeen RP: Contribution of lead to hypertension with renal impairment.  New Eng J Med 1983; 390(1):17-21.

11.     Perry H: Hypertension and the geochemical environment. Ann NY Acad Sci 1972; 199: 202.

12.     Cranton EM: Protocol of the American College for Advancement in Medicine for the safe and effective administration of EDTA chelation therapy.  J Adv Med 1989;  2:296-306.

13.     McDonagh EW, Rudolph CJ, Cheraskin E: The effect of EDTA salts plus supportive multivitamin trace mineral supplementation upon renal function: a study in serum creatinine.  J Hol Med 1982; 4(2): 146-51.

   

Note: Many of the pictures have been taken from and are reproduced with permission from the book, the Scientific Basis for Chelation Therapy by Rozema and Halstead.  In an effort to comply with the rules of truthful advertising and the ACAM settlement agreement with the FTC, this section of the web site was reconstructed and duly referenced with the aid of counsel, in November, 1999.

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