A Textbook on EDTA Chelation Therapy: Second Edition / Edition 2

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A single volume for learning everything health professionals need to administer and advocate chelation therapy, including its protocols and safety.

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Product Details

  • ISBN-13: 9781571742537
  • Publisher: Hampton Roads Publishing Company, Inc.
  • Publication date: 4/28/2001
  • Edition description: Subsequent
  • Edition number: 2
  • Pages: 608
  • Sales rank: 1,011,370
  • Product dimensions: 6.10 (w) x 9.10 (h) x 1.70 (d)

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A Textbook on EDTA Chelation Therapy


Hampton Roads Publishing Company, Inc.

Copyright © 2001 Elmer M. Cranton, M.D.
All rights reserved.
ISBN: 978-1-61283-274-6


Scientific Rationale for EDTA Chelation Therapy in Treatment of Atherosclerosis and Diseases of Aging

Elmer M. Cranton, M.D. and James P. Frackelton, M.D.

ABSTRACT: The widely accepted Free-Radical Theory of Aging has given us a coherent and unifying scientific explanation for the many diverse benefits resulting from EDTA chelation therapy and nutritional supplementation. The Free Radical Theory will be discussed foremost in this chapter. The emerging Cell-Senescence Model of Aging, however, combined with the concept of apoptosis (programmed cell death), adds to the free radical explanation, and gives us a broader scientific rationale for EDTA chelation therapy plus nutritional supplementation. To be valid, the proposed mechanism of action must explain why benefit requires several months to occur and improvement continues long after therapy is completed. The wide range of reported benefits can be explained, at least in part, by reactivation of enzymes that are dependent on metal ions for function and removal of metals that act as catalysts of free radical proliferation. Suboptimal nutriture weakens trace element-dependent antioxidant enzymes. The use of supplemental micronutrients and antioxidants is an integral part of this therapy. EDTA chelation therapy combined with nutritional supplements and modification of health-destroying habits act in unison to prevent and to partially reverse many common age-associated diseases.


The use of chelation therapy with intravenous ethylene diamine tetraacetate (EDTA) for the treatment of atherosclerosis is increasing rapidly worldwide. This practice, which began more than four decades ago, accelerates each year. Many published studies confirm safety and effectiveness of intravenous EDTA for treatment of occlusive atherosclerotic arterial disease and age-related degenerative diseases. A very important basis for the scientific rationale of this therapy is thus the fact that it has been proven effective over and over again in clinical practice. More than one million patients have received more than twenty million infusions with no serious adverse effects—when administered following the approved protocol described in chapter 32. Many years ago, reports of kidney damage and other adverse effects resulted from excessive doses of EDTA, infused too rapidly (greater than 50 mg/Kg/day, infused more rapidly than 16.6 mg/min).

Excessive dose-rates of infusion, especially in the presence of preexisting kidney disease or heavy metal toxicity, were responsible for occasional reports of nephrotoxicity. No such adverse side effects have been reported when the currently approved protocol has been correctly followed.

Research with laboratory animals provides further support for the effectiveness of EDTA chelation therapy.

There has never been a valid scientific study of EDTA chelation that did not show effectiveness, although there have been reports in which positive data were erroneously interpreted as negative. Reports of negative or adverse results from EDTA chelation following the currently approved protocol have been either editorial comments and letters to the editor written by opponents of this therapy or seriously flawed attempts to discredit chelation with biased and unscientific interpretation of data, often by cardiovascular surgeons who freely admit their bias.

In the last ten years, a small cluster of studies has sprouted up in the medical literature purporting to demonstrate that EDTA chelation is not effective in treatment of cardiovascular disease. Although flawed and imperfect, those studies in actuality provide only positive support for chelation. Their negative conclusions are not supported by the data.

The Danish Study

The most controversial and oft cited study of that type was done in Denmark. It was the handiwork of a group of Danish cardiovascular surgeons, with admitted bias against chelation. Results of that study were published in two medical journals, the Journal of Internal Medicine and the American Journal of Surgery. The surgeons' adverse conclusions were also widely publicized in the news media.

The surgeons followed 153 patients suffering from intermittent claudication. The patients had such severely compromised circulation in their lower extremities that walking a city block or less would cause them to stop with pain. An endpoint measured for this study was their maximal walking distance (MWD)—the very longest distance that they could walk before pain of claudication brought them to a halt. Patients were equally divided into an EDTA group and a placebo group. In the pre-treatment phase, the EDTA group averaged walking 119 meters before pain stopped them; the placebo group was less limited at the outset and averaged 157 meters.

Treatment was either 20 intravenous infusions of disodium EDTA or 20 infusions of a simple salt solution, depending on their group. Although the study was purportedly double-blinded (neither patients nor researchers were supposed to know who received placebo and who received EDTA), the researchers later admitted that they broke the code well before the post-treatment final evaluation.

Both groups showed improvement, and the investigators concluded that the improvement was not statistically significant. This Danish study turned many people against chelation; but, in rather short order, the integrity of the study was called into question. It was learned that the researchers had violated their own double-blind protocol. Not only did they themselves know before the end of the study who was receiving EDTA and who placebo, they had also revealed this information to many of the test subjects. Before the study was over more than 64 percent of the subjects were aware of which treatment they had received. This was highly questionable from an ethical and scientific standpoint.

One important aspect of the Danish study is the startling fact that the patients who were given EDTA were much sicker than the patients treated with a placebo. Therefore, the improvements the EDTA group made were harder earned and more significant. The researchers (who had candidly admitted that they undertook the study to convince the Danish government not to pay for chelation) either never noticed that aspect or felt reluctant to reveal it. The evidence is seen in the pre-treatment MWDs: 119 meters for the EDTA group and 157 meters for the placebo group.

Still more significant were the standard deviations. The plus or minus 38 meters SD for EDTA patients versus the plus or minus 266 meters SD for the placebo group represents an enormous variation in walking capacity that is heavily biased in favor of the placebo group. Those standard deviations show that some placebo patients must have walked half a mile before stopping. The placebo group's claudication was therefore markedly less severe, and the EDTA group was much more severely diseased. The design of the study was obviously biased against EDTA chelation from the outset.

Yet, when the six-month study was completed, the mean MWD in the EDTA group increased by 51.3 percent, from 119 to 180 meters, while the mean MWD in the placebo group increased only 23.6 percent, from 157 to 194 meters. The chelation group's improvement was therefore more than twice as great as the placebo group's, even though the chelation group was significantly sicker at the outset. This is a positive study, supporting the usefulness of EDTA chelation. The authors' published negative conclusions are not supported by the data.

The New Zealand Study

Another study—also conducted by vascular surgeons—was done at the Otago Medical School in Dunedin, New Zealand two years after the Danish study. The subjects of this study were also suffering from intermittent claudication. The subjects were divided into two groups, the EDTA group and the control group. The study extended to three months after 20 infusions of either EDTA or a placebo were given. The authors concluded that EDTA chelation had been ineffective. Once again, that conclusion was unsupported by their data.

Absolute walking distance in the EDTA group increased by 25.9 percent; while in the placebo group, it increased by 14.8 percent. The difference was not considered statistically significant. The study, however, had only 17 subjects in the placebo group. One of the placebo patients was what the statisticians call an "outlier," one whose results differ strikingly from everyone else in the group. This patient's walking distance increased by almost 500 meters. All of the statistical gain in the placebo group was due to this one individual's progress. Without him, the placebo group's distance actually decreased.

This illustrates the perils of a small study. The 25 percent gain in the EDTA group compared to no gain in the placebo group would have been very significant statistically.

In addition, the New Zealand researchers conceded that improvement in artery pulsatility (pulse intensity) in the EDTA group's worse leg improved enough to reach statistical significance (p<0.001).

A 25.9 percent improvement in walking is by no means minor and would attract notice if the agent had been a patentable drug. Even that level of improvement is not representative of the much greater improvements claudication patients normally experience after chelation. The below-expected improvement seen in this study can be explained by smoking. Eighty-six percent of the chelated subjects were smokers. Although they were advised to quit smoking when the study began, how many of them actually complied is not known.

The Heidelberg Study

Another study that was carried out with an erroneous negative conclusion is the "Heidelberg Trial," funded by the German pharmaceutical company Thiemann, AG in the early 1980s. A group of patients with intermittent claudication were given 20 infusions of EDTA and compared with a so-called "placebo" group that was actually given bencyclan, a pharmacologically active vasodilating and antiplatelet agent owned by Thiemann.

From a practical commercial standpoint, Thiemann's action was bizarre. If EDTA did well in the trial, Thiemann's well-established drug could only suffer. Nonetheless, the trial went forward and was reported in 1985 at the 7th International Congress on Arteriosclerosis in Melbourne, Australia. Immediately following 20 infusions of EDTA the trial subjects' pain-free walking distance increased by 70 percent. By contrast, patients receiving bencyclan increased their pain-free walking distance by 76 percent. The difference between these two results was not statistically significant, but another result was. Twelve weeks after the series of infusions was completed, the EDTA patients' average pain-free walking distance had continued to increase, going up to 182 percent. No further improvement had occurred in the patients receiving bencyclan. Those percentages were made public, although never published.

An informal report from Thiemann mentioned only the 70 and 76 percent figures. Press releases stated that chelation was no better than a placebo, but failed to mention that the "placebo" was a drug that had been proven effective in the treatment of intermittent claudication. Thiemann never released the actual data on which the Heidelberg Trial based its conclusions, but some German scientists who had access to it, and who were disturbed at the deception they were witnessing, chose to reveal the complete raw data to members of the American scientific community.


Excerpted from A Textbook on EDTA Chelation Therapy by ELMER M. CRANTON. Copyright © 2001 Elmer M. Cranton, M.D.. Excerpted by permission of Hampton Roads Publishing Company, Inc..
All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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Table of Contents

Foreword to the First Edition xiii
Introduction to the First Edition xv
Introduction to the Second Edition xxi
Section I Scientific Rationale
Chapter 1 Scientific Rationale for EDTA Chelation Therapy in Treatment of Atherosclerosis and Diseases of Aging 3
Chapter 2 Iron and Ischemic Heart Disease 62
Chapter 3 The Crosslinkage Theory of Aging As a Predictive Indicator 67
Chapter 4 Possibilities and Limitations of Chelation As a Means for Life Extension 88
Chapter 5 Nutritional Factors in Cardiovascular Disease 100
Section II Clinical Trials
Chapter 6 Current Status of EDTA Chelation Therapy in Occlusive Arterial Disease 120
Chapter 7 EDTA Chelation Therapy: Efficacy in Arteriosclerotic Heart Disease 133
Chapter 8 EDTA Chelation Therapy: Efficacy in Brain Disorders 142
Chapter 9 An Oculocerebrovasculometric Analysis of the Improvement in Arterial Stenosis following EDTA Chelation Therapy 164
Chapter 10 Effect of EDTA Chelation Therapy plus Multivitamin-Trace Mineral Supplementation upon Vascular Dynamics: Ankle/Brachial Doppler Systolic Blood Pressure Ratio 168
Chapter 11 Effect of EDTA Chelation Therapy: Treatment of Peripheral Arterial Occlusion, an Alternative to Amputation 177
Chapter 12 Ninety Percent Reduction in Cancer Mortality after Chelation Therapy with EDTA 195
Chapter 13 The "Clinical Change" in Patients Treated with EDTA Chelation plus Multivitamin/Trace Mineral Supplementation 202
Chapter 14 EDTA Chelation Therapy: A Retrospective Study of 2,870 Patients 210
Chapter 15 Benefits of EDTA Chelation Therapy on Arteriosclerosis: A Retrospective Study of 470 Patients 225
Chapter 16 Visual Field Evidence of Macular Degeneration Reversal Using a Combination of EDTA Chelation and Multiple Vitamin and Trace Mineral Therapy 237
Chapter 17 A Nonsurgical Approach to Obstructive Carotid Stenosis Using EDTA Chelation 247
Chapter 18 The Effect of Intravenous Disodium Ethylenediaminetetraacetic Acid (EDTA) upon Bone Density Levels 259
Chapter 19 Renal Artery Stenosis Reversal in a Hypertensive Individual, Using a Combination of EDTA Chelation and Multiple Vitamin and Trace Mineral Therapy 265
Chapter 20 The Effect of EDTA Chelation Therapy with Multivitamin/Trace Mineral Supplementation upon Reported Fatigue 273
Chapter 21 Clinical Improvements as Judged by the Cornell Medical Index Questionnaire in Patients Treated with EDTA Chelation Therapy 278
Chapter 22 A Pilot Double-Blind Study of Sodium-Magnesium EDTA in Peripheral Vascular Disease 285
Chapter 23 The Correlation between EDTA Chelation Therapy and Improvement in Cardiovascular Function: A Meta-Analysis 294
Chapter 24 EDTA Chelation Treatment for Vascular Disease: A Meta-Analysis Using Unpublished Data 317
Chapter 25 If EDTA Chelation Therapy Is So Good, Why Is It Not More Widely Accepted? 329
Section III Safety
Chapter 26 Kidney Effects of Ethylene Diamine Tetraacetic Acid (EDTA): A Literature Review 345
Chapter 27 The Effect of EDTA Chelation Therapy plus Supportive Multivitamin-Trace Mineral Supplementation upon Renal Function: A Study in Serum Creatinine 352
Chapter 28 The Improvement in Renal Function following EDTA Chelation and Multivitamin-Trace Mineral Therapy: A Study in Creatinine Clearance 361
Chapter 29 The Effect of EDTA Chelation Therapy plus Supportive Multivitamin-Trace Mineral Supplementation upon Renal Function: A Study in Blood Urea Nitrogen (BUN) 366
Chapter 30 Another Look at Renal Function and the EDTA Chelation Treatment Process 376
Section IV History and Protocol for Administration
Chapter 31 Overview, Historical Background, and Current Status of EDTA Chelation Therapy for Atherosclerosis 382
Chapter 32 Protocol for the Safe and Effective Administration of EDTA and Other Chelating Agents for Vascular and Degenerative Diseases 404
Chapter 33 Iron and Copper Supplementation with EDTA Chelation Therapy 462
Section V Laboratory Evaluation
Chapter 34 A Laboratory Method to Measure Plasma EDTA Levels 468
Chapter 35 Monitoring Renal Function during EDTA Chelation Therapy 477
Chapter 36 Urinary Trace and Toxic Elements and Minerals in Untimed Urine Specimens Relative to Urine Creatinine, Part I: Concentrations of Elements in Fasting Urine 484
Chapter 37 Urinary Trace and Toxic Elements and Minerals in Untimed Urine Specimens Relative to Urine Creatinine, Part II: Provoked Increase in Excretion following Intravenous EDTA 503
Chapter 38 Testing for Toxic Elements and Chelation of Mercury 540
Index 549
About Dr. Cranton 565
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  • Anonymous

    Posted December 6, 2001

    Chelation Therapy in detail by Expert Doctor

    This book is a must for anyone with an interest in EDTA chelation therapy! Dr. Cranton is the leading expert in EDTA chelation therapy for treatment of atherosclerosis and age-related diseases. Chelation therapy is an emerging, non-surgical procedure, performed in the doctor's office, that can often avoid the need for bypass surgery---preventing heart attacks, strokes and amputations. This book is clearly the most up-to-date review of how this therapy is done, the historical background, and the scientific data that show its value in the treatment of heart disease and other vascular disease. At first glance this might seem to be a highly technical book of interest only to medical doctors. But it should also be of great interest to victims of atherosclerosis, coronary heart disease, or blocked arteries to the legs or brain. EDTA chelation remains controversial within the medical profession and when patients ask their cardiologists or bypass surgeons about chelation they are commonly and unjustifiably warned against it. Before accepting such biased opinions, you should study the actual scientific facts for yourself. This book provides the best way to do that. I challenge any open-minded person to study the material in this book and not be favorably impressed. Twenty detailed chapters describe many of the clinical trials, including the actual data that prove benefit. The highly flawed and misleading Danish, New Zealand, and Heidelberg studies are analyzed in detail and are shown, in fact, to be quite favorable to EDTA chelation therapy This is a fully-indexed text, with a foreword and endorsement by Dr. Linus Pauling, the only person ever to receive two, unshared Nobel prizes. It contains a detailed protocol with instructions for physicians who wish to administer this therapy in their practices. The medical politics of EDTA chelation and the controversy surrounding its tragically slow acceptance are also explained. The book begins with a lengthy chapter with hundreds of scientific references describing the scientific rationale, which incorporates recent findings on homocysteine, apoptosis, cell senescence, telomeres, and trace elements. The 50-year history of EDTA in treatment of atherosclerosis and age-related diseases is covered in detail. Also included are the latest developments in the emerging area of interest in mercury toxicity. If you are involved in the clinical practice of EDTA chelation therapy you will need to own this new edition, whether you own the earlier edition or not. It affords you the most complete answer to critics of this amazing therapy. It is a reference you will refer to often. If you are merely curious and want to learn the facts for yourself before deciding whether to practice or receive this therapy, this is the book for you.

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