Chelation Therapy is a technique the Doctor McDonagh and Rudolph have been doing together since 1977 (almost 33 years) at McDonagh Medical Center and Doctor McDonagh was doing it 10 years before their partnership in 1977. They have a total combined experience of about 75 years and have written 32 scientific papers on the subject making then the most published physicians in the world on the use of EDTA chelation in patients with heart disease (#30) , hypertension (#17), ruptured discs (in combination with prolotherapy) (#29), blocked leg arteries (#14), blocked carotid (neck) arteries (#23 & #27), blocked renal (to kidney) arteries (#32), macular degeneration (#31), Osteoporosis (#21) Fatigue (#12) and emphysema (#22). 

They have authored two scientific papers that seem to put to rest the rumor that, when used properly, this therapy causes kidney damage (#6 & #18) which traditional practitioners, not familiar with the treatment, use to frighten prospective patients from this therapy. For a detailed analysis on this controversy, see our section on Safety of EDTA. After reading the above, it will be apparent that the kidney function, on the average, improves with our program.

To find out more about the above disorders go to the disorders treated section on the homepage.

There are 3 major areas that I want to focus on in this educational endeavor:

http://www.mcdonaghmed.com/chelation-therapy/

Chelation therapy using intravenous infusion of EDTA is a highly effective treatment for atherosclerotic cardiovascular disease. Safety and effectiveness are well documented in clinical studies, all of which to date are supportive of this therapy. There are no studies showing lack of effectiveness. Strong evidence is presented to support the use of this safe, efficacious, and inexpensive therapy before resorting to surgery and other risky, invasive treatments. 

"This therapy has been proven effective over and over again in clinical practice," says Dr. Cranton.

"More than one million patients have received more than twenty million infusions with great benefit and without serious adverse effects."

Clinical trials all clearly demonstrated improved circulation after chelation. These are the sort of results that any chelation therapist expects―we not only notice improved exercise tolerance, memory, and mental alertness in our patients but even healthy color returning to their cheeks. Many other objectively measured indicators of circulatory health tell similar stories:

Journal of Advancement in Medicine, Volume 2, Numbers 1/2, Spring/Summer 1989

Drs. Casdorph and Farr reported on four patients who had all been recommended to undergo surgical amputation of their gangrenous lower extremities before treatment with EDTA chelation (click here for abstract). Clearly, these were people who had reached end-stage complications of atherosclerosis and poor blood flow. Most of them had deep ulcerations and large areas of dead, necrotic tissue on their feet.

In some cases, circulation to the extremities had become so poor and so much tissue had died that the condition was no longer causing significant physical pain. The patients' pain was now mental―in the clear knowledge that they were about to lose a leg. All four patients chose to postpone amputation (against surgical advice) and receive infusions of EDTA combined with hyperbaric oxygen therapy (BHOT).

Summary:

* Treatment was completely successful in three out of the four cases.

* In the fourth case, the patient did eventually lose only the tips of his second, third, and fourth toes, but the foot and leg were saved. 

* After chelation, all four patients recovered circulation in their lower extremities sufficient to not only protect them from amputation but to also allow them pain-free walking without limitation or handicap.

* Several years after chelation therapy, those four patients continued to be alive and well, walking on their own legs and feet.

* Their recovery―if witnessed by a physician who was unaware of or unwilling to credit chelation's effectiveness―could only be seen as a sort of medical miracle, something comparable to spontaneous remission of an advanced and deadly cancer.

Drs. McDonagh, Rudolph, and Cheraskin took 77 elderly patients with documented narrowing of the peripheral arteries in their legs and measured changes in blood flow after approximately 26 EDTA infusions administered over 60 days. They used the preferred method for such testing: the ankle/brachial Doppler blood pressure ratio.

This method compares the blood pressure and flow in the arms with that in the ankles using Doppler ultrasound. In a person with a youthful circulatory system, the normal pressure in the ankles is equal to or greater than that in the arms. Patients with impaired circulation to the lower extremities have, of course, weaker arterial blood flow and lower blood pressure in their ankles than in their arms.

Summary:

* On average, after chelation therapy, the patients' ankle pressure increased from 55 percent of the arm pressure to 71 percent of the arm pressure, a change so significant that the statistical likelihood of its being due to random chance would be somewhere in the neighborhood of one in 10,000.(1)

* Improvement in Doppler blood pressure reflects only blood flow in larger arteries.

* EDTA also improves capillary circulation, which is especially reduced in diabetes.

H. Richard Casdorph, M.D., Ph.D., is Assistant Clinical Professor of Medicine at the University of California Medical School, Irvine, California. He practices in internal medicine and cardiovascular disease at Long Beach, California. He received his training in cardiovascular diseases at the Mayo Clinic and received his Ph.D. degree in Medicine from the University of Minnesota. He has also taught at UCLA Medical School and has been Chief of Medicine at Long Beach Community Hospital.

Abstract:

Fifteen patients with well-documented impairment of cerebral blood flow were studied utilizing the isotope technetium 99m.

* A highly significant improvement (P = .0005) in cerebral blood flow occurred following approximately twenty intravenous infusions of disodium EDTA.

* All fifteen patients improved clinically, including one with little or no improvement in measured cerebral blood flow.

* EDTA chelates and removes aluminum as well as calcium.

* Aluminum has been incriminated in senile and pre-senile dementia.

* This study is especially noteworthy in view of the fact that medical science has no other effective treatment for many of these conditions.

* Radioactive nuclide studies were performed at the Nuclear Medicine Department of the Lon Beach Memorial Hospital, California.

_____________________________________________

(Data from this study showing large, numerically tabulated and objective improvements in blood flow to the brain. Computerized graphs showing improved blood flow are astounding, even to those untrained in medical science. A scintillation counter and computer were used to generate those sophisticated images, which are perhaps the most convincing objective evidence we have for increased blood flow after chelation. I challenge any open-minded physician to review the data in that article and not come away impressed. - Elmer M Cranton M.D.)

Journal of Advancement in Medicine Volume 6, Number 3, Fall 1993

C. Hancke, MD and K. Flytlie, MD

Claus Hancke M.D. received his medical education at the University of Copenhagen. He is general practice and is president of the Danish Chelation Doctors. He is an ABCT diplomate. Knut Flytlie M.D. received his medical education at the University of Gutenberg, Germany. He is in general practice and operates a clinic for Preventive Medicine and Chelation.
He is an ABCT diplomate.

ABSTRACT:

In a retrospective study we report results of EDTA chelation in 470 patients, using a number of parameters, most of them objective.

* Although the patients acted as their own controls, we observed improvements of 80 to 90%, depending upon the measurement used.

* Of 92 patients referred for surgical intervention, only 10 required ultimate surgery after or during their chelation therapy, thus saving an estimated 3 million dollars of insurance money.

* Our experience covers a period of 6 years and we saw no severe side effects or casualties arising from the treatment.

* We conclude that EDTA chelation therapy is safe, effective and cost-saving.

_____________________________________________

( Drs. Hancke and Flytlie, two Danish doctors with impeccable credentials, published such a study in 1993―a counterblast, as it were, to the Danish bypass surgeons' ineffectual attempt to discredit chelation in the previous year. Hancke and Flytlie measured improvements using a several different criteria in a series of 470 patients who were followed for six years following chelation therapy (click here for abstract).

Of 265 patients with coronary artery disease and narrowing of the blood vessels to the heart, they reported improvement in 90 percent. Sixty-five of those patients had been referred for bypass surgery before chelation. After treatment, 58 of the bypass candidates improved so dramatically that they avoided the surgeon's knife. Among the 207 angina patients using nitroglycerin to control their pain, 189 were able to reduce their consumption. Most discontinued its use altogether. Of 27 patients awaiting foot or leg amputation, 24 avoided surgery.(4)

These results, remarkable as they may seem, fully correspond with what physicians who administer chelation therapy routinely observe in practice. - Elmer M Cranton M.D.)

Journal of Advancement in Medicine, Volume 2, Numbers 1/2, Spring/Summer 1989

Efrain Olszewer, MD and James P. Carter, MD, DrPH

Dr. Olszewer is a cardiologist in Sao Paulo, Brazil, where this study was conducted. Dr. Carter is Professor and Head,
Nutrition Section, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana.

 

ABSTRACT:

Results are presented of a 28-month retrospective analysis of 2,870 patients with documented atherosclerosis and otherdegenerative, age associated diseases who were treated with intravenous disodium magnesium EDTA chelation therapy.

* Observed benefits strongly support the use of EDTA chelation therapy for those conditions.

* Marked improvement occurred in 76.9% and good improvement occurred in 17% of treated patients with ischemic heart disease.

* Marked improvement occurred in 91% and good improvement occurred in 8% of treated patients with peripheral vascular disease and intermittent claudication.

* In patients with cerebrovascular and other degenerative cerebral diseases, 24% had marked improvement, and 30% had good improvement.

* Of four patients with scleroderma, three had marked improvement and one had good improvement.

* 75% of all patients had marked improvement in symptoms of vascular origin.

* Independent of pathology, 89% of all treated patients had marked or good improvement.

J Natl Med Assoc. 1990 Mar;82(3):173-7.

Olszewer E, Sabbag FC, Carter JP. Source: CEMIO, Sao Paulo, Brazil.

Abstract

Ten male patients with peripheral vascular disease, Type 2 (LaFontaine), were randomly assigned in a double-blind study to receive either Na2 ethylene diamine tetra acetic acid (EDTA) plus MgSO4, B complex, and vitamin C, or a placebo of MgSO4, B complex, and vitamin C in Ringer's lactate solution. A total of 20 intravenous infusions were planned for administration to each patient.

* Clinical and laboratory (noninvasive) tests showed dramatic improvements after 10 (EDTA Chelation Therapy) infusions in some patients, and thus was broken the code indicating who was receiving EDTA and who was receiving placebo.

* The group that improved had been receiving EDTA; there was no change in the placebo group.

* The trial was then completed in a single-blind fashion. Patients originally assigned to receive placebo then received 10 EDTA infusions, while the group originally assigned to EDTA received 20 EDTA infusions.

* The group that had formerly received placebo showed improvements comparable to those seen in the first EDTA group after 10 treatments.

_____________________________________________

(Midway through the study they were forced to open up the blind for ethical reasons; five of the patients―these turned out to be the ones receiving EDTA chelation―were doing dramatically better than the placebo group. It was felt to have been unethical to continue giving placebo therapy. The placebo patients were then put on EDTA and they too rapidly began to improve. - Elmer M Cranton M.D.)

The two articles summarized below containing data derived by meta-analysis of all available published studies, with added analysis of unpublished studies, using EDTA chelation therapy. They show a very consistent and high level of benefit in more than 85% of patients

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 FIRST META-ANALYSIS PAPER:

The Correlation Between EDTA Chelation Therapy and Improvement in CardiovascularFunction: A Meta-Analysis

L. Terry Chappell, MD, John P. Stahl, PhD

ABSTRACT:

In order to establish whether there is value in treating cardiovascular disease with intravenous EDTA chelation therapy, a meta-analysis was done, based on currently available scientific literature. A thorough literature search identified 40 articles on the subject.

* Nineteen studies met the criteria for inclusion with data on 22,765 patients.

* The meta-analysis revealed a statistical correlation coefficient of 0.88, which indicates a high positive relationship between EDTA therapy and improved cardiovascular function.

* Eighty-seven per cent (87%) of the patients included in the meta-analysis demonstrated clinical improvement by objective before-and-after testing.

A Textbook on EDTA Chelation Therapy, Second Edition. edited by Elmer M. Cranton, M.D., Charlottesville, Virginia: Hampton Roads Publishing Company; 2001, chapter 23, 294-316.

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 SECOND META-ANALYSIS PAPER:

EDTA Chelation Treatment for Vascular Disease: A Meta-Analysis Using Unpublished Data

L. Terry Chappell, MD, John P. Stahl, PhD, Ronald Evans, MA

ABSTRACT:

The authors previously reported the results of a meta-analysis on the correlation between EDTA therapy and improvement in cardiovascular function where only published data were used in the analysis.  Many analysts suggest that using exclusively published data in a meta-analysis leads to a lowered confidence level in the results because of the possibility of publication bias.  In order to improve the confidence level if possible in the results of their original paper the authors repeated the study using unpublished data. Unpublished "file drawer" data were collected from 32 clinicians who utilize intravenous EDTA with essentially the same protocol as was used in the original study. 

* Various objective measurements demonstrated improvement in 1086 or 88% of the 1241 patients reported with an overall statistical correlation coefficient of 0.88. 

* A comparison of the studies using unpublished data with published data shows that the results are essentially the same. 

* These data provide additional confidence of the effectiveness of EDTA (Chelation Therapy) treatment.

A Textbook on EDTA Chelation Therapy, Second Edition. edited by Elmer M. Cranton, M.D., Charlottesville, Virginia: Hampton Roads Publishing Company; 2001, chapter 24, 317-328.

_____________________________________________

(This is an eagle-eyed observation and comparison of diverse studies that summarizes, as best it may, the total results achieved by many researchers following chelation therapy. Over the course of the last decade, such analytic overviews have grown more reliable and are more relied upon. Chappell and Stahl identified 19 articles in the medical literature that met their criteria for determining chelation's effectiveness in cardiovascular illness. In combination, the articles provided data on 22,765 patients. The meta-analysis determined that 87 percent of these patients experienced favorable outcomes. Only those improvements measured by objective testing were accepted as evidence in their analysis.

Chappell and Stahl were compelled to conclude that there was very strong published evidence for chelation's effectiveness in the treatment of cardiovascular disease. - Elmer M Cranton M.D.)

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

ABSTRACT: 

Twenty-four hour urinary creatinine clearance measurements on ambulatory patients are not reliable. Collection errors are common as outpatients. Serial measurements of serum creatinine and routine urine analyses are more reliable to monitor for renal safety during a course of EDTA chelation therapy. Intravenous EDTA chelation therapy can cause renal impairment, if not properly monitored. An occasional patient will unpredictably be susceptible to transient EDTA nephrotoxicity.

Serum creatinine levels, carefully monitored throughout therapy, will safeguard renal function, and are essential if infusions are given more often than twice weekly or when kidney function is impaired at the outset. The Cockcroft-Gault equation accurately reflects glomerular filtration rate and provides an accurate, computed creatinine clearance estimate. That formula and has been modified, based on blood level measurements of EDTA during therapy, to provide approximately the same blood levels of EDTA in all patients.

Serum Creatinine and Creatinine Clearance

Twenty-four hour collection of urine specimens for creatinine clearance measurement is not reliable in ambulatory patients, especially the elderly and infirm who are commonly treated with EDTA chelation therapy.1-3 Rates of glomerular filtration (approximated as measured creatinine clearance) can more accurately be assessed by measuring serum creatinine alone, and then computing clearance. Serum creatinine levels can thus be used to accurately compute glomerular filtration rate.2,3 The dosing protocol below is designed to provide approximately the same blood levels of EDTA throughout the infusion for all patients, regardless of age, sex, weight or kidney function.

__________________________________________________________

COCKCROFT-GAULT EQUATION, MODIFIED


CrCl = (140 — Age) X (LBW X 1.33)
-----------------------------------------
   (72 X Cr)



This can be formula simplified as follows:


CrCl = (140 — Age) X LBW
--------------------------------
     54 X Cr



CrCl = computed renal glomerular filtration rate in ml/min

Age = patient’s age

LBW = computed lean body weight in Kg, see below.

Cr = serum creatinine in mg/dL

For women, multiply the above result by 0.85

__________________________________________________________

EDTA DOSE TO BE ADMINISTERED IN EACH INFUSION IS COMPUTED AS
  (TO BE ADMINISTERED SLOWLY, NOT LESS THAN THREE HOURS) 


50 mg EDTA per (Kg LBW X 1.33) X (CrCl/100)


The maximum dose is usually 3.0 grams, unless otherwise
individualized a physician


Correct for CrCl/100 only if creatinine clearance
is less than 100 ml/min.


Maximum rate of infusion is 16.6 mg/min X CrCl/100, for a 70 Kg patient

_________________________________________________________

LEAN BODY WEIGHT (LBW) IN KG AS USED IN ABOVE COMPUTATIONS


Lean body weight for males is computed at 50 kg plus 2.3 kg for each inch of height over 5 feet.


Lean body weight for females is computed at 45.5 kg plus 2.3 kg for every inch of height over 5 feet.

Actual weight is used whenever actual weight is less than computed lean body weight.

_____________________________________________________________

As reported by Dr Reidenberg at Cornell Medical School in the New England Journal of Medicine, "Creatinine . . . formation decreases with age. . . Elderly people can have markedly decreased renal function without having serum creatinine levels above the upper limit of normal. . . In patients with stable renal function, who are not massively obese, or edematous . . . we have found the Cockcroft-Gault equation accurate.”3

EDTA is distributed in extracellular fluid. It is not fat soluble and does not significantly enter cells. The safe dose of 50 mg/kg of body weight was originally derived on an average population with approximately 25% of their body weight as fat. To prevent obese patents from receiving an overdose, the administered dose of 50 mg/kg is computed above using lean body weight plus 33 percent, which produces the equivalent of 25 percent body fat. Similarly, the Cockcroft-Gault formula was found to be inaccurate for obese patients. Cockcroft and Gault derived their formula using average Americans who had approximately 25% of their body weights as fat. By using 1.33 times LBW to compute renal clearance using the Cockcroft-Gault equation, that source of error is also minimized. In the original ACAM Protocol, that correction for body fat was inadvertently omitted, causing inappropriately reduced doses in smaller patients.

Derivation of the above protocol is somewhat counter-intuitive, since weight seems to enter into the computation more than once. Weight is actually used three times, but is canceled out in the Cockcroft-Gault computation. The 72 constant in the denominator actually represents kg and produces a correction factor to adjust for the weight of a patient who weighs more or less than that amount. Without that adjustment, the final computation would only be accurate for a person who weighs 72 kg. By limiting weight of obese patients to 1.33 times LBW when computing creatinine clearance, we prevent erroneously high computations for obese patients

Most medicines enter into cellular metabolism and remain active for many hours. EDTA is different and unique in the following ways:

1) EDTA is inert and leaves the body unaltered. It does not react or interact chemically with metabolism, other than to bind, redistribute or remove loosely attached, polyvalent, cationic metal ions in the urine.

2) EDTA has a very short half-life in the body with normal renal function, approximately 42 minutes, and is passed out in the urine unchanged in a very short time.

3) EDTA distribution in the body is solely extracellular. Because EDTA is not fat-soluble and does not cross cell membranes, its distribution is restricted to plasma and extracellular fluid (ECF)—approximately 8 to 10 liters in volume.

4) Although EDTA remains outside of cells, much of its beneficial effect relates to removal, redistribution and balancing of metal ions within cells. Benefit will therefore be enhanced by maintaining a concentration in plasma and ECF adequate to produce a high diffusion gradient across cell membranes lasting several hours.

5) Disodium EDTA infusion causes a temporary lowering of plasma calcium concentration, which causes a pulsitile increase in parathyroid hormone. This  sequence of events is thought to be partially responsible for long term benefit.However, if the computed dose of disodium EDTA is infused too rapidly, plasma calcium drops too low, causing undesirable side effects. Decades of experience tell us that by slowly infusing the dose of disodium EDTA  computed using the formula above,  optimal benefits an be achieved with minimal side effects. 

Extracellular fluid exists largely in lean tissues. Adipose tissue has very little water or blood flow. The protocol dose of EDTA for patients with normal renal function is 50 mg EDTA per kg of LBW X 1.33, infused over 3 hours. That dose has been found by experience to be the maximum safe dose for patients with normal kidney function. When kidney function is normal (creatinine clearance 100 or higher), no further adjustment is made.

When renal clearance is reduced, the fact that EDTA is otherwise lost in urine at a very rapid rate during the 3-hour infusion becomes an important variable. This is best understood by visualizing a large container of plasma (extracellular fluid). That plasma is continuously being pumped through a filter (kidneys) that totally removes EDTA from approximately 130 ml per minute of solution. That represents the normal rate of glomerular filtration (creatinine clearance) in a young, healthy male of average weight. At that rate, 50-percent of a bolus dose of the EDTA would be removed in 45 minutes, 75-percent in two hours, and so forth. The goal of chelation therapy is to bathe cells of the body with a therapeutic concentration of EDTA for three hours or longer. That is achieved by continuously infusing EDTA at a constant, safe rate over 3 hours, to compensate for rapid loss in urine during that time. Decades of experience tell us that a dose of 50 mg of EDTA per kg body weight, infused over 3 hours, provides optimum benefit, and is safe when given at a maximum infusion rate of 16.6 mg/min in an adult of average weight and normal kidney function.

In a large series of patients with varied kidney function and body weight, plasma EDTA levels were measured 45 minutes after beginning each infusion (one half-life) and again at 3 hours, at the end of each infusion. By adjusting the dose of EDTA using the formula above, it was documented that equivalent plasma levels of EDTA were measured in all patients.(7) 

Total volume of extra cellular fluid is directly proportional lean body weight. Assume, for example, that the volume of plasma and extracellular fluid is 9 liters in a average, elderly 72 Kg patient. Assuming that EDTA would be totally removed from 6 liters of blood per hour, at a filtration rate of rate of approximately 100 ml/min, EDTA would be removed from 4.5 liters of plasma every 45 minutes. The half-life in blood of EDTA would therefore be 45 minutes. That corresponds exactly to the observed half-life as reported in the scientific literature. The EDTA initially infused has been largely eliminated by 90 minutes, half way though a 3-hour infusion, in an adult patient of average weight with reasonably healthy kidneys.

The blood level is continuously replenished by infusing EDTA at a rate of 16.6 mg/min throughout the infusion. If kidneys are impaired and renal clearance is reduced to 50 ml/min, for example,--as often occurs in chronically ill elderly patients--EDTA would be cleared from only 3 liters of plasma per hour. In such a patient, with creatinine clearance reduced to 50 ml.min, it is therefore necessary to reduce the dose-rate of infusion by half to achieve approximately the same blood level during that same period of time. If the blood level becomes excessive, EDTA in the renal filtrate becomes excessive, potentially causing renal tubular cells to swell. This can lead to further renal impairment.

Cockcroft and Gault, who derived the original equation, found that it gives a correlation coefficient between computed and actual measured creatinine clearance of 0.83.2 The Cockcroft-Gault equation was found to overestimate renal function in very obese or edematous patients and in patients with rapidly deteriorating kidney function. It is possible, however, to correct at least partially for such overestimates by limiting weight in the computation to 1.33 times LBW.2,3

Although rare, there are well documented instances of patients suffering serious renal impairment as a result of intravenous EDTA. Careful monitoring of serum creatinine is therefore essential to insure safety during therapy. Technology has progressed to the point where rapid and accurate creatinine determinations can be performed inexpensively in a physician's office. Serum creatinine can be measured quickly and easily using the Refletron®, or a similar dry-reagent laboratory instrument. Accurate results may be obtained within a few minutes and can conveniently be done prior to a chelation infusion, if kidney function is in doubt. If dry-reagent chemistry is not used, lipemic serum must first be ultracentrifuged to clear chylomicrons, which will otherwise cause erroneous measurements.

Safety of EDTA


Intravenous EDTA, properly administered, is relatively safe in comparison to most other prescription drugs.4,5 It is unjustified, however, to state that EDTA is not potentially nephrotoxic. Nephrotoxicity remains a risk for some patients; primarily the elderly with preexisting impairment of renal function.4-6 Serum creatinine levels should be carefully monitored throughout a course of chelation therapy. If a longer time is allowed between infusions, and if the dose-rate of EDTA is reduced to a safe level compatible with renal function, using the above protocol, most patients can safely benefit from a series of EDTA infusions, despite mild to moderate pre-existing renal impairment-—up to a serum creatinine level of 3.0 mg/dL if great care is used. Continued treatment in the face of rising creatinine levels, however, can result in progressive renal impairment and, in rare instances, has lead to temporary renal dialysis.

In one published report, a patient required renal dialysis to prevent death from EDTA chelation therapy.6 That same patient was later reported to be recovered with marked improvement of symptoms of atherosclerosis for which chelation therapy was administered. Renal function eventually returned to a state better than existed prior to administration of EDTA.

If chelation therapy is temporarily withheld in the face of a progressive rise in serum creatinine, kidney function can be expected to slowly return to baseline levels--and not uncommonly to an even more favorable level, reflecting improvement from therapy. McDonagh and associates reported that in a series of 383 chelation patients, six had pre-existing elevations of serum creatinine at the beginning of therapy. Infusions of EDTA were given approximately once each week. One of the six patients who began therapy with an elevated serum creatinine experienced relatively rapid deterioration in kidney function shortly after therapy was begun (this occurred even though treatments were given only once each week). Serum creatinine doubled after only a few infusions.5 Therapy was then discontinued and serum creatinine slowly returned over three months to a level that was even closer to normal than before therapy.

If serum creatinine had not been closely monitored during therapy, that patient might have suffered far more serious renal impairment. It is not uncommon for elderly patients and those with atherosclerosis to have mild to moderate impairment of renal function at the onset of EDTA chelation therapy. Most such patients tolerate chelation without difficulty if closely monitored. An occasional patient, however, will be unpredictably sensitive to EDTA and will show a transient deterioration of serum creatinine, sometimes after only a few infusions. It is not possible to predict in advance which patients will be unduly sensitive to EDTA and which will tolerate the infusions without difficulty. Only by serially measuring serum creatinine can potential renal complications be avoided. Patients with renal impairment and elevated serum creatinine should have serum creatinine measured at the time of every EDTA infusion.

Patients who are found less tolerant to EDTA should wait longer between infusions, often two weeks or more. In addition, it may be necessary to administer a lower dose and with a reduced infusion rate of four or more hours.

References

* 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. 



* CURRENT STATUS OF EDTA CHELATION THERAPY IN OCCLUSIVE ARTERIAL DISEASE
Elmer M. Cranton, MD and James P. Frackelton, MD 



* EDTA CHELATION THERAPY: EFFICACY IN ARTERIOSCLEROTIC HEART DISEASE
H. Richard Casdorph, MD, PhD 



* EDTA CHELATION THERAPY: EFFICACY IN BRAIN DISORDERS
H. Richard Casdorph, MD, PhD 



* AN OCULOCEREBROVASCULOMETRIC ANALYSIS OF THE IMPROVEMENT IN ARTERIAL STENOSIS FOLLOWING EDTA CHELATION THERAPY
Edward W. McDonagh, DO, Charles J. Rudolph, DO, PhD, and E. Cheraskin, MD, DMD 



* EFFECT OF EDTA CHELATION THERAPY PLUS MULTIVITAMIN TRACE MINERAL SUPPLEMENTATION UPON VASCULAR DYNAMICS: ANKLE/BRACHIAL DOPPLER SYSTOLIC BLOOD PRESSURE RATIO
Edward W. McDonagh, DO, Charles J. Rudolph, DO, PhD, and E. Cheraskin, MD, DMD 



* EDTA CHELATION THERAPY: TREATMENT OF PERIPHERAL ARTERIAL OCCLUSION, AN ALTERNATIVE TO AMPUTATION
H. Richard Casdorph, MD, PhD, and Charles H. Farr, MD, PhD 



* NINETY PERCENT REDUCTION IN CANCER MORTALITY AFTER CHELATION THERAPY WITH EDTA
Walter Blumer, MD and Elmer M. Cranton, MD 



* THE "CLINICAL CHANGE" IN PATIENTS TREATED WITH EDTA CHELATION PLUS MULTIVITAMIN/TRACE MINERAL SUPPLEMENTATION
Edward W. McDonagh, DO, Charles J. Rudolph, DO, PhD, and E. Cheraskin, MD, DMD 



* EDTA CHELATION THERAPY: A RETROSPECTIVE STUDY OF 2,870 PATIENTS
Efrain Olszewer, MD and James P. Carter, MD, DrPH 



* BENEFITS OF EDTA CHELATION THERAPY ON ATHEROSCLEROSIS: A RETROSPECTIVE STUDY OF 470 PATIENTS.
Claus Hancke, and Knut Flythe 




* VISUAL FIELD EVIDENCE OF MACULAR DEGENERATION REVERSAL USING A COMBINATION OF EDTA CHELATION AND MULTIPLE VITAMIN AND TRACE MINERAL THERAPY.
Charles J. Rudolph, DO, PhD, R. T. Samuels, and Edward W. McDonagh, DO 



* A NONSURGICAL APPROACH TO OBSTRUCTIVE CAROTID STENOSIS. USING EDTA CHELATION.
Charles J. Rudolph, DO, PhD, and Edward W. McDonagh, DO, and R.K. Barber 



* THE EFFECT OF INTRAVENOUS DISODIUM ETHYLENEDIAMINETETAACETIC ACID (EDTA) UPON BONE DENSITY.
Charles J. Rudolph, DO, PhD, and Edward W. McDonagh, DO, D. G. Wussow 



* RENAL ARTERY STENOSIS REVERSAL IN A HYPERTENSIVE INDIVIDUAL, USING A COMBINATION OF EDTA CHELATION AND MULTIPLE VITAMIN AND TRACE MINERAL THERAPY.
Charles J. Rudolph, DO, PhD, and Edward W. McDonagh, DO 



* THE EFFECT OF EDTA CHELATION THERAPY WITH MULTIVITAMIN/TRACE MINERAL SUPPLEMENTATION UPON REPORTED FATIGUE.
Edward W. McDonagh, DO, Charles J. Rudolph, DO, PhD, and E. Cheraskin, MD, DMD 



* CLINICAL IMPROVEMENTS AS JUDGED BY THE CORNELL MEDICAL INDEX QUESTIONNAIRE IN PATIENTS TREATED WITH EDTA CHELATION THERAPY
H. D. Riordan, MD, E. Cheraskin, MD, DMD, and M. Dirks, BD 



* A PILOT DOUBLE BLIND STUDY OF SODIUM-MAGNESIUM EDTA IN PERIPHERAL VASCULAR DISEASE.
Efrain Olszewer, MD, F. C. Sabbag, and James P. Carter 



* THE CORRELATION BETWEEN EDTA CHELATION THERAPY AND IMPROVEMENT IN CARDIOVASCULAR FUNCTION: A META-ANALYSIS.
L. Terry Cha ppell, and J.P. Stahl 



* EDTA CHELATION TREATMENT FOR VASCULAR DISEASE: A META-ANALYSIS USING UNPUBLISHED DATA.
L. Terry Chappell, J.P. Stahl, and R. Evans 



* IF EDTA CHELATION THERAPY IS SO GOOD, WHY IS IT NOT MORE WIDELY ACCEPTED?
James P. Carter, MD, DrPH 



* KIDNEY EFFECTS OF ETHYLENE DIAMINE TETRAACETIC ACID (EDTA): A LITERATURE REVIEW
Elmer M. Cranton, MD 

* THE EFFECT OF EDTA CHELATION THERAPY PLUS SUPPORTIVE MULTIVITAMIN‑TRACE-MINERAL SUPPLEMENTATION UPON RENAL FUNCTION: A STUDY IN SERUM CREATININE
Edward W. McDonagh, DO, Charles J. Rudolph, DO, PhD, and E. Cheraskin, MD, DMD 



* THE IMPROVEMENT IN RENAL FUNCTION FOLLOWING EDTA CHELATION AND MULTIVITAMIN TRACE-MINERAL THERAPY: A STUDY IN CREATININE CLEARANCE
Keith W. Sehnert, MD, A. F. Clague, and E. Cheraskin, MD, DMD 



* THE EFFECT OF EDTA CHELATION THERAPY PLUS SUPPORTIVE MULTIVITAMIN-TRACE MINERAL SUPPLEMENTATION UPON RENAL FUNCTION: A STUDY IN BLOOD UREA NITROGEN (BUN)
Edward W. McDonagh, DO, Charles J. Rudolph, DO, PhD, and E. Cheraskin, MD, DMD 



* ANOTHER LOOK AT RENAL FUNCTION AND THE EDTA CHELATION TREATMENT PROCESS
H. D. Riordan, MD, E. Cheraskin, MD, DMD, M. Dirks, BD, MA, M. Schultz, ARNP, and P. Brizendine, ARNP 

HISTORY AND PROTOCOL FOR ADMINISTRATION:


* Overview, Historical Background and Current Status of EDTA Chelation Therapy for Atherosclerosis
Michael B. Schachter, MD 



* THE PROTOCOL FOR THE SAFE AND EFFECTIVE ADMINISTRATION OF EDTA AND OTHER CHELATING AGENTS FOR VASCULAR AND DEGENERATIVE DISEASES
Theodore C. Rozema 



* IRON AND COPPER SUPPLEMENTATION WITH EDTA CHELATION THERAPY
James P. Frackelton, MD and Elmer M. Cranton, MD 

SECTION V: LABORATORY EVALUATION 


* A LABORATORY METHOD TO MEASURE PLASMA EDTA LEVELS.
Zheng Xian Liu, K. C. Harich, and Elmer M. Cranton, MD 



* MONITORING RENAL FUNCTION AND DOSE COMPUTATION DURING EDTA CHELATION THERAPY
Elmer M. Cranton, M.D. and James P. Frackelton, MD  (Full text available for download)



* URINARY TRACE AND TOXIC ELEMENTS AND MINERALS IN UNTIMED URINE SPECIMENS RELATIVE TO URINE CREATININE, PART I: CONCENTRATIONS OF ELEMENTS IN FASTING URINE
Elmer M. Cranton, MD Zheng Xian Liu, MS, and Ivy M. Smith, MT 



* URINARY TRACE AND TOXIC ELEMENTS AND MINERALS IN UNTIMED URINE SPECIMENS RELATIVE TO URINE CREATININE, PART II: PROVOKED INCREASE IN EXCRETION FOLLOWING INTRAVENOUS EDTA
Elmer M. Cranton, MD Zheng Xian Liu, MS, and Ivy M. Smith, MT 



* TESTING FOR TOXIC ELEMENTS AND CHELATION OF MERCURY
Elmer M. Cranton, M.D.

It's very difficult to test real people using chelation therapy and not come away impressed. Nevertheless, some physicians have achieved that feat. Let's look at their research:

Every now and then puzzled patients tell me that a friend, relative, or skeptical physician has told them that chelation was fairly tested and fell flat. I can usually guess what they're referring to. In the last ten years, a small cluster of studies sprouted up in the mainstream medical literature purporting to demonstrate that EDTA chelation was a fizzle when it came to treating cardiovascular ailments.

The curious thing is that those studies―flawed and imperfect though they are―only succeed in offering us still more positive data to support this therapy (click here for analysis).

The most controversial and oft cited study was done in Denmark. It was the handiwork of a group of Danish cardiovascular bypass surgeons. Results of that study were published in two medical journals, the Journal of Internal Medicine and the American Journal of Surgery. The results were also widely publicized in the news media.

The surgeons had taken 153 patients suffering with intermittent claudication. These were people with such severely compromised circulation in their lower extremities that walking across a parking lot could challenge their fortitude. One measurement of their condition was their maximal walking distance (MWD)―the very longest distance that they could walk before intolerable leg pain brought them abruptly to a halt. The patients were divided into an EDTA group and a placebo group. In the pre-treatment phase, the EDTA group could on average walk 119 meters before colliding with their MWD; the placebo group averaged 157 meters.

Treatment began with the patients receiving either 20 intravenous infusions of EDTA or 20 infusions of a simple salt solution, depending on their group. The study was purportedly double-blinded, that is, neither the patients nor the researchers knew which person was receiving which infusion until after the study was complete. Progress was measured periodically. In particular, we will analyze their results at three months following treatment, when full benefit from chelation would be expected to occur.

Both placebo and treatment groups showed improvement. However, the investigators concluded that the improvement was not statistically significant and―equally important―that the difference in response rate between the EDTA group and the placebo group was roughly similar. Obviously, a drug that fails to achieve more than the placebo effect is presumed to be a dud.

The Danish study impressed many people; 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 patients. Before the study was over the researchers and more than 64 percent of the patients were aware of which treatment they had received.

This was unorthodox and since it had not been reported in the published study, extremely questionable from an ethical standpoint.

Many people had also been struck by the study's relatively small size. Intermittent claudication is a very unpredictable disease, and, unless enough patients are included in a trial, the results tend to be statistically unreliable.

The most interesting aspect of the Danish study, however, was hidden away in the numbers. This is the startling fact that the patients who were given EDTA were certainly a good deal sicker than the patients tested with a placebo. Therefore, the improvements they made were harder earned and more significant. The researchers, who 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 in the pre-treatment MWDs. The EDTA patients' longest average distance before claudication pain stopped them in their tracks was 119 meters, while for the placebo patients it was 157 meters.

Still more significant was the standard deviation. Standard deviation is a statistical abstraction, which reflects the amount of variability among a collection of raw scores. In essence, standard deviation reflects how widely diverse the numbers are in each group. A high standard deviation indicates that measurements were spread out toward the extremes of a wide range, rather than closely clustered near the average. Without going further into the arcane science of statistics, it is enough to say that the plus or minus 38 meters for EDTA patients versus plus or minus 266 meters for placebo group represents an enormous difference in walking capacity that is heavily biased in favor of the placebo group. The standard deviation numbers show that some placebo patients must have walked half a mile before stopping. The EDTA group's claudication was therefore much more severe. The EDTA group was much sicker. The design of the study was therefore catastrophically biased against EDTA chelation from the outset.

Yet, when the six-month study was completed, the MWD in the EDTA group rose by 51 percent, from 119 to 180 meters, while the mean MWD in the placebo group rose only 24 percent, from 157 to 194 meters. In plain English, looking at all the published data, the chelation group's improvement was more than twice as great as the placebo group's, even though they were significantly sicker at the outset.(8,9)

I believe the Danish study must be interpreted as another solid demonstration of the effectiveness of chelation. If it were not for its relative smallness, I would be happy to quote from its results at any time. I hope the Danish surgeons can be persuaded to undertake another study with five times as many subjects. If they take the trouble to hire an academic statistician to oversee design and interpretation of the study, and refrain from violating the double blind, they may yet do good work, and we shall all be much in their debt.

Another study―also conducted by vascular surgeons―was done at the Otago Medical School in Dunedin, New Zealand, two years later. The subjects of this study were also suffering from intermittent claudication manifested by leg pain and walking difficulties beyond a very limited distance. Chelation subjects were compared to controls. The study extended to three months after 20 infusions of either EDTA or a placebo had been administered. Upon examining the results, the authors of the study concluded that chelation had been ineffective. Once again, that conclusion seems ill founded.

 The absolute walking distance of the EDTA group increased by 26 percent; in the placebo group, it increased by 15 percent. This was not considered statistically significant. The study, however, was so small that there were only 17 subjects in the placebo group. One of these was what the statisticians call an "outlier." That is a person whose results differ strikingly from everyone else in the group. That placebo 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, their placebo distance decreased slightly.

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

Meanwhile, even the New Zealand researchers conceded that the improvement in artery pulsatility (measurement of pulse intensity) in the EDTA group's worse leg reached statistical significance. In statistical terms, there was less than a one in a thousand chance that that improvement was not a benefit of EDTA. (10)

I would note only two other things. First, a 26 percent improvement in walking is by no means minor and would attract notice if the agent had been a patentable drug. Second, even that level of improvement is in no sense representative of the much greater improvements claudication patients normally experience after chelation.

There is a simple reason for the difference: smoking.

Smoking so dramatically undermines cardiovascular function, especially in people who are already seriously sick with claudication, that it negates much of the gain that chelation provides. In the New Zealand study, 86 percent of the chelated subjects were smokers. They were advised to quit smoking when the study began, but how many of them actually stopped is, I fear, a subject for skeptical speculation. A demonstration of chelation's full potential requires a much higher percentage of non-smoking subjects at the outset.

Just as this book goes to the printer, another small study alleging to disprove EDTA chelation therapy is being widely reported by the news media. This recent study was conducted by cardiologists in Calgary, Canada, who freely admit their bias against chelation. They seem to have set out to discredit a therapy that they oppose by studying a few patients with heart disease. Because the study has not yet been published in a scientific journal, it is not possible to provide a meaningful critique. I feel certain, however, that when we finally do have an opportunity to conduct a detailed review of that study's design and data, the final assessment will be very similar to that of the Danish and New Zealand studies, as described in detail in this chapter―another hatchet job.

It's relatively easy to design a study specifically to discredit an unpopular therapy, and to make that study superficially appear to be scientific. The United States Congress once commissioned its Office of Technological Assessment to analyze all published medical research for scientific merit. After a careful review of research studies from leading medical journals, they concluded that, "more than 75 percent of all published medical research has invalid or insupportable conclusions as a result of statistical problems alone." The final report to Congress stated, "few published clinical trials are well enough designed to yield valuable results."

And it's not merely intellectual dishonesty. Many doctors who oppose chelation therapy firmly believe that it is ineffective. That is what they have been told. So they attack, with no personal knowledge about what they are attacking. Perhaps they feel threatened because very few doctors have the time to thoroughly read and analyze published studies in medical journals. They usually skim the abstract and jump to the authors' conclusions, accepting them without question.

I have also found medical doctors to be naive and unaware that the peer review process is often used as a form of editorial censorship―a way to maintain the status quo and protect the professional reputations and practices of the reviewers. Also, because medical journals so often depend heavily on advertising by major pharmaceutical companies, studies that are unpopular with that industry are rarely published; while brief letters to the editor and unsupported editorial opinion attacking opposed therapies quickly find their way into print. Journals tend to be reluctant to bite the hand that feeds them.

 Powerful psychological defense mechanisms also come into play. If doctors are not taught about EDTA chelation therapy in medical school (and they are not), and if those doctors therefore do not routinely use or prescribe chelation therapy for patients, then they believe one of two things: 1) either their medical educations were deficient and they are not providing the best of care for patients; or, 2) other doctors routinely using and prescribing chelation therapy for medical conditions that are not FDA-approved must be "quacks," exploiting desperate patients. Which do you think their choice will be? It's apparently difficult for many medical doctors to shed an attitude of God-like omniscience and admit that they simply do not know everything there is to know.

One final study that was carried out with what I am forced to call negative intent is such a curious oddity that it also deserves discussion, although it remains unpublished. It is usually referred to as the "Heidelberg Trial" and was conducted at the behest of the German pharmaceutical company Thiemann, AG, in the early 1980s. Once again using patients with intermittent claudication, it compared the effects of 20 infusions of EDTA with 20 infusions of bencyclan, a vasodilating and antiplatelet agent owned by Thiemann.

Needless to say, from a practical commercial standpoint, Thiemann's action was bizarre. If EDTA did well in the trial, Thiemann's own already well established drug could only suffer. Nonetheless, the trial went forward and was reported before the audience in 1985 at the 7th International Congress on Arteriosclerosis in Melbourne, Australia. That study showed that immediately following 20 infusions of EDTA, pain-free walking distance increased by 70 percent. By contrast, the patients receiving bencyclan had increased their pain-free walking distance by 76 percent. The difference between these two results was, of course, not statistically significant, but another result was. It turned out that 12 weeks after the series of infusions was completed, the EDTA patients' average pain-free walking distance had continued to increase, going up by an astounding 182 percent. No further improvement had occurred in the patients receiving bencyclan, however.(11)

A report from Thiemann only mentioned the 70 and 76 percent figures, and press releases stated that chelation was no better than a placebo without mentioning that the "placebo" was a drug that had been proven effective in the treatment of intermittent claudication. Thiemann never released the actual data from the Heidelberg Trial, but some German scientists who had access to it, and who were disturbed at the deception they were witnessing, chose to reveal the data to members of the American scientific community.

The complete data showed that four patients in the EDTA group experienced more than a 1,000-meter increase in their pain-free walking distance following treatment.(12) This highly favorable data from those four patients mysteriously disappeared before the final results were made public. As sponsor and by funding the study, Thiemann had a legal right under terms of their contract to edit the final results and to interpret the data in any way that suited them. An analysis of the complete data showed an average increase in walking distance in the EDTA-treated group of 400 percent at three months after therapy―five times the 76-percent increase of the group receiving bencyclan.

These three ineffectual attempts discredit chelation with flawed research represent pretty much the sum total of scientific involvement that the establishment has had with this extraordinary therapy over the past thirty years.

In January, 2002, the American Medical Association published yet another junk-science study in a seeming further attempt to discredit EDTA chelation therapy. If anything, that so called PATCH study, conducted in Calgary Canada, was one more positive study with a misleading negative conclusion.

However, the darkest moment for chelation actually came way back in 1963. This was when Drs. J. R. Kitchell and L. E. Meltzer co-authored an article reassessing their support for EDTA chelation.

Although it was hardly in widespread use, chelation had been surprisingly uncontroversial up until that moment. Beginning in 1953, Dr. Norman Clarke, Sr., and his associates at Providence Hospital in Detroit began using EDTA chelation to treat coronary heart disease. In 1956, they reported that they had treated 20 patients suffering from chest pain (angina pectoris). Nineteen of the 20 patients had had a "remarkable" improvement in symptoms.(13)

Soon other physicians became interested, among them Drs. Kitchell and Meltzer, who specialized in cardiology at Presbyterian Hospital in Philadelphia. From 1959 to 1963, Kitchell and Meltzer reported on their consistent good results treating cardiovascular diseases with EDTA. Their early reports were all very positive.(14-16)

But in April of 1963, shortly after their last favorable report, they published a "reappraisal" in the American Journal of Cardiology that questioned chelation's value.

That reappraisal article included ten original patients on whom they had previously published data, and 28 patients with coronary heart disease who were treated subsequently. Treated patients in this report were all severely ill. The authors state that the patients were, " . . .referred to us because of severe angina. The patients had previously been treated with most of the accepted methods, and their inclusion in this study resulted from wholly unsuccessful courses. Each of the patients was considered disabled at the start of therapy." This was therefore a very high-risk group with any form of therapy.

Seventy-one percent of patients treated had subjective improvement of symptoms, 64 percent had objective improvement of measured exercise tolerance three months after receiving 20 chelation treatments, and 46 percent showed improved electrocardiographic patterns. Kitchell and Meltzer then went on to conclude that chelation was not effective because some patients eventually regressed more than a year after treatment. However, considering the poor health of the patients, there is no other treatment about which the same statement could not be made. Eighteen months following therapy, 46 percent of those patients remained improved. Theresults were very favorable even though the authors' conclusions were not.(17)

I believe that this "reappraisal" article was largely responsible for termination of academic research into chelation as a treatment for cardiovascular ills. Rather than analyzing the data for themselves, most physicians simply accepted the mistakenly negative conclusion at face value. We will probably never know what prompted those early researchers to change their position so abruptly. We can only speculate that it was an unrealistic expectation the emergence of bypass surgery would be a final solution.

The years that followed were filled with astonishing demonstrations of surgical inventiveness; and, for at least the next two decades, cure by the knife dominated the medical landscape. Then came balloon angioplasty. Those surgical and high-tech discoveries were splendid in themselves; but what was tragic was to regard them as the preferred, if not the exclusive, approach to complex cardiovascular problems.

As for chelation, its future is now bright because its effectiveness is incontrovertible. Biased or uninformed physicians may call it untested, but no scientifically informed person can read the studies on which this chapter is based without realizing that EDTA chelation therapy is a formidable antagonist to cardiovascular disease.

A major upsurge in demand for chelation is now coming from the many people who have heard first-hand from friends or relatives who benefited from this remarkable therapy.