Saving a Million Hearts

In 2013 a group of ICIM members gathered to discuss an integrative, preventative approach to the Saving a Million Hearts initiative, including chelation therapy. Here are video clips of their conversations. The event was organized by Terry Chappell MD, and Jeannette Soriano MD is the facilitator.

Jeannette Soriano

Saving a Million Hearts Outline

Saving a Million Hearts Introduction from an Integrative Medicine Perspective

Dr. Terry Chappell, Dr. Lambert Parker, and Dr. James Carter discuss the “Saving a Million Hearts” initiative of the CDC and other medical groups. These three integrative doctors talk about the importance of going beyond pharmaceuticals.

Saving a Million Hearts: Stress and Lifestyle

Dr. John Wilson, Dr. James Carter, Dr. Ellie Campbell discuss diet, stress, and lifestyle as they relate to cardiovascular disease. Includes reference to an Alpha-Stim study by ICIM member William Eidleman MD.

Saving a Million Hearts: Informed Consent

Dr. Terry Chappell and Dr. Russ Jaffe discuss the importance of having informed consents as part of the patient education process for integrative medicine and chelation therapy for cardiovascular disease.

Saving a Million Hearts: Testing for Risk Factors

Dr. Conrad Maulfair, Dr. Ellie Campbell, Dr. Robban Sica, and Dr. Joe Hickey discuss what cardiovascular risk factors should be explored for effective prevention of heart attack and stroke.

Saving a Million Hearts: Metabolic Syndrome

Dr. Joe Hickey, Dr. Robban Sica, Dr. Ellie Campbell, Dr. Conrad Maulfair talk about the testing they do to screen for Metabolic Syndrome in their integrative practices, and discuss what treatments they recommend to their patients.

Saving a Million Hearts: Testing and Treating Cholesterol

Dr Rick Mason, Dr. Joe Hickey and Dr. Garry Gordon discuss cholesterol’s role in heart disease- to test or not to test! What is the dietary impact? What kind of cholesterol should we focus on? HDL, LDL, lipids, proteins, triglycerides… what wisdom will the future of medicine hold? Is there a cholesterol propaganda scheme? What are treatment strategies?

Saving a Million Hearts: Blood Pressure

Dr. Joe Hickey, Dr. Lambert Paker, Dr. Muhammad Ashraf discuss blood pressure tips for check ups, monitoring and treatment.

Saving a Million Hearts: Toxic Metals Q&A

Dr. Robin Bernhoft, Dr. Jim Smith, Dr. John Wilson answer questions from some of the most experienced chelation doctors in the country about diagnosing and treating heavy metal toxicity, with a focus on EDTA chelation.

Saving a Million Hearts: Chelation Protocols I

Dr. Robban Sica, Dr. Terry Chappell, and Dr. Garry Gordon discuss the IV chelation protocols that they have used.

Saving a Million Hearts: Chelation Protocols II

Dr. Robban Sica, Dr. Terry Chappell, and Dr. Garry Gordon discuss the IV chelation protocols that they have used.

Saving a Million Hearts: Micronutrients 

Dr. Chuck Mary and Dr. Rick Mason, CoQ10, Magnesium, Copper and other micronutrients’ role in the body and for prevention of cardiovascular disease.

Saving a Million Hearts: Women’s Health and Allergy Testing in Cardiovascular Disease

Dr. Robban Sica, Dr. Russell Jaffe, Dr. Ellie Campbell, and Dr. John Wilson discuss the role allergies can play in cardiovascular disease, laboratory testing, and special considerations for women’s health.

Dr. Chappell’s article “Saving a Million Hearts can be found here



Mercury Toxicity and Treatment: A Review of the Literature

I can’t thank you enough for your excellent participation in a landmark meeting “Saving a Million Hearts.” The structure was an experiment that we definitely want to repeat, and it reminds us again about the quality of our membership and attendees.

Here is one more resource:

Dear Dr. Bernhoft,

I am pleased to let you know that your article has been published in its final form in the “Journal of Environmental and Public Health:”

Robin A. Bernhoft, “Mercury Toxicity and Treatment: A Review of the Literature,” Journal of Environmental and Public Health, vol. 2012, Article ID 460508, 10 pages, 2012. doi:10.1155/2012/460508.

You may access this article from the Table of Contents of Volume 2012, which is located at the following link:

Alternatively, you may directly access your article at the following location:

“Journal of Environmental and Public Health” is an open access journal, meaning that the full-text of all published articles is made freely available on the journal’s website with no subscription or registration barriers.

Best regards,

Noha Hany
Journal of Environmental and Public Health
Hindawi Publishing Corporation.

Magnesium deficiency or composition of the infusate used in the load test?

Robert Waters MD


Mg Man Cal tiss-04-17-08

Serum/plasma measurements do not reflect magnesium deficits in clinical situations and magnesium load tests are used as a more accurate method to identify magnesium deficiency in a variety of disease states as well as in subclinical conditions. The objective of this study was to determine if people are indeed magnesium deficient or if the apparent magnesium deficiency is due to the composition of the infusate used in the load test.

Magnesium load tests were performed on 7 patients using three different Mg solution infusions- a Mg-EDTA (ethylene diamine tetraacetic acid)-nutrient cocktail used in EDTA chelation therapy containing several components including vitamins and minerals and the same cocktail without EDTA and an infusion of an identical amount of magnesium in normal saline solution.  There was no significant difference in the amount of magnesium retained in the 24 hours after infusion among the three infusates.  All infusates resulted in very high magnesium retention compared to previous published magnesium load studies.  Magnesium deficiency may be widespread and the relationship of Mg deficiency to related diseases requires further study.


Mg is the fourth most abundant cation in the body and its intracellular concentration is exceeded only by potassium [1].  Mg activates more than 300 enzymes in the human body [2].  Deficiency of Mg has been linked to a variety of clinical disease states including hypertension, myocardial infarction, cardiac dysrhythmias, coronary spasm and premature artherosclerosis [3].  In addition, patients with diabetes have been found to be at particular risk for Mg deficiency [4].  Conditions related to the deficiency of Mg may be linked to its functions as a cofactor for enzymes related to cell respiration, glycolysis and ion transport (e.g. Na-K-ATPase).  In fact, the central position of Mg in its role in energy storage, transfer and utilization is mediated through its function in the formation of Mg-ATP, the ultimate form of stored energy in biological systems.  In addition, Mg has functions related to protein synthesis through its action on nucleic acid polymerization, binding of ribosomes to RNA and the synthesis and degradation of DNA [5].  Mg is also an integral player in calcium biology via its ability to maintain low resting concentrations of intracellular calcium ions.  It competes with calcium for membrane binding sites and as such has been described as a “calcium channel blocker” [6].

In degenerative diseases, Mg deficiency has been shown to be related to the generation of free radicals [7].  Mg deficiency has also been shown to negatively influence the generation of nitric oxide and therefore the impact of such deficiency may be responsible in part for the pathogenesis of endothelial dysfunction and its relationship to vascular disease, diabetes and other diseases associated with aging [8].

In a previous study, we showed that after the infusion of 686 mg of elemental Mg as Mg sulfate, in an EDTA chelation “cocktail”, 83% of the infused Mg was retained in the initial 24 hours following infusion [9]. This degree of retention of Mg has generally been recognized to represent evidence of severe Mg deficiency.  However, in that study, it was not clear if the apparent Mg retention was due to a true Mg deficiency or if the components of the chelation cocktail affected Mg retention.  Guldager et al. [10] infused 3 g of EDTA in saline, without any Mg, into a group of peripheral vascular disease patients and collected 24 hour urines of the patients and controls.  There was a highly significant decrease in the Mg in the 24 hour urines of the EDTA patients vs the controls indicating that the EDTA increased Mg retention.  The serum Mg in these patients did not increase so it is probable that the EDTA caused Mg to enter intracellular compartments.  This present study was designed to determine the effects of components of the Mg infusates on Mg retention.


The study was approved by the Clinic Human Studies Review Board, Wisconsin Dells, WI.  The study was explained to the subjects and patients signed an informed consent before the study.  Data are available to the participants upon request.  Participants did not incur any medical fees as a result of their participation and were not paid for their participation.

At the onset of the study, patients were instructed in the accurate collection of 24-h urine specimens to avoid metal contamination.  Twenty-four-hour urine samples were collected in 4-L sample containers (Fisher Scientific Co., Pittsburgh, PA) 2d prior to chelation therapy (d 1 and d 2), the day of chelation therapy (d 3), and the following day (d 4).  Control urine samples were collected on Monday and Tuesday and the post-infusion urine samples on Wednesday and Thursday.  In Phase 1 of the study, on Wednesday morning of the study week, an intravenous infusion of 2.25 g of EDTA mixed in sterile water with 5 g of sodium ascorbate, 2500 units of heparin, 3 mL of 2% procaine, 100mg pyridoxine HCl, 4 meq KCl, 1 mL of 8.4% sodium bicarbonate, 1000 µg hydroxycobalamin, 1 mL vitamin B complex, and 7 mL magnesium sulfate equivalent to 686 mg of elemental magnesium was given in an arm vein over a 2.5 hour period. During phase 2, patients received an identical infusion without any EDTA and during phase 3 subjects received 686 mg elemental Mg in saline [9] [11].  Order of the phases was random.  The procedures were two to four weeks apart.  Magnesium contents of the urine samples were measured and the Mg retention calculated using the following formula modified from Jeppesen [12]:

%Mg retention = [infused Mg – (urine Mg on day 3 – average urine Mg on days 1 and 2)/ infused Mg] X 100.

Day 3 was the following day after the infusion; days 1 and 2 were baseline days immediately preceding the infusion. In addition, Mg content was also measured on day 4.

Since the time of our original chelation study, published and anecdotal data have revealed that the clinical efficacy of EDTA chelation therapy could be achieved with a smaller dose of EDTA with fewer potential side effects.  Therefore, we reduced the dose of EDTA to 2.25 g.

Magnesium concentrations in the urine were determined using flame atomic absorption using a Perkin-Elmer 5000 flame atomic absorption spectrometer using standard techniques (Perkin-Elmer, Norwalk, CT) and reference materials as described [13].

Statistics: Statistical analyses of the data were performed using 2-Way Analysis of Variance (SAS Institute, Cary, NC, version 9.1).  The main effects were the variable components of the infusions in the 3 Phases.  Values are mean ±  SEM.


Means for magnesium losses among the three Phases were not statistically different.  Approximately 70% of the infused Mg was retained during the 24-h period after the infusion (day 3) in Phase 1.  Retention of Mg in Phases 2 and 3 were similar.  By day 4, the 24-h Mg excretion was not significantly different from the averages of days 1 and 2 in all three Phases of the study.


In this study, Mg retention was greater than 70% for all infusates.  High Mg retention is probably not due components of the infusate since infusion of Mg added to saline also led to significant Mg retention. The presence of EDTA in the cocktail did not increase the retention of Mg and retention was still approximately 72% when Mg sulfate was added to saline alone and infused.  Suboptimal Mg status appears to be present in essentially all of the subjects.

From analyzing the data on Mg load tests published over the last 30 years, it appears that there is great variation in the percentage of Mg that can be expected to be retained by normal patients vs. patients with various medical conditions.  It is clear that serum/plasma Mg measurements do not necessarily reflect Mg deficits in clinical situations [14].  Thus alternative measurements of Mg status were attempted and ultimately the Mg retention test was suggested as a more accurate method to identify Mg deficiency in a variety of disease states as well as in subclinical conditions.  Other methods including bone Mg, muscle Mg, NMR spectroscopy, single ion channel analysis, leukocyte Mg, intraerythrocyte Mg and Mg balance studies are more expensive and/or invasive but may not be more informative than the Mg load test.  Even the intracellular Mg measurements have shown inconsistent correlation with serum levels and other tissue levels as well as Mg load test data [15].

Table 2 summarizes the data from a number of intravenous load tests.  In most of the studies, the demarcation in Mg retention between patients and controls is roughly 20%.  In our present study, all groups of patients had Mg retention of at least 70%.  The presence of EDTA at a dose of 2.25g in the infused Mg preparation did not explain the high retention since when EDTA was omitted from the infusate, Mg retention remained high.  However, we cannot, with certainty, conclude that EDTA results in no greater Mg retention since we only used 2.25g of EDTA in the infusions vs the prior study of 3.0g which resulted in an even greater retention of 83% [9].   The results of Guldagner, et al also suggest a causal Mg retention by 3g of EDTA without any Mg added to the infusate [10].

Components of the infusate in the present study also appear to have little influence on magnesium retention since the Phase 2 Mg retention cocktail without EDTA, but otherwise the same vitamins and minerals, was not different from the cocktail containing only Mg and saline.  Patients in our earlier study [9] all had evidence of degenerative diseases and retained even greater amounts of Mg than the patients in our present study and the dose of EDTA in that study was 3 g. Earlier studies of the therapeutic effects of EDTA used 5 g of EDTA per treatment, 5 days per week, and showed dramatic positive clinical effects as well as objective evidence of benefits such as improved EKG’s, reduction in the calcification of heart valves and dissolution of metastatic calcification in the kidneys [16] [17]. Only further studies on the dose dependent effects of EDTA  as well as careful choice of “normal” vs. “diseased” patients can help resolve the issue of whether EDTA can influence calcium and magnesium dynamics in vivo in correlation with clinical and biochemical findings.

A number of studies using the Mg retention test have shown that patients with corornary heart disease are Mg deficient compared to controls.  Jeppesen reasoned that Greenlanders have a lower rate of myocardial infarction as a result of their high serum Mg, low serum calcium and prolonged bleeding time (known to be induced by Mg administration) [12].   After administering 30 mmoles of intravenous Mg over 12 hours in patients with acute myocardial infarction, the infarction patients retained 42% of the infused Mg over the next 24 hours compared to only 22% in the control group.  He also obtained quadricep muscle biopsies, which revealed an increased Mg content in the control group vs the acute myocardial infarction groups but differences were not statistically significant.

Sjogren et al. [18] showed patients with Crohn’s disease had lower tissue concentrations of Mg compared with controls and after IV infusions of 60 mmole Mg, the Crohn’s patients had significantly higher Mg retention than the controls.  Gullestad et al. [19] showed that Mg retention in the 24 hour urine was 3-4% in a group of individuals without known predisposition for Mg deficiency after an infusion of 30 mmoles Mg sulfate.  This was significantly lower than that for 661 hospitalized patients with known predisposition to Mg deficiency (cardiovascular disease, alcoholism, etc. whose percent retention varied from 16 – 38%).  Interestingly, the serum Mg was similar in the patient groups and the controls except for the alcoholics, hypertensives and young healthy controls who had significantly reduced levels.

This later finding, particularly in reference to “young healthy” controls, brings up the probability that dietary intake of Mg is suboptimal and Western diets may be contributing to an increasing problem of Mg deficiency which may be a component of the growing epidemic of the metabolic syndrome and related diseases.

This possibility is supported by manuscripts of Resnick and associates spanning from 1984  to 2000 [20] [21].  Using Mg-specific selective ion electrode apparatus and 31P-NMR spectroscopy, there was a significant correlation between intracellular ionized Mg as well as intracellular free Mg and the presence of NIDDM [22].  Other studies reported increased intracellular calcium, decreased intracellular Mg and decreased cytosolic pH with the presence of essential hypertension [23].  A 1992 study revealed that oral glucose loading, even in normal subjects, elevates free calcium and suppresses free Mg [24].  These data suggest, in the author’s words, “an ionic hypothesis of cardiovascular and metabolic disease in which a generalized defect in cell ion handling is present in all tissues.”  This trend leads to, in different tissues, the features of the metabolic syndrome, hypertension, obesity, insulin resistance and left ventricular hypertrophy, the latter related both to hypertension and, independently, vasoconstriction and increased contractility caused by high cytosolic calcium and lowered free Mg [24].  Arterial stiffness, as measured by High Frequency Ultrasound analysis, is known to correlate with hypertension and coronary heart disease [25].  Resnick et al. [26] showed, using direct magnetic resonance determination of aortic distensibility, that in essential hypertension, there are statistically significant correlations between fasting glucose, abdominal visceral fat and in situ intracellular Mg.

In a rat model, Barbagallo et al. [27] showed that glucose, at increasing mM concentrations, caused a significant increase in cytosolic free calcium in vascular smooth muscle.  The authors suggest that these cellular effects of hyperglycemia may underlie the predisposition of patients with diabetes and patients with insulin resistance to hypertension and vascular diseases.  The same group of investigators showed that aging itself is associated with the onset of the elevation of intracellular calcium and reduction of intracellular Mg that is indistinguishable from effects seen in essential hypertension and diabetes mellitus independent of age [28].  These changes may predispose older persons to cardiovascular and metabolic diseases.

Wells et al. [28] identified a previously unknown genetic defect in Mg metabolism in salt-sensitive essential hypertension.  This Mg binding defect results in the inhibition of Mg entry into the cell thereby reducing Mg dependent enzymes from operating efficiently.  The resulting lowering of Mg ATP results in the inability to extrude sodium ions and hypertension develops as a consequence of smooth muscle dysfunction.  The authors also found the Mg binding defect was found in every one of 24 patients with type 2 diabetes suggesting that this defect in Mg transport may be a contributor to NIDDM.  These findings are of possible importance when considered in conjunction with the studies described above [18] [21-24 [26] [27].

Gullestad et al. evaluated 88 healthy Norwegians ages 18 to 66 years using a 30 mmole intravenous Mg load test over 8 hours and measured the 24 hour urinary Mg excretion [29].  They found no correlation between Mg retention and serum Mg or basal urinary Mg.  The Mg retention in these healthy patients was 10.6 to – 4%.  The lowest and highest second standard deviation values were -19.5% and 27.5% respectively.  This result agrees well with the above historical consensus.

Another study by Gullestad et al. [30] on “healthy free-living elderly Norwegians,” mean age 73 ± 6, using the same load test of 30 mmoles of  Mg revealed a retention of 28% compared to 6% in younger controls.  This finding also roughly agrees with the literature and is very interesting when considered in the light of the findings of Barbagallo et al. [27] that elderly people show intracellular calcium and Mg ion concentrations similar to those found in hypertensives and people with diabetes.

A study of Mg deficiency using the “short-term” Mg loading test by Rob et al. [31] revealed that even low dose (0.1 mmole Mg per Kg of body weight) infused over one hour was still able to differentiate Mg adequate patients from renal transplant patients with known Mg deficiency. After treatment with 5 mmoles of Mg per kilogram body weight for four months, a cohort of the latter group reduced their Mg retention from 47% on average to 16%.  The placebo transplant patients continued to retain the infused Mg at 58% of the dose.  The utility of this short-term, low dose Mg retention test can clearly help identify Mg deficiency and help ensure that patients are adequately repleted.

Finally, we could ask which tissue cells are the benefactors of the increased Mg retention in the patients studied.  Bone may be a tissue compartment that may have taken up the infused magnesium since two-thirds of the total body Mg content is contained in skeletal tissue[32].  This is especially likely since it is known that the Mg content of bone falls with age [33] and in the osteoporotic state [34].  If the diet is Mg deficient and the small intestine and kidney can’t effectively increase Mg absorption, bone releases the element into the extra cellular fluid to maintain the serum level [35].


These data demonstrate that Mg deficiency may be widespread.  The composition of the infusate used in magnesium load tests appears to have minimal influence on magnesium retention and does not explain the reported magnesium deficiency.  The importance of dietary factors, especially Mg, in the causation of the present epidemic of metabolic syndrome and its associated complications calls for additional efforts to identify and treat patients at risk of magnesium deficiency.

Table 1:  EDTA and cocktail effects on magnesium losses and retention on the day of the infusions (day 3) minus average of days 1 and 2


1 263 285 345
2 245 156 50
3 203 116 116
4 193 144 198
5 182 210 276
6 133 80 96
7 205 289 268
MEAN ± SEM 203 ± 16 182 ± 31 193 ± 41
% Retention of infused magnesium 70.3 ± 2.3 73.3 ± 4.5 71.9 ± 6.0


Values are mean ± SEM.  All infusates contained 686 mg of Mg.

Values for COCKTAIL, COCKTAIL MINUS EDTA and SALINE are urinary magnesium losses (mg) on day 3 minus the average for days 1 and 2.  There were no significant differences among the three different infusates tested.





Table 2:  Intravenous magnesium load tests in patients and controls

Reference Country Patients, Mg Retention, % Disease/Condition Controls, Mg Retention, %
Thoren [36]
Caddell et al. [37]
Bohmer & Mathiesen [38]
Ryzen et al. [39]
Fort & Lifshitz [40]
Jeppesen [12]Sjogren et al. [18]
Rasmussen et al. [41]
Martin [42]
Gullestad et al.  [19]
Gullestad et al.  [29]
Gullestad et al. [30]
Ozono et al. [43]
Toral Revuelta et al. [44]
Hebert et al. [45]
Papzachariou et al. [46]
Waters et al. [9] 
No patients
G.I. fluid loss
Post partum women
IDDM children
MICrohn’s disease
Various diagnoses
No patients
Malnourished elderly
Intensive care patients
Not given

Citations are in chronological order.

*NC denotes no controls.



The authors would like to thank the late Dr. Mildred Seelig for her advice and encouragement during the initial stages of this study.




Reference List


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  4. Walti MK, Zimmermann MB, Walczyk T, Spinas GA, Hurrell RF (2003) Measurement of magnesium absorption and retention in type 2 diabetic patients with the use of stable isotopes. Am J Clin Nutr 78:448-453
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  8. Mak IT, Komarov AM, Wagner TL, Stafford RE, Dickens BF, Weglicki WB (1996) Enhanced NO production during Mg deficiency and its role in mediating red blood cell glutathione loss. Am J Physiol 271:C385-C390
  9. Waters RS, Bryden NA, Patterson KY, Veillon C, Anderson RA (2001) EDTA chelation effects on urinary losses of cadmium, calcium, chromium, cobalt, copper, lead, magnesium, and zinc. Biol Trace Elem Res 83:207-221
  10. Guldager B, Jorgensen PJ, Grandjean P (1996) Metal excretion and magnesium retention in patients with intermittent claudication treated with intravenous disodium EDTA. Clin Chem 42:1938-1942
  11. Anderson RA, Bryden NA, Waters R (1999) EDTA chelation therapy does not selectively increase chromium losses. Biol Trace Elem Res 70:265-272
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  20. Resnick LM, Gupta RK, Laragh JH (1984) Intracellular free magnesium in erythrocytes of essential hypertension: relation to blood pressure and serum divalent cations. Proc Natl Acad Sci 81:6511-6515
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  37. Caddell JL, Saier FL, Thomason CA (1975) Parenteral magnesium load tests in postpartum American women. Am J Clin Nutr 28:1099-1104
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  41. Rasmussen HS, McNair P, Goransson L, Balslov S, Larsen OG, Aurup P (1988) Magnesium deficiency in patients with ischemic heart disease with and without acute myocardial infarction uncovered by an intravenous loading test. Arch Intern Med 148:329-332
  42. Martin BJ (1990) The magnesium load test: experience in elderly subjects. Aging (Milano) 2:291-296
  43. Ozono R, Oshima T, Matsuura H, Higashi Y, Ishida T, Watanabe M, Yoshimura M, Hiraga H, Ono N, Kajiyama G (1995) Systemic magnesium deficiency disclosed by magnesium loading test in patients with essential hypertension. Hypertens Res 18:39-42
  44. Toral R, Jr., Martinez HD, Martinez RM, Llobell SG, Peralba Vano JI, Ribera Casado JM (1996) Intravenous magnesium load test in elderly patients with protein-energy malnutrition. Magnes Res 9:293-298
  45. Hebert P, Mehta N, Wang J, Hindmarsh T, Jones G, Cardinal P (1997) Functional magnesium deficiency in critically ill patients identified using a magnesium-loading test. Crit Care Med 25:749-755
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Address all correspondence to:

Dr. Robert S. Waters, Waters Preventive Medical Center, PO Box 357,Wisconsin Dells, WI 53965, Phone: 608-254-7178, FAX: 608-253-7139, Email:



An Open Letter to Cardiologists

Dear Cardiologist,

dooleyMy name is Dr. Bruce Dooley and have I practiced in Fort Lauderdale and Naples for twenty years. Having recently arrived in Palm Beach County, I am writing to all the local Cardiologists to both personally introduce myself as well as seeking your cooperation and participation in an outcomes study involving EDTA Chelation Therapy. I will describe this in more detail in a minute.

You may be aware of the recent significant clinical results of the 7-year Trial to Assess Chelation Therapy (TACT). This randomized, double-blinded, placebo-controlled study was funded by the NIH and headed up by Dr. Tony Lamas (Chief of Cardiology, Miami Mt. Sinai Hospital). At the November 2012 Annual meeting of the AHA, Dr. Lamas announced that the study proved that EDTA intravenous therapy was both clinically effective and safe. Regrettably, the response from the Cardiologists on the panel was that “more studies were needed“.

Having personally supervised the administration of over 10,000 EDTA infusions, I and other physicians knowledgeable on this therapy were not surprised by the positive results of the TACT study: Improvements in circulation are the norm and were first discovered in the early 1950’s followed by much interest and investigation of this intravenous therapy . But when EDTA (ethylene diamine tetra acetate, (commonly used to chelate lead and other metals) lost its patent and became generic in the 1960’s, Abbott Labs dropped their research for its approval as a cardiac drug. It is also important to note that it was during this period that Dr. Michael DeBakey performed the first CABG in Houston. Thus, for the past 50 years, physicians like me have performed this therapy, formed medical associations to develop safe protocols, and train other physicians. Many office-based outcome studies were published and the vast majority showed significant improvements in circulation. But a properly constructed study was needed to convince other physicians of the effectiveness and safety of EDTA chelation.

So here our present dilemma and my reason for requesting your help: Getting the NIH to fund this $35 million TACT study in 2003 was difficult enough. We seriously doubt that further monies will be forthcoming. There was also the problem of patient recruitment (ask a person to sit in a recliner chair for 40 treatments for three hours each with a 50% chance it is a placebo). The question then arose as to how to gather more data now that EDTA chelation therapy has been proven clinically effective and safe. One consideration was to seek other physicians help to enrol their eligible patients in an outcomes study. Our belief is that if enough evidential outcomes are positive as reviewed and submitted by respected Cardiologists, then this therapy may gain acceptance as a recommended treatment.

So we see this happening as such:

1. Participating cardiologists refer a patient for a series of twenty EDTA chelation infusions with the cost of the program being born by the patient, who is given full informed consent.

  1. The participating referring cardiologist completes both a pre and post chelation program evaluation for which he/ she will be directly reimbursed $500 as remuneration for their time spent on the evaluations (total of 20-30 minutes). This will be paid to the physician at the onset of the twenty treatment program by their patient.
  2. On a national level, this program would generate a significant number of reports from Cardiologists which would eventually be collated into a report and submitted to the American Heart Association for their consideration.

    I am seeking your help by becoming a participating physician in this important project. To better get acquainted with each other, and to further explain the therapy, please allow me the opportunity to meet with you outside of your busy office practice. It would be my pleasure to show you our beautiful center and answer any questions you might have over dinner if you like.

To help facilitate this, I would request that you please return the enclosed, stamped response card indicating your decision to either accept or decline participation. If you would like to participate, I will have my staff do a follow- up call to your office to schedule an afternoon visit/dinner.

Thank you very much for your time and attention and I look forward very much
to hearing back from you.

Kind regards,
Dr. Bruce Dooley

A Comprehensive Integrative Approach to Diabetes

By L. Terry Chappell, T. Rae Neal, Natallie Paphanchith

Incidence and Cost

medic-alert-bracelet-1316095-639x412Diabetes is a growing epidemic in the United States. According to the National Diabetes Statistics report for 2014, 21 million people in the United States have been diagnosed with type 1 or type 2 diabetes. It is estimated an additional 8.1 million people are undiagnosed. In addition to diabetes, 86 million Americans were diagnosed with the precursor, pre-diabetes in 2012. Treatment and management of this disease is costly. The estimated annual cost of diabetes per year in the US is 245 billion dollars.

More alarming than diagnosis and cost is the impact diabetes has on our overall health and wellbeing. Diabetes was listed as the 7th leading cause of death in the United States in 2010. When diabetes is controlled we reduce the risk of co-existing diseases. Unfortunately, many patients remain with an elevated hemoglobin A1C. Uncontrolled diabetes leads to multiple micro and macro vascular complications. Co-morbidities secondary to diabetes include: hypertension, hyperlipidemia, coronary artery disease, cerebral vascular accidents, chronic kidney disease, amputation, retinopathy, and neuropathy (1).

Conventional Approach to the Treatment of Diabetes

Type 2 diabetes mellitus (T2DM) is clearly linked to obesity. As obesity rates climb, so does the diagnosis. 80-90 percent of patients diagnosed with type 2 diabetes are classified as obese. The International Diabetes Foundation was quoted, “Diabetes and obesity are the biggest public health challenges of the 21st century”. The link here is clear; obesity drives insulin resistance and an inflammatory response. Prolonged insulin resistance puts an extreme amount of stress on the pancreas. When resistance is accompanied by dysfunction of the pancreatic islet b cells that is what ultimately leads to the disease (2).

A dietary goal should be to minimize refined sugars and starches. Modern carbohydrate staples, like potatoes, breads, and cereals, have a high glycemic index (GI) and a very strong link to chronic disease (3). Foods low on the GI scale like sweet potatoes, winter squash, and beans help to stabilize blood glucose levels.   This can be achieved with whole structured foods and lower GI.     Clinical trials support low GI diets with greater fat content as more effective than low fat diets at preventing complications associated with cardiovascular disease. Often a low fat diet contains the highest GI content, which leads to increased insulin resistance. Low GI diets improved whole body insulin sensitivity throughout the trials with no increase in LDL cholesterol (3).   Whole rice and seeds decrease circulating levels of glucose, insulin, LDL cholesterol, and fructosamine, while refined sugar and high fructose corn syrup lead to increased risk for T2DM. Large amounts of fructose result in insulin resistance and could accelerate the development of T2DM and associated complications. Avoiding processed foods is an important step in preventing and managing diabetes (4).

Many treatment options are available to treat diabetes. Since discussing obesity in the previous paragraph, lifestyle modifications are the initial target. Nutritional planning, weight loss and diabetic education are a top priority. However, despite efforts of diet and exercise many patients will require additional therapies. There are multiple oral medications. Metformin is the initial medication of choice if liver and kidney function remain stable. However if the hemoglobin A1C remains elevated after 3 months of therapy an additional agent may be selected. Treatment of diabetes has greatly changed in the last 10 years. Use of Sulfonylureas, Meglitinides and Alpha-glucosidase inhibitors are less common as innovative medications are integrating to the market.

Emerging drug classifications include Thiazolidinediones, DPP-IV inhibitors, GLP agonists, and SGLT2 inhibitors. If insulin resistance remains high and oral medications and injectable non-insulin medications are not effective in maintaining glycemic control, insulin may be added. Likewise, if chronic medical conditions arise and prevent the use of certain medications, a basal bolus regimen of insulin may be more appropriate.

Goals of Treatment

As previously mentioned, treatment goals are targeted by the hemoglobin A1C. The A1C is a 3 month average of the patients’ blood sugar. An A1C less than 5.7 percent is normal, prediabetic range is 5.7-6.4 percent and diabetes is diagnosed if the A1C is greater than 6.5 percent. For patients diagnosed with diabetes The American Diabetes Association recommends an A1C goal less than 7 percent. However, many randomized trails that examined the effects of glycemic control excluded the frail elderly (5).

Newer data points to higher health threats in the elderly population with tight glycemic control. The most common risk is severe hypoglycemia. Hypoglycemia leads to increased falls, injury, trauma, and hospitalizations (6). Also, elderly patients are more likely to experience adverse effects from their medications. The American Geriatric Society recommends the targeted A1C to be 8% in the elderly (7). However, the A1C target is controversial among various organizations. Ultimately, goals should have an individualist approach and target.

Complementary Treatment Options and Lifestyle Measures

Complementary, alternative, integrative, or comprehensive, whatever term you choose, these additional approaches to medicine offer many options for the prevention and treatment of T2DM. The California Institute of Integral Studies and Integrative Medicine presented a paradigm shift in our health care system at the International Congress for Clinicians in Complementary and Integrative Medicine in 2013 (8). Collaborative practice and interaction between disciplines will provide valuable insight toward a new health care model. It is estimated that as much as 40% of adults use complementary and alternative medicine (CAM) with up to 34% of those patients having a chronic disease. These figures are deceptive when disclosure of CAM use is often withheld due to conflict with other providers (9).

Personal responsibility is essential for prevention and management of diabetes. Awareness of recommended caloric intake and ideal body weight prevent the buildup of excess body fat, which can lead to cellular insulin resistance. Maintaining ideal body weight and modifying the diet to include important nutrients, limit less beneficial ingredients, and eliminate harmful options will lead to improved glycemic control(4). Organic pollutants also accumulate in adipose tissue and carry destructive consequences.   Sorbitol accumulation caused by environmental exposure leads to cell death and contributes to diabetic complications (4). Weight loss and detoxification will improve insulin sensitivity and glucose tolerance. Losing as little as 5% of body fat leads to marked improvement in glycemic control and reduces the incidence of T2DM by up to 50% (10).

Gaby also identified a gluten free diet as delaying or preventing the development ofT2DM due to the preservation of beta cells.   Vegan diets improve glycemic control. Coffee is associated with a decrease risk of developing T2DM. Oolong tea is associated with a mean decrease in plasma glucose concentrations. This could be due to reducing iron absorption, which might improve glycemic control. Modest increases in body iron stores have an adverse effect on glucose metabolism. Iron depletion enhances glucose utilization. Phlebotomy treatments have effectively reduced iron concentration to vegetarian levels and caused a 40% increase in insulin sensitivity (4). Deferoxamine, an iron-chelating agent, was used in poorly controlled diabetic patients with elevated ferritin levels successfully to improve blood glucose and HbA1c levels (4).

Increased dietary fiber from legumes, carrots, artichokes, peaches, strawberries, and grapefruit can improve glycemic control.   Obtaining fiber from food is preferred. If supplementation is necessary, unprocessed wheat bran or apple fiber are recommended.   Legumes have an ability to flatten blood sugar response for over four hours, when eaten at breakfast. The blood sugar remained consistent four hours after ingestion (4).

The temperature and manner in which food is cooked plays a role in the development of diabetes. The advanced glycation end products (AGE) remain in food after the cooking process. These products cause modifications in protein structure, which promote inflammation (4).   Less AGE formation results from cooking techniques using water at low temperatures for a longer period of time. An emphasis on boiling, poaching, and stewing over frying, broiling, and roasting can decrease AGE by up to 50%. AGE products play a role in the pathogenesis of insulin resistance and diabetic complications (4).

Effect of acidic environment on the advanced glycation end product (AGE) content of beef. Beef (25 g) was roasted for 15 minutes at 150°C with or without premarinating in 10 mL vinegar (A) or lemon juice (B) for 1 hour. Samples were homogenized and AGE (Nε-carboxy-methyl-lysine) content was assessed by enzyme-linked immunosorbent assay as described in the Methods section. Data are shown as % change from raw state. White bars represent raw state, hatched bars roasted without marinating and black bars marinated samples. *Significant changes compared to the raw state (P<0.05). #Significant changes compared to cooked without marinating samples. 1=raw beef. 2=roasted beef with no vinegar or lemon. 3=roasted beef after marinating with either vinegar or lemon for 1 hour.

Consuming raw fats such as sesame, coconut, avocado, flax seed and olive oil help to reduce HbA1c.   Esposito et al. found that a low carb Mediterranean diet effectively reduced HbA1c, achieved diabetes remission, and delayed the need for medications (11). Harokopio at the University of Athens found eating plenty of olive oil, fish, and whole grains was more effective at slowing the progression of T2DM than a low fat diet.   The key factor in the Mediterranean diet is that more than 30% of daily calories are from fat. Olive oil is high in oleic acid and monounsaturated content providing antioxidant and anti-inflammatory properties (12).

Mind body medicine, recognized by the National Center for Complementary Medicine, includes, yoga, Tai Chi, and meditation. These techniques are used to influence the mind body connection. Movement, breathing, meditation, and chanting can be used to achieve life style changes, stress relief, and allow inner focus. The American Diabetic Association recommends 150 minutes a week of moderate to intense physical activity; these mind body activities can be considered moderate exercise. No real improvement in glycemic control was seen but beneficial effects on behavior, mood, stress, and quality of life were identified as positive outcomes (9).   Because chronic stress has been implicated as an increased risk factor for the development of T2DM and we know stress induced inflammatory cytokines could be the cause of this finding, it is easy to see how daily practice of mind body medicine would have a positive effect.   Many improvements have been documented with daily yoga training. Reduced fasting blood sugar and post-prandial levels, better glycemic control, and stable autonomic control are possible with daily yoga training.


Nutritional supplementation has been effective with diabetes management.   As mentioned above various antioxidants are beneficial in preventing complications related to diabetes. The goal is to attempt to include as many fresh nutrient dense ingredients as possible and supplement as needed. High levels of oxidative stress have been found in diabetic patients, increasing the need for antioxidant supplementation. Deficient levels of vitamin C in diabetic patients are compounded by an impaired cellular uptake promoting hyperglycemia, which further decreases intracellular vitamin C levels. This localized deficiency contributes to end organ damage. Vitamin C supplements given at 1000 mg daily decreased urinary albumin and slowed the progression of diabetic nephropathy.

Electrolyte disorders have been found to play an important role in the complications of diabetes and are associated with increased mortality and morbidity. Several factors affect the bodies ability to utilize nutrients including; nutritional status, absorption, acid base imbalances, pharmacokinetics, renal disease, and acute illness. This might explain why diabetic patients are found to be low in several important nutrients. Hypomagnesaemia is commonly identified in diabetic patients. Magnesium is involved with more than 300 enzymatic reactions and is vital to glucose metabolism and insulin homeostasis. Low serum and plasma levels of magnesium are associated with alterations in nerve, muscle, and cardiac conduction. This contributes to nephropathy and end stage renal disease. Increased dietary intake of magnesium improved metabolic control and reduced the risk of T2DM and dyslipidemia (4).

The trace element chromium aids glucose with transport into the cell. Chromium deficiency induces hyperglycemia and impaired glucose tolerance. Normal chromium intake is <20 ug/day. Diet recall was used to determine the daily dietary intake of chromium. Low daily intake led to supplementing with 200 ug chromium picolinate or chromium rich yeast, which resulted in improved glucose tolerance.   The findings held true in cases of gestational diabetes as well. Chromium is found in whole grains, broccoli, and grapes.   Normal dietary intake ranges from 20-35ug/day, based on sex and age.   Reduced HbA1c and fasting blood sugar levels were achieved with chromium supplementation. A large meta-analysis confirmed these results with a combination therapy of 600 ug chromium picolinide and 2 mg biotin (4).

Biotin is a B vitamin that enhances chromium absorption and is involved with intracellular metabolism of glucose. Biotin administration of 9-16 mg/day improved glucose tolerance and decreased mean fasting blood sugar by 45% (4).   Inositol, D-chiro-Inositol and D-pinitol are found naturally in legumes and citrus fruits. D-pinitol mediates the action of insulin. When given at 20 mg/kg of body weight, a 5% decrease in plasma glucose is seen (4). Vitamin D deficiency has been associated with increased glucose tolerance and diabetes. Supplementation has shown improvement in endothelial function, glucose tolerance, and an increase in insulin secretion. Doses varied from 800- 300,000 IU/day (4).

a-Lipoic acid (ALA) is an antioxidant. One of its many benefits includes helping to avoid vitamin C and E deficiency which are important to prevent and treat T2DM. Supplementing with 600 mg of alpha lipoic acid effectively increased insulin sensitivity, slowed the progression of complications, and prevented renal damage in T2DM patients.   ALA is naturally occurring in broccoli, brussel sprouts, peas, potatoes, and yeast (4).

Herbal Preparations

Bitter melon (momordica charantia) is a plant native to India and Asia. It has been used medicinally for over 600 years. Evidence has shown positive effects on glucose levels, glucose uptake, and glycogen synthesis and glucose oxidation (13).   Active ingredients include charantin, vicine, and polypetide-p. Doses ranged from 150 and 2000 mg daily.   Fruit, juice, and seed extracts were also used in some studies (12). Minimal side effects have been reported, although the ingredients are contraindicated in pregnancy. Four specific compounds identified provide the biological evidence for the benefits witnessed. An example of traditional or complementary medicine providing new and effective treatments for T2DM is metformin, which originated from goats rue (Galega Officinalis). Tan et al. identified bitter melon as one of the most popular botanical treatments for T2DM (14).

Another promising biologic T2DM treatment is Fenugreek, Trigonella foenum-graecum. Commonly used in Traditional Chinese medicine for glucose control, digestive aid, and relief of menopausal symptoms, Fenugreek given at 100 mg improved fasting blood glucose levels. Fifteen grams of ground fenugreek seed power with a meal lowered postprandial glucose levels (4).

Small trials have yielded promising results for Gymnema sylvestre or gurmar . The leaves of this plant are used in Ayurveda medicine to treat DM, cholesterol, and obesity. Significant improvement in fasting blood sugar and HbA1c levels were obtained with doses from 200 mg to 800 mg of an extract daily (4).

Cinnamon, Cinamonum cassia, gui zhi, Traditional Chinese Medicine, this differs from the common spice Cinnamonum verum. C cassia has been used for thousands of years to treat DM. The herb activates insulin receptors and increases glycogen synthesis. Five clinical trials evaluated doses from 1 – 6 grams daily and saw decreases in fasting blood glucose levels from 18 – 29 % (4).

Red Korean Ginseng was found to improve glucose tolerance test results, fasting plasma glucose, and blood sugar levels. American ginseng (AG) along with an herb called Konjac-Mannan (KJM) may improve T2DM control and associated complications. KJM affects the nutrient absorption rate in the small bowel while AG affects the post absorption activity, they work in unison to increase sensitivity and enhance secretion.   Doses ranged from 100 – 200 mg BID reductions in fasting plasma glucose and HbA1c were documented (15).

Berberine is a compound found in golden seal, Oregon grape, barberry, and other plants. Some research as shown it to be as effective as metformin (16).   Doses up to 1000 mg twice daily along with life style modifications lead to a 7% reduction in HbA1c. Glucose and lipid lowering properties were identified.   Future T2DM treatment may have been identified by targeting free fatty acid metabolism.

Publication trends in Iranian endocrinology outlined highly cited articles effective in treating T2DM.   Of the 44 articles found in PubMed, Scopas, and Google Scholar, a few of the relative topics include silybummarianum, Gaertn silyonarin, or milk thistle, as an effective treatment for T2DM and decreased serum glucose and HbA1c levels in diabetic outpatients using psyllium (4).

Shenyan Kangfu, based on Traditional Chinese Medicine and Zhao Enjian’s valuable therapeutic knowledge, is a traditional herbal preparation that has been improved and formulated into tablets.   SYKFT tablets consist of 11 herbal ingredients with a synergic effect to nourish the kidney and spleen by detoxifying the body.   Widely acclaimed shenya kangfu, has been used for DM nephropathy based on the qi-yin deficiency syndrome; swelling, fatigue, and weak limbs (25). Five sites in four major cities in mainland China have been identified. Enrollment is planned for 80 patients in stage III or IV diabetic nephropathy. Enrollment began in November 2012, 20 participants had been enrolled by March 2013 (17).

As outlined, there are many alternative treatments for T2DM that have been recognized as safe and effective.   Small trials, meta-analyses, and anecdotal evidence provide recommendations and document safety concerns while outlining the need for additional research to improve the care that clinicians provide.     The Natural Medicine Comprehensive Database confirms that many treatments outlined in this article are safe and effective. The U.S. Department of Health and Human Services contends that there is no high-quality evidence of benefit from alternative or supplemental treatments for diabetes.   We as health care providers must use good judgment and available evidence to offer patients the best options for maintaining optimum health. Chandra and associates make it clear that we will never have absolute clarity on which therapies are effective and which are not. So much depends on patient preferences and available alternatives. He calls this the “gray zone” of medicine (18).

Chelation Therapy

Perhaps the most promising advance for the treatment of diabetes since insulin came from the Trial to Assess Chelation Therapy (TACT) (19). This trial emerged from a hearing of the Oversight committee of Congress and a subsequent call for proposals by the National Institutes of Health. TACT was designed to determine if future cardiac events could be reduced for patients at least 50 years of age who had already suffered at least one heart attack. It was a randomized, double-blind, clinical trial of 1708 patients, who were given more than 55,000 intravenous treatments. Half of the patients were given high dose vitamins. Thus there were four groups in the study: double placebo, high dose vitamins without chelation, chelation with placebo vitamins, and chelation with high dose vitamins (20). All of the patients were given evidence-based conventional care for their coronary artery disease. At the beginning of the five years that patients were followed, they were given 30 weekly IV’s and then 10 more treatments at monthly intervals.

The benefit of EDTA chelation was shown to be statistically significant. All of the cardiac events (death, re-infarction, stroke, coronary artery revascularization, and hospitalization for severe angina) were less in the EDTA groups than in the groups that received IV placebos. All cause mortality was also less in the treated patients. Further analysis showed that 37% of the patients had diabetes (322 EDTA and 311 placebo). For those patients with diabetes, there was a 41% reduction in cardiac events, a 52% drop in recurrent MI, and a 43% reduction in deaths. Those who received both chelation and high-dose vitamins had the best results, but even with chelation and placebo vitamins, the NNT for major cardiac events for diabetic patients over the 5 years was 6.5. For statins in such patients the NNT is considered to be highly effective at 17. Chelation was shown to be extremely safe when given according to protocol (18).

A major action of EDTA chelation is its removal of toxic heavy metals, such as lead, cadmium, arsenic, and mercury. Such metals are proven to be toxic to the vascular tree by their free radical activity (21). Carlos Lamar published numerous case studies in the mid-to-late1960 on chelation’s positive effects for diabetes (22). Paul Cutler found significant improvement in diabetic control with the use of the iron chelator, desferoxamine, in diabetic patients who also had high ferritin levels (23). EDTA also chelates iron, but not as effectively as desferoxamine. Therapeutic phlebotomies are more effective than either desferoxamine or EDTA. The vast majority of studies on chelation therapy and vascular disease were not randomized clinical trials and were of insufficient power to draw conclusions. Most of the studies did not identify patients who had diabetes.

The authors of TACT state that the magnitude of benefit for diabetic patients, calls for urgency to replicate their study (24). TACT-2 has been planned. At the same time, other forms of vascular disease, especially peripheral vascular disease, should be studied. Hancke and Flytlie published a remarkable study demonstrating that 24 out of 27 patients on the waiting list for amputation were able to cancel their surgery and save their legs (25).

Patient Decision-Making

In the meantime, TACT is clearly the best evidence available showing that chelation therapy might benefit vascular disease. The new guidelines for vascular problems call for the treating physician to have a conversation with his or her patients explaining the risks and potential benefits of all options of therapy. Then it is imperative that the patient decides what mode of therapy sounds best to him or her. This is the new “gold standard” (26). The patient is the decision-maker, not the doctor. Chelation therapy should be discussed in light of the evidence of TACT. If TACT-2 replicates TACT-1, chelation might be suggested for all diabetic patients. With the current status of evidence, chelation therapy should be offered to patients as an option for treatment, especially if they have signs of vascular disease.

Physicians trained in providing intravenous chelation report better overall results than TACT (27). One reason that clinical practice might be better is that continued monthly maintenance is commonly offered after the basic course of treatment. TACT treated patients intravenously only for the first 20 months, but followed them for 5 years. Another reason could be that TACT did not follow patients with challenge tests for heavy metals or vascular testing to assess progressive improvement. A re-accumulation of toxic metals is not unlikely. Finally, other nutritional therapies are often added by integrative physicians. All of these measures contribute to the best care for each individual patient and would likely improve the overall results.

Chelation therapy has been opposed by many conventional doctors for many years. In 1980, the AMA effectively said to the chelation community, “Put up some evidence, or stop doing the therapy”. With the help of NIH funding and cooperation among doctors familiar with the therapy and a group of courageous cardiologists, the evidence has arrived. As clinical scientists who continually advocate evidence-based medicine, physicians are obligated to accept good evidence when it conflicts with their beliefs (28). The rest of this article puts forth a comprehensive approach to diabetic patients that includes chelation therapy and alternative medicine as therapeutic options for prevention, control of the disease, avoidance of complications, and a longer lifespan.

A Comprehensive Integrative Approach to Diabetes

First, patients must realize it when they have either pre-diabetes or diabetes. This requires screening tests by their doctors’ orders or at health fairs, especially for anyone who is overweight or has a family history of diabetes. Patients with hypoglycemia not infrequently convert to diabetes as they grow older. Fasting blood sugars are a reasonable start but HbA1C tests are more accurate. Those who are overweight should be encouraged to eat less and better, and exercise more. Obesity is a major cause of gene expression into active diabetes.

As soon as pre-diabetes or diabetes is detected, a careful reassessment of lifestyle factors should be instituted. The patient and the family must embrace responsibility for controlling the disease. A healthy diet is crucial, with a special emphasis on low carbs if high triglycerides or the metabolic syndrome is present. Regular exercise and an effective way to deal with stress are important. Smoking and excessive environmental pollution are to be avoided as much as possible. Regular monitoring of lipids, HbA1C, kidney function tests such as creatinine with GFR and micro-albumen, vitamin D3 levels, annual eye exams, vascular screenings, and careful attention to the feet are all required. The sensitive CRP, homocysteine, and ferritin levels should be checked at least once. A challenge test is the best way to screen for toxic metals.

Nutritional supplements can help control the disease and avoid complications. Vitamin C, biotin, chromium, magnesium, zinc, selenium, B-complex, inositol, and alpha lipoic acid should all be considered. Several herbal supplements could also be selected if further control of the blood sugar is needed. Good candidates include cinnamon, bitter melon, and berberine. Fenugreek, Gymnema Sylvestre, Korean or American ginseng, KJM, and combinations of herbs from India or China also might have therapeutic benefit. Milk thistle might help by its detoxification of harmful chemicals. Psyllium is also good for detox, and aids constipation. Generally, herbals are safer and less likely to cause hypoglycemia than medications.

Medications are next on the list. Oral medicines are discussed above, and insulin is a reasonable choice if needed, whether or not the patient is insulin dependent. Doctors must be careful to avoid over-medication that can lead to HbA1C readings that are too low, hypoglycemic episodes, and severe injuries, especially in the frail elderly. Control of the disease is imperative. Therapeutic goals for the HbA1C should be 6.5-7.0 for most patients and 8.0 for unstable elderly patients. Of course, lower levels of HbA1C are desirable if they are achieved without the help of medications.

The most dramatic evidence of treatment success in the last few years came with TACT. Chelation therapy reduced future cardiac events and lowered the death rate for patients with diabetes who had a previous myocardial infarction.   The magnitude of benefit was perhaps greater than any intervention other than considerable weight loss or insulin therapy. The probable mechanism has to do with free-radical activity and inflammation caused by toxic metals, which are removed with chelation. Confirmatory research is coming with TACT-2, but cardiologists and endocrinologists should at least describe the remarkable evidence generated by TACT-1 and let patients choose whether they want chelation, either before or after significant vascular disease has developed. After all, most of the complications from diabetes are vascular, which can lead to devastating disabilities and/or premature death.


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26.Krumholz H.M. Variations in health care, patient preferences, and high-quality decision-making. JAMA 2013;311:151-152.

27.Chappell LT, Shukla R, Yang J, Blaha R, et al. Subsequent cardiac and stroke events in patients with known vascular disease treated with EDTA chelation therapy: a retrospective study. Evid Based Integrative Med 2005;2:27-35.

28.Maron DJ, Hlatky MA. Trial to assess chelation therapy (TACT) and equipoise: when evidence conflicts with beliefs. Published on-line from Mosby, inc. Department of Medicine, Stanford University. Email requests from 2014

Subsequent Cardiac and Stroke Events in Patients with Known Vascular Disease Treated with EDTA Chelation Therapy

Dr L. Terry Chappell, Rakesh Shukla, Jun Yang, René Blaha, Tammy Born, Claus Hancke, William Mitchell, Efrain Olszewer, Peter van der Schaar, James Ventresco;

Chappell23 Aug 2012


Myocardial infarction (MI) and strokes are leading causes of death in the US. Surgical and medical treatments can be helpful, but carry risks of morbidity and mortality.


To evaluate whether cardiac events were reduced for patients with known vascular disease who were treated with intravenous ethylene diamine tetra-acetic acid (EDTA) chelation therapy.


Retrospective study with a 3-year follow-up, compared with similar patient groups by use of meta-analysis.

Population and setting

A total of 220 consecutive patients with known vascular disease were treated with chelation therapy during 1992–2001. Eight outpatient centres were included: five from the US and one each from Denmark, the Netherlands and Brazil. Average patient age was 64 years, 72.3% were males and 18.2% were smokers. Average number of treatments was 58.

Main outcome measures

MI, stroke and death from any cause were primary outcome measures. Secondary measures were resolution of symptoms and need for coronary artery bypass surgery (CABG) and percutaneous transluminal coronary angioplasty.


According to the meta-analysis, expected outcomes in a 3-year follow-up period for 220 patients with coronary artery disease treated only with conventional therapies would be 15 MIs and six deaths. There were no deaths and no MIs in this group of patients who received chelation therapy. Four patients had strokes but recovered well. There were two angioplasties and six CABG procedures. Compared with similar patient populations treated with conventional therapies, patients who also were chelated had a 93.6% lesser need for angioplasty and a 62.5% reduced need for CABG. Of the patients that initiated treatment with symptoms, 68.7% had complete resolution of symptoms.


This study indicates that the administration of intravenous EDTA chelation therapy for patients with vascular disease resulted in fewer subsequent cardiac events than primary treatment with CABG, angioplasty or conventional medical therapy. EDTA chelation therapy for vascular disease is a reasonable, off-label adjunct, especially for patients who refuse or are not eligible for surgery. Clinical trials such as the Trial to Assess Chelation Therapy (TACT) are needed for definitive proof.

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Managing Cardiovascular Diseases

Ramblings of a Maniacal Frenetic: Pragmatic Reflections on Helping Patients Understand Their Illnesses and Treatments

by John Parks Trowbridge, MD, FACAM

John 2My father told me, in early 1979, that he was going to see a doctor about doing chelation therapy. I went only slightly berserk, insisting that I would have heard about it in my training or residency if it had any value for cardiovascular diseases. He “wisely” stayed away from that charlatan. Then my mother needed drastic surgery for a bleeding ulcer in the fall of 1982. As I needed to fill my days while seeing her in San Francisco, I visited the office of Robert Haskell, MD. We discussed nutritional medicine and dietary programs … and then he asked, “Well, you do chelation therapy, of course?” I explained my reservation about doing any treatments that were exaggerated in their claims of helping … especially with a wide variety of illnesses. He said simply: “Come with me.” We climbed up one flight of stairs. “Here,” he said, “is my nurse. And my charts. And my patients. Have a good day.” And what a day it was! I could barely believe the documented results of patients who had barely been able to walk due to shortness of breath or chest pains or calf pains. And I got to hear their stunning stories, in person – and to lay my hands on their bodies. I was hooked. I spent the next five months studying everything that I could find on chelation, so that I would “ace” the written exam. At the training, I met Warren Levin, MD, of New York City, clearly the best lecturer at the meeting. I spent two glorious learning days in his office; the same for Milan Packovich, MD, of Pittsburgh; also for Charles Farr, PhD, MD, of Oklahoma City; and for another eight doctors who generously offered to share their best ideas with me, so that I could strive from the start “to be the best.” H. Ray Evers, MD, of Dothan, Alabama, graciously hosted me for three days to see the best of the past. And thus began my saga, to “learn more and do better than anyone else.” At the very least, each of my parents and I myself benefited greatly.

Pump, Pipes, and Performance
Cardiovascular diseases (CVD), in order to be adequately evaluated and treated, need to be classified according to the likely etiology or explanation. Simply stated, CVD are associated with the pump (the heart), the pipes (arteries of whatever size and location), and performance (impaired function despite adequate anatomy). One last classification – pediatric – will be ignored for this article, since congenital heart diseases, as genetic or developmental irregularities, have their own unique considerations. When the “pipes” involve the venous system, such as with thrombophlebitis, this is treated as a special case of inflammation.

Hey, Buddy, Can You Really Treat That?
If we have incomplete or missing diagnoses, should you proceed with treatment? In fact, that complaint has been leveled at chelation therapists for years, that we fail to do “enough” diagnostic workup. If you want the details of your problem delineated down to the molecular level, go to your local university cardiologist. But if you want to feel better now and get on with your life, why not consider a treatment that works for most heart and blood vessel problems (and those of many other systems) that plague most people? Problems that don’t improve can continue to be evaluated. The only heart problems that don’t reliably show desired improvement are pediatric, because of their distorted anatomic features. The only peripheral (or central) blood vessel problems that don’t show expected improvement are ….. sorry, can’t recall any.

What Do People Really Need to Know?
For the most part, medical explanations use technical terms that confuse or oversimplifications that mislead. Using the framework presented here, concepts can easily be offered that lead patients into a fair understanding of the treatments proposed and what to expect. (Much of “doctoring” is teaching, which improves compliance dramatically.)

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Prevention of Lower-Extremity Amputation with EDTA Chelation Therapy

By H. Joseph Holliday, MD, FACAM, RVT; 2000


This patient review was designed to compare the lower-extremity amputation rate of patients treated with traditional surgery interventions with those who received EDTA chelation for treatment of peripheral vascular insufficiency. The patient populations were similar and the follow-up period was compatible between chelation patients and those progressing to amputation after surgery. All amputations occurred within 1 year after surgery. The chelation-treated group was observed for 36 months. 89 patients were treated surgically with 8 failures leading to amputation (9% amputation rate). Rest pain was relieved in 9 of 14 patients after surgery. Therefore, 64% of the patients who presented with rest pain experienced improvement in quality of life with no rest pain after surgery. Five patients with continued rest pain after surgery required amputation. Seventy-six patients (87%) were able to walk without claudication after surgery. Twenty-two chelation patients received a combined total of 750 treatments. Four patients presented with rest pain and all but 1 patient received total relief after an average of 12 treatments; consequently, 75% of patients with rest pain were improved. The patient who experienced no improvement in rest pain stopped chelation after 12 treatments. Twenty-one patients completed 30 or more EDTA treatments; of those patients, 20 experienced an increase in walking distance without pain. The patient who did not experience an increase in walking distance without pain received complete relief from rest pain. None of the patients receiving chelation therapy progressed to amputation. Chelation treated patients were found to have a lower amputation rate than surgically treated patients with comparable lower-extremity arterial disease. Symptom relief with chelation is excellent. Therefore, EDTA chelation can be considered an option to surgical intervention for the initial and complete treatment of patients with lower-extremity arterial occlusive disease.

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Holliday, MD: Carotid Restenosis: A Case for EDTA Chelation

By H. Joseph Holliday, MD, FACA, RVT


Carotid restenosis has been found in up to 25% of patients after carotid endarterectomy. The most common cause of restenosis is continuation of the atherosclerotic process. Surgery can be beneficial in stroke prevention and should be considered in those patients at high risk for stroke. However, surgery does not arrest the disease of atherosclerosis. This report demonstrates a 10% reduction in the degree of stenosis in a patient treated with EDTA chelation for restenosis of a carotid artery after endarterectoy. EDTA chelation does arrest and reverse atherosclerosis and should be used in conjuction with surgery or as a primary treatment for carotid restenosis as well as for vascular occlusive disease in any artery whether initial or recurrent.

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Effect of chelation therapy on progressive diabetic nephropathy in patients with type 2 diabetes and high-normal body lead burdens.

Chen KH1, Lin JL, Lin-Tan DT, Hsu HH, Hsu CW, Hsu KH, Yen TH., 2012


A previous study in type 2 diabetic patients with high-normal body lead burdens showed that EDTA chelation therapy for 3 months slows progressive diabetic nephropathy during a 12-month follow-up. The effect of a longer course of therapy on kidney function decrease over a longer follow-up is not known.


A 12-month run-in phase, then a randomized single-blind study with a 27-month intervention.


University medical center; 50 patients (serum creatinine, 1.5-3.9 mg/dL) with high-normal body lead burden (≥80-<600 μg) were randomly assigned to the treatment and control groups.


The treatment group received weekly chelation therapy for 3 months to reduce their body lead burden to <60 μg and then as needed for 24 months to maintain this level. The control group received placebo for 3 months and then weekly for 5 weeks at 6-month intervals for 24 months.


The primary end point was change in estimated glomerular filtration rate (eGFR) over time. A secondary end point was a 2-fold increase in baseline serum creatinine level or the requirement for renal replacement therapy.


Body lead burdens were assessed by EDTA mobilization tests and eGFR was calculated using the equation for Chinese patients with type 2 diabetes.


Mean baseline eGFRs in the treatment and control groups were similar. After 3 months of chelation therapy, the change in eGFR in the treatment group (+1.0 ± 4.8 mL/min/1.73 m(2)) differed significantly from that in the control group (-1.5 ± 4.8 mL/min/1.73 m(2); P = 0.04). In the subsequent 24-month intervention, the yearly rate of decrease in eGFR (5.6 ± 5.0 mL/min/1.73 m(2) per year) in the treatment group was slower than that (9.2 ± 3.6 mL/min/1.73 m(2) per year; P = 0.04) in the control group. 17 (68%) control-group patients and 9 (36%) treatment-group patients achieved the secondary end point.


Small sample size, not double blind.


A 27-month course of EDTA chelation therapy retards the progression of diabetic nephropathy in type 2 diabetic patients with high-normal body lead burdens.