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



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.)

To Continue Reading on PDF, Click Here

Protocol Controversies for Treating Cardiovascular Disease with EDTA Chelation Therapy

L. Terry Chappell and Jeanne A. Drisko, Reprinted from the Townsend Letter with permission


The Trial To Assess Chelation Therapy (TACT) is the only large, randomized clinical trial to provide statistically significant evidence that EDTA chelation therapy with high-dose multivitamins can reduce future cardiac events in patients with known cardiovascular disease(1,2).  TACT utilized the published protocol(3) that is used by organizations such as the American College for Advancement in Medicine (ACAM), the International College of Integrative Medicine (ICIM), the American Board of Clinical Metal Toxicology (ABCT), and the International Board of Clinical Metal Toxicology (IBCMT), all of which teach physicians how to administer the therapy and/or test them to provide certification.

TACT used an intravenous dose of 3 Gm of disodium EDTA with magnesium, adjusted downward if kidney function was compromised, 7 Gm of vitamin C, 500 cc of sterile water, and several minor additives, all infused over a minimum of 3 hours(1,2). See Table 1. The published protocol is more flexible, allowing for 1.5 Gm-3 Gm of disodium magnesium EDTA over no more than 1 Gm per hour and varying amounts of vitamin C, as long as the osmolality of the treatment solution is not hypotonic and not so hypertonic as to cause problems.  Calcium EDTA has also been used in various forms with claims of effectiveness for vascular disease.  The use of Calcium EDTA, especially in the oral form, to treat cardiovascular disease has been criticized by the teaching organizations mentioned above.  Concerns have also been raised about high doses of vitamin C, which becomes a pro-oxidant instead of an anti-oxidant at certain levels(4).

The purpose of this article is to discuss the rationale, evidence, and experience of physicians who are acknowledged experts in the use of EDTA for treating cardiovascular disease.  We hope to clarify whether Calcium EDTA should be used to treat vascular disease and how much EDTA and vitamin C are effective and safe to use.

The Published Protocol

 TACT used the 3 Gm basic dose of disodium EDTA with magnesium to treat patients who had a history of documented myocardial infarction.  The basic protocol for TACT is shown in Table 1.  {Insert Table 1} The 3 Gm dose for disodium EDTA has been taught for years, and many doctors who provide intravenous chelation therapy use it routinely.  However, there is evidence that a lesser dose might be just as effective(6,7,8,9).  As a result, a substantial number of treating physicians use the lesser dose, based on these reports.  Obviously, a lesser treatment time is more convenient for patients.  Neither dose puts the kidneys at risk as long as the required rate of administration is followed.  For patients with congestive heart failure, a lesser fluid volume for the treatment might be advantageous.

Chappell and Stahl performed a meta-analysis of studies showing objective improvement for patients with cardiovascular disease treated with intravenous EDTA chelation therapy(5).  Nineteen published studies involving 22,765 patients met the inclusion criteria.  All of these studies used the 3 Gm dose of EDTA with one exception.  Olszewer and Carter treated 2,482 patients with the 1.5 Gm dose, and 2,379 improved(6).  In the meta-analysis, 87% of patients improved, and there was a correlation coefficient of 0.88 between improvement in vascular function and treatment with EDTA.  Patients of the physician who used the 1.5 Gm dose did as well as those from the other sites combined.

Chappell and associates did a follow-up meta-analysis of 32 unpublished reports on 1241 patients(7).  1086 or 88% showed measurable improvement. 778 patients were treated with the 1.5 Gm bottle.  A comparison of the 1.5 Gm and 3 Gm doses in this study showed almost identical results. 

Born and Geurkink published a retrospective, randomized study comparing patients with peripheral artery disease treated with the 3 Gm dose of EDTA to those treated with the 1.5 Gm dose(8).  20 treatments were given to 15 patients in each group.  Those treated with the lower dose improved using Doppler ultrasound by an average of 123%.  The patients in the 3 Gm group improved by an average of 70%.  The results were statistically significant.  One patient treated with 1.5 Gm improved 715%.  That patient was omitted from the study as an outlier.

Chappell and associates compared 220 vascular patients treated with a basic course and maintenance chelation to matched controls from the literature(9).  An average of 58 treatments were given. Subsequent cardiac events were much less in the EDTA-treated group.  The patients treated with the 1.5 Gm dose had virtually the same results as those with the 3 Gm dose.

An in vitro study published in Surgery in 1962 showed the mobilization of calcium from atherosclerotic plaque with EDTA in the laboratory(10).  The results demonstrated that the longer the tissue is exposed to EDTA, the more calcium was removed.  To our knowledge, this finding has not been confirmed in vivo.

Blaurock-Busch observes that the German Chelation Society approves both a 2 Gm and 3 Gm dose(11).  Gordon wrote the first American Academy of Medical Preventics (AAMP) chelation protocol in 1972, based on the work of such pioneers as Clark and Lamar.  It was not published, but it was used in coursework for many years.  He listed the EDTA dose of 50 mg/ Kg.  Cranton’s 1989 Textbook refers to a maximum of 3 Gm dose, except for large patients who could receive up to 5 Gm at 50 mg/Kg.  The textbook was updated in 2001(12).  Rozema’s protocol for EDTA(3) lists both a 3 Gm and 1.5 Gm dose, as does van der Schaar’s 2012 Textbook(13).  The latter has a maximum of 4 Gm for large patients.  All of these protocols insist on an infusion rate of disodium EDTA not faster than 1 Gm per hour to avoid overloading the kidneys.

Because of TACT, the best evidence for treatment of vascular disease with intravenous disodium EDTA lies with the 3 Gm dose.  However, the published studies cited above that compare the 3 Gm dose to the 1.5 Gm dose show the latter to be as effective.  As noted, one study showed the 1.5 Gm dose to be more effective for peripheral vascular disease.  Future large clinical trials will be necessary to determine the lowest amount of EDTA that can produce the best outcome in cardiovascular disease.

Mechanisms of action for EDTA

Proposed mechanisms of action for EDTA chelation therapy have been documented(14), but no consensus exists as to which mechanism(s) are most important to treat vascular disease.  It is well known that both disodium EDTA and calcium EDTA can remove heavy metals.  Such metals as lead, cadmium, and mercury increase the risk of vascular diseases by increasing free radical activity(15).  Reduction of free radicals by EDTA infusions reduces inflammation, which might lesson the likelihood of the rupture of unstable plaques(16).  The clot that occurs as a result of this rupture is the accepted mechanism for most myocardial infarctions and strokes.  A small study by Chappell and Angus showed a reduction of brachial artery stiffness with chelation(17).  Iron deposits have been found in macrophage foam cells, which further increase free radicals and inflammation.  Excessive copper also increases free-radical activity.  EDTA chelates both iron and copper(18).

Lowering blood calcium levels with intravenous boluses of disodium EDTA can inhibit platelet aggregation for weeks at a time(19).  Intravenous EDTA has been proposed as a safer substitute for clopidogrel to prevent clotting after inserting drug-eluting stents(20).  The anti-clotting effect is likely to be an important mechanism for chelation’s cardiovascular benefits.  Selye demonstrated harmful deposition of calcium in soft tissue when a sensitized individual is exposed to a new challenge after a suitable interval(21). The drop in serum calcium that occurs almost immediately upon IV infusion of disodium EDTA stimulates parathyroid activity.  Parathormone mobilizes calcium from soft tissue deposits, but the effect is irregular.  Although there are case reports that plaque can be reduced with disodium chelation(22,23), studies have not shown a predictable improvement in lumen size for arteries blocked with plaque.  It is possible that the calcium reduction cascade stabilizes vulnerable plaques, but this also has not been proven. 

High doses of magnesium are put into the intravenous treatment solution, which prevents adverse effects from the brief drop in calcium levels.  Improved levels of intracellular magnesium might reduce irritable foci that cause arrhythmias and lower blood pressure. To prevent progressive calcium depletion, it is important that IV infusions of disodium EDTA be given no more often than 2-3 days per week, with at least 24 hours between treatments.  With 60 years of use of intravenous disodium EDTA for vascular disease, no fatalities have been attributed to EDTA when the protocol has been followed.  However, there have been isolated fatalities when disodium EDTA was administered by rapid IV push.

Nitric oxide(NO) is an important signaling molecule that is anti-atherosclerotic.  NO production declines with age and is worse with a high fat diet.  Lead inhibits NO formation.  EDTA not only removes lead but also independently increases NO production(24).  This might be an important mechanism for improved circulation for both disodium EDTA and calcium EDTA.

Vitamin K2 also might help remove metastatic calcium from arterial walls.  It has been suggested as an oral supplement to augment the decalcifying effect of disodium EDTA(25).  However, vitamin K2 is not currently included in the chelation therapy protocol

Calcium EDTA

Intravenous calcium EDTA is approved for removing lead and is used to treat accumulations of other toxic metals.  Since there is no reduction of serum calcium as is seen with disodium EDTA, certain mechanisms that are proposed for treating vascular problems do not apply.  Specifically, metastatic calcium is not mobilized and platelets are not inhibited.

 Oral, sublingual, transdermal, and rectal EDTA all consist of calcium EDTA. Oral EDTA is only about 5% absorbed.  Rectal EDTA might be absorbed as much as 35-37% (26).

Intravenous calcium EDTA is used widely as a challenge test and a treatment for toxic metals.  It was used in a small study by Lin that showed that non-diabetic patients with moderate kidney disease might progress less rapidly with EDTA treatment than without(27).  Chen and associates showed that diabetic nephropathy in the presence of high lead levels progressed at a slower rate than controls when their lead levels were reduced and kept under control with 1 Gm calcium EDTA treatments IV(28).  High levels of lead have been shown to be associated with lower blood pressure and an increased risk of vascular disease(29).  Reducing the lead burden might result in improved blood pressure and better circulation to the kidneys.  However, without a drop in serum calcium, decalcification of the arterial wall is highly unlikely.  The many published studies showing improvement in vascular disease, including TACT, all have used disodium EDTA with magnesium.

Garry Gordon has proposed that calcium EDTA combined with lecithin and other nutrients improves blood viscosity, and he cites the work of Lowe (30) and others.  One might expect this to be the case since lavender-top tubes with EDTA are used to anti-coagulate blood drawn from patients for testing.  However, the EDTA used for that purpose is potassium EDTA (K2EDTA), not calcium EDTA.  We were unable to find evidence that calcium EDTA reduces platelet activity directly.  One mechanism for inhibition of platelet aggregation is a depletion of calcium ions.  However, another probable mechanism that applies to calcium EDTA is its stimulation of the production of NO.  Several oral nutrients that can lesson platelet aggregation, such as vitamin E and gingko, can be given orally along with calcium EDTA.

Cranton points out a potential danger of oral chelation on his website(31).  Some toxic metals that are ingested might not be absorbed into the body if calcium EDTA is present, but many more essential minerals will also not be absorbed.  Depletion of zinc, chromium, copper, manganese, and other minerals can reduce antioxidant defenses and endocrine function.  Cranton stresses the importance of the rapid decrease in both toxic metals and calcium with disodium EDTA.  This occurs extracellularly since EDTA does not enter the cells.  A re-equilibration results so that calcium is mobilized as described above and toxic metals are brought out of storage in the bone, brain, and fat cells.

Calcium EDTA is widely sold and advertised as an ingredient in various nutritional supplements.  Claims of effectiveness for calcium EDTA in treating vascular disease are often made based on research that was done for intravenous disodium EDTA.  Calcium EDTA and disodium EDTA are two separate compounds that act on calcium differently in the body.  Although useful mechanisms of action might apply for calcium EDTA, we did not find any clinical trials that support the use of calcium EDTA for treating vascular problems.

Van der Schaar’s textbook describes many toxic metals and chelating agents(13).  DMSA, DMPS, and the two forms of EDTA are commonly used in clinical practice at this time.  DMSA is available orally and is used to chelate lead and mercury in adults and children.  DMPS is a compounded substance for oral or IV use, mostly for lead and mercury, but it is not an FDA-approved medication.  DFO is sometimes used for iron overload parentally but serial phlebotomies are generally more effective.  D-penicillamine can be helpful as a challenge test and occasional treatment.  These medications can be used in combination if the prescribing physician is experienced. The two forms of EDTA are broader chelators and are especially effective for lead.  EDTA has perhaps the weakest affinity for mercury.  If mercury is elevated with a challenge test, it might be prudent to treat with DMSA or DMPS before prescribing intravenous EDTA.  Maintaining good levels of beneficial minerals is important no matter what chelation agent(s) is/are prescribed.  Treatment with DMSA or DMPS reduces free radical activity by binding and excreting heavy metals, which might be beneficial.  However, we did not find any clinical trials that have studied either one as a treatment or preventative for vascular disease.

Vitamin C

As with any medical practice, whether conventional or alternative, different approaches and individualized styles of practice evolve. Some of the differences in approaches relate to experience and some are based on growing evidence from the scientific literature. And so it is with EDTA chelation therapy with certain groups giving differing amounts of EDTA over varying times and by different routes of administration, while others advocate using different formulations and combinations of additives in the mix. One proposed change has been the recent suggestion that vitamin C or ascorbic acid be removed from EDTA chelation therapy(4,32) because of its known action as a pro-oxidant in the extracellular space in living systems(33,34).

Seminal findings regarding the unexpected pro-oxidant action of intravenous vitamin C were discovered in the National Institutes of Health (NIH) lab of Mark Levine, MD along with his colleagues, Qi Chen, PhD and others(33,34).  Levine and colleagues clearly defined that oral vitamin C was a vitamin with tight physiologic control and anti-oxidant properties, while intravenous vitamin C administration bypassed tight control and through Fenton chemistry became pro-oxidative in the extracellular space(35-37). In people with normal G6PD status, the pro-oxidative nature of vitamin C does not occur in the vascular space(34).

It is interesting that another well-known anti-oxidant, glutathione, does not behave like vitamin C when injected in high doses(38).  Glutathione maintains its anti-oxidant properties even when injected at increasing concentrations and has led to the recommendation against adding IV vitamin C and IV glutathione together at the same setting(38).  To date, other anti-oxidants such as alpha lipoic acid have not been evaluated in this manner to determine if they might exhibit a dual nature like vitamin C.

The pro-oxidative nature of intravenous vitamin C has led some to postulate that adding vitamin C to EDTA chelation therapy might have a deleterious effect on patients with already high oxidative burden, as seen in diabetes(4,32).  The hypothesis is that patients with oxidative disease processes may not be able to tolerate the additional oxidative burst that briefly occurs after intravenous vitamin C.  Roussel and colleagues conducted a small uncontrolled trial in 6 adults where EDTA chelation therapy was administered according to standard protocol except for elimination of the vitamin C from the infusate(4).  In the reported trial, markers for oxidative damage were evaluated in the absence of added vitamin C and were found not to be present. The group concluded that EDTA chelation therapy without added vitamin C decreases oxidative stress. But as Roussel and colleagues clearly stated, the small trial was not designed to test the curative effects of the chelation therapy. They acknowledged they were focusing solely on anti-oxidative effects.

The Roussel trial is in contrast to the TACT trial where 1,708 participants with known cardiovascular disease were enrolled(2).  The sample size was chosen so that the effect of EDTA chelation therapy on cardiovascular outcomes could be evaluated. The standard accepted protocol was chosen and this included 7 grams of vitamin C injected at each infusion(1).  An unexpected and remarkable finding at the conclusion of the TACT trial was the marked reduction in cardiovascular events in diabetic participants (2).  This has prompted the NIH to ask researchers to focus on the positive effects in the standard EDTA infusate that may have promoted such beneficial outcomes(39). However, the belief that intravenous vitamin C is a harmful pro-oxidant has led other experienced practitioners of chelation therapy to abandon the addition of vitamin C to the mix(32).  The trial findings with the small sample size and the concerns raised by Roussel and colleagues are contradicted by the positive outcomes of TACT.

What then is the effect that vitamin C plays in the chelation infusate? Is it related to the pro-oxidative burst? Is it related to other as of yet undescribed effects, apart from Fenton chemistry? It is advisable to remember that in the vascular space, when there is normal G6PD status, there are no significant detectable levels of hydrogen peroxide and no detectable pro-oxidant effect(33,34,40).  Any hydrogen peroxide that might be formed after infusion of vitamin C is quickly and effectively quenched in the vascular space, unlike what occurs in the extracellular space. Is it possible that vitamin C at increased concentrations has an effect on the endothelium? Or on the function of blood elements like the red blood cells that are so critical for oxygen mobilization? Unpublished research carried out by the Levine team points to this possibility.

The epidemiology literature shows that vitamin C is critical for improvement of HbA1c and avoiding untoward effects in diabetics(41).  However, it can easily be argued that this is a vitamin effect not a pharmacologic effect. In the tobacco literature it has been shown that the prolonged and destructive exposure to tobacco smoke markedly reduces available vitamin C levels in vivo that are only replenished effectively with intravenous infusion(42-46).  Functional effects on the microvascular bed can be reversed with IV vitamin C(43,45).  It can be argued that tobacco smoking is a model for highly oxidative chronic diseases such as diabetes.  Benefits of infused vitamin C could have positive effects on microvasculature function. This would certainly be a good model for future research.

Other nonvascular effects of IV vitamin C also come into play such as the effects of ascorbate in steroidogenesis, vascular tone, adrenal gland function during stress, and general well-being(47-50).  Taking the narrow view that vitamin C acts only a pro-oxidant or an anti-oxidant may result in the risk of excluding vitamin C with its various positive functions, both known and as yet unknown, in the beneficial treatment of cardiovascular disease with EDTA chelation therapy.


Scientific evidence, especially with TACT, supports intravenous disodium EDTA with magnesium, along with oral multivitamins, to treat vascular disease.  Disodium EDTA can only be given by slow intravenous drip, at a rate no faster than 1 Gm per hour.  Under no circumstances can this preparation be given by intravenous push because of its effect to rapidly lower serum calcium.  Evidence supports treatment doses of 1.5 or 3.0 Gms of disodium EDTA.  The dose should be reduced if kidney function is impaired.  Kidney function should be monitored during the course of treatment. Treatments should be limited to no more than 2 or 3 days per week with at least 24 hours between treatments.  20-30 treatments are needed to complete a basic course of treatment for vascular disease(3).  More treatments may be required in difficult cases.  Most experts recommend monthly maintenance after the basic course is completed.  If the published protocol is followed, safety is not an issue(2).  Disodium EDTA with magnesium effectively removes heavy metals from the body.  Other likely mechanisms of action include reduced platelet aggregation, mobilization of metastatic calcium by parathormone, increased NO production, and antioxidant activity.

Calcium EDTA can be given intravenously or by other routes of administration to remove toxic metals.  Oral absorption is only 5% and rectal absorption might be as high as 35-37%.  Calcium EDTA does not have all the mechanisms of action that disodium EDTA does to reduce or prevent vascular disease.  However, calcium EDTA with multivitamins increases NO production and decreases free radical activity.  Moderately impaired kidney function might improve with IV Calcium EDTA.  Clinical trials have not been done to support calcium EDTA as a treatment for vascular disease at this time.  Calcium EDTA should not be given on a continuing basis without being careful to avoid depletion of essential mineral nutrients. Optimal mineral balance might be difficult to accomplish with oral preparations given on a daily basis.

At this juncture because of the positive TACT outcomes, vitamin C should not be excluded from or reduced in the infusate. The hypothesis that IV vitamin C results in a significant deleterious oxidative burst has not been born out and as part of the total chelation component seems to provide an additional benefit in patients with diabetes and cardiovascular disease. As shown in other conditions with high oxidative environments, IV vitamin C can provide protection and vascular stability. Exciting research opportunities in parsing out the effect of the various chelation components in treating cardiovascular disease lie ahead. 

*See responses from physicians below References section


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TABLE 1: Infusate used in TACT Trial




3 grams

Magnesium Chloride

2 grams

Procaine HCl

100 mg


2,500 Units

Ascorbate (Vitamin C)

7 grams


2 mEq

Na Bicarbonate

840 mg

Pantothenic Acid

250 mg


100 mg


100 mg

Sterile Water

To 500 mL


The mixture of components given in the TACT Trial was based on committee consensus bewteen the TACT Trial investigators and representatives of the chelating community. The agreed upon solution was selected as the representative mixture that had been in use. The amount of EDTA administered to the trial participants was tailored to the individual renal function based on the Cockgroft-Gault equation. Reference: (1,2,3)

Comments from a few experts:

MirandaRalph Miranda— I suspect that the most consistently effective dose is the 3 Grams of disodium-magnesium EDTA in the 500 ml bag/bottle infused over 3 hours. I believe that the attraction of metal ions and ligands causes enough of a shift in pools of metal ions, that previously inhibited enzymatic reactions are liberated from the effects of toxic metals and permitted to contribute to normal and desirable repair processes for which they are suited. Remove the poisons from the systems, and the systems work closer to their innate abilities, to clean up the damage inherent to everyday life. 

Of course, some patients are too frail to withstand the higher dose or the greater fluid volumes, so the 1.5 Gm dose infused at the same rate over half the time or a bit longer suits them well. I’m convinced that the patients who get the “half dose” get far more than “half” the benefit. This dose also works well for patients who are not at liberty to spend as much time away from work, or in my office. Another reason to tread lightly would be patients on multiple pharmaceuticals or with multiple intertwined medical condition.

 I will also use the calcium disodium EDTA, especially when the sole focus of treatment is removal of specific toxic metals. I am not a fan of the rapid infusion of this mixture, even though many chelating doc’s recommend the rapid push due to the absence of risk for hypercalcemia. I believe there is plenty of potential for disruption of physiologic levels of Zn, Mn, Cr, and other trace metals from too rapid an injection. Oral EDTA and rectal suppositories share the lack of significant absorption for purposes of CVD and reducing metals. These are the least effective choices and I reserve them for those who cannot, for whatever reason, use the IV therapies.

Michael Schachter— I generally follow the ACAM protocol, using Cockgroft-Gault to calculate the proper dosage with a maximum of 3 grams of EDTA. My infusions are generally 3 hours. We have used catheters exclusively for many years to avoid butterflies’ tendency to come out of the vein when the patient moves around. If my primary goal is removing lead or cadmium, I use calcium EDTA instead of disodium EDTA and usually run the infusion over 20 to 30 minutes.

Claus Hancke— Since 1987 I have been using the same protocol with great success and not one single fatality or serious side effect in nearly 100.000 infusions.  Nothing is added that can be given as effectively orally.  My carrier solution is 250cc of isotonic glucose.  This does not create problems with diabetic patients and avoids a saline load for those with heart failure.  Magnesium and bicarbonate avoid infusional pain and tremor. I use 3 Gm of EDTA and have recently reduced from 5 Gm to 2 Gm of vitamin C.  My infusions last 3 hours.

We EDTA-doctors of the world have been using the EDTA chelation protocol mainly unchanged from 1987.  Now after 25 years we have succeeded against our opponents and can show the TACT study with significant results.  So I don’t think it is politically wise to change the protocol right now.  Let’s make serious trials to see the efficacy of different infusion modalities, but never give up what we have established.

RozemaTed Rozema–Hans Seyle comments in his book, Calciphylaxis, about how PTH is a direct producer of calcium deposition in arterial walls.  My personal take on the deposition of calcium in arterial walls leading to atherosclerosis is that as we age, the fundus of the stomach does not produce the gastric acid needed to imbed a marker on the calcium molecule so it can be seen by the gut villi cells and be invited into the blood stream. This will cause not enough calcium to be absorbed to maintain the tightly controlled calcium balance in the blood stream. Over time, there is a miniscule parathyroid hormone release to take calcium from the bone to make up the shortfall.  This produces the sensitization to put some of the calcium into arterial walls.  Over many years, the clinical picture of early death and other vascular conditions result.

The issue of using calcium EDTA (instead of magnesium disodium EDTA to reduce metastatic calcium and treat vascular disease) is imbedded in the use of magnesium disodium EDTA.  Once the latter molecule hits the blood stream, the magnesium is dropped for chelation of calcium.  The resulting decrease in free serum calcium is what triggers the parathyroid action (and the platelet effect).  The resulting calcium disodium EDTA will then do all the toxic metal binding that calcium disodium EDTA does when given as a short IV infusion….

Joe Hickey—I believe that mercury is chelated with EDTA.  The resulting mercury EDTA rapidly vaporizes from urine and thus is difficult to measure.  If one believes that neither CaNa2EDTA or MgNa2EDTA effectively chelates mercury, then one must account for mercury with DMSA or DMPS.  If urine and fecal measurements are done, the largest amount of heavy metals removed is by far mercury with lead a distant second place.  If only urine is collected, lead is usually the highest excretion with mercury second, in my patients. Therefore, I also use DMSA if tolerable with either form of EDTA to account for mercury.  I will give 10 mg/kg of DMSA for three days, starting on the day of the IV with EDTA.  DMSA is less likely to vaporize in the stool. 

When treating primarily for vascular disease, I use MgNa2 EDTA 1.5 Gms over 1.5 hours with the addition of the DMSA.  I have found this regimen to be successful in patients who have had recurrent angina, post bypass, and stent closure.  I am rarely able to talk patients into consistently sitting for the 3 Gm/3 hour infusion.  I believe there is probably an additional effect for the 3 hour infusion in cases of calcific valvular disease and scleroderma, because of the parathyroid effect but I am not convinced that the 3 Gm dose is the sole treatment for vascular disease.  In younger patients with fibromyalgia or neuropathy, I will usually use CaNa2EDTA in combination with DMSA.  If DSMA is not tolerated, I will alternate with DMPS.

John Trowbridge— What are we trying to accomplish with chelation treatmenDr._John_Trowbridgets?  If a patient is substantially ‘loaded’ with toxic metals, treatment goals will be different than those for one with high-grade blockage disease in critical arteries. Patients suffering with crippling inflammatory and/or auto-immune diseases might require a another approach. 

Injectable and oral medication alternatives to EDTA should be considered, depending on a variety of factors.  However, 60 years of beneficial and safe reports regarding EDTA would argue for that to be the basic IV chelator.  Others could be added in ways that maximize their safety considerations as well, such as oral DMPS, DMSA, and d-penicillamine, as well as IM DFO.

With different stability constants and side effects, using two or more chelating agents at the same time, poses potential risks to the patient.  The simplest way to avoid such unpredictable interactions is to administer one chelating drug at a time. In 1993 I developed the idea of administering different chelating drugs on an intermittent, pulsatile schedule.  This protocol avoids the potential of interaction of two or more chelation drugs but still allows for exploiting the ‘preferences’ of each drug for different toxic metals.  Extra physiologic minerals would, of course, be needed to handle the additional chelator load.

To minimize side effects, I have patents take one 250 mg tablet each evening during the week.  For example, a patient might be advised to take d-Pen 250 mg each bedtime on days 1-7 of the month, then DMSA 250 mg each bedtime on days 8-14, then d-Pen again on days 15-21 and DMSA again on days 22-28, with a ‘break’ until day 1 of the next month.  I do not mix IV EDTA with DFO, nor do I give d-penicillamine  or DMSA within 4-6 hours of EDTA IV.  

With the changing urinary elements test reports, a patient might be told to take just d-Pen or DMSA every day of the month.  Now that oral DMPS is readily available, it might be inserted into the ‘weekly’ protocol as well, especially when mercury levels are substantially elevated on the test report.

By 1997, I had confirmed that our reduction of toxic heavy metal body burden – as measured by the d-Pen challenge urinary elements test – was proceeding at a rate at least one-third faster than with IV EDTA alone.

Two serious mistakes that beginning doctors often make when giving chelation therapy are insufficient attention to mineral depletion and too rapid reduction of cardiovascular medications.  Ample minerals must be supplied, either orally or IV, and gradual reductions of meds are required in order for the body to “relearn” more normal functions.         

Conrad Maudrmaulfairlfair—With calcium being an important factor in the aging process and in the atherosclerotic disease process, we want to have the maximum benefit from its removal that is possible.  I personally am a strong advocate of the 3-4 hour chelation treatment simply based on clinical experience.

Patients suffering from end-stage chronic degenerative diseases are misled when they read or are told that oral application of chelating agents and in particular EDTA can be an alternative to a comprehensive chelation therapy program including the parenteral administration of EDTA.  A patient having significant end-stage disease opting to take an oral chelation product because it is cheaper and does not require a personal commitment of time and involvement is most assuredly going to experience a poor outcome.  A practitioner who encourages a patient with significant disease to think that using oral chelation is better than doing nothing is being as irresponsible as allowing a patient uncontested to continue to smoke one pack of cigarettes a day because it is better than the two packs a day he/she had previously smoked.

Trowbridge, MD: Cardiovascular Chelation

John 2by John Parks Trowbridge, MD
Reprinted from the May 2010 Townsend Letter with permission

Personal Pollution and Matters of the Heart
“This can’t be happening” is often the first thought. Gripping, gnawing chest pains give way to a heavier, crushing feeling that generates fear. The idea of “indigestion” soon gives way to “impending doom.” In this setting, 9-1-1 is sometimes a reluctant last resort, after antacids and resting produce only a pitiful response.

The arrival of paramedics brings reassurances from technicians who methodically start oxygen, apply EKG leads, and prepare for transport. Nurses and doctors in the emergency room go about their duties calmly and with dispatch – starting IVs, administering medications that relieve the urgent worry. Transfer to the coronary care unit is swift and easy, and monitors beep with the soothing monotony of a metronome.

From A to Z, everything about the medical team responses engenders trust and dependence in the patient: “These folks really know what they’re doing. Thank God I got here in time.” Trusting eyes gaze into the cardiologist’s face, searching for any clues that the situation is worse than it might appear. Again, reassurance: “You’re here, you’re safe – we need to do some tests to figure out how best to fix you now.”

Slippery slope? Conveyor belt? One-way road to a “dead” end? Many terms have been applied to the “work-up” and “treatments” offered in modern cardiology and cardiovascular surgery. In point of fact, major studies 30 years ago showed that one in six bypass operations are life-saving, when high-grade blockage is worsening in the left main artery or early in the left anterior descending (LAD) artery (the “widow-maker” or “artery of sudden death”).1

Then what of the other five in every six patients? Therein lies the rub.

‘Treating’ with Tests
Everyone knows about the routine resting heart tracing: 12-lead EKG, often with a “rhythm strip” of several seconds. The predictive value is minimal in the absence of symptoms or an irregular pulse.2 A 24-hour (or longer) Holter monitor gives valuable insights into rhythm disturbances but has little use in confirming “ischemic” disease, where blood flow to regions of the heart muscle is becoming compromised. Worthy of comment is that ischemic patterns can be documented in patients without blockage in the heart arteries but with magnesium deficiency or other conditions creating episodes of heart artery spasm. Vasospasticity can constrict blood flow transiently, and chest pains, shortness of breath, weakness, pale complexion, and sweating can mimic heart “angina pains” or even “myocardial infarction (MI).”

Angina simply means reversible chest pain events, often responding to nitroglycerin-type medications. The success of these drugs produces further patient trust that the cardiologist “knows how to treat me.” Myocardial infarction results from sudden blockage of blood flow to a (small or large) portion of the heart muscle. A heart artery already narrowing from deposits of plaque is more easily blocked completely by sudden formation of a platelet plug, also called a “thrombosis” (ACS or “acute coronary syndrome”). More recent studies show that the gunk in plaque is more likely to break off if a smooth hardened surface has not formed (so-called vulnerable plaque). Such free-floating chunks will always find a smaller arteriole and lodge there, blocking blood flow beyond … a heart attack.3

Vasospastic episodes can occur in patients who have artery blockage disease and in those who do not. When tests show minimal blockage that should not be causing angina episodes, cardiologists are sometimes stumped and nevertheless recommend “revascularization” procedures: balloon angioplasty, stents, even heart artery bypass. Each of these operations is based upon a “Roto-Rooter” plumbing concept of heart disease: open the plugged pipes or simply route around them.

This “conventional cardiology concept” comes from the tests upon which they rely in figuring out how to fix heart disease.4 Simply stated, “If the only tool you have is a hammer, then all the problems you see look like nails.” Since many cardiology tests look at the “plumbing,” the treatments advised are designed to address flow blockages that can be seen. That viewpoint creates the fundamental restriction – blinders, if you will – preventing well-trained cardiologists from being able to see the value of treatments other than those in their “plumber’s toolkit.”

One of the most widely known heart tests is the “stress EKG.” A blood pressure cuff is applied, patches with electrical leads are placed on your body, you begin to walk on a treadmill, and the workout is gradually increased to a jog.5 If your legs become fatigued, if you become short of breath, or if the heart tracing shows certain changes – “flags” that indicate problems – then the test is concluded; otherwise, you race along to a calculated heart rate. Comparing your blood pressure changes to the exercise heart tracing gives a hint of how well your heart muscle is working; in other words, how well your blood is flowing to your heart and other muscles.

Even a “negative” (“normal”) stress test is often followed by a “nuclear stress test,” simply because your cardiologist “wants to be sure.” This examination starts with a stress test followed immediately by a radioactive “tracer” injected just as a fancy Geiger counter is placed over your heart. About four hours later, you are placed under the Geiger counter again. Images “after exercise stress” and “at rest” are compared – if the tracer pictures after exercise show “holes” that later “fill,” you have blockage disease restricting the blood flow. If the “holes” don’t “fill” later at rest, then you have had one or more heart attacks where muscle tissue has been replaced by thickened scar. No “holes” after exercise? Then you appear to have adequate blood flow to your heart muscle.

Even a “negative” (“normal”) nuclear stress EKG is often followed by a “coronary angiogram” (heart artery “pictures” – also called an “arteriogram” or “catheterization”), simply because your cardiologist is “being complete” in your evaluation after being admitted for chest pains. Trusting your doctor – and reassured by your test reports so far – you naïvely consent to this much more invasive test. A catheter (tube) is placed into a large artery (as in your groin) and advanced to your heart, where X-ray dye can be injected to outline the pattern of your heart arteries. One tiny technicality: the severity of diameter narrowing is commonly overestimated by 30% to 60%.6 [As the “gold standard” for coronary artery disease, angiograms have several limitations. Recently developed computerized coronary angiography instruments (not yet widely available) will help to work around some of these errors of interpretation.]

Bingo! Narrowing is likely to be identified, since you did come in with chest pains. Now your cardiologist has a reason to recommend “balloon angioplasty” (another tube, this one with a blow-up tip that crushes blockage against the wall of the artery), often with placement of a “stent” (sort of a Chinese finger-trap in reverse, where it is inserted stretched out then “springs open” to press against the wall of the blood vessel). Modern stents are “radioactive” or coated with “chemotherapy,” to reduce your body’s attempt to cover over this strange device, thereby narrowing the artery again.

Balloons? Chemotherapy? Radio­activity? You might have a few questions, but your cardiologist is reassuring that you’ll probably be able to avoid “open heart surgery” (a bypass operation). Now that’s appealing! Once again, you innocently consent to another procedure, hoping that your future will be bright and comfortable. But the results from surgery can’t ever be guaranteed.

Speaking of surgery – what happens if your cardiologist invites a cardiovascular surgeon to discuss a bypass operation with you? For the vast majority of patients, the answer is simple: your lack of knowledge about options will mean that you trustingly agree to have the surgery. Americans are suffering in droves, like lemmings to the sea: in the US in 2005, 469,000 coronary artery bypass procedures were performed on 261,000 patients. An estimated 1,265,000 “stent” procedures were performed; approximately 69% of these were performed on men and approximately 50% on people aged 65, according to the National Center for Health Statistics. During 2006, some 2,192 heart transplantations were performed.7

But What If You’re ‘One of Those Five’?
If only one in six patients has a heart bypass operation8 that is life-saving or life-extending, what is the situation for those other five patients who also often undergo the surgery? Most survive, some do not, many feel better … but their improvements might well have been possible with modern medications and lifestyle changes alone.9 Virtually every “open-heart” patient will suffer some slight or significant degree of “pump syndrome,” neurological or mental changes associated with the heart-lung pump.10 About 1 in 20 bypass patients will die during or soon after surgery. Of those who survive, over half can be expected to suffer fairly dire concerns over the next 12 months: heart attack, stroke, heart rhythm disturbance, congestive heart failure, or rising blood pressure. And each of these events will force these patients back into the trusted arms of their cardiologists and consulting medical specialists.

Perhaps one of the best reviews of the limitations, side-effects, and outright hazards of angioplasty, stents, and bypass surgery can be found in several chapters of the book, Is Heart Surgery Necessary? What Your Doctor Won’t Tell You, by Julian Whitaker, MD.1 Before undergoing any of these procedures, every patient owes his family – and him- or herself – the time to read and understand these risks, in order to question his doctors appropriately and be able to give an actual informed consent, should he so choose.

What About Treating the Patient?
Wait! Can you actually afford to wait, do you have the time – the luxury – to read this and other books, to get the true details for yourself? While doctors sometimes give the impression that “you’re a ticking time bomb, we’ve got to move quickly,” published studies have shown quite the opposite conclusion. Harvard cardiologist Peter Graboys showed, 20 years ago, that patients who chose to wait before having bypass surgery suffered no deaths from heart disease over the next 2½ years.11 A second study showed only a 1.1% annual death rate from heart disease over the following five years for those who politely (or not so!) declined to have an angiogram, likely concluding that this was just “a map for surgery” that they were reluctant to undergo.12 This rate is far below an estimated up to 5% death rate for bypass surgery. Balloon angioplasty surgery offers an estimated 1% deaths, but recurrent procedures are quite likely.

Recognize that Harvard’s cardiology staff used only routine medications available at that time, along with “usual” lifestyle changes – diet, exercise, and so on. As conventional physicians, they had little interest (or faith) in integrative technologies such as nutritional supplements or chelation therapy. The combined use of (even more modern) medications now, along with specific “orthomolecular nutrition” and chelation, would be predicted to enhance further the startling results that they obtained with minimal effort, and clinical experience supports that expectation.

Rather than progressing rapidly to invasive and potentially risky tests, an integrative physician sometimes will order a set of echocardiograms, basically “sonar” ultrasound pictures of heart muscle performance. When valves and heart muscle function appear reasonably normal and the “ejection fraction” (percentage of blood pumped from the heart with each beat) is normal or almost so, then performance has been preserved even though blockage disease might be present. Activity or exercise might display reduced capacity, consistent with blood flow reduction. A patient with frequent angina, and especially with chest pains at rest, is more likely to have blockage changes best treated first by surgery unless he or she refuses and an aggressive nonsurgical treatment program is pursued.13

The recent availability of “heart scanners” (EBT, or electron beam tomography) has helped to quantify the degree of blockage present as well as its location. This 10-minute test uses minimal radiation and gives reasonably reliable pictures, from which a heart artery diagram of calcium-hardened blockage can be constructed. Again, “high-grade” (severe) blockages early in the left-side heart arteries can move a patient toward the “surgical option” for best survival, with follow-up chelation to treat the underlying cause.

An integrative physician offering chelation therapy will, of course, review and consider cardiology tests available from other specialists in order to best plan a treatment program. Angiogram pictures, though, will rarely be required.

Nonsurgical Treatment of Heart Disease?

Can blockage disease be effectively and safely treated without surgery? The answer, as demonstrated by dozens of clinical studies and case reports over the past 50 years, is an unreserved “Yes!”

However, reduction of blockage should be considered only a possible and desirable side effect and not the goal of a chelation treatment program. An early thought in the late 1950s was that chelation “worked” by removing artery blockage. This seemed a logical way to explain observed improvements in heart function, EKG patterns, congestive heart failure, chest X-ray images, angina chest pains, shortness of breath, and activity levels.14 Without question, some patients do show reduced blockage, as demonstrated by before-and-after-treatment heart scan images in two patients reported to the American Chemical Society in 1994.15 Of interest is that virtually 9 out of 10 patients show improved heart performance – but not all of those show reduced blockage disease by any test performed.16

Another factor to recognize is that our tests are less than precise in quantifying the degree of blockage present, whether improving or worsening patterns. Several assumptions are made in each test setting (heart, carotid neck arteries, abdominal aorta, legs, and so on). The presumed “gold standard” – such as heart angiograms – are difficult to interpret at best … and the same test can be read differently on different days … by the same cardiologist. If blockage doesn’t disappear with chelation, then what could explain the obvious and dramatic clinical improvements in the vast majority of patients? In actual fact, blockage probably is reduced in many arteries: a 10% to 15% increase in “cross-sectional diameter” (the area through which blood can flow, where larger diameters have less resistance to flow) produces double (or more) blood volume delivered to tissues downstream.17 Current tests fail to reliably detect such small reductions in blockage with increases in blood vessel diameter – but the patients can clearly feel and enjoy the improvements, as overwhelmingly noted with chelation therapy. The use of artery bypasses and stents is based upon increasing the diameter of a “feeding” vessel, but such operations involve many risks and the duration of improvements can be limited. Indeed, the diameter increases of bypasses and stents are noted only at the operation site and not generalized throughout the arterial system as with chelation therapy.

Studies documenting patient improvements with chelation are well summarized elsewhere.18-20 What has received very little attention is how much these improvements can be attributed to decreased toxic metal burdens – coincidentally reducing inflammation – and other mechanisms. When platelets have less free radical inflammatory injury, they become less “sticky,” less likely to form sudden “clots” or “plugs” and completely block ailing arteries. When magnesium is provided in large doses, blood vessels more readily dilate to increase flow volume and have less spastic tendency to restrict flow. Vitamins B6 and C, amino acids lysine and proline, essential fatty acids, zinc – these and other nutritional supports that are provided during a series of chelation treatments clearly help to stimulate improved clinical function, detoxification, and tissue repair. Even nattokinase (or lumbrokinase), which lowers blood flow “viscosity” by reducing free-floating monomer fibrin strands, might help explain some of the benefits seen in advanced chelation programs.

What About ‘Personal Pollution’?
All chelating medications share in common one key property: forming a particular chemical bond with certain positively charged ions (metal atoms).21 This drug–metal complex allows for easier removal of the metals through the kidneys. In many cases, the chelating drug prefers to bond with so-called heavy metals that are toxic to the body. Reducing the presence of toxic metals allows for usual “physiologic” chemical reactions to proceed more normally.

Toxic metals insert themselves in place of appropriate metals (such as magnesium or zinc), “sitting” on active sites in enzymes and blocking needed chemical reactions. In addition, they stimulate a tremendous increase in the rate of production of “free radicals” (also described as “oxidants” or “ROTS,” “reactive oxygen toxic species”) that inflict lasting damage to body cell structures, especially those involved in the mitochondria, the tiny “energy-factories” that produce the ATP that powers all cell processes in all cells. (Antioxidant vitamins – such as vitamins C and E and beta-carotene – glutathione, and other molecules help to protect vital molecules from free radical injury.22) Another concept to describe free radical production is inflammation, the destructive and powerful process that creates the pain of arthritis, of heat and chemical burns, and basically all departures from normal function and physiology. Blockage within blood vessels, of course, is one of these “departures.”

A better understanding of how toxic metals lead to suffering and death is found in several observations over the past 40 years, almost from the time humans began in earnest to poison the planet. Animal studies have shown that heavy metals are uniformly neurotoxic, immunotoxic, carcinogenic, and directly harmful to all vital organ systems. The onset and severity of suffering depends, of course, on the dose and exposure patterns as well as cellular compartmentalization and tissue equilibration. Death follows slowly or rapidly based on the same criteria. Toxic heavy metals are throughout the environment (air, food, water, objects) and there is no way to avoid them entirely. Since they come into your body easily but leave much more slowly, all of them accumulate over time and increasingly interfere with body metabolism.

Every person will suffer some (slight or increasingly significant) degree of impairment among his or her many organ systems, based upon his or her exposures, nutritional status, biochemistry, physiology, and so on. Basically, the “weakest link” in each individual will begin to show toxic damage first. In a more global wholistic view, virtually all human ailments (including expression of genetic aberrations) can be aggravated by – or even directly attributed to – increasing burdens of toxic heavy metals.23 Since bioaccumulation from the environment cannot be avoided, attention must be directed to minimizing exposure and removing those that have gained entry. The medical procedure of removing them, of course, is called “chelation therapy.”

A general idea of the magnitude of “toxicity” can be gleaned from providing tainted cage water to rodents, where their only liquid source is laced with a heavy metal. Daily water intake is based on animal weight. Thus, calculations can be made regarding how much of a particular toxic metal was required to kill any individual animal. The lowest dose that killed the first one is noted. Amounts are recorded all the way up to the highest dose, the one that finally killed the last remaining animal in a group of 100. These name for this group of concentrations is lethal dose (LD), and a number is appended, to indicate the population percentage that has succumbed to that amount of toxic metal. For example, the LD1 is the concentration to kill the first animal; LD50 is enough dosage to kill half of the subjects (50 out of the 100). The LD100 dose is the amount that will kill all of the animals.

Of greater concern to people who think they have only minimal exposure to toxics is that small amounts of different toxic heavy metals can combine to create ever more destructive changes. The overwhelming majority of people are lulled into a false sense of security that they “don’t have too much toxics on board, their levels are really ‘low.'” One rodent study showed that combining the LD1 level of mercury with 1/20th the LD1 level of lead in the cage water did not kill just 2 animals (addition), it did not kill 4 or even 8 animals (multiplication) – this seemingly inconsequential combination killed all 100 of the rodents (amplification).24 Extending the implications to human beings is sobering, particularly when we are making our environment increasingly toxic. Modern medicine has no other method to remove toxic metals (as or after they enter) than the chemical process of chelation. Indeed, this is the only FDA-approved method of detoxifying from this heavy-metal toxic body burden.

Treating the ‘Personal Pollution’
The question, does chelation work? was well answered in the very earliest studies, in the 1950s, by Norman E. Clark Sr., MD, the “father of chelation therapy in America.”25 Subsequent studies have confirmed his early observations, with rare exception (and those often criticized as having faulty scientific design or controls). But two questions arise: first, will chelation help all blood vessel problems? And second, what about over-the-counter oral products that might work just as well as the intravenous treatments?

The range of occlusive (blockage) blood vessel disorders – in the heart, neck, brain, central core (including kidneys), and legs – has been widely studied. The results are uniformly positive, though the percentages of those areas that improve rise with increasing distance from the brain. As a clinical rule-of-thumb, “brain” and “eye” problems improve significantly about 75% of the time, heart problems about 88%, and leg problems about 92%. (Some studies have suggested even better results.26,27) The differences deserve further investigation, but suffice it to say that they probably relate in some degree to different forms of calcium deposition (“hardening”) in the different artery walls.

The most common diseases causing significant blood vessel blockages are diabetes (both types, especially when poorly controlled) and high blood pressure (“hypertension”). In both conditions – as in most others – the improvements with chelation can be startling. Legs scheduled for amputation – a frequent conclusion for diabetics – have been largely saved by chelation treatments.28,29 Clinical experience confirms that blood sugar control is often improved, sometimes dramatically, and dosages of insulin or oral hypoglycemics can be reduced for many patients … reducing side effects, of course.

The sugar-control implications for “metabolic syndrome” (an inaccurate title for “insulin resistance syndrome”) are overwhelming. Also misnamed “cardiometabolic syndrome,” this pattern shows elevating blood pressure, blood sugar, and triglycerides, lowered HDL (“heart protective”) cholesterol, along with enlarging waistline. This cluster of disease findings is associated with higher incidences of heart attacks and strokes, two of the top three leading killers in the US. Chelation therapy produces impressive results in these patients. Results in other disease conditions (such as Raynaud’s phenomenon, scleroderma, sys­temic lupus, rheumatoid arthritis, Parkinson’s, and so on) are similarly encouraging.30

So the second question – “over-the-counter” items that might help – raises some interesting concerns. For example, when people order the latest hyped-up bottle from a newsletter or other brochure, are they really worsening inside while they delay seeking actual, scientific, evidence-based chelation therapy? Younger people, with lesser exposures to toxics and fewer degenerative issues, might “buy some time” with such readily obtained “nutritionals.” Older folks – especially those with degenerative diseases or (even unknown) history of prolonged or extraordinary exposures – are walking straight into the lions’ den. While any one individual might live a long and fruitful life without actual chelation, the vast majority are likely to succumb to the common killers, usually at the common ages. Even sequential “negative” (“normal”) test reports showing minimal blockage changes in arteries are no protection against sudden blockage from “sticky” platelets or other results of localized inflammation.

The longer-lived European (especially Mediterranean and Baltic) societies, particularly those whose citizens remain vital and active late in life, can offer some hints as to useful dietary counsel. Sulfur – found in onions, garlic, many grains, legumes, red meats, eggs, nuts and seeds, broccoli, cabbages, even milk and asparagus – readily binds with toxic heavy metals, but only weakly. Selenium – found in brazil nuts and a variety of meats – also can bind to heavy metals. When foods are grown (or animals are raised) in sulfur- or selenium-deficient soils, they have minimal amounts of these valuable minerals. Their use as significant “chelators” – even in the form of alpha-lipoic acid or methyl-sulfonyl methane (“MSM”) or N-acetyl-cysteine (“NAC”) – has not been adequately studied.

Some publicly promoted products have cilantro, chlorella or other algae, and other botanical nostrums and are widely touted as helping to remove toxic metals. Again, their use as significant “chelators” has not been persuasively studied. Claims are made for EDTA in various products administered orally, but none of these have been subjected to rigorous scientific studies in any ways that successful intravenous EDTA chelation has been evaluated. Indeed, a number of formulas also have the nutritional element chromium listed as an ingredient in the same capsule or tablet. Once EDTA “finds” the included chromium, it binds more strongly than with almost anything else and is only slowly released. So, you get virtually no benefit from the chromium or chelation value from the oral EDTA.

If neither foods nor over-the-counter “oral chelators” offer much prospect of demonstrable lasting improvement, then what options exist other than intravenous chelation therapy? Here we are treading on “unstudied ground” once again. Heavy toxic metals interfere in so many ways – blocking enzyme and other metabolism reactions, creating inflammation, making “sticky” platelets, “rusting” the inner linings of blood vessels and thereby encouraging blockage, damaging brain and nerve functions, impairing immune defenses, encouraging the development of cancer, and so on. Theoretically the reduction of the total body burden, by any means, should aid the restoration of more normal functions.

Several chelation medications – such as D-penicillamine and DMSA – have been given orally, safely, for many years. Perhaps the detoxification of heavy metals cannot work nearly as successfully as intravenous EDTA. However, speculation can be offered: carefully prescribed use of various oral chelation medications might, over long periods of time, offer important benefits to people unable or unwilling to take in-the-vein treatments; however, they might forego some (possibly critical) improvements with artery blockage disease. In the near future, this would be a fruitful area for study by the National Center for Complementary and Alternative Medicine (in the US National Institutes of Health).

When Hot Dogs Are Banned …
Based on the studies available over the past 60 years, should we be optimistic regarding chelation therapy – whether intravenous EDTA or various oral chelator medications – finally becoming available for the majority of Americans? Absolutely not.

At a recent trial, where I was serving as an expert witness for the defense, the state medical board attorney noted: “Since EDTA and other chelation medications are approved by the FDA for removal of toxic metals, then really their use is ‘conventional’ medicine practice, not ‘alternative’ or ‘integrative,’ right?” My reply: “Well, yes, except for one teeny-tiny technicality.” “What’s that?” asked the prosecutor. “The state medical boards.” “Why do you say that?” he asked, surprised. “Isn’t that why we’re in this trial? All of the medical boards ignore approval by the FDA, ignore the clear evidence found in the medical literature, and ignore the overwhelming reports of patient benefits from chelation – and they prosecute the doctors offering the treatment, just as you are today.”

A recent pediatrics study claims that 10,000 emergency-room visits are made each year for children who are choking on hot dogs. Some six dozen reportedly die. Each year. If that many patients suffered death as a result of chelation therapy properly administered, the treatment would have been banned several dozen years ago. In sharp contrast to the “wiener losers,” whenever any single patient complains of “side effects” or – as happens every few years, when a patient ill enough to finally seek chelation treatments dies anytime during the therapy program – the state launches a full-scale investigation, usually seeking to remove the “offending” doctor’s license to practice medicine.31 As a society, we tolerate dozens of deaths from the lowly hot dog – at the same time we tolerate dozens of millions of preventable deaths and untold suffering from heart attacks, strokes, high blood pressure, kidney failure, macular degeneration, and amputations for gangrene, among the many disease conditions that could have been helped by chelation. When will the public demand a change of policy that we can believe in?