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From the Townsend Letter
May 2014

Protocol Controversies for Treating Cardiovascular Disease with EDTA Chelation Therapy
by L. Terry Chappell, MD, and Jeanne A. Drisko, MD, CNS
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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 because of its known action as a prooxidant in the extracellular space in living systems.4,32-34
Seminal findings regarding the unexpected prooxidant 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 antioxidant properties, while intravenous vitamin C administration bypassed tight control and through Fenton chemistry became prooxidative in the extracellular space.35-37 In people with normal G6PD status, the prooxidative nature of vitamin C does not occur in the vascular space.34
It is interesting that another well-known antioxidant, glutathione, does not behave like vitamin C when injected in high doses.38 Glutathione maintains its antioxidant 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 antioxidants 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 prooxidative 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 antioxidative effects.
The Roussel trial is in contrast to TACT, wherein 1708 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 g of vitamin C injected at each infusion.1 An unexpected and remarkable finding at the conclusion of TACT 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 prooxidant 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 prooxidative burst? Is it related to other as 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 prooxidant 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 such as 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 as only a prooxidant or an antioxidant 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 g 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 g 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 to 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% to 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 borne 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 lie ahead in parsing out the effect of the various chelation components in treating cardiovascular disease.

Comments from a Few Experts
Ralph 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 g 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 conditions
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 docs 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 250 cc 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 g of EDTA and have recently reduced from 5 g to 2 g 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.

Ted 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 embed a marker on the calcium molecule so it can be seen by the gut villi cells and be invited into the bloodstream. This will cause not enough calcium to be absorbed to maintain the tightly controlled calcium balance in the bloodstream. 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 embedded in the use of magnesium disodium EDTA. Once the latter molecule hits the bloodstream, 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 CaNa2 EDTA nor MgNa2 EDTA 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 g 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 g/3-hour infusion. I believe that 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 g dose is the sole treatment for vascular disease. In younger patients with fibromyalgia or neuropathy, I will usually use CaNa2 EDTA in combination with DMSA. If DSMA is not tolerated, I will alternate with DMPS.

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