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From the Townsend Letter
May 2013

Chelation Therapy: Stepping Into the Next 60 Years
A Historical Commentary

by John Parks Trowbridge, MD
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Mind-body medicine, a term well known in medicine, has major roots in observations made in the 1960s by one of my lab directors at Stanford, George Solomon, MD. Intensive study of the "relaxation response," "healing touch," "acupuncture," and similar "soft science" technologies has led to widespread acceptance in the medical and lay communities. At about the same time, startling observations were being made of reversals of increasingly prevalent coronary and peripheral vascular maladies by chelation therapy with intravenous EDTA. Despite "hard science" showing that these beneficial discoveries have been replicated time and again, chelation remains largely unknown or, at worst, vigorously defiled. Paul Dudley White, MD, President Eisenhower's cardiologist, encountered similar resistance for over two decades to his introduction of the EKG. René Laënnec was more fortunate in securing wide acceptance of the scientific results available with his new "stethoscope" within a decade in the early 1800s. Given a world increasingly aware of pollution with toxic heavy metals, and given a population with younger onset of serious degenerative diseases, and given 60 years of overwhelmingly successful results, why have conventional medicine and regulatory government tossed chelation aside, onto the trash heap of so-called fraudulent diversions?

Going to the Dogs – and Nowhere Else?
What we now unquestioningly call "modern medicine" was largely invented since the late 1940s. Houston cardiovascular surgeon Denton Cooley, MD, studied pediatric procedures in postwar Europe, and his research efforts have saved countless children. Coronary endarterectomy was tried for occlusive disease, but most patients had diffuse involvement and were poorly qualified. Other partners of Houston cardiovascular surgeon Michael Debakey, MD, were Ed Garrett Sr., MD, and Jimmy Howell, MD. In the early 1960s, they were in the forefront of perfecting a technique of removing a peripheral vein and inserting it as an aortocoronary bypass on the heart … of dogs. Endless hours spent in the dog lab led to skills and procedures hitherto unknown. Other complementary technologies were arising at the same time, including selective coronary angiography (to identify and locate high-grade occlusion), the cardiopulmonary bypass "pump" ("heart/lung" machine), and startling advances in anesthesia and antibiosis. Still, the dogs were their only bypass "patients," and their survival was not the object of the research.

Despite sharing with their cardiology colleagues the potential for success of their new surgical approach, no patients were forthcoming. Finally, cardiologist Ed Dennis, MD, endorsed a last-ditch effort to salvage patients moribund after their infarction. In 1964, Garrett led the team to perform the first successful coronary artery bypass procedure, at Baylor University. The early patients, already preterminal, failed to survive. With the prospect of revascularization too tantalizing to resist, stable patients with severe angina were then referred for surgery. The first two died. The third survived. And a new era of surgical success emerged.

But … Banished Forever to the Pound?
Intravenous EDTA chelation therapy was welcomed directly into patient practice in a most unusual way: in the emergency room. A child presented to the Georgetown University Hospital in 1952, clearly suffering with lead poisoning (from chewing paint off a window sill?). Pediatrician S. P. Bessman, MD, recalled a recent conference wherein neurology researcher Martin Rubin, PhD, described exchanging lead for calcium by a new "chelating" compound … in the test tube. "Can I use it in this kid? How do I dose it?" Serendipity led to clinical success and the child recovered. The case was reported in the Medical Annals, District of Columbia, later read by Norman E. Clarke Sr., MD, a cardiologist in Detroit. He was seeing plumbism (lead intoxication) in battery-factory workers, and thought to try this new chelation treatment. Soon, his patients were reporting less use of nitroglycerin, fewer angina pains, and increased activity without dyspnea. Why not, he thought, try this on "heart patients" who were not suffering with lead toxicity. They, too, dramatically improved with chelation. And a new era of medical success emerged … and was soon to be banished like an old dog.

The NIH TACT Results
Almost 60 years after the first discovery that EDTA chelation therapy could be effective in the treatment of heart and blood vessel diseases, results of the first large randomized double-blind trial were reported at the American Heart Association meeting in November 2012. A number of commentaries have identified "problems" with the 7-year-long National Institutes of Health (NIH) study, under the direction of cardiologist Gervasio Lamas, MD, of the Mt. Sinai Medical Center, Miami Beach, Florida. An 18% reduction of cardiovascular events in the entire treated group suggests a beneficial effect. However, one cadre accounted for substantial improvements: diabetic patients enjoyed a 39% decrease in adverse events compared with placebo (usual medical treatment) controls.

Given the increase in diabetes in the American population – including the younger age of onset for many victims – any treatment offering significant benefit should, in the best of possible worlds, be readily embraced.

Diabetic Complications
Research at the NIH in diabetics during the 1970s showed that normalization of blood sugars preserves endovascular and end-organ tissues, approaching the baseline health seen in normoglycemic populations. Over the past 30 years, there has been an alarming increase of obesity. Enlarging girth is often accompanied by the ominous signs of cardiometabolic syndrome, emphasizing the critical need for early and aggressive control of blood sugar. Nevertheless, ingrained societal patterns – including nutritional debasement in daily food selections – complicate efforts to achieve the lifestyle changes essential for nondrug hyperglycemic control. Drugs, of course, impose the risk of side effects and even hypoglycemic episodes, so many physicians are comfortable allowing patients to float with higher-than-normal fasting and postprandial patterns … and thus tolerating the commensurate development of occlusive changes affecting end organs.

Chronic renal dialysis is one of the most expensive repetitive procedures in modern medicine, and diabetics claim an inordinate volume of these resources. The NIH TACT trial excluded renal failure patterns in order to simplify data analysis. A seminal 2003 study by Lin and Lin-Tan, published in the New England Journal of Medicine, matched patients developing nondiabetic renal failure and carefully treated the intervention group with intravenous EDTA chelation. While the untreated observation group devolved toward dialysis, the treated patients improved toward normal kidney function, presumably due to reduction of lead in the kidneys. Many experienced chelation physicians have seen serum creatinine levels reduce over time in both their diabetic and nondiabetic patients, but a conclusive study remains to be done – and is sorely needed and could be done easily with pooled data.

Beyond Diabetes
Reports of chelation improvements in diabetics have been peppered throughout the medical literature over the past 50 years. In 1964, Carlos P. Lamar, MD, offered his diabetic patients a real chance at a more normal life, saving limbs scheduled for amputation, saving vision in those going blind, and lowering insulin dosages. Kansas City, Missouri, chelation specialists Ed W. McDonagh, DO, and Charles J. Rudolph, DO, PhD, were joined by research professional Emanuel Cheraskin, MD, DMD, to publish 31papers documenting their clinical practice experience over the 1980s and 1990s. Topics included significant improvements of vital importance to diabetics and nondiabetics alike: blood sugar, cholesterol, HDL cholesterol, triglycerides, kidney function and serum creatinine levels, artery blockage disease (even of the aorta), severe heart artery blockage, blockage of neck carotid arteries, hardening of the arteries, platelet clotting functions, fatigue, pulse rate and blood pressure, serum calcium and iron levels, trace element patterns in degenerative diseases, psychological status, and general "clinical change" (improvements) observed in chelation patients. Perhaps of more interest to many readersis the demonstrated reversal of macular degeneration (commonly seen in diabetics) reported by McDonagh and Rudolph's group in 1994. Their evidence included retina photographs, documenting improvement consistent with increased circulation to the eyes. Pooled objective data from practicing ophthalmologists could easily document a pattern of improvement, offering hope where there is no other treatment.

Coronary Occlusive Disease
The "end organ" of most concern for diabetics and nondiabetics alike is the cardiac muscle. Heart disease "statistics" 60 years ago were generally reported as reduction in symptoms, in angina and infarction, and improvement in EKG patterns. For the past 20 years, we've had benefit of the ultrafast CT "heart scan," helping outline the anatomy of calcified plaque in coronary vessels and allowing for earlier identification of those at risk. For over 50 years, selective coronary angiography has provided "a map for surgery" – but its extensive use in postoperative bypass patients has created an industry ripe for challenge as generally unnecessary and sometimes fallible. For almost 50 years, coronary artery bypass grafting (CABG) has been shown to provide a life-saving alternative for those with significant diffuse disease or "left main" or "left anterior descending" artery occlusion. The 50-year-old technologies of coronary "ballooning" and "stenting" – now impregnated for drug elution – remain popular despite the frequency of restenosis or other complications. The question of whether ultrafast CT is suitable for documenting improvements with chelation remains elusive, since some symptomatically successful patients continue to show advancing calcium scores. Collateral channels are not readily seen in these pictures or even in angiograms, so perfusion studies with stress-and-rest thallium scans can be more revealing.

Salvage of cardiac muscle is the sine qua non of all interventions. Indeed, kinase infusions within the early hours of acute infarction have preserved countless organs with minimal or no damage. Various drugs have found popularity in the conventional cardiology community as possibly reducing or delaying development of coronary occlusions. These include, of course, the "statin" drugs and antithrombotics such as clopidogrel. A number of concerns have been raised regarding their extensive side effects, including interruption of physiologic biochemistry (such as with statins, impaired synthesis of vitamin D, bile acids, coenzyme Q10, and so on). Chelation avoids these challenges to normal functions. Further, chelation has greatest success when occlusion has not progressed to tight stenosis or to the point where unstable plaque threatens to block distal flow. Coronary angiography is still risky, especially with regard to vulnerable plaque. Additionally, it is limited in not being able to discern plaque reduction that yields very slight increases in cross-sectional vessel caliber, a situation wherein fluid dynamics produces a much greater increase in flow volumes. Once again, clinical improvement is one of the best measures of success.

So the question remains: besides lifestyle changes to minimize risks, what actual treatments could enhance myocardial salvage? The almost 60-year history of consistent reports suggests that EDTA chelation has already established itself as an unrecognized but viable alternative, with patient satisfaction and clinical improvements routinely in the 90% range in published studies.

EDTA Chelation and Cardiac Disease
Beginning with Clarke's initial reports in 1955, anecdotal papers have repeatedly documented that "heart patients" improve with a wide variety of symptoms. Angina episodes, dyspnea on exertion, blood pressure elevations, rhythm disturbances, electrocardiogram patterns – all these were shown to improve in reports over the first 10 years. Other small group reports over the past 50 years have continued to confirm these early findings. The usual critique is that they involve a small number of patients or that double-blinding is absent. These criticisms, of course, ignore that proposed CABG surgery was canceled in the majority as no longer needed, and that people are still walking on limbs scheduled for amputation.

The importance of a nonsurgical alternative for coronary disease is highlighted by a recent report on war fighter deaths over 10 years in the Middle East. Autopsies on 3832 service members, killed at an average age of 26, showed that almost 9% had some blockage forming in their heart arteries. About a quarter of these had severe blockage, yet they were asymptomatic and deployed into combat. As more sensitive diagnostic modalities are developed and widely employed, an increasing percentage of the population will "qualify" for treatment of their clinically silent diseases. In such cases, early and consistent use of chelation might dramatically lower medical care costs while improving overall health outcomes.

Anatomy vs. Microphysiology
Perhaps of greatest interest is the effort to understand why – or how – EDTA chelation is responsible for such dramatic cardiac (and other) benefits. Borrowing from the engineering concept of "opening the pipes," such as with bypass or stenting, early explanations focused on a "Roto-Rooter" effect of "dissolving" the atherosclerotic blockage. While this effect has been observed and documented in some chelation patients over the years, such a view is probably severely limited.

Much more likely is that chelation acts in just exactly the way that it is "approved" by the Food and Drug Administration: it reduces the body burden of toxic heavy metals such as lead, arsenic, cadmium, mercury, and so on. Sadly, the conventional medical community sets the standards and those lab parameters are for acute intoxication (as reflected in blood levels) rather than for total body burden (as reflected in hair or nail clippings or by collecting urine after challenging with a chelating drug). Since the "acute exposure" tests fail to "show toxicity," insurance carriers decline claims for reimbursement.

The significance of reducing toxic metals cannot be overstated. But the mechanisms by which this result could produce dramatic improvements remain open to rampant speculation.

An early explanation suggested that, in states of impaired antioxidant levels, cholesterol serves as an electron sponge to help protect the endothelium. Oxidized cholesterol, being a "sticky" molecule, then deposits along the vessel margin, especially at sites of branching or disrupted flow. Having a weak activity similar to that of vitamin D, oxidized cholesterol invites calcium to be deposited in a noncovalent binding. Over time, accretion of more cholesterol, calcium, and cellular detritus results in a discrete volume of occlusive plaque, subintimal and medial. Pathologist Rudolph Virchow, MD, called this metastatic calcium, since it was out of the bones and teeth but not bonded in place. Accordingly, EDTA was thought to "pinch" these available calcium atoms and thereby initiate dismantling and dissolution of the plaque. A more sophisticated view might relate to lowering of ionized calcium in circulation, stimulating release of parathyroid hormone, leading indirectly to mobilization of "releasable" calcium in hardened plaque and body tissues.

One fascinating result of such speculation is the inclusion of calcium as a toxic element when it is abnormally deposited in organs through a variety of aging and degeneration mechanisms. While babies are "soft and rubbery," aging individuals are increasingly hardened and brittle. This one feature – reduction of metastatic calcium depositions, peppered throughout organelles and cells and interstitium as well as in plaque – might be "the key" to results with intravenous EDTA chelation. This speculation receives support from the realization that "sick mitochondria" accumulate excessive calcium and swell (especially in magnesium deficiency), disrupting the stereochemical alignment of the electron transport chain on the cristae shelves, markedly reducing the efficiency of oxidative phosphorylation and, hence, the health of the cell. One way that mitochondria "get sick" is through the selective deposition of lead and other heavy metals, disrupting mitochondrial DNA expression as well as energy production. Reversal of these mitochondrial modifications could explain many (if not most) of the clinical improvements demonstrated with EDTA treatments.

Chelation patients often report significant symptom improvement within the first half-dozen or dozen treatments, long before a major improvement in blood flow "through the pipes" is likely. When reviewing organ failings – as seen with liver, kidneys, and brain in addition to heart – such mitochondrial inefficiency might be a primary mechanism. Similarly, removal of toxic heavy metals by chelation is much more biologically cost effective than the body's detoxification effort that leads to depletion of intracellular glutathione. Thus, chelation can help to preserve cellular antioxidant status and a more robust ability to regenerate vitamins C and E as electron donors.

Recall also that all other toxic metals are accumulating throughout the tissues as well – mercury, lead, cadmium, arsenic, and so on – with their separate contributions to free radical production and functional impairment. Iron is an essential element that can be present in excess (iron "storage" disorders, even polycythemia), where it also stimulates the generation of free radicals, which are especially toxic in metabolically active tissues such as liver and heart. Jukka T. Salonen, MD, PhD, MScPH, of Finland, reported in 1992 a large prospective study of men with no symptoms of heart disease. Over the next 3 years, the lifetime total of cigarettes smoked was the primary risk factor in those suffering myocardial infarction. The second factor was an elevated blood ferritin level (possibly correlated with a shift toward tissue acidosis). This provides an easy laboratory test to discover those at higher risk – levels rising higher above 100 ng/ml are directly associated with an increasing incidence of coronary events. The iron story is, however, complicated, and ferritin only slowly declines over dozens of EDTA chelation treatments.

A side issue is coming to the forefront: the expanding use of injectable diagnostic imaging contrast agents, such as gadolinium, iron (Feridex), and manganese (Teslascan). Urinary challenge tests with D-penicillamine in some patients have shown very high excretion levels of gadolinium. The clinical significance of these findings is unclear, but the use of chelation treatments in patients who have had repeated contrast studies might prove valuable. Gadolinium use has been linked to onset of nephrogenic systemic fibrosis.

Another factor deserving study is the effect that chelation might have on the improvement of tissue perfusion by reducing constriction of the tiniest arterioles, which serve as a large bed of peripheral resistance vessels. Where increased arteriolar resistance opposes the systolic pressure, relaxation of these "flow-limiter" muscles can raise tissue perfusion volume considerably. Increasingly sensitive vascular lab studies and digital thermography are two inexpensive and noninvasive methods that can be used to document improved perfusion.

McDonagh and Rudolph, among others, have shown that chelation produces a more normal reduced platelet volume and increased pliability. Ease of flow through capillary beds provides increased perfusion and oxygenation help to maintain normal tissue alkalinization. Reduction of acidotic microenvironments slows the production of free-floating single fibrin fibrils from fibrinogen, further lowering viscosity in the narrow capillaries. Any combination of these microphysiologic changes could explain improved tissue viability and marked improvement in clinical symptoms and organ function.

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