Chelation Therapy for Cardiovascular Disease:
A Dozen Issues Worth Considering
by L. Terry Chappell, MD
Introduction
Intravenous EDTA chelation therapy is a treatment for cardiovascular disease that is frequently embraced by doctors who offer their patients alternative medicine and is rejected and ridiculed by many physicians who limit themselves to conventional, “evidence-based” medicine. This article examines key issues in the controversy and presents guidance to those who are concerned with effective prevention and treatment of cardiovascular disease.
1.
The conventional approach to prevention and treatment of cardiovascular disease that emphasizes drugs and surgery is slowly getting better but is still only minimally effective.
Coronary artery disease is far and away the leading cause of death. Strokes are third. From 1996 to 2006, we saw a 12.9 % drop in cardiovascular deaths. There were still 831,272 people who died of cardiovascular disease during 2006, which is 1 out of every 2.9 total deaths that year. All the bypasses, stents, beta blockers, ACE inhibitors, platelet inhibitors, and statins together had minimal impact on death rates from cardiovascular diseases.1
2.
Lifestyle factors are more powerful than drugs for treating and preventing cardiovascular disease.
Estimates are that 57% to 62% of improvements in cardiovascular death rates are due to lifestyle changes, including smoking cessation, improved diet, and regular exercise. Persistent obesity, inadequate stress coping skills, and environmental toxins have lessened the impact of lifestyle factors. Only 5% to 30% of the improvement in vascular death rates are attributed to prescription medications. One reason why medications have been a disappointment is our reliance on double-blind studies for evidence. It is not uncommon to have to treat 100 patients with a specific drug for years in order to prevent 1 cardiac event in 1 patient. In a large trial, such results can still be statistically significant. An individualized assessment of lifestyle factors is much more likely to benefit a patient than a drug that helps a few more people than a placebo does2.
3.
The vulnerable plaque is the cause of most heart attacks and strokes.
Eighty percent of heart attacks and strokes begin with a “vulnerable plaque,” which is an unstable plaque, usually blocking less than 50% of an arterial lumen, that leaks some fatty material.3 The body responds with a sudden clot at the site or one that dislodges and moves downstream to block the artery. The resulting lack of blood flow, if not abated promptly, causes ischemia and tissue death (e.g., myocardial infarction). Most bypasses and angioplasties are performed on areas of well-established, slow-forming plaque that is not vulnerable. Thus they do not address the cause of the vast majority of coronary events and strokes. Interestingly, a small study showed that chelation therapy might improve brachial artery stiffness, which correlates at least to some degree with a vulnerable arterial plaque.4
4.
Clopidogrel (Plavix) is the most powerful oral platelet inhibitor available to treat and prevent clotting in patients with cardiovascular disease, but it also has dangerous side effects.
Clopidogrel is a standard treatment for those who have had or threaten to have bypasses, stents, strokes, and myocardial infarctions. The drug does prevent a small number of blood clots that can lead to infarctions. However, clopidogrel also has the unsettling side effect of hemorrhage in almost as many patients who are protected from clotting.5 Informed consents ask patients to choose between the risk of heart attack or stroke and a somewhat lesser risk of brain hemorrhage. A safer regimen might include fish oils, nattokinase, EDTA, and/or low-dose aspirin, all of which inhibit platelet aggregation with a lesser risk of hemorrhage. To date, comparative studies for safety and efficacy have not been done.
5.The open artery study (OAT) showed that angioplasty with stents did no better in preventing future cardiac events after a heart attack than medical therapy).6
Most cardiac surgeons continue to perform surgery after heart attacks, contrary to the evidence. Except in special circumstances, such as prominent triple vessel disease and major blockage in the main vessel to the left ventricle, scientific evidence does not support the use of surgery. Medical therapy and lifestyle changes are the best treatments that conventional medicine has to offer. A vulnerable plaque is the most likely source for future problems. We need to study and embrace therapies that stabilize such plaque. Chelation therapy might have exactly that mechanism of action.
6.
The best scientific evidence we have today supports the use of EDTA chelation therapy, but does not yet provide large, controlled clinical trials with statistical significance.
Many studies have been published showing improvement with EDTA treatment in patients with cardiovascular diseases.7 A few studies performed by opponents of the therapy came to negative conclusions even though at least some of their data showed positive results. None of the clinical trials had nearly enough power for statistical significance. All but one had surrogate end points, such as test results, decreased use of medication, and walking distance. One cardiac events study, published by the author, had myocardial infarction, the need for cardiac surgery, and death as solid primary end points.8 Patients treated with EDTA and conventional therapies were compared with similar groups from the literature that did not receive chelation. There were fewer heart attacks, bypasses, and angioplasties and no deaths in the 220 patients who received chelation. The Trial to Assess Chelation Therapy (TACT) is a large, double-blind prospective trial that also has cardiac events as primary end points. Enrollment with 1708 patients was completed in June 2010. The results of TACT are expected in 2 to 3 years.
7.
Lead is a significant risk factor for cardiovascular and other chronic degenerative diseases.
EDTA removes lead from the body.
Many studies in prominent medical journals have documented that only slight elevations of lead increase the risk not only of cardiovascular disease but also other chronic degenerative diseases, such as cancer.9 The amount of lead in the body is directly proportional to the amount of elevation of blood pressure.10 EDTA was approved by the FDA to remove lead from the body. One would assume that removing lead by administering EDTA would decrease the incidence of degenerative disease, including cardiovascular disease. Logically, the NIH (National Institutes of Health) would fund such studies as a priority. The studies would be simple to perform and relatively inexpensive, but no proposals have been submitted and funded.
8.
Blood tests for the body burden for lead are inaccurate.
Once absorbed through the digestive system, lead stays in the blood for only a few days. Thus a blood test for lead is fine to assess recent exposure, such as workplace contamination in adults and regular ingestion of chips of lead-based paint by young children. But episodic or periodic exposure from the food supply or other environmental sources are often not detected because the lead is stored in fat cells, bone, and brain tissue. To assess and monitor the body burden of lead, we must use a challenge test. The most commonly used one utilizes intravenous EDTA, with subsequent urine collection. Other chelators, such as DMPS and DMSA, are sometimes added to improve the sensitivity of the test.
9.
Oral EDTA effectively prevents absorption of lead, but there is no evidence to support its use in the treatment of vascular disease.
There are many studies from the 1960s that show that those who work with lead can reduce their absorption by taking oral EDTA. Only 5% of EDTA is absorbed. Thus the remaining 95% attaches itself to lead in the GI tract and carries it out of the body before it can be absorbed. The use of oral EDTA to prevent the absorption of lead makes some sense, but the effect is not enough to treat established cardiovascular disease. Another problem with oral EDTA is that it is calcium salt and thus does not cause a temporary dip in the serum calcium, as does disodium EDTA, which is most commonly given for intravenous therapy. Temporary calcium reduction is the proposed mechanism for improved platelet aggregation.11 Most importantly, there are no published studies indicating that oral EDTA might reverse vascular disease.
10.
Intravenous EDTA chelation therapy is a safe treatment when given according to protocol, and it has been shown to improve kidney function in patients with mild kidney failure.
Many studies have shown that, when given according to the published protocol, intravenous EDTA chelation therapy is extremely safe. Side effects are rare. Kidney strain is the most common side effect cited, but an adjustment in dosage rapidly corrects early signs of kidney strain. Studies published in major journals show that patients with compromised kidney function actually improve with EDTA treatment, presumably because circulation to the kidney improved.12 We do not yet know the results of TACT, but the monitoring committee has given multiple reports that no safety concerns have been detected.
11.
Patients who receive chelation therapy often feel better and have a better quality of life.
Of the many studies that have been reported in the literature, few have targeted quality of life as a primary end point. But the ones that have administered questionnaires to determine whether changes in quality of life have occurred usually show significant improvement. People with cardiovascular disease who undergo chelation therapy usually feel much better and are able to decrease symptom-controlling medications substantially.
12.
Chelation therapy is less expensive than drugs and surgery for the treatment of cardiovascular disease.
No published studies compare the actual expenditures of the therapies discussed. However, cardiac surgeries can easily run $60,000 to $100,000, and medications routinely prescribed can total $500 to $1000 per month. Cardiac surgeries are much more common in the US than anywhere else in the world, and yet our cardiovascular death rate is no lower than that of other countries. Our total costs for cardiac care are much higher than in other countries. Obviously, we are not providing cost-effective care. The cost of intravenous chelation ranges from $3000 to $4000 for a basic, office-based course of 30 treatments. Often one treatment a month is then suggested for maintenance. Nutritional supplements are additional, but their cost is much less than for patented cardiovascular drugs.
Conclusion
Looking at all these issues together, it is clear that treatment for cardiovascular disease is less effective than it should be. The cost of current treatments is rising fast and becoming prohibitive. Lifestyle changes should be at the top of our list for both primary and secondary prevention. We recognize that the vulnerable plaque is the main culprit for vascular events, but we do little to treat it effectively. We routinely use clopidogrel, despite its side effects and cost. We are aware of the environmental dangers of lead but choose to ignore lead and other heavy metals once they enter the body. EDTA chelation therapy has been shown to be safe, and patients usually feel significantly better after treatment. The evidence for effectiveness is not yet conclusive with the double-blind statistical standard. But TACT is in progress, and many lesser studies have indicated the effectiveness of intravenous chelation therapy.
By putting into practice evidence-based medicine, we would substantially reduce the number of cardiac surgeries. Most patients do just as well with medications and lifestyle changes. Unfortunately, our disease-care system is economically entrenched by the need to continue the revenue stream of surgery. Only the threat of financial collapse of the system is likely to withstand the power of concentrated economic interests.
Is there enough evidence to include chelation therapy under Medicare and other agencies that approve payment for services? Not yet. If TACT shows definite benefit, will chelation therapy immediately become an approved therapy? Hopefully so, but not for certain. Those who publish guidelines might well demand another lengthy study to confirm the results, knowing that a second $30 million grant is unlikely to come from NIH or anywhere else.
All patients should be given the evidence for both benefits and risks of taking conventional, well-accepted therapies. They should be told how many patients must be treated to prevent one cardiac event. They have the right to choose not to utilize any of these therapies, because of weak evidence that it will help their individual case, because of potential side effects, or because of cost. Alternative treatments should be presented in exactly the same way. When we carefully examine the issues discussed in this article, it appears that all patients deserve to be informed about chelation therapy as an option. We will have additional information when TACT is completed, but patients at risk now should not have to wait for that to happen. The results from currently approved treatments are simply not acceptable. Patients at risk might suffer a catastrophic heart attack or stroke that could have been prevented with chelation therapy.
Notes
1. American Heart Association. Cardiovascular disease statistics [online document]. http://www.americanheart.org/presenter.jhtml?identifier=4478. Accessed February 13, 2011.
2. Chiuve SE, McCullough ML, Sacks FM, et al. Healthy lifestyle factors in the primary prevention of coronary heart disease among men: benefits among users and nonusers of lipid-lowering and antihypertensive medications. Circulation. 2006;114:160–167.
3. Heistad DD. Unstable coronary artery plaques. N Engl J Med. 2003;349:2285–2287.
4. Chappell LT, Angus RC, Stahl JP, Evans RE. Brachial artery stiffness testing as an outcome measurement for EDTA treated patients with vascular disease. Clinical Prac Alt Med 2000;1:225–29.
5. Chappell LT. Should EDTA chelation therapy be used instead of long-term clopidogrel plus aspirin to treat patients at risk from drug-eluting stents? Altern Med Rev. 2007;12:152–158.
6. Hochman JS, Lamas GA, Buller CE, et al. Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med. 2006;355:2395–2407.
7. Cranton EM, ed. A Textbook on EDTA Chelation Therapy. 2nd ed. Charlottesville, VA: Hampton Roads: 2001.
8. Chappell LT, Shukla R, Yang J, Blaha R, et.al. Subsequent cardiac and stroke events in patients with known vascular disease treated with EDTA chelation therapy. Evid Based Integrative Med. 2005;2:27–35.
9. Menke A, Muntner P, Batuman V, et al. Blood lead below 0.48 micromol/L (10 microg/dL) and mortality among US adults. Circulation. 2006;114:1388–1394.
10. Nash D, Magder L, Lustberg M, et al. Blood lead, blood pressure and hypertension in perimenopausal and post menopausal women. JAMA. 2003;289:1523–1532.
11. Zucker MB, Grant RA. Nonreversible loss of platelet aggregability induced by calcium deprivation. Blood. 1978;52:505–513.
12. Lin JL, Lin-Tan DT, Hsu KH, et al. Environmental lead exposure and progression of renal diseases in patients without diabetes. N Engl J Med. 2003;348:277–286.
L. Terry Chappell, MD, is a board-certified family physician in private practice in Bluffton, Ohio. He is past president of ACAM (American College for Advancement in Medicine)and ICIM (International College of Integrative Medicine) and serves as adviser to the American Board of Clinical Metal Toxicology. He is a clinical investigator for TACT (Trial to Assess Chelation Therapy).
Corresponding address is P.O. Box 248, Bluffton, OH 45817; e-mail: chappell@wcoil.com. He reports no financial conflicts of interest.
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