EDTA May Help Remove Calcium
Is There Too Much
Calcium in Your Arteries?
Excessive calcium can be a risk factor
for heart attack, even with cholesterol under control
By Dr. Edward R. Rosick
f you asked most people what disease is the number one killer in America today, the answer would probably be cancer. However, although cancer does strike one in three Americans, it’s not the top lethal disease—that dubious distinction belongs to cardiovascular disease. According to the American Heart Association, over 60 million Americans suffer from some form of this multifaceted disease, and a significant percentage of them—about 13 million—have coronary artery disease (CAD), the leading cause of death in America. It is estimated that over 600,000 Americans will die from CAD this year. The financial impact of cardiovascular disease on health care is also staggering, with expenditures running over $200 billion annually.
Pharmaceutical companies have poured hundreds of millions of dollars into their endless search for medications to decrease cholesterol levels. High levels of LDL-cholesterol (the “bad cholesterol”) put us at high risk for heart disease—most probably in the form of CAD. That is because high LDL levels can lead to atherosclerosis—the buildup of cholesterol-containing plaque inside our blood vessels. This restricts blood flow, increases blood pressure, and damages the vessels themselves. Ultimately, it can lead to all kinds of damage throughout the body, including the heart and brain.
Statins Are Excellent Drugs, but …
Many doctors (and their patients) believe they have found the medication for high LDL levels, in the form of prescription drugs called statins, which are now among the world’s top-selling pharmaceuticals. A number of recent studies have shown convincingly that statins can dramatically reduce LDL levels, and with them, the risk for cardiac “events,” such as angina pectoris, heart attack, and surgical revascularization (e.g., coronary artery bypass grafting). The evidence for the extraordinary efficacy of statins in this regard is overwhelming—and they are generally quite safe.*
… Heart Disease Is Not All About Cholesterol
Despite their efficacy and safety, statins have an Achilles heel: they are very expensive. This provides a strong incentive for many people to seek nutritional supplements that can help reduce their risk for heart disease. There are different avenues for pursuing this goal. Although there is no doubt that high LDL-cholesterol levels (along with low levels of HDL-cholesterol, the “good cholesterol”) are a major factor in the genesis and progression of CAD, cholesterol is not the only factor. CAD is a multistage process that takes years to develop and manifest, and other factors, such as inflammation and oxidative stress, are important as well.
Statins, whose primary function is to inhibit cholesterol biosynthesis in the liver, do not work equally well (and, in some cases, perhaps not at all) in everyone. It has been shown in both primary and secondary prevention trials that users of statins enjoy a 30 to 33% reduction in risk of heart attack and death—a favorable statistic, but by no means the ultimate solution to the problem.
Coronary Artery Calcification May Be an Independent Risk Factor
One reason why statins are not universally effective may be calcium, an important component of arterial plaque (which has a complex composition—it’s not just cholesterol). A new study by researchers at the Tulane University School of Medicine in New Orleans has shown that calcium deposits in the plaques in our coronary arteries—called coronary artery calcification, or CAC—may be an independent risk factor for CAD, even in those of us who have our cholesterol levels under control.
EBCT images of two human hearts: a normal heart and a heart with advanced coronary artery disease (CAD), showing coronary artery calcification (CAC).
The study was conducted with 495 initially asymptomatic male and female patients (aged 49–65) who were free of CAD but who had known risk factors for it, such as hypertension and high cholesterol. All the patients had significant CAC at the outset. The researchers followed the progression of their CAC using a noninvasive imaging technique called electron beam computed tomography (EBCT), which can measure the volume of the calcium deposits in the plaques. EBCT scans were done at the initial visit, after which all the patients were started on cholesterol-lowering statin therapy. The average interval between scans was 1.9 years, with a range of 1 to 6 years. The interval from the time of the first scan to the time of the follow-up contact averaged 3.2 years.
Calcification Can Increase Even If Cholesterol Does Not
The amount of calcification in the patients’ coronary arteries was expressed as a calcium volume score (CVS). The CVS values of most patients increased substantially during the course of the study, even if their LDL levels did not increase—meaning that CAC was progressing even if cholesterol levels were under control. There was, however, a distinct correlation between the two measures: CVS values increased about twice as rapidly in patients whose LDL levels were 100 mg/dL or greater than in those whose LDL levels were below that figure.
This suggests that cholesterol levels alone may not be very reliable as an indicator of arterial health, and that CAC might provide a useful, independent measure for assessing cardiovascular risk. The validity of this idea is underscored by other results of the same study. During the course of the study, 41 patients experienced fatal or nonfatal myocardial infarction (MI), or heart attack. Analysis of the data subsequently showed that the CVS scores for these patients were much higher, on average, than for those who did not have an MI. Furthermore, whereas there was a net regression in CAC in 20% of the patients who were event-free (no MI), this was not true in any of the MI victims.
Calcification Correlates Strongly with Heart Attacks
For technical reasons, the authors chose to define an increase in CVS of 15% per year or greater as significant; conversely, an increase of less than 15% per year was deemed not to be significant. Based on this criterion, it turned out that, for all patients who were event-free during the course of the study, those who did have a significant yearly increase in CAC (as measured by CVS) had a survival rate of only 66%, whereas those whose CAC did not increase significantly had a survival rate of 97%. And the remarkable bottom line was that the risk for having an MI was 17 times greater (i.e., 1600% greater) in those patients who did have a significant increase in CAC than in those who did not.
EDTA Chelation Therapy Is a Popular Alternative
With the role of CAC as a risk factor for MI looming ever larger, it seems all the more desirable to try to control it by any reasonable means. One method that has a large following in the alternative medical community is chelation therapy with EDTA (ethylenediaminetetraacetic acid), a synthetic amino acid that is considered to be extremely safe. Its use is approved by the FDA for removing toxic heavy-metal ions from the blood.* (For an explanation of how chelation works, see the
sidebar on page 24 of this issue, in the article on turmeric.)
EDTA is also used by approximately 100,000 people annually for the unapproved treatment of CAD. The therapy is most commonly performed via intravenous infusion, but EDTA can be taken orally as well. Proponents of the therapy state that it helps dissolve plaques by removing the calcium ions. Although there have been numerous case studies extolling the efficacy and safety of EDTA chelation therapy for CAD, there have as yet been no convincing scientific studies that demonstrate this. To that end, the National Institutes of Health initiated a major placebo-controlled, double-blind study in 2003, being conducted at over 100 research sites across the country; it should be complete in 2008. It is hoped that this comprehensive study will resolve many of the long-standing questions regarding the therapeutic value of chelation therapy.
EDTA, Tetracycline, etc.—A Curious Therapy
A new study has reported a beneficial effect, on coronary artery calcification (CAC), of a combination therapy consisting of EDTA and tetracycline, along with a wide array of supplemental nutrients. The rationale for this unusual mix was the authors’ belief that something they call “unconventional apatite-forming bacteria-like nano-organisms” (“nanobacteria” for short) may be involved in the development of CAC and, therefore, of CAD (coronary artery disease).* Some evidence in support of this theory has been published recently.
The authors, who are affiliated with a private company in Florida, used a proprietary therapy they call “comET,” which consists of: (1) a 15-ingredient nutraceutical powder; (2) EDTA (1500 mg taken rectally once daily); and (3) tetracycline hydrochloride (500 mg taken orally once daily). Oddly, one of the 15 ingredients in the nutraceutical powder is EDTA (in an unspecified amount); the other 14 are an assortment of vitamins, minerals, antioxidants, amino acids, enzymes, and herbal extracts (also in unspecified amounts). According to the authors, this formulation was designed to be “nanobacteriocidal,” i.e., lethal to the nanobacteria, which they believe act as triggers for the calcification process.
In this non-placebo-controlled study, 77 patients (aged 42–81) with stable CAD and positive CAC scores were given the comET therapy over a 4-month period. According to the authors, 44 patients (57%) were “responders” in terms of having significant decreases in CAC scores, with an average reduction of 14%. The patients’ angina pectoris and lipid profiles improved as well. Although the presence of nanobacteria was detected serologically in all 77 patients at the outset of the study, no evidence of the postulated nanobacteriocidal effect was observed.
What are we to make of this unconventional study, which claims to be the first to demonstrate a significant decrease in CAC scores with any therapeutic regimen? It’s hard to say. Considering the study’s obvious weaknesses, healthy skepticism is in order … but who knows? Let’s keep an open mind and hope to see confirmation of these results in a more convincing fashion.
- Maniscalco BS, Taylor KA. Calcification in coronary artery disease can be reversed by EDTA-tetracycline long-term chemotherapy. Pathophysiology 2004 Oct;11(2):95-101.
- Miller VM, Rodgers G, Charlesworth JA, et al. Evidence of nanobacterial-like structures in calcified human arteries and cardiac valves. Am J Physiol Circ Physiol 2004;287:H1115-24.
- Ciftcioglu N, Miller-Hjelle MA, Hjelle JT, Kajander EO. Inhibition of nanobacteria by antimicrobial drugs as measured by a modified microdilution method. Antimicrob Agents Chemother 2002;46(7):2077-86.
Bigger Guns Are Better
Meanwhile, it might pay to try oral EDTA for yourself, as it holds the potential for gain with virtually no risk. Your arteries are the vessels of your lifeblood, literally, and it’s wise to treat them with the utmost respect and care. EDTA is not a “magic bullet” for the health of your arteries, but it might improve their caliber, so to speak, by helping to remove some of the unwanted plaque that narrows their bore.
- Blumenthal RS. Statins: effective antiatherosclerotic therapy. Am Heart J 2000;139(4):577-83.
- Raggi P, Callister TQ, Shaw LJ. Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy. Arterioscler Thromb Vasc Biol 2004;24:1272-7.
- NIH launches large clinical trial on EDTA chelation therapy for coronary artery disease. Press release, Aug. 7, 2002. http:/nccam.nih.gov/news/2002/chelation/pressrelease.htm.
- Questions & answers: the NIH trial of EDTA chelation therapy for coronary artery disease. Press release, Oct. 9, 2003. http://nccam.nih.gov/news/2002/chelation/q-and-a.htm.
Dr. Rosick is an attending physician and clinical assistant professor of medicine at Pennsylvania State University, where he specializes in preventive and alternative medicine. He also holds a master’s degree in healthcare administration.