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Chelation with EDTA and the Hidden Causes of Heart Disease

Chelation with EDTA and the Hidden Causes of Heart Disease

By Ward Dean, MD

Previously, we have discussed the benefits of oral chelation therapy in heart health by virtue of its ability to remove heavy metals from the body. Recently, however, much research has addressed the role inflammation and infections have to play in heart disease as well as another little known factor known as vulnerable plaque. Therefore, I would like to first recap oral chelation’s benefits, discuss the “hidden” factors that cause heart disease and then touch upon the importance of using chelation while simultaneously reducing inflammation linked to cardiovascular concerns.

Chelation therapy typically uses the synthetic amino acid, ethylene diamine tetraacetic acid (EDTA). It is thought to help support cardiovascular health by means of its removal of heavy metals.

The Food and Drug Administration has approved EDTA as a pharmaceutical agent for the treatment of lead and other heavy metal poisoning or exposure. In older literature, the FDA also approved EDTA as being “possibly effective in occlusive vascular disorders…arrhythmias and atrioventricular induction defects…and in the treatment of pathologic conditions to which calcium tissue deposits or hypercalcemia may contribute other than those listed above.”1

These “possibly effective” indications were removed from FDA-approved literature in the late 1970s for unknown reasons. Today, the FDA has approved EDTA as a food additive that is generally recognized as safe (GRAS). However, many people opt to use EDTA chelation—both intravenously and orally—as an alternative, or in addition, to more traditional/widely accepted approaches such as angioplasty or bypass surgery.

Beneficial Uses of Oral EDTA in Cardiovascular Disease

In addition to the controversial but widespread recognition of EDTA’s intravenous benefits are its less well-known clinical uses when administered orally. Early clinical studies with EDTA reported loss of fat in rats, reduction of cholesterol in rabbits, and reduced blood pressure in humans. Consequently, a study of the effects of oral EDTA on patients with atherosclerosis and/or hypertension was conducted on 10 patients. Four of these patients had hypertension, four had angina pectoris, one had peripheral vascular disease (intermittent claudication), and one was recovering from a heart attack. All were treated with one gram of oral EDTA daily for three months. Seven of the ten patients experienced significant reductions in their cholesterol levels, and blood pressure was reduced in all ten. The most marked change occurred in the patient with intermittent claudication, whose cholesterol dropped from 278 mg per 100 ml to 128! This patient also reported improved exercise tolerance, and the researchers found improved pulsations in the extremities. The four patients with angina pectoris also all reported improvement.2

In another series of 20 patients who suffered from hypercholesterolemia, hypertension, angina or peripheral vascular disease, one gram of EDTA was administered orally every day for 3 months. During that short time, elevated cholesterol levels in nine of the patients dropped to within the normal range. No adverse results were experienced by any of the patients. Angina attacks were reduced in frequency and severity in five individuals. One person who previously had suffered a heart attack and experienced several angina attacks daily thereafter, obtained complete relief.3

Cholesterol mg. percentIn another study, two patients with extremely elevated cholesterol were treated with oral EDTA. One patient took EDTA in progressively large doses ranging from 500 mg to 4 grams daily for one year, and the other took 1,000 mg daily for three years (Fig. 1.). Although the first patient suffered a heart attack after three years of therapy, she recovered uneventfully, and had reduced angina pains and improved sense of well-being with continued use of EDTA. The second patient—in addition to hypercholesterolemia—had a condition known as xanthomatosis (yellowish papules in the skin, related to elevated blood lipids). She not only experienced dramatic reductions in her cholesterol levels with oral EDTA treatment, but her skin lesions completely resolved.4 Other laboratory studies (including kidney and liver function) remained normal throughout the study for both patients. This is further confirmation of the safety of oral EDTA, considering that doses as high as 4 grams daily were consumed.

Further support of the anti-atherosclerotic effects of oral EDTA are provided by Italian researchers who found that two grams of oral EDTA daily were effective in reducing blood cholesterol.5 Scientists at Wayne State University quantified reversal in atherosclerotic plaque in rabbits that were treated with daily subcutaneous EDTA injections.6

Heart Disease and Inflammation

Dr. Garry Gordon, one of chelation therapy’s Founding Fathers, recently has developed an appreciation for the volume of research indicating that inflammation plays an important role in heart disease. In addition, he points to the evidence that chronic infections are strongly linked to heart disease. Consequently, he recommends a multi-pronged approach that includes both oral EDTA chelation and other substances to reduce inflammation.

I agree wholeheartedly that inflammation is a factor—perhaps even the primary factor—behind heart disease. Even the American Heart Association recommends that patients at intermediate or high risk of coronary heart disease may benefit from measurement of the inflammatory marker CRP to help determine their individual risk prediction.7

The link between the inflammatory marker C-Reactive Protein and cardiovascular disease has been firmly established in the medical literature in a variety of studies. In one study, researchers followed thousands of subjects and determined that CRP showed a significant association with coronary heart disease risk in men. Another inflammatory marker, TNFalpha, also predicted coronary heart disease as well as total mortality among men.8

The researchers concluded, “These findings provide further support to the important role of inflammation in the pathogenesis of cardiovascular disease.”

Inflammatory mediated heart disease may, in part, be triggered by chronic infections and may explain why research has linked chronic infections to cardiovascular disease. Recent reports indicate that chlamydia pneumoniae, Helicobacter pylori, Cytomegalovirus, and the herpes virus all may instigate the development of cardiovascular disease.9

The respiratory infection, chlamydia pneumoniae (CP), is one of the strongest predictors of cardiovascular disease. A number of studies have established this link, including one meta analysis of the medical literature10 that concluded “CP infection may be one of the risk factors of coronary heart disease.” Additionally, postoperative white blood cell count predicts atrial fibrillation after cardiac surgery,11 further cementing the correlation between immunity and cardiovascular health.

In addition to inflammation and infections, another “hidden” cause of cardiovascular disease is what’s known as non-calcified vulnerable plaque. This issue is especially relative to chelation because even people who demonstrate dramatic improvement in symptoms after undergoing chelation, sometimes still show calcified plaque on their arteries during standard tests. However, many of the standard tests, such as angiograms, do not detect vulnerable, non-calcified plaque, the rupture of which may be responsible for up to 85 percent of sudden cardio- and cerebrovascular deaths.12

Vulnerable Plaque occurs when an active infection caused by one of the viruses or bacteria mentioned earlier takes hold in the arterial wall. Due to the infection, platelets aggregate more easily into clumps of this vulnerable plaque, which ultimately ruptures and causes a blood clot.

After EDTA chelation, patients who are still showing calcified plaques on their arteries often opt for surgery. However, Dr. Gordon theorizes—and I concur—that given all the research that exists on vulnerable plaques, traditional surgery to correct calcified plaques may actually be operating on the wrong plaques! Given chelation therapy’s known ability to help patients easily sustain a far higher level of physical activity and the fact that improved exercise tolerance is a sign of improved oxygenation of ischemic tissues, the reduction of traditional, calcified plaque is not the only measurement of chelation therapy’s success.

EDTA and Anti-inflammatory Support

An extensive amount of evidence suggests cardiovascular disease may be inflammation driven and that this inflammation may have a viral or bacterial etiology. Heavy metals such as lead and aluminum have been known to trigger inflammation and their removal from the body with chelation can go a long way in helping to reduce the inflammatory response. However, other agents besides heavy metals—including viruses, bacteria and even stress—can produce inflammation. Therefore, I recommend combining oral and intravenous chelation therapy with natural anti-inflammatory and immune-boosting agents.

A combination of Stephania tetrandra extract, Holy Basil, 5-Loxin® (from Boswellia) and Luteolin can help lower inflammation. Stephania tetrandra’s active components have been shown to suppress multiple inflammatory cytokines and mediators and to suppress nuclear factor kappa beta (NFkB) activation in human T cells (immune cells).13 5-Loxin inhibits 5-Lox, which converts arachidonic acid (made within the body from linoleic acid in vegetable oils) to the highly inflammatory leukotrienes.14 Luteolin possesses strong anti-inflammatory and anti-allergic activity in vivo (living organism).15 In mice with induced sepsis, luteolin increased the survival rate from 4 percent (untreated) to 48 percent (luteolin-treated).16 Holy basil leaves contain various compounds that are effective COX-2 inhibitors.17 In rats, holy basil was about 60 percent as effective as sodium salicylate (an aspirin-related compound) in reducing inflammation in various tests.18

In cases of viral or bacterial inflammation, I consider Thymic Protein A19 and Beta-Glucan20 to be two of the most effective immune-boosting supplements.

Taking oral chelation one step farther by combining it with any of these supplements can ensure that several aspects of cardiovascular health are addressed.

Absorption of Oral EDTA

In 1954, Dr. Harry Foreman and his colleagues performed a landmark study to determine how much orally administered EDTA the body absorbs.21 The scientists found that the body absorbs about five percent of orally consumed EDTA (Fig. 2) and that it can take up to three days for the EDTA to be totally excreted. If someone consumed nutritional supplements that contained 1,000 mg of EDTA (used as a stabilizer of the ingredients in the supplement), then we can assume from Dr. Foreman’s research that about 50 mg will be absorbed each day and that 1,500 mg will be absorbed each month. That equates to almost the same amount of EDTA administered in one intravenous chelation treatment.22

Conclusion

Those unable to obtain intravenous chelation therapy due to financial, occupational, geographical or other restraints, or who wish to undergo a less-intensive preventive approach may be able to obtain many of the same benefits of intravenous chelation therapy by consuming food-additive EDTA that is used as a stabilizer in food supplements. Many physicians are augmenting weekly or monthly intravenous infusions with daily oral EDTA.

Furthermore, due to new research that indicates inflammation and chronic infections are linked to heart disease, a combined protocol of oral chelation together with anti-inflammatory and immune-boosting supplements can prove especially effective.

Because of concern that long-term use of EDTA might result in depletion of certain elements, Drs. Ira Manville and Robin Moser recommended that a potent vitamin and mineral formula be administered during treatment with EDTA.23

I recommend that the supplemental minerals should be taken with meals and not with the EDTA formula because of the possibility of EDTA binding to nutritional as well as to unwanted metallic elements.

References

1. Calcium disodium edetate and disodium edetate. Federal Register, Volume 35, No. 8, Tuesday, January 13, 1970, 585-587.

2. Mitchell PH, Schroeder HA. Depression of cholesterol levels in human plasma following ethylenediamine tetracetate and hydralazine. J Chronic Diseases. 1955;2(5):520-532.
3. Schroeder HA. A practical method for the reduction of plasma cholesterol in man. J Chronic Diseases. 1956;4:461-468.

4. Perry Jr. and Camel G. Some effects of CaNa2EDTA on plasma cholesterol and urinary zinc in man, in: Metal Binding in Medicine, by Marvin J. Seven and L. Audrey Johnson (eds), 1960, J.B. Lippincott Company, Philadelphia, 209-215.

5. Mariani B, Bisetti A, Romeo V. Blood-cholesterol-lowering action of the sodium salt of calciumethylenediaminotetraacetic acid. Gazz Intern Med e Chir. 1957;62:1812-1823.

6. Wartman A, Lampe TL, McCann DS, Boyle AJ. Plaque reversal with MgEDTA in experimental atherosclerosis: Elastin and collagen metabolism. J Atherosclerosis Res. 1967;7:331-341.

7. Pfutzner A, Forst T. High-sensitivity C-reactive protein as cardiovascular risk marker in patients with diabetes mellitus. Diabetes Technol Ther. 2006 Feb;8(1):28-36.

8. Tuomisto K, Jousilahti P, Sundvall J, Pajunen P, Salomaa V. C-reactive protein, interleukin-6 and tumor necrosis factor alpha as predictors of incident coronary and cardiovascular events and total mortality. A population-based, prospective study. Thromb Haemost. 2006 Mar;95(3):511-8.

9. Fudal M, Wilczewski P. [Atherosclerosis and inflammation–role of chlamydia pneumoniae infection what do we know to date?] [Article in Polish]. Wiad Lek. 2004;57(3-4):151-5.

10. Wang SK, Wang JZ. [Meta-analysis on the relationship of chlamydia pneumonia infection and coronary heart disease]. [Article in Chinese]. Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2005 Jun;27(3):349-53.

11. Lamm G, Auer J, Weber T, Berent R, Ng C, Eber B. Postoperative white blood cell count predicts atrial fibrillation after cardiac surgery. J Cardiothorac Vasc Anesth. 2006 Feb;20(1):51-6.

12. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Eng J Med. 2000 March 23:836.

13. Ye J, et al. On the role of hydroxyl radical and the effect of tetrandrine on nuclear factor-kappa B activation by phorbol 12-myristate 13-acetate. Ann Clin Lab Sci. 2000;30:65-71.

14. Uz T, et al. Aging-associated up-regulation of neuronal 5-lipoxygenase expression: putative role in neuronal vulnerability. FASEB J. 1998;12:439-49.

15. Ueda H, et al. Luteolin as an anti-inflammatory and anti-allergy constituent of Perilla frutescens. Biol Pharm Bull. 2002; 25:1197-1202.

16. Kotanidou A, et al. Luteolin reduces lipopolysaccharide-induced lethal toxicity and expression of proinflammatory molecules in mice. Am J Respir Crit Care Med. 2002;165:818-23.

17. Kelm M, et al. Antioxidant and cyclooxygenase inhibitory phenolic compounds from Ocimum sanctum Linn. Phytomed. 2000;7:7-13.

18. Godshani S, et al. Ocimum sanctum: an experimental study evaluating its anti-inflammatory, analgesic and antipyretic activity in animals. J Ethnopharmacol. 1987;21:153-63.

19. Hays EF, Beardsley TR. Immunologic effects of human thymic stromal grafts and cell lines. Clin Immunol Immunopathol. 1984 Dec;33(3):381-90.

20. Cramer DE, Allendorf DJ, Baran JT, Hansen R, Marroquin J, Li B, Ratajczak J, Ratajczak MZ, Yan J. Beta-glucan enhances complement-mediated hematopoietic recovery after bone marrow injury. Blood. 2005 Sep 22.

21. Foreman H, Trujillo T. The metabolism of C14 labeled ethylenediaminetetraacetic acid in human beings. J Lab Clin Med. 1954;43:566-571.

22. Born GR, Geurkink TL. Improved peripheral vascular function with low dose intravenous ethylene diamine tetraacetic acid (EDTA). Townsend Letter for Doctors. 1994 July;132:722-726.

23. Manville I, Moser R. Recent developments in the care of workers exposed to lead. AMA Arch Indust Health. 1955;12:528-538.

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