Dr. Jonathan Collin, MD
     

About Dr. Jonathan Collin EDTA Chelation Therapy

A Clinical Study: EDTA Chelation Therapy
in the Treatment of Arteriosclerosis
and Atherosclerotic Conditions

by Jonathan Collin, MD

(Data Submission to the Public Health Service, May 1981, unpublished report)

One approved usage of EDTA (di-sodium-ethylene-di-amine-tetra-acetic acid) sanctioned by the Food and Drug Administration is in the treatment of acute lead poisoning. Most of the clinical reports documenting EDTA Chelation as an appropriate tool in lead intoxication originated in the early 1950s (Belknap, 1952; Butler, 1952; Foreman, 1953). Not until 1955 did Clarke, Clarke and Mosher report the clinical observation of EDTA influencing the process of atherosclerosis. This observation was a medical serendipity: the Clarke team was not seeking a change in the cardiovascular process. They were involved in the clinical therapy of lead detoxification and made the observation that older patients with known atherosclerotic disease changed vascularly under EDTA chelation.

The initial Clarke, Clarke, Mosher report of 1955 was followed by further clinical documentation in 1956 of EDTA's use to treat angina pectoris. Other medical investigators made similar observations of EDTA's role in the treatment of cardiovascular disease (Bechtel, 1956; Bessman, 1957; Perry, 1961; Szekely, 1963; Wenig, 1958: and Wilder, 1962). In the midst of the research work on chelation therapy's role in clinical medicine, Seven (1960) discussed toxicology problems with a variety of chelating agents. Nephrotoxicity (kidney poisoning) had been observed by some workers in the usage of EDTA (Foreman, 1956). Chelation therapy investigation slacked off during the mid-sixties to some extent. However, the Clarke team pursued chelation therapy as a primary cardiovascular therapy throughout this period and into the seventies at Providence Hospital in Detroit. Recent clinical activity with EDTA has led to extensive literature reviews on chelation and more fundamental documentation of its use in atherosclerosis (Harper and Gordon, 1975; Halstead 1919).

The United States Public Health Service, in collaboration with the National Institutes of Health, organized a study of EDTA Chelation in 1981. This study was relegated to an office in the Public Health Service dealing with modern health technologies. Substantial data was offered to this department by many members of the American Academy of Medical Preventics (Los Angeles) for scientific review. Although no formal explanation was given, none of the reports submitted were properly examined by any scientific boards, nor was the data published. At a later date, without any well-documented summary, the Public Health Service concluded that EDTA Chelation Therapy for arteriosclerosis should be considered experimental and without substantial evidence to support its clinical use. This decision came, apparently, without the support of double-blind studies or peer-review publications. It was based on the opinions of various spokespersons of the American Heart Association, the American College of Cardiology, the AMA, and the National Institutes of Health. The Medicare decision of 1982, to deny reimbursement for EDTA chelation therapy, was based primarily on this Public Health Service study. In large part, then, the medical community and national health agencies have done very little serious scientific study on EDTA Chelation therapy.

The purpose of this report is to provide documentation of the experiences of one clinic using EDTA Chelation in the treatment of arteriosclerosis. The research design does not control for EDTA and placebo; it is simply gathering clinical results using each individual patient as his/her own before and after. Criticism concerning lack of scientific control and statistical analysis are granted. However, recent comments by the medical community in the peer-review journals and to the press indicate a pervasive opinion that EDTA Chelation has no validity whatsoever. This report establishes significant pre- and post- chelation changes, suggesting that orthodox medical opinion of EDTA may be seriously wanting.

Clinical Design
EDTA Chelation Therapy is administered to individuals with documented arteriosclerotic disease of the heart, head and neck, or peripheral circulation. The diagnosis of circulatory disease, using invasive and non-invasive cardiovascular techniques, is made prior to accepting the patient for consideration of the therapy. Once the lesion(s) in the circulation have been defined, the patient is apprised of all medical and surgical therapies appropriate to manage the disease. Consultation with the cardiologist and cardiovascular surgeon is advised, and followup with the medical specialist is recommended. If the individual decides to consider EDTA Chelation therapy, laboratory testing must be undertaken to identify potential toxicity risks. All EDTA patients need to show adequate kidney and liver functioning, stable electrolyte levels, normal blood count, and no evidence of underlying tumor. Evident tuberculosis or infectious disease contraindicates chelation. The patient is scrutinized for any factors that present undue risks that would make EDTA treatment inappropriate.

Once these steps have been satisfactorily attended to, a thorough evaluation of the individual's nutrition and metabolic status is undertaken. A thorough physical and history establishes deficiencies and dietary excesses. Insufficient calories, protein, fat, carbohydrates, vitamins, mineral elements, and amino acids are defined through dietary survey and history, and laboratory testing of the serum, urine, and blood cell. Nutritional deficiencies are corrected as expediently as possible and monitored. Equally likely are dietary excesses of fat, cholesterol, refined carbohydrates, and salt. Individuals are strongly encouraged to increase their unrefined food stuffs, vegetables and whole grains to build up their fiber ingestion while restricting their intake of animal fat, sugar and salt. Obvious over-indulging in caffeine, nicotine, and alcohol is eliminated to the best of the patient's ability.

Supplementation with vitamin and mineral food supplements, usually in the form of tablet or capsule, is ordered to make up for difficult deficiencies. In view of the aggressive effect EDTA has on the biochemistry, particularly in chelating minerals that may already be potentially deficient, mineral supplementation is advised in mega-quantities. The use of analyses to monitor minerals in the body is supported in spite of literature arguing against this clinical testing. In short, every effort is made to thoroughly analyze the nutritional and metabolic function and to correct the diagnosed shortcomings before initiating the chelation treatment.

Certain cardiovascular studies are completed prior to initiating the chelation including electrocardiogram (ECG), and the plethysmogram of the peripheral pulses end carotids. The plethysmograph provides a non-invasive study of the pulse contour, showing reduction in the pulse amplitude and alteration in the upslope and downslope of the pulse. An obstruction in the artery, a plaque-induced restriction in the blood flow, will usually be observed on plethysmography. Invasive studies can then be ordered to precisely define the lesion. The chemistry SMA-18 specifies kidney and liver function: BUN and SGOT can be used as markers for each system respectively. Since EDTA Chelation actively binds metal elements, the excretion of lead and arsenic can be studied by a 24-hour urinary study. Increases in such 24-hour excretions suggest heavy metal intoxication.

The EDTA Chelation itself is administered to the patient on an out-patient basis in the office during the morning or afternoon. One session of EDTA is given in a two to three hour period. A patient can have one to three chelations in a one-week period. Rules on the frequency of EDTA chelation are required to ensure that the possibility of nephrotoxicity is reduced. Peer-review literature concerning EDTA Chelation's toxic effect on kidneys does not, however, call for a restriction on the quantity of EDTA a person may be given in a specified time. Recent studies by Halstead (l979) and others clarify that the earlier problems with toxicity are totally negated when EDTA Chelation is given slowly and less frequently.

The quantity of EDTA given is 1 to 3 grams depending on the weight, sex, age, and condition of the patient. The EDTA is diluted in a buffered solution such as Ringer's Lactate, Fructose or Dextrose in Water, Half Normal Saline, etc. Because EDTA has substantial ligand-forming activity in living systems, every EDTA solution receives at least 1,000 milligrams of magnesium chloride (or magnesium equivalent). This brings about an initial binding of much of the EDTA to magnesium, lessening the pain of administering EDTA. Other additives to the EDTA solution include 5,000 IU of heparin, one to ten grams of ascorbic acid, and one to two milliliters of 2% lidocaine. Usually vitamins are also added to the EDTA solution, including thiamine, pyridoxine, B-Complex and B-12. Other additives, appropriate for the patient's management, may be injected.

The patient receives the solution under the observation of the nurse and doctor while sitting in the office, reading or talking to a fellow patient. Blood pressure, weight, pulse, and other vital signs are measured at each visit. During the chelation process, alterations are made in the rate of infusion depending on the patient's condition. Relaxing background music, comfortable chairs and pillows to prop the patient's arms on, nice lighting, and nursing TLC help in reducing the anxiety of having an infusion. Patients are encouraged to snack on wholesome food and drink during the process. In the rare circumstances when patients experience reactions, intranasal oxygen is usually administered, and this suffices to bring about stabilization. It is extremely rare when resuscitation procedures are necessary (probably no higher than the number experienced in any general practice office during non-surgery treatment).

The usual arteriosclerotic patient is recommended a series of twenty to thirty chelations over several months. In the course of this treatment, repeat cardiovascular and laboratory testing is made to study changes in blood flow and metabolic functioning. Further, the possibility of toxicity is studied in these blood tests. Any patient having abnormal liver or kidney functions has his chelation discontinued, and thorough investigation of toxicity is made. Our protocol demands that monitoring is made continuously to ensure that no harmful effects go undetected.

Clinical Summary
Twenty-six patients, fourteen males and twelve females, aged from 34 to 85 years of age, underwent EDTA Chelation Therapy at the clinic from 1975 through 1981. All patients receiving this therapy were diagnosed with atherosclerosis or some significant cardiovascular process (Table 1).

Of the twenty-six patients, twenty-three received at least 20 separate chelation treatments. Fifteen patients received thirty or more individual infusions. Each of the twenty-six patients underwent non-invasive plethysmograph before EDTA chelation. Understandably, the plethysmogram demonstrated arteriosclerotic disease in each of the patients; all twenty-six were previously diagnosed with arteriosclerotic heart, peripheral, or cerebral disease. Plethysmography carried out following chelation revealed at least 20% improvement in cardiovascular functioning in all twenty-six patients. In fourteen of the twenty-six patients, the plethysmogram demonstrated 50% improvement in pulse amplitude and contour. Ten of the twenty-six patients showed a continued documentation of this improved circulatory plethysmogram when the test was repeated yearly over five years. (Table 2).

A review is made of evidence of nephrotoxicity and hepatotoxicity. In zero of twenty-six patients was the BUN found to change from a normal to abnormal elevation. In only one patient of twenty-six was there a change in the SGOT; evidence to support hepatotoxicity in chelation patients was insignificant. To the contrary, the data strongly suggests that EDTA improved both hepatic and renal functioning in these patients (Table 3).

Table 4 confirms the expected activity of EDTA in inducing an effective diuresis of lead. It also substantiates the ability of EDTA to chelate arsenic.

Conclusion
The data charted on these twenty-six individuals receiving EDTA chelation therapy strongly suggests that EDTA is efficacious in the treatment of arteriosclerosis. Through the use of an effective, cautious protocol, no incidents of toxicity were observed in this group of chelating patients. No evidence was found for significant nephrotoxicity, a key criticism against the medical use of EDTA. Inasmuch as the EDTA was observed to bring about a significant diuresis of lead and arsenic, while improving the cardiovascular status of most patients by at least 20%, the original observations of the Clarke and Clarke group (1955) has been again confirmed in 1981. This report argues for the role of EDTA in treatment of cardiovascular diseases and calls for serious scientific study of EDTA chelation to be initiated at the university level in the near future.

References

1. Bechtel, JR, White, JE, Estes, EH Jr. (1956). The electrocardiographic effects of hypocalcemia induced in normal subjects with edathamil sodium. Circ 13:837.

2. Belknap, EL (1952). EDTA in the treatment of lead poisoning. Ind Med Surg 21(6):305.

3. Bessman, SP, Doorenbos, NJ (1957), Editorial. Chelation. Ann Int Med 47(5):1036.

4. Butler, AM (1952), Use of calcium ethylene-diaminetetraacetate in treating heavy-metal poisoning. Arch Ind Hyg Occ Med 7:137.

5. Clarke, NE, Clarke, CN, Mosher, RE (1955). The "in vivo" dissolution of metastatic calcium. An approach to atherosclerosis. Am J Med Sci 229:142.

6. Clarke, NE, Clarke, CN, Mosher RE (1956). Treatment of angina pectoris with disodium ethylene diamine tetraacetic acid. Am J Med Sci 232:654.

7. Foreman, H, Finnegan, C, Lushbaugh, CC (1956). Nephrotoxic hazard from uncontrolled edathamil calcium-disodium therapy. J Am Med Assoc 160(12):1042.

8. Foreman, H, Hardy, HL, Shipmen, TL, Belknap, EL (1953). Use of calcium ethylenediaminetetraacetate in cases of lead intoxication. Arch Ind Medx 7:148.

9. Halstead, B (1979). The Scientific Basis of EDTA Chelation Therapy. Colton (CA): Quill Publishers.

10. Harper, HW, Gordon, GF (1975). Reprints of Medical Literature on Chelation Therapy. Los Angeles: American Academy of Medical Preventics.

11. Perry, Jr. HM (1961). Chelation therapy in circulatory and sclerosing disease (discussion). Fed Proc 20(3), Pt II Suppl 10:254.

12. Seven, MJ (1960). Observations on the toxicity of intravenous chelating agents in: Metal-binding in Medicine (Ed. Seven, MJ and Johnson, LA). Philadelphia: Lippincott.

13. Szekely, P, Wynne, NA (1953). Effects of calcium chelation on digitalis-induced cardiac arrythmias. Br Heart J 25:589.

14. Wenig, E, Schwerd, W (1958). Nil noarel Gafahren bei der Behandiung der Bleintoxikation mit Calcium versenat. Munch Med Wsch 100:1788.

15. Wilder, LW, DeJode, LR, Milstein, SW, Howard, JM (1962). Mobilization of atherosclerotic plaque calcium with EDTA utilizing the isolation-perfusion principle. Surg 52(5):793.

Table 1
Distribution of Medical Patients According to
Age, Sex, Weight, and Medical Diagnosis

1. 63 M 194 Peripheral Vascular Disease; Arterial Ulcer

2. 62 M 163 Hypertensive Cardiovascular Disease

3. 66 M 163 Ischemic Heart Disease

4. 63 M 175 Angina Pectoris

5. 53 F 104 Rheumatic Mitral Valve Disease, Mitral Stenosis

6. 60 F 123 Congestive Heart Failure, Mitral Stenosis

7. 62 M 249 Hypertensive Cardiovascular Disease

8. 34 F 161 Hypertensive Cardiovascular Disease

9. 68 M 185 Peripheral Vascular Disease

10. 85 M 164 Congestive Heart Failure, C.V.A.

11. 67 M 146 Atherosclerosis, DOPD

12. 66 F 144 Basilar Artery Disease

13. 61 M 154 Angina

14. 68 M 137 Ischemic Heart Disease, Peripheral Arteriosclerosis

15. 50 M 163 Cerebral Arteriosclerosis

16. 71 F 102 Ischemic Heart Disease, C.V.A.

17. 78 F 123 Hypertension, Angina Pectoris

18. 54 M 127 Angina, Post Myocardial Infarction

19. 36 F 120 Hyperlipidemia, Atherosclerosis

20. 48 M 177 Lead Toxicity, Atherosclerosis

21. 72 F 135 Ischemic Heart Disease

22. 57 F 125 Hypertension, Hyperlipidemia, Atherosclerosis

23. 81 F -- Post Myocardial Infarction, Diabetes, DJD

24. 49 F 171 Hyperlipidemia, Arteriosclerosis

25. 57 M 183 Ischemic Heart Disease, Peripheral Arteriosclerosis

26. 69 F 137 Hypertension, Peripheral Arteriosclerosis

Table 2
Pre- and Post-Chelation Plethysmography
*Delay in crest

# of Chelations Artery Site Abnormal Amplitude Reduction? Contour Flattened? Change in Pulse Contour

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

52

23

30

42

45

44

30

25

28

17

20

68

40

30

30

41

12

23

10

20

29

54

29

30

70

30

Carotids

Supra-Orbital

Left Carotid

Carotids

Carotids

Carotids

Ocular

Supra-Orbital

Carotids, S-O

Carotids, S-O

Supra-Orbital

Carotids

Carotids

Carotids, Extr.

Carotids

Carotids

Ocular, S-O

Ocular, S-O

Carotids

Ocular, S-O

Carotids, Extr.

Extremities

Carotids

Supra-Orbital

Carotids

Carotids

Both

Both

Both*

Both

Both

Both

Amplitude

Both

Both

Both

Both

Both

Both*

Both

Both*

Both*

Both

Both

Both*

Both

Both

Both

Both*

Both

Both

Both

+60%

+50%

+20%

+60%

+50%

+20%

+50%

+30%

+30%

+20%

+75%

+60%

+60%

+30%

+30%

+60%

+20%

+20%

+20%

+30%

+20%

+20%

+30%

+30%

+50%

+60%

Table 3
Liver and Kidney Function Studies

 

Pre-Chelation Bun

Post Bun

Pre-Chelation SGOT

Post SGOT

Post Bun

 

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

 

17 mgm%

11.5

14

22

15

41(H)

8.6

16.6

15

28(H)

19

15

16

2

17

28(H)

20.2

15

14

13

27(H)

13

19

14.3

16.4

17

 

19 mgm%

15

19

18

13

17

20

16

17

19

18

18

18

16

20

16

13

19

21

17

20

9

15

13

14

16

 

25 units

18.5

27

47(H)

3

31

21.6

23.8

27.8

68(H)

18

22

32

--

34

28

14

--

31

3

22

47(H)

--

--

19.6

33 

 

units

16

--

--

15.4

48(H)

--

--

--

--

--

--

--

50(H)

32

13

--

10

--

--

10

12

--

--

26

18

 

19 mgm%

15

19

18

13

17

20

16

17

19

18

18

18

16

20

16

13

19

21

17

20

9

15

13

14

16

Table 4
Effect on Heavy Metal Excretions

 

24 Hour Urinary Lead (Normal: less than 80 ugm)

24 Hour Urinary Arsenic (Normal: less than 40 ugm)

 

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

 

--

28

93

--

28

17

230

132

182

--

154

--

51

--

54

99

140

39

--

175

105

68

--

188

102

--

 

--

72

151

--

112

6

--

61

384

--

28

185

31

--

81

159

71

29

--

69

70

92

--

60

328

--

 

Visit the Townsend Letter online.

 

About Dr. Jonathan Collin | EDTA Chelation Therapy | Medical Offices of Dr. Jonathan Collin | EDTA Chelation Therapy links

©1996-2014 Jonathan Collin, MD
All rights reserved
Webmistress: Sandy Hershelman