EDTA Chelation: A Misunderstood Therapy for
Atherosclerosis and other
By using nutritional therapy and lifestyle
modifications, many of these risk factors can be reduced or eliminated. However, despite their best efforts, some people may
still develop coronary artery disease, carotid artery disease or
other vascular illness. These conditions may be manifested by chest pain with exertion (angina); (2) memory loss or temporary
disorientation or sensory loss due to reduced blood flow to the
brain, (transient ischemic attacks temporary or pain in the calves after walking
relatively short distances which is relieved by rest (intermittent
Vitamin Research Products Inc. 2001
Chelation: A Misunderstood Therapy for Atherosclerosis and other
The two leading causes of death for men and women over the age of 50
are heart attacks and strokes. Atherosclerosis, or "hardening
of the arteries," is usually involved in the pathogenesis of
these conditions. A significant focus of nutritional therapy is to
reduce various risk factors that predispose an individual to
atherosclerosis. These risk factors include: (1) a high ratio of
total cholesterol to high density lipoproteins; (2) elevated blood
levels of homocysteine, fibrinogen, lipoprotein a, glucose, or
insulin; (3) family history; (4) cigarette smoking; (5) obesity; and
(6) sedentary lifestyle. By using nutritional therapy and lifestyle
modifications, many of these risk factors can be reduced or
eliminated. However, despite their best efforts, some people may
still develop coronary artery disease, carotid artery disease, or
other vascular illness. These conditions may be manifested by: (1)
chest pain with exertion (angina); (2) memory loss or temporary
disorientation or sensory loss due to reduced blood flow to the
brain, (transient ischemic attacks temporary
"mini-strokes"); or (3) pain in the calves after walking
relatively short distances which is relieved by rest (intermittent
claudication). All of these symptoms or conditions, which should be
evaluated by a physician, are worrisome indicators that there may be
significant arterial narrowing in the affected portions, as well as
elsewhere in the body.
The problem with the
"mainstream" approach to vascular disease is that, for the
most part, it's like putting a band-aid on a major traumatic injury.
Certainly, surgeons can bypass a few "blockages" with a
vein graft or prosthesis, or literally smash arteries open with a
balloon angioplasty, but these approaches appear primitive and crude
when one realizes that atherosclerosis is not a localized injury; it
is a systemic disease. This disease is present not only in the
coronary or carotid arteries, but also in the brain, lungs, kidneys,
and legs. (Fig. 1) Furthermore, the blockages not only occlude the
larger vessels that can be seen and manipulated by surgeons and
cardiologists, but the smaller vessels as well. And it is in the
capillaries of the micro-circulation where the oxygen exchange to
the tissues takes place. Clearly, the optimum treatment for
atherosclerosis would be a biological approach which removes plaque
and restores blood flow throughout the entire arterial system and
which treats the micro as well as the macro vessels. But is there
such a biological approach that really works?
Common sites of Atherosclerotic lesions
<------ abdominal aorta
Chelation therapy is
a controversial therapy that is administered by approximately 2,000
to 3,000 physicians in the U.S. It consists of the intravenous
infusion of a solution containing ethylene diamine tetraacetic acid
(EDTA), a synthetic amino acid, as well as vitamins, minerals, and
other substances. The one- to three-hour treatments (depending on
the dose) are administered to a patient who sits comfortably in an
easy chair, reading, talking, watching TV or even sleeping. The
treatments are administered as often as several times per week to as
infrequently as one every other month, depending on the degree of
illness and the patient's length of previous treatment. Usually a
course of twenty to thirty treatments are adequate to reverse
significant blockages, whereupon the patient is put on a less
frequent maintenance regimen.
Proponents of EDTA
chelation therapy of which I am one believe that it is highly
beneficial in the prevention and treatment of atherosclerosis as
well as other chronic degenerative diseases. On the other hand, its
detractors (most of the mainstream medical establishment) claim that
it is worthless at best and may even constitute medical fraud.
EDTA Chelation Therapy
EDTA was synthesized
in Germany in 1935, and first patented in the U.S. in 1941. Its
first uses were in industry as a chelating agent, as an
anticoagulant for clinical laboratory use, and as a treatment for
lead poisoning. In 1955, Dr. Norman Clarke, then Director of
Research of Providence Hospital in Detroit, Michigan, reported on
his use of intravenous EDTA to dissolve what he referred to as
"metastatic calcium"; (i.e., calcium that has been
deposited where it was not wanted, as in arteries [atherosclerosis],
joints [arthritis], kidneys [kidney stones], and the bony ossicular
system in the ears [otosclerosis]), with generally favorable
results. Since then, hundreds of papers have been published on the
effects of chelation therapy in a variety of chronic diseases, with
the vast majority reporting favorable results. The numbers of papers
on EDTA chelation therapy are too numerous to cite here. However,
many can be found in the books and papers that are referenced at the
end of this article.
I believe the most
extensive confirmation of the beneficial cardiovascular effects of
EDTA chelation therapy have been two massive
"meta-analyses" of both published and unpublished
studies.1,2 These papers evaluated the results of over 24,000
chelation patients, in which 88% demonstrated clinical improvement.
Typical of these studies was that of Hancke and Flytlie3 which
described improvements in 80-91% of a series of 470 patients with
coronary artery disease. The report included 92 patients who were
referred for surgical intervention, but of whom only 10 ultimately
required surgery either during or after their chelation therapy. The
authors estimated that EDTA chelation therapy not only resulted in
an improvement in overall cardiovascular health, but saved over $3
million in insurance money as well!3
Perhaps one of the
reasons for the controversy surrounding EDTA is that even its
strongest proponents can't seem to agree on the mechanism by which
it works. The first, and probably most widely held belief, is that
the benefits are due to EDTA's ability to bind with ionic calcium in
the blood. This temporarily lowers the blood calcium level, which
stimulates the parathyroid gland to release parathyroid hormone (PTH).
PTH in turn stimulates osteoclastic and osteoblastic activity of the
bone, mobilizing calcium from unwanted parts of the body (i.e.,
arteries, joints, etc). This mechanism is described in detail in Dr.
Garry Gordon's, The Chelation Answer.4
However, in another
popular "bible" about chelation, Bypassing Bypass,
Dr. Elmer Cranton dismisses the "calcium-chelation
misconception." He believes that removal of toxic heavy metals
and normalization of mineral metabolism are secondary mechanisms and
proposes that the benefits of chelation are due primarily to its
free radical-fighting effects.5
Dr. Johan Bjorksten,
father of the "cross-linkage theory of aging," believes
that the benefits of EDTA are due to its ability to dissolve inter-
and intra-molecular cross-linkages.6
Frackelton reported several years ago that EDTA has a profound
effect on thrombin-induced platelet aggregation. Platelet
aggregation is an essential step in the formation of a blood clot.
Intra-arterial blood clots are a major cause of heart attacks and
strokes, especially when the vessel has been narrowed by
atherosclerotic plaque. Kindness and Frackelton demonstrated that
this physiological anti-clotting property of EDTA is superior to
that of aspirin, without the dangers inherent in aspirin therapy.7
I believe that one of
the least-touted but most significant mechanisms of EDTA may be that
of its ability to "resuscitate mitochondria." Mitochondria
are the "power plants" of every cell in the body. (Fig. 2)
It is within the mitochondria that the process of oxidative
phosphorylation takes place, which generates energy-producing ATP
without which life could not exist. Loss of mitochondrial function
has long been considered to be one of the primary causes of the
aging process.8,9,10 Recently, the role of impaired mitochondrial
function in the pathogenesis of many diseases has been increasingly
recognized.11,12,13 EDTA was recognized as early as the 1950's to
have the ability to stabilize mitochondria.14 Hunter and colleagues
suggested that this effect of EDTA was likely to be due to its
combining with the mitochondrial membrane rather than its chelating
with metal ions.15 Gallagher's studies tended to confirm their
Structure of a Mitochondrion
Mechanisms aside, the
one issue that all chelating physicians overwhelmingly agree on is
the tremendous benefits that can be obtained in a variety of
degenerative, age-related conditions, using this safe, non-invasive,
relatively inexpensive therapy.
Are there any
Adverse Effects of Chelation Therapy?
The most serious
potential adverse effect of EDTA chelation is nephrotoxicity (kidney
damage). This is dependent on the dose, the rate of infusion, the
patient's kidney function, and the patient's body burden of toxic
heavy metals. Kidney damage was not uncommon in the early days of
chelation therapy, when doses of EDTA in the range of 5-10 grams per
day were used, and treatments were administered as often as 5 days
per week. Kidney damage can be easily prevented, however, by
carefully adjusting the frequency, dose and rate in which the EDTA
is administered. In addition, I have found that judicious
administration of EDTA over prolonged periods (three to six months
and longer) actually improves kidney function.
adverse effects include hypocalcemia (excessively low blood levels
of calcium) due to EDTA's binding excessively with calcium in the
blood; hypoglycemia (low blood sugar), believed to be due to
accompanying hypocalcemia; and phlebitis (inflammation of the vein)
usually due to improperly prepared solutions. Rarely reported side
effects include chills and fever following infusion, exacerbation of
congestive heart failure due to fluid overload, fatigue (usually due
to hypoglycemia or hypocalcemia), seizures, arrythmias, or rash.
Although these have been reported occasionally by others, I have
never observed any of these rare side effects despite having
administered thousands of IV EDTA treatments.
The risk of incurring
any of the above adverse effects has further been greatly reduced by
the recent finding of Drs. Grant Born and Tammy Geurkink16 that even
greater benefit can be obtained by most patients who are treated
with only 1.5 grams of EDTA per treatment, rather than with the
standard dose of three grams. These physicians randomly divided 30
patients into two groups, each of which consisted of eight males and
seven females. One group was treated with "high dose" EDTA
(3 grams), and the other was treated with "low dose" (1.5
grams). All patients' vascular status was determined using a
non-invasive, hand-held Doppler ultrasound instrument which measured
blood flow in the lower extremities. After 20 EDTA treatments, every
patient in the high dose group improved significantly. Strikingly,
every patient in the low dose group also improved, and this group
had an even greater degree of overall improvement! Consequently, I
now use only the low dose EDTA in all of my patients, and I believe
the benefits that my patients have experienced parallel those of
Drs. Born and Geurkink. So, not only are the benefits of EDTA
apparently increased with the low dose therapy, but the minimal
risks of adverse side effects are even further reduced.
source of nutrients and supplements.
did we qualify them ?
Chappell, L.T., and Stahl, J.P. The correlation between
EDTA Chelation therapy and improvement in cardiovascular
function: A Meta-Analysis. J Adv Med, 1993, 6: 3,
Chappell, L.T., Stahl, J.P., and Evans, R. EDTA Chelation
treatment for vascular disease: A Meta-Analysis using
unpublished data. J Adv Med, 1994, 7: 3, 131-142.
Hancke, C. and Flytlie, K., Benefits of EDTA Chelation
Therapy in Arteriosclerosis: A retrospective study of 470
patients. J Advancement in Medicine, 1993., 6: 3,
Walker, Morton, and Gordon, Gary. The Chelation Answer.
M. Evans and Company, New York, 1982.
Cranton, Elmer. Bypassing Bypass (2d Ed). Medex
Publishers, Trout Dale, VA 24378-0044, 1992.
Bjorksten, Johan. The crosslinkage theory of aging as a
predictive indicator, in: A Textbook on EDTA Chelation
Therapy, 1989, by Elmer M.Cranton (ed). Available
from: American College for Advancement in Medicine, Laguna
Niguel, CA, 1989.
Kindness, G., and Frackelton, J.P. Effect of EDTA on
platelet aggregation in human blood. J Adv Med,
1989, 2: 4, 519-530.
Harman, D. The biologic clock: The mitochondria? J Am
Geriatr Soc, 1972, 20: 145-147.
Miquel, J., Economos, A.C., Fleming, J., and Johnson, J.E.
Mitochondrial role in cell aging. Exp Gerontol,
1980, 15: 575-591.
Miquel, J. An update on the mitochondrial-DNA mutation
hypothesis of cell aging. Mutation Research, 1992,
Wallace, D.C. Mitochondrial genetics: a paradigm for aging
and degenerative diseases? Science, 1992,
Shoffner, J.M. and Wallace, D.C. Oxidative phosphorylation
diseases and mitochondrial DNA mutations: diagnosis and
treatment, Ann Rev. Nutr, 1994, 14: 535-568.
Flier, J.S. and Underhill, L.H. Mitochondria, DNA and
disease, New England J of Medicine, 1995,
Gallagher, C.H. Aging of mitochondria. Nature,
1960, 187: 732, 566-568.
Hunter, F.E., Malison, R., Bridgers, W.F., Schutz, B., and
Atchison, A. J Biol Chem, 1959, 234: 693.
Born, G.R., and Geurkink, T.L. Improved peripheral
vascular function with low dose intravenous ethylene
diamine tetraacetic acid (EDTA). Townsend Letter for
Doctors. July, 1994, # 132, 722-726.
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