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The Role of Chelation Therapy: Antibioticsand Mycoplasms
Harold W. Clark, Ph.D.
(Portions taken from the book Why Arthritis? Searching for the
Cause and the Cure of Rheumatoid Disease
by Harold W. Clark. Ph.D.)
Submitted by The Arthritis Trust of America, 7376 Walker Road,
Fairview, TN 37062; www.arthritistrust.org
Harold W. Clark, Ph.D.
Why are some doctors and patients speaking & shout-
ing out for Chelation therapy? The recent hearing held in Tampa
by a committee of the Florida Board of Medicine attracted pa-
tients and doctors from Florida and across the country. A mix-up
in scheduled time provoked the president of the Pro-Chelation
Alliance for Medical Freedom to accuse the committee of being a
“Kangaroo Court”?
What is so special about Chelation therapy that has been
used and promoted for over 50 years, but never clinically tested in
chronic diseases? Another similar form of chelation therapy that
has been used and promoted for over 50 years is treatment of
arthritis with tetracycline antibiotics. The tetracyclines were re-
cently clinically tested and found to be safe and effective in rheu-
matoid arthritis and the inhibition of metallic enzymes such as
collagenase that destroys tissue collagen.
Chelation is a chemical term given to molecules that
combine or complex with metals such as lead, mercury, copper,
iron, calcium, etc. The term is taken from ‘chela’ the pincerlike
claws of crabs. Such agents hold metals making them ineffective
by limiting their availability for metabolic activity. One such
chelating agent that is widely used is a synthetic amino acid, eth-
ylene diamine tetra-acetic acid, or EDTA that chelates the toxic
metals such as lead & mercury, as well as calcium and the other
essential trace metals. As chelating agents the other amino acids
(protein fragments), vitamins A, C and E, are also used in chela-
tion therapy as antioxidants.
Aspirin and other antinflamatory (NSAIDS) chelates
convey a variety of benefits to multiple organ systems. Most no-
tably by combining with Calcium as an anticoagulant improves
the cardiovascular and macular degeneration. By reducing arte-
rial plaque formation with an increased blood supply relieves pa-
tients from angina, claudication, and dizziness. However with long
term and extensive use the benefits of chelates are lost with the
nonspecific removal and reduction of the essential trace metals.
Chelation therapy can be a double edge sword like steroid therapy
that can help or put the patients at greater risk with the temporary
control of symptoms and not the primary causes. The reduction
and elimination of arterial plaque formation by dietary and chela-
tion means can have life saving benefits but does not, eliminate
the suspected infectious and persisting causes. Treatment of vas-
cular disorders of microbial causes such as mycoplasmas and
chlamydia with the chelating tetracycline antibiotics can provide
a multiple action affect.
Whether mycoplasmas or other microbes are the per-
sistent sensitizing pathogens in collagen vascular disorders remains
to be demonstrated. The primary concern is a safer and more ef-
fective treatment of the toxic forms of therapy that impose a greater
danger and economic burden. The tetracyclines are potent chelat-
ing (eomplexing) medications and as such have been found to act
as antiinflammatory, immmosuppressive, and anti-metallic en-
zymes as well as antimicrobial. When tetracyclines complex with
copper they become active antioxidants and antiinflammatory
agents (electron scavengers) by neutralizing the damaging oxy-
gen free radicals produced by the activated leucocytes. By com-
bining with the copper, zinc, iron and other trace metal elements
in enzymes such as collagenase, tetracyclines can inhibit the en-
zymatic destruction of tissues. Consequently the mode of tetracy-
cline or chelate administration, intravenous or oral, could have a
pronounced effect on their complexed state and thus their reactiv-
ity. Prescribing some medications “Between Meals” or with meals
is an attempt to provide optimum conditions for the utilization of
each drug. Even between meals the gastro-intestinal tract contents
provide a much greater diversification of chemicals and acidity
than the blood. Thus when tolerable the more direct intravenous
administration of tetracyclines and other chelating drugs will be
more constant and effective than oral medication. The intermit-
tent administration or pulse doses, 2-3/week rather than daily is
more effective by giving the tissues time to normalize.
The beneficial effects of tetracyclines and other chelat-
ing agents such as EDTA, aspirin, and vitamins C, E, or A, are
attributed to their metal complex and their resulting multiple ac-
tions, including antimicrobial. The administration of multiple
acting chelating drugs could enhance or inhibit their activity and
effectiveness depending upon their relative affinity. For example
EDTA with a greater affinity for Calcium than tetracyclines could
have a greater anticoagulant action. On the other hand tetracycline’s
greater affinity for nucleic acids and lipids than most chelates
results in a greater inhibition of protein synthesis and microbial
growth. It is of interest to note that for many years the combina-
tion of Vitamin E and Selenium, a metal chelate, was a favorite
arthritis medication used by veterinarians. Perhaps Bayer’s plain
aspirin was touted as faster acting because it was not prechelated
and neutralized with less effective metals.
Although not accepted clinically perhaps the preformed
copper-aspirinate would be more effective in the control of
inflamation and the preformed copper-tetracyclinate would con-
trol the collagen vascular disorders of microbial origin. In contrast
the chelate D-penicillamine medication used to chelate copper and
treat rheumatoid arthritis was found to inhibit mycoplasma growth
when complexed with copper. Another aspect of chelation to con-
sider is the potential adverse or beneficial affects of two or more
chelating medications administered similtaneously. Excesive use
of the EDTA or tetracycline chelates could inhibit the copper/zinc
superoxide dismutase enzyme that protects against the tissue de-
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