DMSA is Di-Mercapto Succinic Acid C2-2(COOH)-2(SH). As a
di-thiol molecule (the 2 SH groups) it is effective at forming coordination
compound bonds with metallic ions. This type of bond is known as a "chelate"
bond. Single thiol molecules, such as many of the so-called "natural" chelators
will indeed form chelate bonds, but they are capable of only binding one of
the two available valence electrons on the metal ion, thus leaving the second
one free to latch on to other opportunistic thiol groups and part company
with the original coordination complex. This phenomenon is called
"re-distribution" when mercury is the target ion of interest, as the single
thiol will latch and drag the mercury ion from its resting place only to
drop it somewhere else in the blood stream so that it is free to find another
structure to damage. Entropy being what it is, this will almost universally
be a worse place than where it came from. Thus, redistribution is almost
always a bad and dangerous thing, and, hence, single thiol molecules, although
they DO form chelate bonds, are not called "chelators" because they are weak
and ineffective at completing the job.
Even di-thiol chelators, like DMSA, are governed by the
laws of equilibrium dynamics. That is, in any complex chemical environment,
like the body, many, many different metal ions are in competition for the
same corrdination complex ligand (or bond site). The overall mix of
chelated metals in a large soup of trillions and trillions of chelator molecules
and trillions and trillions of available metal ions will represent a probabilistic
bell curve. That is, some metals, like mercury, will have a much higher
"equilibrium potential" for the thiol bond than will other metals, like say
calcium. The average mix of bound metals in the soup will be ratioed based
on the numeric value of the relative equilibrium potentials. Thus, even di-thiol
chelators tend to cause some redistribution of metals within the body, i.e.,
some will be stirred up to action by the presence of the bond potential but
will not actually be permanently bound due to the competition of other
in-vivo metals.
What I've just explained to you in the above paragraph
(read it again if you fell asleep halfway through) is why the half-life of the
chelator drug is SO important in safe chelation and why most people here
have selected the Andy Cutler protocol (because his is the only protocol
currently available that understands and handles this important but widely
overlooked element of the therapy). When the chelator drug, DMSA in this
example, starts to be metabolized and excreted by either the kidney or
the liver, and its blood concentration falls to half the original amount
after dosing, the stirred-up but unbound mercury will begin to settle out
in random places within the body, poisoning new structures and disrupting
new biochemical pathways. It is at this very critical time that the Cutler
protocol instructs the patient to re-dose another alotment of chelator to
maintain the blood level of the drug. As such, it "mops up" the stirred but
unbound mercury left by the previous dose.
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