I do not need to do "the research." Anything on the internet is
SUSPECT! It is not research. It is mostly HYPE.

There is no point in debating horse linament for dentistry. Its
already in the literature. Its nonsense!

By the way, you may want to refer to DMSO as DMSO, not DMSA.

Joel

Welcome to the Dimethyl Sulfoxide (DMSO) information center. Select
one of the buttons to the left for additional information about this
versatile treatment option.

Dr. Jacob can be contacted at jacobs@ohsu.edu. Dr. Jacob is no longer
seeing patients. He is taking this time to write a six-volume
encyclopedia on DMSO, its mixtures, and its compounds, including MSM.

For information about treatment, please contact Dr. Jeffrey Tyler at
www.portlandvitality.com.

Dr. Jacob's son, Jeff, can be contacted at 1.866.375.2262 or
www.jacoblab.com. Jeff has worked side by side with Dr. Jacob over the
last two decades in production of the DMSO & MSM formulations.

....and of course, in toxicology, the DOSE is the poison!

KIDDING ABOUT THE DMSO, but try it anyway!
You appear to like HORSing around!

Joel

**

Dimercaptosuccinic Acid (DMSA), A Non-Toxic, Water-Soluble Treatment
For Heavy Metal Toxicity

by Alan L. Miller, N.D.

--------------------------------------------------------------------------------

Abstract

Heavy metals are, unfortunately, present in the air, water, and food
supply. Cases of severe acute lead, mercury, arsenic, and cadmium
poisoning are rare; however, when they do occur an effective,
non-toxic treatment is essential. In addition, chronic, low-level
exposure to lead in the soil and in residues of lead-based paint; to
mercury in the atmosphere, in dental amalgams and in seafood; and to
cadmium and arsenic in the environment and in cigarette smoke is much
more common than acute exposure. Meso-2,3-dimercaptosuccinic acid
(DMSA) is a sulfhydryl-containing, water-soluble, non-toxic,
orally-administered metal chelator which has been in use as an
antidote to heavy metal toxicity since the 1950s. More recent clinical
use and research substantiates this compound's efficacy and safety,
and establishes it as the premier metal chelation compound, based on
oral dosing, urinary excretion, and its safety characteristics
compared to other chelating substances. (Altern Med Rev
1998;3(3):199-207)

--------------------------------------------------------------------------------

Introduction

Contamination of water, air, and food by numerous chemicals and
non-essential elements, such as heavy metals, is an unfortunate
byproduct of a complex, industrialized, high-tech society. The
resultant accumulation of heavy metals in the human body poses a
significant health risk, leading to a wide array of symptomatology,
including anemia, learning deficits, reduced intelligence, behavioral
and cognitive changes, tremor, gingivitis, hypertension, irritability,
cancer, depression, memory loss, fatigue, headache, hyperuricemia,
gout, chronic renal failure, male infertility, osteodystrophies, and
possibly multiple sclerosis and Alzheimer's disease.

Although human lead toxicity has decreased in the United States since
discontinuation of the use of lead as a gasoline additive, it
continues to be a significant problem, especially in urban areas,
where lead-based paint exposure is still an issue, and in areas where
lead is mined and/or smelted. Chronic mercury toxicity from
occupational, environmental, dental amalgam, and contaminated food
exposure, is a significant threat to public health. Other heavy
metals, including cadmium and arsenic, can also be found in the human
body due to cigarette smoke, and occupational and environmental
exposure. Diagnostic testing for the presence of heavy metals, and
subsequently decreasing the body's burden of these substances, should
be an integral part of the overall treatment regimen for individuals
with the above-mentioned symptomatology or a known exposure to these
substances.

It has long been acknowledged that sulfhydryl-containing compounds
have the ability to chelate metals. The sulfur-containing amino acids
methionine and cysteine, cysteine's acetylated analogue
N-acetylcysteine, the methionine metabolite S-adenosylmethionine,
alpha-lipoic acid, and the tri-peptide glutathione (GSH) all
contribute to the chelation and excretion of metals from the human
body.

Meso-2,3-dimercaptosuccinic acid (DMSA), is a water-soluble,
sulfhydryl-containing compound which is an effective oral chelator of
heavy metals. Initial studies over forty years ago identified DMSA as
an effective antidote to heavy metal poisoning. DMSA was subsequently
studied for twenty years in the People's Republic of China, Japan, and
Russia before scientists in Europe and the United States "discovered"
the substance and its potential usefulness in the mid-1970s.1

DMSA is a dithiol (containing two sulfhydryl, or S-H, groups) and an
analogue of dimercaprol (BAL, British Anti-Lewisite), a lipid-soluble
compound also used for metal chelation (see Figure 1). DMSA's water
solubility and oral dosing create a distinct advantage over BAL, which
has a small therapeutic index and must be administered in an oil
solution via painful, deep intramuscular injection.2 DMSA, on the
other hand, has a large therapeutic window and is the least toxic of
the dithiol compounds.3

--------------------------------------------------------------------------------

Lead

Lead exposure is still a public health problem in the United States,
being found in approximately 21 million pre-1940 homes. Dust and soil
lead, derived from flaking, weathering, and chalking paint, also
contribute to chronic exposure.

Lead competes in the body with calcium, causing numerous malfunctions
in calcium-facilitated cellular metabolism and calcium uptake and
usage, including inhibition of neurotransmitter release and blockade
of calcium channels and calcium-sodium ATP pumps.

The central nervous system (CNS) appears to be affected the greatest
by lead. Children in particular are susceptible to its devastating
effects on mental development and intelligence. Neurobehavioral
deficits resembling attention deficit disorder have also been found in
lead-exposed children.4 Blood lead concentrations of 20-25 µg/100 ml
can cause irreversible CNS damage in children.5

Poor quality nutrition, including deficiencies in iron and calcium,
are known to exacerbate the manifestations of lead exposure, including
its CNS effects. Acute adult lead exposure leads to renal proximal
tubular damage; chronic exposure causes renal dysfunction
characterized by hypertension, hyperuricemia, gout, and chronic renal
failure.6

Inorganic lead is absorbed, distributed, and excreted. Once in the
blood, lead is distributed primarily among three compartments ­ blood,
soft tissue (kidney, bone marrow, liver, and brain), and mineralizing
tissue (bones and teeth). Mineralizing tissue contains about 95
percent of the total body burden of lead in adults.

After lead is absorbed in the human body, it reacts with thiol
(sulfhydryl) groups on peptides and proteins, inhibiting enzymes
involved in heme synthesis and interfering with normal
neurotransmitter functions.7 This natural reaction with thiols is also
the body's method of eliminating lead, especially from the liver.
Hepatic glutathione attaches to lead and enhances its excretion in the
feces. Unfortunately, hepatic glutathione can be depleted in this
manner, resulting in less glutathione being available for conjugation
of other toxic substances. In addition to these hepatic effects,
individuals with higher concentrations of blood lead have been noted
to have lower levels of erythrocyte reduced glutathione.8 Decreased
erythrocyte glutathione is due to the fact that 99 percent of lead in
the blood is attached to red blood cells; the remaining one percent is
in the plasma. Lead stored in bone has a half-life of 25 years,
although lead in bone can be mobilized into the blood, and
subsequently to other tissues.

--------------------------------------------------------------------------------

Mercury

Humans are exposed to mercury primarily in two forms: mercury vapor
and methyl mercury compounds. Unfortunately, mercury is a ubiquitous
substance in our environment. Mercury vapor in the atmosphere makes
its way into fresh and salt water by falling in precipitation. Methyl
mercury compounds are created by bacterial conversion of inorganic
mercury in water and soil, which subsequently concentrates in seafood
and fish. Dietary fish intake has been found to have a direct
correlation with methyl mercury levels in blood and hair.9,10

"Silver" amalgam dental fillings are the major source of inorganic
mercury exposure in humans.11 This term, however, is a misnomer, as
this compound is not predominately silver; the proper term should be
"mercury amalgam." The most common dental filling material, amalgams
contain approximately 50 percent liquid metallic mercury, 35 percent
silver, 9 percent tin, 6 percent copper, and a trace of zinc.12 As
they are prepared and placed in the patient's mouth, the dentist and
the person preparing the amalgam,13,14 as well as the patient are
exposed to mercury vapor (HgO). The patient is further exposed to
mercury vapor as the amalgam releases HgO when the individual
chews,15-17 brushes,18 or drinks hot beverages.16-18 Studies of
mercury content in expired air of those with and without amalgams have
found significantly higher baseline mercury levels in subjects with
amalgams, and up to a 15.6-fold increase in mercury in expired air
after chewing.15,16 Mercury release was found to be greater in
corroded amalgams compared to new, polished fillings.18 Mercury vapor
from amalgams enters the bloodstream after being inhaled into the
lungs.

Comparisons of blood levels of mercury and the number of amalgams show
a direct correlation between number of amalgam fillings and
concentration of blood17,19 and urine mercury.13,14,20 In addition, a
statistically significant correlation was found between the number of
dental amalgam fillings and mercury content of the kidney cortex (p
<0.0001) and the occipital lobe cortex of the brain (p <0.0016) in
cadavers.21

After removal of all amalgams, there is a transient increase in
mercury concentration in the blood, plasma, and feces, followed by a
decrease in blood levels below the pre-removal baseline.11,19,22,23

Mercury vapor is lipid soluble, freely passing through cell membranes
and across the blood-brain barrier. Methyl mercury also easily crosses
the blood-brain barrier and the placenta.7 Inorganic and methyl
mercury have a high affinity for sulfhydryls, reacting intracellularly
with the sulfhydryl group on glutathione and cysteine, and histidine
residues in proteins, and allowing transport out of the cell. In rats,
it was found that mercury secretion into the bile was dependent on
glutathione secretion into the bile, suggesting the biliary secretion
of mercury is in large part dependent on the biliary transport of
GSH.24-26 In humans, 90 percent of mercury elimination is via the
feces, with only 10 percent normally being excreted in the urine.12 A
decrease in hepatic glutathione content secondary to excretion of
mercury can decrease hepatic cell viability by mechanisms stated
earlier.

--------------------------------------------------------------------------------

Arsenic and Cadmium

Environmental arsenic and cadmium exposure comes from pollutants
discharged from industries utilizing these metals, including herbicide
and battery manufacturers. These metals are also found in cigarette
smoke.

Cadmium, as well as lead and mercury, can interact metabolically with
nutritionally essential metals. Cadmium interacts with calcium in the
skeletal system to produce osteodystrophies, and competes with zinc
for binding sites on metallothionein, which is important in the
storage and transport of zinc during development.

Biliary excretion seems to be an essential factor for the fecal
elimination of cadmium and arsenic, although these metals may be also
excreted in the urine.27,28

--------------------------------------------------------------------------------

Pharmacokinetics of DMSA

In healthy individuals, approximately 20 percent of an oral dose of
DMSA is absorbed from the gastrointestinal tract. Ninety-five percent
of the DMSA that makes it to the bloodstream is bound to albumin. Most
likely, one of the sulfhydryls in DMSA binds to a cysteine residue on
albumin, leaving the other S-H available to chelate metals. In healthy
fasting men, 90 percent of the DMSA recovered in the urine was found
to be mixed disulfides of DMSA (DMSA attached to one or two cysteine
molecules), and 10 percent was free unchanged DMSA. No mixed
disulfides were found in the blood.29-31 It is thought these are
formed as albumin releases DMSA in the kidney.32

In three children with lead poisoning, free DMSA was found in the
blood of all subjects, while it was found in only one out of five
healthy adult subjects. It is not known whether this is an age-related
phenomenon, or exactly what the significance of this finding might be.
It is unknown if these pharmacokinetic parameters are different in
other metal toxicities or concomitant disease processes. For instance,
if the patient has increased gut permeability, does this increase DMSA
absorption?

Studies addressing the possibility that DMSA may chelate metal stored
in the gut, because a significant percentage of an oral dose is not
absorbed, have yet to be done. A study of whole body retention in mice
of radioactively-tagged, orally-administered mercuric chloride
revealed DMSA and its analogue DMPS (2,3-dimercapto-propanesulfonate)
(see Figure 1), given orally at the same time as the mercury,
significantly decreased the absorption and whole body retention of the
metal.33 This is an important finding which suggests administration of
DMSA a short time after an acute ingestion of mercury will chelate the
metal and decrease the amount absorbed. It does not, however, answer
the question of whether DMSA will bind gut reservoirs of mercury or
whether it will assist the liver in elimination of mercury due to
chronic exposure.

--------------------------------------------------------------------------------

DMSA Treatment in Lead Toxicity

DMSA has been used since the 1950s as an antidote for lead poisoning
in Russia, Japan, and the Peoples Republic of China. DMSA has been
shown in recent studies to be a safe and effective chelator of lead,
reducing blood levels significantly.1,34,35 At a dose of 10 mg/kg for
five days in adult males, DMSA lowered blood lead levels 35.5 percent;
a more aggressive approach utilizing a 30 mg/kg dose lowered blood
lead 72.5 percent. Clinical symptoms and biochemical indices of lead
toxicity also improved.35

An animal study indicated DMSA is an effective chelator of lead in
soft tissue, but it may not chelate lead from bone.36 Another found
DMSA or calcium disodium ethylenediamine tetraacetic acid (CaNa2EDTA)
produced significant reductions in kidney, bone and brain lead levels,
but DMSA produced greater reductions of bone lead.37

In a preliminary animal study, combination therapy with DMSA and
CaNa2EDTA was more effective than either individual chelator at
increasing urinary and fecal elimination of lead, and reducing
hepatic, renal, and femur lead concentrations in rats.38

It has been suggested that chelating agents, including BAL and
CaNa2EDTA, may mobilize and redistribute lead to soft tissue,
including the brain. Lead-exposed rats given CaNa2EDTA showed an
initial decrease in bone and kidney lead, and an increase in hepatic
and brain lead concentrations, indicating redistribution to these
organs.39 Rats administered DMSA in combination with CaNa2EDTA showed
increased urinary lead output and decreased tissue burden versus use
of these therapeutic substances individually. No redistribution of
lead to the brain was observed with the combined therapy. A decrease
in blood zinc level was noted with the combination, as has been
observed with CaNa2EDTA monotherapy.40

In a study of lead's pro-oxidant activity and the effect of thiol
substances as antioxidants, five weeks of lead exposure in mice
depleted hepatic and brain glutathione (GS) levels, and increased
malondialdehyde (MDA), a marker of lipid peroxidation. DMSA
administration for seven days resulted in a reduction in blood, liver,
and brain lead levels. N-acetylcysteine supplementation decreased MDA
levels, indicating amelioration of oxidative stress by NAC, but it did
not decrease lead levels.41

In an animal study, co-administration of ascorbic acid (vitamin C)
with DMSA enhanced the urinary excretion of lead in rats compared to
DMSA alone.42

A suggested protocol for lead toxicity is to identify and remove the
environmental exposure, and use DMSA 10 mg/kg three times a day for
the first five days, followed by 14 days at 10 mg/kg twice a day.

--------------------------------------------------------------------------------

DMSA Treatment in Mercury Toxicity

DMSA has been in recent use as a treatment for mercury poisoning since
Friedheim reported on DMSA treatment of experimental toxicity in mice
in 1975, noting its low toxicity and favorable efficacy compared to
BAL and D-penicillamine.43 Since that time, numerous animal and human
studies have shown DMSA administration increases urinary mercury
excretion and reduces blood and tissue mercury
concentration.3,33,44-47

In a comparison study of chelating agents, eleven construction workers
with acute mercury poisoning were treated with either DMSA or
N-acetyl-D,L-penicillamine (NAP), another sulfhydryl-containing metal
chelator. DMSA treatment resulted in greater urinary excretion of
mercury than NAP.48

In a study of single-dose, DMSA-induced urinary excretion in
occupationally-poisoned workers, a significant increase in urinary
mercury excretion was noted, especially in the first 24 hours. Mercury
excretion was greatest in the first eight hours after oral DMSA
administration.49

After methylmercuric chloride administration in rats, DMSA, DMPS, and
NAP were studied for their ability to remove mercury from blood and
tissue. DMSA was the most effective at removing mercury from the
blood, liver, brain, spleen, lungs, large intestine, skeletal muscle,
and bone. DMPS was more effective at removing mercury from the
kidneys.50

--------------------------------------------------------------------------------

Chelation of Mercury from the Brain

In rats, following intravenous administration of methyl mercury, DMSA
was found to be the "most efficient chelator for brain mercury."51

In another animal study, DMSA was given four days after methyl mercury
injection in mice, and continued for eight days. DMSA removed
two-thirds of the brain mercury deposits, NAP removed approximately
one-half, while DMPS did not remove significant amounts of mercury
from the brain.44

DMSA has also been used effectively in arsenic and cadmium
poisoning.2,3,53

--------------------------------------------------------------------------------

Mercury Diagnostic and Treatment Protocol

Hair analysis is an inexpensive and valuable tool for evaluating prior
mercury exposure.10,53 An effective way to evaluate mercury toxicity
quantitatively is to determine the amount of mercury excreted in the
urine after a challenge dose of DMSA. A baseline 24-hour urine is
collected before the challenge, then again on day three of a three-day
dosing of 200 mg three times a day.

The therapeutic dosage of DMSA for mercury toxicity is not well
defined in the literature. Doses as high as 30 mg/kg per day have been
used, with no serious side effects noted.34 One DMSA treatment
protocol suggests 10 mg/kg day taken in divided doses for three days.
The patient then discontinues taking DMSA for 14 days, then takes it
again for 3 days. Five to 10 treatment cycles may be necessary.54
Another protocol suggests 500 mg per day on an empty stomach, every
other day for a minimum of five weeks. For very sensitive patients,
250 mg per day, every other day may be necessary, with an increase to
500 mg after two to three weeks, for a total of five weeks of
therapy.55 More studies need to be done to define optimal dosing
strategies for this substance. Be aware that sulfhydryl compounds in
DMSA will make urine smell very sulfurous. Adequate communication with
the patient regarding this issue is important, so they are not taken
by surprise.

Adjunctive nutrient therapy includes hydrolyzed whey protein, as it
contains cysteine and cysteine residues which can be of benefit while
using DMSA. Cysteine is the rate-limiting step in glutathione
production, necessary for fecal heavy metal excretion and
hepatoprotection. Whey also contains branched-chain amino acids, which
will occupy transport sites at the blood-brain barrier, effectively
keeping bound metals from being re-deposited in the brain.
Supplemental dosing of N-acetylcysteine, 500 mg three times per day,
can also be helpful.54 A multi-mineral supplement can be taken between
cycles.

--------------------------------------------------------------------------------

References

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24. Ballatori N, Clarkson TW. Biliary secretion of glutathione-metal
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25. Ballatori N, Clarkson TW. Dependence of biliary secretion of
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26. Gregus Z, Varga F. Role of glutathione and hepatic glutathione
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zinc: a study with enzyme inducers and glutathione depletors. Acta
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27. Gregus Z, Klaassen CD. Disposition of metals in rats: a
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28. Ishihara N, Matsushiro T. Biliary and urinary excretion of metals
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29. Aposhian HV, Maiorino RM, Rivera M, et al. Human studies with the
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30. Maiorino RM, Bruce DC, Aposhian HV. Determination and metabolism
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mixed disulfides of meso-2,3-dimercaptosuccinic acid with L-cysteine
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31. Maiorino RM, Akins JM, Blaha K, et al. Determination and
metabolism of dithiol chelating agents: X. In humans,
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32. Aposhian HV, Maiorino RM, Dart RC, Perry DF. Urinary excretion of
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33. Nielson JB, Andersen O. Effect of four thiol-containing chelators
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34. Fournier L, Thomas G, Garnier R, et al. 2,3-Dimercaptosuccinic
acid treatment of heavy metal poisoning in humans. Med Toxicol Adverse
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35. Graziano JH, Siris ES, Lolacono N, et al. 2,3-dimercaptosuccinic
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36. Cory-Slechta DA. Mobilization of lead over the course of DMSA
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37. Jones MM, Basinger MA, Gale GR, et al. Effect of chelate
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38. Tandon SK, Floras SJS. Therapeutic efficacy of dimercaptosuccinic
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39. Cory-Slechta DA, Weiss B, Cox C. Mobilization and redistribution
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40. Flora SJ, Bhattacharya R, Vijayaraghavan R. Combined therapeutic
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41. Ercal N, Treeratphan P, Hammond TC, et al. In vivo indices of
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42. Tandon SK, Singh S, Jain VK. Efficacy of combined chelation in
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43. Friedheim E, Corvi C. Meso-dimercaptosuccinic acid, a chelating
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44. Aaseth J, Friedheim EA. Treatment of methyl mercury poisoning in
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Acta Pharmacol Toxicol 1978;42:248-252.

45. Aaseth J, Alexander J, Raknerud N. Treatment of mercuric chloride
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46. Grandjean P, Guldager B, Larsen IB, et al. Placebo response in
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47. Ramsey DT, Casteel SW, Faggella AM, et al. Use of orally
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48. Bluhm RE, Bobbitt RG, Welch LG, et al. Elemental mercury vapour
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49. Roels HA, Boeckx M, Ceulemans E, Lauwerys RR. Urinary excretion of
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Med 1991;48:247-253.

50. Planas-Bohne F. The influence of chelating agents on the
distribution and biotransformation of methylmercuric chloride in rats.
J Pharmacol Exp Ther 1981;217:500-504.

51. Butterworth RF, Gonce M, Barbeau A. Accumulation and removal of
Hg203 in different regions of the rat brain. Can J Neurol Sci
1978;5:397-400.

52. Lenz K, Hruby K, Druml W, et al. 2,3-Dimercaptosuccinic acid in
human arsenic poisoning. Arch Toxicol 1981;47:241-243.

53. Schweinsberg F. Risk estimation of mercury intake from different
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54. Quig, David, PhD. Doctor's Data, Chicago, IL. Personal
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55. Frackelton JP, Christensen RL. Mercury poisoning and its potential
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observations using a new therapeutic approach. J Adv Med 1998;11:9-25.

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Return to

Although extremely rare, mercury poisoning has been implicated in
cases where people are excellent break dancers one day, and very
suddenly they find themselves completely unable to break dance the
very next morning.

Joel

Not with dentistry Dude. You cannot chelate out 17 micrograms!

Joel

Right. The altie.alties kill themselves with their goofie therapies.

I see you making an ASSumption based on...on...on...hmmm, on what are you
basing this assumption? Your preconceived notions? And where did you pull
the "Suppose one in 500 develops significant amalgam toxicity" statement
from? One could just as easily guess the third person didn't come back
because my advice was correct, and they were too embarrassed to come back
and admit that. I don't know, and neither do you.

T

Go to the alties and stop annoying the
dentists about chelation and stuff.

We do dentistry not alchemy.

Joel