MERCURY, SCIENCE AND POLITICS

January 2009

Dr. Boyd Haley

Professor Emeritus of
Chemistry/Biochemistry
University of Kentucky
 Visualization of Mercury Vapor Escaping
from an Aged Dental Amalgam
• From: www.
uninformed
concent.com
• David
Kennedy’s
IAOMT tape
IN SPITE OF THE
OBVIOUS
EMISSION OF Amalgam is 50%
Hg VAPORS Mercury, inches from
FROM DENTAL your brain and
AMALGAM olfactory tissues.
THE FDA HAS
STEADFASTLY
REFUSED TO
TEST THEM
FOR SAFETY!
 Mercury from Dental Amalgam
1. Pro-amalgam ADA spokespersons “estimate” that
about 0.03 mcg mercury are emitted from a single
amalgam per day. Estimate that it would take
several hundred amalgams to provide a toxic
exposure.
2. A new IAOMT study shows that different
amalgam types emit more mercury and that a
single spill (very small amalgam) emits between
4.0 to 20 mcg of mercury per day at room
temperature and without abrasion of any sort.
This is about 133 to 666 times more than was
estimated by the ADA!
 IAOMT AMALGAM STUDY PROCEDURE
• Nine dentists across the USA volunteered to make 10
cylindrical, one spill amalgams in a provided plexiglass
mold.
• The IAOMT provided new amalgam kits directly from the
manufacturers to each dentist.
• The amalgams in the molds were sent to Dr. Haley at the
University of Kentucky for Hg analysis.
• The amalgams were allowed to age for over one month to
eliminate any surface mercury.
• The amalgams were placed in 10 ml of distilled water which
was changed daily.
• Aliquots of this water were removed at days indicated and
analyzed for mercury content.
Micrograms Hg released/24hrs/cm2 at 25oC from amalgams kept in a sealed test tube.

DENTISTS BRAND DAY1 DAY4 DAY8 DAY11 DAY15 DAY18 DAY22 DAY25

BASCIANO Valiant 9.921 9.677 9.580 9.463 8.700 8.873 9.392 9.311

9.751 9.262 8.886 8.202 8.074 8.014 9.563 10.322

8.075 7.288 7.054 7.288 7.558 7.311 7.315 6.956

ECCLES Dispersalloy 9.966 9.620 10.851 10.590 11.260 9.070 9.280 9.014

7.322 7.922 9.913 9.279 8.639 6.809 7.542 8.672

9.206 8.685 8.599 8.480 7.783 8.270 7.936 8.997

FISCHER Valiant 5.958 5.829 4.408 4.533 4.266 4.473 5.136 4.460

5.280 4.762 4.492 4.279 4.801 4.505 4.300 4.862

4.596 4.704 4.929 4.867 6.147 5.798 5.936 5.468

GRUBE Valiant 6.841 6.904 6.788 5.782 8.158 7.740 7.893 8.026

12.458 11.878 11.771 12.404 12.146 10.693 10.484 10.221

13.911 13.421 12.618 11.176 11.669 13.439 13.208 13.090

MESSERMAN Dispersalloy 11.357 11.238 11.887 12.086 15.335 14.712 14.473 15.859

17.796 17.484 16.765 19.584 19.321 20.716 20.696 19.995

15.336 14.602 14.086 18.625 17.759 12.389 16.285 15.580

 From a study funded by NIH done on orphans in Lisbon, Portugal.

GIRLS
BOYS

J. Woods, et al., Environmental Health Perspectives (2007) 115;10, 1527-1531.

• The previous slide shows that prolonged
exposure to mercury vapor decreases the
child’s ability to excrete mercury through their
kidneys. Especially affects BOYS.
• This is consistent with the well known toxic
effects of mercury on kidneys.
• This explanation is consistent with the reports
by the EPA and National Academy of
Sciences that 8 to10% of American women
have such high Hg body levels that would
render increased susceptibility to neurological
damage any child they would give birth to.
 ELEVATED MERCURY IN IDIOPATHIC
DILATED CARDIOMYOPATHY (IDCM).
WHERE DOES THE Hg COME FROM?
LEVELS ng/g Hg Sb
Controls 8.0 1.5
IDCM 178,400 19.260
Frustaci et al., J. of American College of Cardiology, 33, (6) 1578, 1999. Controls
were patients with valvular or ischemic heart disease.
ATHLETIC YOUTH DIE OF IDCM.
WHY HASN’T NIH REQUESTED PROPOSALS FOR
RESEARCH TO STUDY THIS??
THIS IS PROOF THAT MERCURY CAN CONCENTRATE IN
SPECIFIC TISSUES OR ORGANS OF THE BODY, EVEN IF Hg
BLOOD LEVELS ARE FOUND TO BE IN THE NORMAL
RANGE.
Activated Matrix Metallo Proteinase (MMP) is involved in
numerous inflammatory diseases. Our new research shows
MMP is activated by mercury and organic mercury!
• Atrial fibrillation (AF) produces changes in atrial structure and extracellular matrix composition, which is regulated by matrix
metalloproteinases (MMPs) and often occurs in the setting of congestive heart failure.
• Matrix metalloproteinases (MMPs) are thought to participate in the pathogenesis of coronary artery disease (CAD), particularly
in the occurrence of acute coronary syndrome (ACS).
• Matrix metalloproteases (MMPs) are important in many physiological processes including development, reproduction, and
wound repair. Conversely, aberrant MMPs expression can be detrimental, promoting the pathologic destruction of extracellular
matrix components in numerous disease states including breast and squamous cell carcinoma.
• The significance of circulating matrix metalloproteinases -2 and -9 (MMP-2, MMP-9), as well as their tissue inhibitors -1 and -2
(TIMP-1, TIMP-2) in ovarian cancer were studied to assess the possibility of using them in clinical decision-making. Within
malignant neoplasias, high circulating TIMP-1 correlated to the aggressive phenotype and unfavorable prognosis.
• Matrix metalloproteinases (MMPs) are implicated in the pathogenesis of diseases such as Alzheimer's Disease (AD) and
amyotrophic lateral sclerosis (ALS). Increased expression of MMP-9 and TIMPs has been reported in postmortem AD and ALS
brain tissue, as well as in ALS cerebrospinal fluid (CSF) and plasma.
• In active MS patients, both with relapsing-remitting and chronic progressive disease MMP-9 mRNA and plasma protein levels
were significantly increased compared to healthy controls.
• Abdominal aortic aneurysms are characterized by degradation of the extracellular matrix, with a reduction in the elastin
concentration of the arterial media. These changes are mediated by increased levels of endogenous metalloproteinases (MMPs)
within the aorta.
• These data suggest that the balance of MMP-2 and MMP-9 to TIMP-1 and TIMP-2 expression is an essential factor in the
aggressiveness of renal cell carcinoma.
• Several solid tumors display enhanced expression of matrix metalloproteinases (MMPs), and recently MMP-inhibitors have
entered clinical trials. The obtained results support the hypothesis that MMPs and their endogenous inhibitors participate in the
invasive process of human osteosarcoma.

NUMEROUS DISEASES INCLUDING SEVERAL CANCERS AND

NEUROLOGICAL ILLNESSES ARE ASSOCIATED WITH THE
ACTIVATION OF SPECIFIC MATRIX METALLO PROTEINASES
(MMP). Hg2+ AND ETHYL-Hg (as thimerosal) BOTH ACTIVATE A
COMMON FORM OF MMP.
g2+ AND THIMEROSAL ACTIVATE MMP-9, AN
E THAT DIGESTS COLLAGEN AND LEADS TO
 Amalgams and General Health
•The constant release of mercury from dental
amalgams would lead to the constant activation of
the enzyme MMP (matrix metallo proteinase) that
degrades collagen and disrupts cell to cell
contacts.
•This would lead to rapid aging and exacerbate the
many diseases that are associated with elevated
MMP activity.
•Anti-aging treatments should all include the
removal of dental amalgams, a fact based on
science not irrelevant “estimations”.
Axonal Transport - A Process Essential
for the Survival of Neurons
Dendrite

Membrane
Bound Organelle
Axon Dynien

Microtubule

Kinesin
 Only Hg2+ Induces Aberrant [32P]8N3GTP-ß-
Tubulin Interactions In Normal Brain Mimicking
the Observation seen in AD Brain

Alzheimer’s Normal Brain

Disease Brain without and with
Hg2+.
EDTA Prevents Cd, Cu & Zn But Not Hg Inhibition
of [32P]8N3GTP Photolabeling of Brain ß-Tubulin
 Water in Which an Aged Amalgam has been Soaked Induce
Abnormal Tubulin in Normal Brain Homogenates: Mimics the
Observation in Alzheimer’s Diseased Brain

120
Placing amalgams in water makes it toxic
100 to brain tubulin just like adding Hg2+.

80
% Active
Tubulin 60
40

20

0
l

1
o2

o4

o8

12 2

24 4

72 2
48 8

96 96
tro

0
o1

12
o
0t

1t

2t

4t

to

to

to

to
n

8t

to
co

Hours of Amalgam Soak

Degenerating Neurons into Neurofibillary Tangles by Treatment with
Nanomolar Levels of Hg2+. Leong et al. NeuroReports 2001,12 (4):733-
737.

MERCURY, AND ONLY

MERCURY COULD CAUSE THE
FORMATION OF NFTs, THE
MAJOR DIAGNOSTIC
HALLMARK OF ALZHEIMER’S
DISEASE!
Immunostaining for Tubulin in Neurons treated with Hg2+.
Leong et al. University of Calgary.
Alzheimer's Metal Concentrations in Plasma and Cerebrospinal
Fluid in Patients with Disease. Dement Geriatr Cogn Disord. 2008 May 5;25(6):508-
515 [Epub ahead of print]
Gerhardsson L, Lundh T, Minthon L, Londos E.
The homeostasis of essential metals such as copper, iron, selenium and zinc
may be altered in the brain of subjects with Alzheimer's disease (AD).
Methods: Concentrations of metals (magnesium, calcium, vanadium, manganese, iron,
cobalt, nickel, copper, zinc, selenium, rubidium, strontium, molybdenum, cadmium, tin,
antimony, cesium, mercury and lead) were determined in plasma and cerebrospinal
fluid (CSF) by inductively coupled plasma mass spectrometry in 173 patients with AD
and in 87 patients with the combination of AD and minor vascular components (AD +
vasc). Comparison was made with 54 healthy controls. Results: The plasma
concentrations of manganese and total mercury were significantly higher in
subjects with AD (p < 0.001) and AD + vasc (p </= 0.013) than in controls. In CSF,
however, the concentrations of vanadium, manganese, rubidium, antimony, cesium and
lead were significantly lower among subjects with AD (p </= 0.010) and AD + vasc (p
</= 0.047) than in controls. Strong positive correlations were noted between plasma Cs
versus CSF Cs in subjects with AD (r(s) = 0.50; p < 0.001), and AD + vasc (r(s) = 0.68;
p < 0.001). Conclusion: Besides the raised plasma mercury concentrations, no
consistent metal pattern in plasma or CSF was observed in patients with AD.
Maternal amalgam dental fillings as the source of mercury
exposure in developing fetus and newborn. Palkovicova L,
Ursinyova M, Masanova V, Yu Z, Hertz-Picciotto I. J Expo Sci Environ Epidemiol. 2007 Sep 12.
Dental amalgam is a mercury-based filling containing approximately 50% of metallic mercury
(Hg(0)). Human placenta does not represent a real barrier to the transport of Hg(0); hence, fetal
exposure occurs as a result of maternal exposure to Hg, with possible subsequent
neurodevelopmental disabilities in infants. This study represents a sub-study of the international
NIH-funded project "Early Childhood Development and polychlorinated biphenyls Exposure in
Slovakia". The main aim of this analysis was to assess the relationship between maternal dental
amalgam fillings and exposure of the developing fetus to Hg. The study subjects were mother-
child pairs (N=99). Questionnaires were administered after delivery, and chemical analyses of
Hg were performed in the samples of maternal and cord blood using atomic absorption
spectrometry with amalgamation technique. The median values of Hg concentrations were 0.63
mug/l (range 0.14-2.9 mug/l) and 0.80 mug/l (range 0.15-2.54 mug/l) for maternal and cord
blood, respectively. None of the cord blood Hg concentrations reached the level considered to be
hazardous for neurodevelopmental effects in children exposed to Hg in utero (EPA reference
dose for Hg of 5.8 mug/l in cord blood). A strong positive correlation between maternal and cord
blood Hg levels was found (rho=0.79; P<0.001). Levels of Hg in the cord blood were
significantly associated with the number of maternal amalgam fillings (rho=0.46,
P<0.001) and with the number of years since the last filling (rho=-0.37, P<0.001); these
associations remained significant after adjustment for maternal age and education.
Dental amalgam fillings in girls and women of reproductive age should be used with caution, to
avoid increased prenatal Hg exposure.
•Mercury, and only mercury, can mimic the abnormal
biochemistry observed in Alzheimer’s Diseased brain
as detected in comparison to normal human brain.
The vaporous form of mercury is the most effective as
it crosses the blood-brain barrier with ease as shown in
a study with living rats.
•Amalgams are only inches from the brain and the
olfactory nerves and constantly release mercury vapor.

•Yet our FDA and ADA constantly contend that these

vapors, shown to accumulate in the brain and other
organs, is safe. Today the FDA is reevaluating the
safety of dental amalgam. Contact them!
Federal Register / Vol. 73, No. 82 / Monday,
April 28, 2008 / Proposed Rules
SUMMARY: The Food and Drug Administration (FDA)
is reopening for 90 days, the comment period for the
proposed rule, published in the Federal Register of
February 20, 2002 (67 FR 7620), on the classification of
encapsulated amalgam alloy and dental mercury, the
reclassification of dental mercury, and the issuance of
special controls for amalgam alloy.
Consumers Dental Choice lawyers had to sue the FDA and
certain officials to get them to take action. The lawsuit is
currently underway. It has been over 30 years that the FDA
has refused to evaluate and classify dental amalgams.
Classification of amalgams is being fought by the American
Dental Association.
Thimerosal Is Composed of Thiosalicylic
Acid And Ethyl Mercury, A Known
Neurotoxicant
Water soluble
Water
insoluble

1. The Merck Index, 12th ed., p. 1590, #9451 (1996).

2. Martindale The Extra Pharmacopoeia, 30th ed., 804 (1993).
Organ Mercury Levels in Infants with Omophaloceles Treated with
Thimerosal. Fagan et al. Archives of Disease in Childhood 52, 962-64, 1977
• Between 1969-75, 13 cases were treated, 10 died. Mercury
analysis of organs ranged from 65 to 2,700 times normal levels. This
appears to be from 9 to 48 topical applications of 0.1% thimerosal
applications. NOTE; These children were most likely on
antibiotics. Consider the effect on their immune system!
• “Paradoxically, (in another study) 3 infants exposed postnatally (Iraq, Methyl-Hg
by ingestion) did not exhibit signs or symptoms, though their blood levels were
>1,000ppb, and one was >1,500ppb.” No antibiotics involved! Blood levels
are not a measure of toxicity.
• CONCLUSION IN 1977: “Organic mercurial antiseptics should
be heavily restricted or withdrawn from hospital use, and the fact
that mercury readily penetrates intact membranes and is highly
toxic seems to have been forgotten.” Result: Merthiolate
(thimerosal) was removed from the market by the FDA due to its
inherent toxicity to infants.
RAPID BLOOD TO BRAIN MOVEMENT OF [203Hg]-THIMEROSAL.
Gasset et al. Tetratogenicities of Opthalmic Drugs. Arch. Opthalomology 93, 52-55,
1975.
• Pregnant rabbits were injected subcutaneous with [203Hg]-
thimerosal.
• From hour 1 post injection to hour 6 the cpm of 203Hg in
the blood decreased from 100,000 to less than 25,000 cpm,
or over 75%.
• From hour 2 post injection to hour 6 there was increased
cpm of 203Hg in the fetal brain (2 fold), liver (4 fold) and
kidney (3 fold).
• Yet the IOM/CDC/AAP state that the rapid loss of
mercury from thimerosal from the blood makes it
unlikely to be toxic enough to cause autism.
Pichichero et al. Lancet 360:1737, 2002
 THE BIG MISTAKE!
• YET SOME INDIVIDUALS AT THE CDC AND
FDA DECIDED IT WAS OK TO INJECT
THIMEROSAL INTO A NEWBORN INFANT AT
LEVELS THAT WOULD BE EPA SAFE IF THE
INFANT WEIGHED 275 POUNDS!
• The EPA “safe level” was based on mercury
exposure from eating fish and whale meat.
• Most of the heavy metal protection in humans is in
the intestinal area as we evolved eating and drinking
contaminated food and water. This is bypassed on
injection of thimerosal or breathing mercury vapor.
 AUTISM IN DIFFERENT AGE GROUPS IN SCOTLAND

THERE IS A LACK OF OLDER AUTISTICS!

Thimerosal is toxic to tubulin and
actin. Combinations of Hg2+ and
thimerosal would be at least
additive.
Thimerosal in vaccines appeared to be more toxic than pure thimerosal!
Most likely due to synergistic effects of other additions like Al3+.

MOST VACCINES
CONTAIN TRACES OF
THIMEROSAL EVEN IF IT
IS NOT ADDED AS A
PRESERVATIVE.

The vaccine thimerosal

concentration was (is) 125,000
to 250,000 nanomolar!
 Hg2+ & THIMEROSAL DISPLAY ADDITIVE TOXICITIES
120 TO NEURONS IN CULTURE.
Neuron Survival (% Initial Number)

100

80
Control
50 nM thimerosal
50 nM thimerosal
60 +10 nM HgCl2

50 nM thimerosal
+ 25 nM HgCl2

40 10 nM HgCl2

25 nM HgCl2

20
0 5 10 15 20 25 30

Time (hr) After Treatment

 SYNERGISTIC EFFECTS OF HEAVY METALS IS
QUITE COMPLEX AND CAN GREATLY ENHANCE
THE TOXICTY OF MERCURY
Shubert et al. Combined Effects in Toxicology--A Rapid systematic
Testing Procedure:Cadmium, Mercury & Lead. J. of
Toxicology & Environmental Health 4:763, 1978.
 “the administration of an essentially no response level
(LD1) of a mercury salt together with a 1/20 of the
LD1 of a lead salt killed all of the animals.”
“Generally, a combination was synergistic when the
most toxic member was present at or near its LD1
dose in the presence of a much less toxic member.”
 Conclusion: Mixing borderline toxic levels of two
toxic metals (Pb2+ & Hg2+) makes an extremely
toxic solution.
 SYNERGISTIC TOXICITIES
120
Control
Al:NEOMYCIN:TESTOSTERONE 50 nM thimerosal
100 EFFECTS 500 nM Al(OH)3
Neuron Survival (% Initial Number)

1.75 µg Neomycin/ml
80 50 nM Thimerosal
500 nM Al(OH)3
50 nM Thimerosal
60 50 NANOMOLAR 1.75 µg Neomycin/ml
50 nM Thimerosal
THIMEROSAL 500 nM Al(OH)3
40 1.75 µg Neomycin/ml

DR. MARK
20
LOVELL
COLLABORATOR
+ TESTOSTERONE
0
0 5 10 15 20 25 30

Time (hr) After Treatment

 Estradiol Reduces Cumulative Mercury and Associated
Disturbances in the Hypothalamus-Pituitary Axis of
Ovariectomized Rats. Oliveria et al. Ecotoxicol. Environ.
Safety Jan.10, 2006
• Methyl-mercury induced a decrease in LHRH in
the medial hypothalmus and a decrease in plasma
levels of LH. These decreases in LHRH and LH
were abolished by estrogenic replacement therapy.

• “The estrogenic effects were associated

with a reduction of mercury content of the
anterior pituitary gland and medial
hypothalmus, suggesting a protective
estrogenic effect.”
 Mercury Effects on the Immune
• System
The mitotic spindle is built on tubulin quite similar
to that found in axons of neurons. Therefore, since
the cells of the immune system must divide for an
effective immune response Hg inhibits this and
actively suppresses the immune system.
• Thimerosal is a very potent inhibitor of
phagocytosis by mononuclear phagocytes,
inhibiting the process at low 1 to 5 nanomolar
levels. (Rampersad et al., Transfusion 45(3):384-
93,2005). This prevents removal of microbes and
ethyl-Hg damaged cells and proteins leading to
greater susceptibility for microbe infection and
widespread autoimmune problems.
Effects of Antibiotics, Diet and other Metals on
Hg Excretion: Found in Published Literature
• Rats exposed to antibiotics were severely impaired
in their ability to excrete mercury.
• Rats on milk versus high protein diets were much
less able to excrete mercury.
• The great enhancement of synergistic toxicity with
Hg and other heavy metals (e.g. lead) is well
documented in the literature. We have many
children with other heavy metals in their bodies.
• The above confounders have rarely been considered
by those who write articles supporting the safety of
thimerosal or dental amalgams.
 MERCURY BIRTH HAIR LEVELS VS. AMALGAM
FILLINGS IN AUTISTIC AND CONTROL GROUPS
AUTISTICS SEEM LESS CAPABLE OF EXCRETING MERCURY AS INFANTS.

14

12

10
Hair Hg level
(mcg/g) 8
Data from A. Holmes,
M. Blaxill & B. Haley,
6 Controls
Int. J. of Toxicology
v22, 2003
4

2
Autistic
0
Number of amalgams: 0-3 4-5 6-7 8-9 >10
Control: autistic ratio: 2.64 6.93 6.70 6.32 17.91
N: 15 22 29 30 43
 Other Epidemiological Studies
• A study on seven-year-old children in the Faeroe Islands
found that blood pressure problems increased with
decreased blood Hg. This implies retention toxicity effects
of Hg in this comparison.
• In the Sechylles study of >700 children, boys with higher
levels of hair mercury performed better on some tests as the
Boston Naming test. This implies that ability to excrete
increases hair Hg levels, not exposure, in this comparison.
• Healthier children seem to be more exposed to mercury if
one believes high blood and hair Hg are measure of
exposure.
• CONCLUSION: Blood and hair Hg levels are not a measure
of exposure at low levels, but rather a measure of both
exposure and ability to excrete mercury.
 The involvement of the 2004 Institute of
Medicine (IOM) report.
• The 2004 IOM committee was funded by the CDC.
• The 2004 IOM report cleared thimerosal as being involved
in autism and recommended that no further research be
done on this issue but to investigate other more fruitful
areas like genetics—which has failed to find a significant
genetic component of autism.
• The 2004 IOM report was based only on 5 epidemiological
studies of questionable value, none lead by an American.
• The 2004 IOM report totally dismissed the basic science
research on thimerosal toxicity and the resultant aberrant
biochemistry possibly caused by mercury-like toxicity
reported by several research scientists.
• A congressionally requested NIH committee looked at
the 2004 IOM report and gave it a very bad evaluation.
• The CDC is living in a state of denial!
Who did the Epidemiological Studies the IOM depended on??
• The Verstraten (Belgium) studies at first showed autism rates were
enhanced by thimerosal exposure but changed with renditions to show
no effect. All the CDC data was lost or destroyed after it was
published. Verstraten now works for a major vaccine producer in
Europe.
• Two studies were done by Danish (Madsen and Hviid) who worked
for the Stantens Serum Institute (SSI). SSI makes thimerosal
containing vaccines and sells them to other countries because they are
not allowed to be used in Denmark since 1992. These studies showed
a 20-fold increase in autism on removal of thimerosal! STUPID!
• One study was done in England by E. Miller. After her results were
made known at the 20004 IOM meeting the National Health Service
removed thimerosal from English vaccines.
• Troubling, that the opinion of the CDC is based totally on foreign,
conflicted opinions. Why couldn’t the CDC find epidemiologists in
the USA to do these studies???
• The Verstraten studies differed from the Danish and English study in
that it did not show the dramatic protection effects of thimerosal
against autism!!!!!
Autism Risks From 5 Sequential Studies by
Verstraten et al. of CDC
Study1 Study2 Study3 Study4 Study5

Indicates thimerosal is causal Conflicts with other CDC

7.62
(1999) for autism. accepted studies from
2.48 Europe!

1.69 Simpsonwood Meeting

1.52
(2001)
1.00*
*i.e., no increased risk of autism compared to low exposure
(2005)
group. Also, no evident protective effect of thimerosal or the
value would have been much less than 1.0. Yet the Danish
studies showed that removal of thimerosal caused a 20 to 25
fold increase in autism. One of these sets of studies has to
be wrong.
After publication in 2005 all of the data for this work was “lost” by the CDC!!!
Evidence of Harm
Go to Safeminds.org to read the FOIA material on the Verstraten studies.
 DANISH STUDY

• In USA rate was 1/150 or 67/10,000!

• Outpatients added in 1995.
• Large Copenhagen Clinic added in1992.
• Autism classification changed in 1994.
• Thimerosal removed from vaccine.

Conclusion; exposure to a potent neurotoxin, thimerosal, prevents autism!!! Nonsense!

•The CDC, AAP and many pro-thimerosal proponents
quote the Danish Studies as showing that thimerosal is
not causal for autism since its removal correlated with
about a 20-fold increase in autism. But this study is
like looking at the involvement of mosquitos with
malaria and doing the research in Alaska!
•These studies are quite unbelievable if one looks at
the content in detail. The major question to the CDC
and AAP is why haven’t the Danes, Swedes and
English replaced thimerosal in their vaccines if it is
proven, as these studies suggest, that thimerosal
prevents autism?????
•Perhaps the medical establishments in these countries
are more concerned about infant health than ours?
 Other Considerations
• In England, between 1970-1980, about 14.7% of
children were not vaccinated as suggested. Yet a
parental autism group there report (Tony Bateson), on
the internet, only two cases of autism in non-vaccinated
children were found in their search of autistics born
during this time frame.
• The UPI series on autism by Dan Olmstead finds:
• Very little, if any, autism in the unvaccinated Amish!
• Healthfirst, a Chicago Clinic that does not vaccinate in
the first year of birth reports no autistic children born
since 1985 from a population of about 35,000 children.
• The dramatic increase in autism in China following the
end of the cold war and the importation of Western
vaccines (Evidence of Harm by David Kirby).
 CRITICAL EXCLUSIONS
THE CDC IGNORING OF THE EARLY REPORT
BY REPORTER DAN OLMSTEAD OF A
GREATLY DECREASED RATE OF AUTISM IN
THE NON-VACCINATED AMISH POPULATION
IS CRIMINAL!
THERE IS NO RATIONAL EXPLANATION FOR
THIS. THEY HAVE PUSHED FOR RESEARCH IN
OTHER AREAS (GENETICS) TO AVOID
FINDING THE POSSIBLE NEGATIVE EFFECTS
OF THE CDC MANDATED VACCINE PROGRAM.

About $25 million has recently been spent to find the

 THE SMOKING GUN STUDY
• Done in Paris, France (since the 2004 IOM committee
recommended NIH not fund thimerosal studies) in a large
autism clinic.
• Investigated porphyrin profiles in autistic versus normal
children because these profiles are the best indicator for
heavy metal toxicity, especially mercury toxicity.
• Found porphyrin profiles that indicated 53% of autistic
children surveyed were mercury toxic.
• Reversed toxic porphyrin profiles by treating autistics with
a mercury chelator. Therefore, the cause was not purely
genetic, but involved mercury toxicity.
• Supporting data from Norway has been reported.
• Dr. Robert Natal and Dr. Richard Lathe were the lead
researchers in this work published in the International J.
Toxicology 2006.
 WHAT ARE PORPHYRINS?
• Porphyrins are a class of compounds that lead to the
synthesis of heme, the iron binding red compound of
hemoglobin that binds oxygen and aids in delivery to cells,
where it is used in the mitochondria to help make energy
(ATP). Lack of heme or hemoglobin leads to a very pale
complexion (ever notice the complexion of autistic
children?)
• Heme has other biological uses. It is in the mitochondrial
electron transport system that makes ATP. A shortage of
heme would prevent adequate energy production and could
increase free radical formation.
• Heme is needed for active P450 enzymes, the enzymes that
modify organic toxins and aid in removing them from the
body. Heme is also needed to remove amyloid protein from
human brain to prevent production of amyloid or senile
plaques as identified with Alzheimer’s diseased brain.
OXIDATIVE STRESS: The single biochemical abnormality found
in essentially all neurological, neurodegenerative, and neurobehavioral
diseases is the increased production of oxidative free radical compounds
and low glutathione levels. This is reflective of oxidative stress.
Oxidative stress is strongly associated with modification of lipids,
proteins, and DNA that can lead to membrane structural problem,
enzyme inhibition and genetic mutations.
James SJ, Cutler P, Melnyk S, et al. Metabolic markers of increased oxidative stress and methylation capacity in children
with autism. Am J Clin Nutr. 2004;80:1611–1617.

Ischiropoulos H, Beckman JS. Oxidative stress and nitration in neurodegeneration: Cause, effect or association? J Clin
Invest.
2003;111:163–169.

Muravchick S, Levy RJ. Clinical implications of mitochondrial dysfunction. Anesthesiology. 2006;105:819–837.

Kern JK, Jones AM. Evidence of toxicity, oxidative stress and neuronal insult in autism. J Toxicol Environ Health B Crit
Rev. 2006;9:485–499.

Larsson HJ, Eaton WW, Madsen KM, et al. Risk factors for autism: Perinatal factors, parental psychiatric history and
socioeconomic status. Am J Epidemiol. 2005;101:916–925.

Deth R, Muratore C, Benzercry J, et al. How environmental and genetic factors combine to cause autism: A
 REACTIVE OXYGEN SPECIES (ROSs)
• Superoxide Anion: O2 + e- O2-.

•Hydrogen Peroxide: O2-. HO2.

(hydroperoxyl radical)
2HO2. H2O2 + O2

•Hydroxyl Radical: O2-. + H2O2 O2 + HO- + HO.

REMOVAL OF ROSs
(Haber-Weiss)
Fe 2+
+ H O Fe 3+
+ HO -
+
SOD or Superoxide Dismutase Catalyzed Reaction.
2 2 HO.

(Fenton)
2O2-. + 2H+ H2O2 + O2 (keeps O2-.
The hydroxyl radical is the most damaging!
<10-11M)

*Catalyase Catalyzed Reaction. 2H2O2 2H2O

+ O2
 Ubiquione (Co-enzyme Q) is a mitochondrial mobile
electron carrier.
Citric Acid Cycle Reducing
equivalents

Both O2-. radical and the quinone radical can leak from damaged
mitochondrial membranes during the electron transport process
involved in making ATP requiring GSH to scavenge them decreasing
 Structures and General
Chemistry of Glutathione
GOOD

BAD

Note the number of charges on GSH. This makes it unlikely that it

could enter any hydrophobic location in a tissue where much of the
damaging oxidation occurs as caused by many toxicants.
 Structures and General
Chemistry of Glutathione
Glutathione (GSH) occurs in all tissues and is the most abundant sulfhydryl (-SH)
containing compound in cells. It protects many enzymes from inhibition by reactive
oxygen species (ROS).
1. Enzyme-SH(active) + ROS + RSH Enzyme-S-S-R(inactive) + H2O2
2. Enzyme-S-S-R(inactive) + GSH Enzyme-SH(active) + G-S-S-R
3. Enzyme-SH(active) + Hg2+ Enzyme-S-Hg+(inactive) + H+
4. Enzyme-S-Hg+(inactive) + GSH Enzyme-SH (active)+ GS-Hg+
5. GS-Hg+ + GSH GS-Hg-SG(excreted form) + H+

GSH PROTECTS THE BODY FROM OXIDATION AND HEAVY METAL

TOXICITY! GS-Hg-SG is probably the major form of mercury that is excreted from
the body by natural means. It leaves through the bilary transport system of the liver
into the feces, not through the kidney. Low GSH levels (oxidative stress) in effect
cause increased enzyme inhibition by ROS and decreases the ability to remove many
toxic metals as well as organic type toxins. YOU CANNOT INCREASE BODY
GLUTATIONE LEVELS BY EATING GLUTATHIONE!
 VIT-C GETS INTO ALL
CELLS AND MITOS.

reduced oxidized

oxidized reduced
 REVERSAL OF LIPID PEROXIDATION BY
GLUTATHIONE PEROXIDASE (GP)

R = CH3CH=CH-CH=(CH)n-COOH (a poly-unsaturated
fatty acid, pufa)

ROOH = CH3CH=CH-CH-(CH)n-COOH (an oxidized fatty

acid or
O-OH a hydroperoxide)

ROOH + 2GSH GSSG (oxidized glutathione) +

ROH + H2O

The ratio of GSH (reduced glutathione)/GSSG (oxidized

glutathione) is a measure of oxidative stress, or simply
put how much GSH is being consumed relative to how
well one can make it. The higher the GSH:GSSG ratio the
better one’s redox system is functioning. It appears as if
 Apoptosis, cell death.
It appears as if oxidation of GSH to GSSG
precedes cell death in two experimental models.
1. Fibroblasts in culture
2. Regressing mammary tissue after weaning.
CONVERSION OF GSH TO GSSG PRECEDES CELL DEATH IN CULTURED
FIBROBASTIC CELLS

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies

in vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
 THE REDOX RATIO OF GSSG/GSH INCREASES BEFORE FIBROBLASTIC
CELL DEATH

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies

in vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
 GSH DROPS AND GSSG INCREASES DURING FIBROBLASTIC CELL
DEATH

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies

in vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
 GSSG AND GSH LEVELS IN REGRESSING MAMMARY GLAND CELLS
AFTER WEANING.

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies in

vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
 CHANGE IN MITOCHONDRIAL GSSG/GSH RATIOS IN REGRESSING
MAMMARY TISSUE.

MITOCHONDRIAL GSSG IS
INCREASING AND GSH IS
DECREASING WITH CELL
DEATH.

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies in

vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
 INCREASED DNA DAMAGE WITH INCREASED OXIDATIVE STRESS IN
REGRESSING MAMMARY CELLS

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies in

vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
 INCREASED H2O2 PRODUCTION IN MITOCHONDRIA FROM APOPTIC
MAMMARY GLAND.

H2 O2
LEVELS

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies in

vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
GLUTATHIONE ESTER DECREASES APOPTOSIS IN CULTURED
FIBROBASTS: THEREFORE THE DEATH IS REDUCED WITH TREATMENT
THAT INCREASES INTRACELLULAR GSH
FCS = fetal calf serum

NO GSH-ester PLUS GSH-ester

Oxidative Damage to mitochondrial DNA and GSH oxidation in apoptosis: Studies in

vivo and in vitro. Esteve et al. FASEB J. 1999 V13, 1055-1064
OLD CONCEPTS: WE NEED TO
DIRECTLY TREAT OXIDATIVE STRESS
• REDUCE THE PRODUCTION OF FREE
RADICALS OR SCAVENGE THEM TO
SALVAGE GSH. (REDUCING VITAMINS)
• INCREASE PRODUCTION OF GLUTATHIONE
BY PROVIDING PRO-GLUTATHIONE
NUTRIENTS (e.g CYSTEINE) AND
REMOVING ANY TOXICANTS (e.g. HEAVY
METALS) THAT PREVENT SYNTHESIS.
• PREVENT AND REVERSE THE DAMAGE
CAUSED BY OXIDATIVE STRESS FACTORS.
•
New Antioxidant Partitioning Concept
Most available antioxidants are water soluble because they
carry ionic charges. DMPS, DMSA, glutathione, and Se2-
are all charged and are rapidly cleared from the body.
Therefore, they are not efficient at removing hydroxyl
radicals that are located in fatty (hydrophobic)
environments or inside of cells, such as the mitochondria.
• Therefore, most toxin generated reactive oxygen species
(ROSs) in the body are not available to DMPS, etc. for
binding as they are intracellular or in hydrophobic locations.
• The new antioxidants are needed that enter hydrophobic
areas. Entering the hydrophobic regions increases the time
spent in the body enhancing the scavenging of hydroxyl
radicals.
• Therefore, the antioxidants need to be both effective in the
ORAC test (oxygen radical absorbance capacity test) and
hydrophobic.
 New Hydrophobic Antioxidant Agents

O O O O
N

NH HN NH HN
Free radical scavenging sites

SH HS SH HS
Potent scavengers of hydroxyl radicals in lipophilic areas.

Benzene bis-amido bis-thiol Pyridine bis-amido bis-thiol

Water insoluble, but lipid soluble, coupling with glutathione
makes this compound water soluble (next slide).
 Glutathione derivative of Antioxidant Agents
OSR compound
O O

O NH O O HN O
HO OH

S NH HN S
NH S S NH

NH2 H2N
O O O O O O

O HO H3C CH3 OH O

Note: Molecule would be charged and

water soluble at pH 7.4.

Glutathione Glutathione
Very water soluble
AN OXYGEN RADICAL ABSORBANCE STUDY OF ONE OF THE NEW
ANTIOXIDANTS DONE IN AQUEOUS SOLUTION.

CT1 Dose Response

60
y = 0.1487x + 3.0744
50
R2 = 0.9994
40
Trolox Eq uM

30
20
10
0
0 50 100 150 200 250 300 350
CT1 uM
 Toxicity Study of Lipid Soluble Antioxidant
• Group A B C D
• Test 1 0 100 200 300
• Test 2 0 200 300 400
• Test 3 0 300 400 500
• Total 0 600 900 1,200

• Test 4 0 - 1,500 1,500

• Procedure: Rats were injected under the skin in the stomach

area with compound to the amount in μMoles/kg body
weight. Three days pause was between each treatment.
• Result: No toxicity or weight loss was observed at any
level of exposure
 TOXICITY TESTING BY ORAL
DELIVERY
•A commercial toxicology laboratory has confirmed
that the new antioxidant is not toxic at 5grams/kg
body weight when given orally, the highest testing
level! This is equivalent to a 100 lb person taking
227grams.
Nor did mice given 1.0g/kg body weight for 28
straight days demonstrate any toxic effects.
•The compounds are not mutagenic as determined by a
FDA approved laboratory.
•This research was done for the purpose of submission
 CONCLUSIONS
• A NON-TOXIC, LIPID SOLUBLE, FREE
RADICAL SCAVENGING ANTIOXIDANT HAS
BEEN DEVELOPED AND FOUND TO BE
WITHOUT TOXICITY IN TEST ANIMALS.
• THESE ANTIOXIDANTS SCAVENGE
HYDROXYL RADICALS.
• THIS ANTIOXIDANT IS EFFECTIVE IN
HELPING MAINTAIN A HEALTHY
GLUTATHIONE LEVEL.