Transcript Conference with IOM and NIH

www.medicalvoices.org
PRESENTS:
A Tidal Wave of Terror:
Thimerosal in Vaccines
Boyd Haley, PdD
Professor of Chemistry,
University of Kentucky
This vaccine webinar series is provided as a community service by Homefirst Natural Pharm Source
www.homefirst.com
TOXICITÉ DU MERCURE ET SA
RELATION AUX MALADIES
NEUROLOGIQUES
DR. BOYD E. HALEY
PROFESSEUR ET PRÉSIDENT DU
DÉPARTEMENT DE CHIMIE
UNIVERSITÉ DU KENTUCKY
WHAT CAUSED THE USA AUTISM EPIDEMIC?
•IT IS NOT CAUSED BY GENETICS.
•IT IS LIKELY A GENETIC SUSCEPTIBILITY TO AN
ENVIRONMENTAL TOXICANT.
•THE TOXICANT HAD TO INCREASE IN ALL 50 STATES AT
APPROXIMATELY THE SAME TIME (1988-90).
•EXPOSURE HAS TO OCCUR BEFORE AGE 2.
•THE TOXICANT HAS TO EFFECT BOYS MUCH MORE THAN
GIRLS! (ONLY MERCURY IS KNOWN TO DO THIS!)
•ANY SUGGESTED TOXICANT HAS TO EXPLAIN THE
MULTIPLE CELLULAR AND BIOCHEMICAL
ABNORMALITIES OBSERVED CLINICALLY IN AUTISTICS.
•ONLY THE THIMEROSAL EXPOSURE FROM THE CDC
MANDATED VACCINE PROGRAM FITS THIS CRITERIA.
Important Observations
1. Today, the USA has the highest infant
vaccination rate in the world, yet the USA is
number 41 on the infant mortality list.
2. The USA has a very high rate of aged individuals
being vaccinated, yet we are now number 28 on
the longevity list.
3. A recent report by Generation Rescue clearly
shows the USA has the highest vaccine rate and
the highest level of autism of 5 major countries.
4. If vaccines decrease the rate of childhood death
due to infectious diseases what types of death are
occurring that make the USA place #41?
AUTISM AND THE RATE OF ASD IN EIGHT YEAR OLDS FROM 1992, 1994 AND 1996 AND
RELATIONSHIP TO COMPLIANCY IN RECEIVING THE HEPATITIS-B VACCINE
VACCINE DATE
1992
1994
1996
2000
YEAR EVALUATED
2000
2002
2004
2008
ASD/10,000(ADDM)
67
74
>100
???
HEP-B % (CDC DATA)
8%
27%
82%
Thimerosal removed(?) from infant vaccines in 2003. ADDM (Autism& Developmental Disabilities Monitoring network,
CDC’s Morbidity and Mortality Weekly Report). Hep-B introduced in 1991 with 25mcgs thimerosal. Hep-B rates were from
National Immunization Survey.
FACTS
•Hepatitis B vaccine to newborn baby boys more than triples the risk of ASD. Annals of
Epidemiology.
•Infant male primates who received one dose of the Hepatitis-B were far more likely to
display developmental delays than unvaccinated controls. Neurotoxicology.
•Boys getting the 3-shot HepB vaccine series were eight times more likely to require
early intervention services than boys who did not have the series. Toxicological and
Environmental Chemistry.
•Children who received the Hepatitis B vaccine series were 50% to 74% more likely to
develop "central nervous system inflammatory demyelination" than children who did
not receive the vaccine depending on the vaccine manufacturer. Neurology.
HEPATITIS B VACCINATION OF MALE NEONATES AND AUTISM
CM Gallagher, MS Goodman, Graduate Program in Public Health, Stony Brook University Medical Center, Stony Brook,
NY Annals of Epidemiology Vol. 19, No. 9 ABSTRACTS (ACE) September 2009: 651–680 p. 659 P24
PURPOSE: Universal newborn immunization with hepatitis B vaccine was
recommended in 1991; however, safety findings are mixed. The Vaccine Safety
Datalink Workgroup reported no association between hepatitis B vaccination at birth
and febrile episodes or neurological adverse events. Other studies found positive
associations between hepatitis B vaccination and ear infection, pharyngitis, and
chronic arthritis; as well as receipt of early intervention/ special education services
(EIS); in probability samples of U.S. children. Children with autistic spectrum disorder
(ASD) comprise a growing caseload for EIS. We evaluated the association between
hepatitis B vaccination of male neonates and parental report of ASD. METHODS: This
cross-sectional study used U.S. probability samples obtained from National Health
Interview Survey 1997–2002 datasets. Logistic regression modeling was used to
estimate the effect of neonatal hepatitis B vaccination on ASD risk among boys age 3–
17 years with shot records, adjusted for race, maternal education, and two-parent
household. RESULTS: Boys who received the hepatitis B vaccine during the first month
of life had 2.94 greater odds for ASD (Nz31 of 7,486; OR Z 2.94; p Z 0.03; 95% CI Z
1.10, 7.90) compared to later- or unvaccinated boys. Non-Hispanic white boys were
61% less likely to have ASD (ORZ0.39; pZ0.04; 95% CIZ0.16, 0.94) relative to nonwhite boys.CONCLUSION: Findings suggest that U.S. male neonates vaccinated with
hepatitis B vaccine had a 3-fold greater risk of ASD; risk was greatest for non-white
boys.
Enhanced toxicity for mice of pertussis vaccines when preserved
with Merthiolate (aka thimerosal).
Nelson, E.A. Gottshall, R.Y. Appl Microbiol. 1967 May;15(3):590-3.
Pertussis vaccines preserved with 0.01% Merthiolate
(thimerosal) are more toxic for mice than unpreserved
vaccines prepared from the same parent concentrate and
containing the same number of organisms. The toxicities of
both Merthiolate (0.01%)-preserved and unpreserved vaccines
increased when the number of organisms injected was
increased. An increase in mortality was observed when
Merthiolate (thimerosal) was injected separately, before or
after an unpreserved saline suspension of pertussis vaccine.
PMID: 6035051 [PubMed - indexed for MEDLINE]
Le thimérosal est composé d’acide
thiosalicylique et d’ éthyl de mercure, une
substance toxique bien connue
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 of
mercury vapor.
FIGURE 1: VACCINE MERCURY BURDEN AND AUTISM RISK: UNITED STATES
California
autism
prevalence
(cases per
10,000)
Vaccine
200 mercury
exposure
(micrograms)
20
California's reported
rates of autism
by year of birth
15
150
100
10
50
5
Cumulative mercury(1)
exposures through
childhood vaccines in
19-35 month olds surveyed
0
0
Year of birth
85
86
87
88
89
90
91
92
93
94
95
96
97
98
Year of survey
87
88
89
90
91
92
93
94
95
96
97
98
99
00
(1) Includes DPT, haemophilus influenza B and hepatitis B exposures weighted by survey year compliance
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.
1. “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.”
2. Conclusion: Mixing borderline toxic levels of two
toxic metals (Pb2+ & Hg2+) makes an extremely
toxic solution.
TOXICITÉS SYNERGÉTIQUES
Neuron Survival (% Initial Number)
120
Control
Aluminum;Neomycin;Testosterone Effects.
50 nM thimerosal
100
500 nM Al(OH)3
1.75 µg Neomycin/ml
50 nM Thimerosal
500 nM Al(OH)3
80
50 nM Thimerosal
1.75 µg Neomycin/ml
50 NANOMOLAR
TESTOSTERONE
60
40
50 nM Thimerosal
500 nM Al(OH)3
1.75 µg Neomycin/ml
20
DR. MARK LOVELL
COLLABORATOR
+ TESTOSTERONE
0
0
5
10
15
20
Time (hr) After Treatment
25
30
LE Hg ET LE THIMÉROSAL MONTRENT DES TOXICITÉS
ADDITIVES.
Neuron Survival (% Initial Number)
120
100
80
Control
50 nM thimerosal
60
50 nM thimerosal
+10 nM HgCl2
50 nM thimerosal
+ 25 nM HgCl2
40
10 nM HgCl2
25 nM HgCl2
20
0
5
10
15
20
Time (hr) After Treatment
25
30
TAUX NANOMOLAIRES ESTIMÉS DE THIMÉROSAL (POUR
NOURISSONS) APRÈS VACCINATION: VALEURS EXPRIMÉES EN
Kg, 16% ( % sang sain), 50 % OU 75 % ACCÈS DU VOLUME SUPPOSÉ
1 kg = 1 litre en volume
Hg 
12.5 g
50 g
67.5 g
1kg(2.2#) 84;125;391 335;500;1,562
453;676;2,106
2kg(4.4#) 42;62;196 167;250;781
226;338;1,053
3kg(6.6#) 28;42;130 111;166;520
151;226;701
5kg (11#) 17;26;78
67;100;312
91;136;421
10kg(22#) 8;12;39
34;50;156
45;68;210
15kg(33#) 5;8;26
23;34;104
31;46;140
NOTE: 1 nM thimerosal inhibits the enzyme methionine
synthetase and phagocytosis.
INFANT
WEIGHT
CALCULATED THIMEROSAL;
CONCENTRATION NANOMOLAR
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.”
Gender-selective toxicity of thimerosal
Donald R. Branch Departments of Medicine and Laboratory Medicine and Pathobiology, University of
Toronto, 67 College St., Toronto, Ontario, Canada M5G 2M1 Experimental and Toxicologic Pathology
(accepted 22 July 2008)
A recent report shows a correlation of the historical use of thimerosal in therapeutic
immunizations with the subsequent development of autism; however, this association
remains controversial. Autism occurs approximately four times more frequently in
males compared to females; thus, studies of thimerosal toxicity should take into
consideration gender-selective effects. The present study was originally undertaken to
determine the maximum tolerated dose (MTD) of thimersosal in male and female CD1
mice. However, during the limited MTD studies, it became apparent that thimerosal has
a differential MTD that depends on whether the mouse is male or female. At doses of
38.4–76.8 mg/kg using 10% DMSO as diluent, seven of seven male mice compared
to zero of seven female mice tested succumbed to thimerosal. Although the
thimerosal levels used were very high, as we were originally only trying to determine
MTD, it was completely unexpected to observe a difference of the MTD between
male and female mice. Thus, our studies, although not directly addressing the
controversy surrounding thimerosal and autism, and still preliminary due to small
numbers of mice examined, provide, nevertheless, the first report of gender-selective
toxicity of thimerosal and indicate that any future studies of thimerosal toxicity should
take into consideration gender-specific differences.
r 2008 Elsevier GmbH. All rights reserved.
ÉMISSION GAZEUSE DU MERCURE À
PARTIR D’UN AMALGAME DENTAIRE
• Source :
www.
uninformed
consent.com
• David
Kennedy’s
IAOMT tape
From a study funded by NIH done on orphans in Lisbon, Portugal
which concluded amalgams were safe for use in children!
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, who are 4 times more likely to become autistic
than are girls, many times more likely to have ADHD.
• The observation is consistent with testosterone causing
retention of mercury.
• 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.
TAUX ÉLEVÉ DE MERCURE SOUS
CARDIOMYOPATHIE DILATATIVE
IDIOPATHIQUE (CMDI).
QUELLE EST LA SOURCE DE MERCURE?
LEVELS ng/g
Controls
IDCM
Hg
8.0
178,400
Sb
1.5
19.260
Frustaci et al., J. of American College of Cardiology, 33, (6) 1578, 1999.
Controls were patients with valvular or ischemic heart disease.
Question is ‘where does this mercury come from?’ Athletic
youth die of IDCM.
TAUX DE MERCURE DANS LES CHEVEUX
(de naissance) POUR DES PATIENTS
AUTISTES ET SAINS
20
18
HIGH
Female
16
Hair Hg level
(ppm)
Male
14
12
AMALGAM COUNT
10
Data from Amy
Holmes, Mark Blaxill
& Boyd Haley, Int. J.
Toxicology v22, in
press, 2003
8
6
4
2
LOW
0
Non-autistic
Mean=3.79
n=34
Autistic
Mean=0.47
n=94
TAUX DE MERCURE DANS LES CHEVEUX (de naissance) EN
FUNCTION DES AMALGAMES POUR LES SUJETS
ATTEINTS DE LA MALADIE D’ALZHEIMER ET LES SUJETS
SAINS
14
Control
12
10
Hair Hg level
(mcg/g)
8
Data from A. Holmes,
M. Blaxill & B. Haley,
Int. J. of Toxicology
v22:1-9, 2003
6
4
2
0
Number of amalgams:
Control: autistic ratio:
N:
Autistic
0-3
2.64
15
4-5
6.93
22
6-7
6.70
29
8-9
6.32
30
>10
17.91
43
CONTRASTE ENTRE LE TAUX DE Hg DANS LES
CHEVEUX (de naissance) ET LE TAUX DE Hg DANS
LE CORPS
• Les enfants autistes ont un taux de Hg beaucoup plus bas
dans leur cheveux de naissance.
• De nombreux physiciens ont rapporté que les enfants
autistes présentaient un taux plus élevé de Hg dans le corps
(par rapport aux enfants sains).
• L’explication la plus simple serait dût à la susceptibilité
génétique de retenir le mercure.
• Il existe également une différence évidente entre Genre
(Hommes & Femmes). Ceci peut être expliqué par les
effets de la testostérone sur la toxicité-T.
CONCLUSIONS IMPORTANTES
• IL EXISTE DONC UN CLASSE DE POPULATION QUI
NE PEUT PAS EFFICACEMENT ÉLIMINER LE
MERCURE.
CES
PERSONNES
SONT,
PAR
CONSÉQUENT, SOUMISES À DE PLUS GRANDS
RISQUES D’EXPOSITION AU MERCURE PAR
RAPPORT AU RESTE DE LA POPULATION.
• ILS POURRAIENT ÊTRE DES PORTEURS DE L’APOE4,
DES
PERSONNES
PRÉSENTANT
UNE
DEFFICIENCE DE MÉTALLOTHIONINE, UNE
DIMINUTION DE GSH, OU ENCORE DES
ANOMALIES GÉNÉTIQUES.
• EST CE QUE CECI RESTE VALIDE POUR LA
MALADIE D’ALZHEIMER ET POUR D’AUTRES
MALADIES NEUROLOGIQUES?
IMPORTANTES CONCLUSION
• THERE APPEARS TO BE A SUBSET OF THE
POPULATION THAT CANNOT EFFECTIVELY
EXCRETE MERCURY AND ARE AT GREATER RISK
TO EXPOSURES TO MERCURY THAN ARE THE
GENERAL POPULATION.
• THESE MAY BE APO-E4 CARRIERS OR
METALLOTHIONINE DEFICIENT, GSH DEPLETED,
OR OTHER GENETIC DIFFERENCES.
• DOES THIS HOLD ALSO FOR AD AND OTHER
NEUROLOGICAL DISEASES?
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):38493,2005). This prevents removal of microbes and
ethyl-Hg damaged cells and proteins leading to
greater susceptibility for microbe infection and
widespread autoimmune problems.
Examples of Some Abnormal Biochemistries
Routinely Observed in the Autistic Child
1. Decreased methylation of biomolecules like DNA, RNA,
proteins: Cause; Inhibition of Methionine Synthetase. (Dr.
R. Deth)
2. Suppressed Immune System: Hg binding to phagocytes
inhibiting phagocytosis. (Dr. Rampersad)
3. Abnormal digestion of casein and gluten at proline rich
sites. Hg inhibition of intestinal P-IV protease. (Dr. Reichlt)
4. Abnormal urinary porphyrin profiles. Hg induced changes.
(Dr. R. Nataf, Dr. J. Woods)
5. Abnormal sulfate levels (Dr. R. Waring)
6. Abnormal oxidative stress (Dr. J. James)
7. Low molybdenum, high neopterin levels.
Molybdopterin
O
O
O
H
N
S
Mo
High Hg2+ ,
Pb2+, Cd2+ and
arsenic affinity.
S
NH
O
O
H2N
N
N
H
P
O
O
-
O
Mo is a essential mineral for conversion of sulfite to sulfate by the
enzyme sulfate oxidase. Autistic children are lower in Mo and
sulfate than control children, and higher in excreted neopterin.
1.
2.
3.
4.
5.
WHAT WOULD REPLACEMENT OF Mo
BY Hg ON MOLYBDOPTERIN DO?
Inhibit the enzyme sulfite oxidase leading to
decreased sulfate levels and higher toxic sulfite
levels.
Cause a depletion of Mo.
Cause a more rapid breakdown of Molybdopterin
to neopterin.
Decrease the removal of toxins, like tylenol, which
require sulfation for removal.
Inhibit other pathways that require sulfation and
increase sulfite sensitivity. Sulfite decreases
mylenation of white matter in the CNS.
CONCLUSIONS
•SULFITE INDUCED IMPROPER MYLENATION OF THE
CNS LEADS TO SEIZURES.
•DEMYLENATION IS OBSERVED IN MANY
NEUROLOGICAL ILLNESSES INCLUDING MULTIPLE
SCLEROSIS AND AUTISM.
•ANYTHING (Hg) THAT WOULD INHIBIT THE
PROCESS OF CONVERTING SULFITE TO SULFATE
COULD INTERFER WITH THE LAYING DOWN OF
WHITE MATTER (MYLENATION) AND COULD BE
CAUSAL FOR MANY NEUROLOGICAL ILLNESSES.
•INDIVIDUALS WHO CANNOT TOLERATE WINE
(CONTAINS SULFITES) SHOULD CONSIDER TAKING A
MOLYBDENUM SUPPLEMENT. ENJOY!
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 vitamins, 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.
Deth R, Muratore C, Benzercry J, et al. How environmental and genetic factors combine to cause
autism: A redox/methylation hypothesis. Neurotoxicology. 2008;29:190–201.
GLUTATHIONE & OXIDATIVE
STRESS
The effect of most toxicants and infections on humans
are:
1. most likely to occur in individuals who are already
suffering from oxidative stress.
2. induce oxidative stress in the process of causing the
medical symptoms they express.
3. reduced or prevented, by various mechanisms, if
the body can maintain a healthy redox status.
HOW TO DETECT AND EVALUATE
LEVEL OF OXIDATIVE STRESS
•A BLOOD GLUTATHIONE TEST IS THE MOST DIRECT
MEASURE OF OXIDATIVE STRESS.
•OXIDIZED DNA BASES (8-OH-deoxyGUANOSINE) AND
OXIDIZED LIPID FRAGMENTS IN URINE ARE ALSO
RELIABLE.
•A URINARY PORPHYRIN PROFILE CAN HELP
IDENTIFY POSSIBLE TOXINS.
•URINARY NEOPTERIN LEVELS SEEM TO
CORRELATE ALSO.
•One of the main sources of free
radicals are damaged, toxic or
dysfunctional mitochondrial which
may result from toxic damage.
•Glutathione (GSH) is the major
compound that scavenges hydroxyl
free radicals and protects the cell
from oxidative damage.
REACTIVE OXYGEN SPECIES (ROSs)
• Superoxide Anion: O2 + e-
O2-.
•Hydrogen Peroxide: O2-.
2HO2.
HO2. (hydroperoxyl radical)
H2O2 + O2
•Hydroxyl Radical: O2-. + H2O2
O2 + HO- + HO. (Haber-Weiss)
Fe2+ + H2O2
Fe3+ + HO- + HO. (Fenton)
The hydroxyl radical is the most damaging!
NATURAL REMOVAL OF ROSs
SOD or Superoxide Dismutase Catalyzed Reaction.
2O2-. + 2H+
H2O2 + O2 (keeps O2-. <10-11M)
*Catalyase Catalyzed Reaction. 2H2O2
2H2O + O2
Peroxidase Catalyzed Reaction. H2O2 + AH2
2H2O + A
“A” could be glutathione (GSH) with glutathione peroxidase.
*Catalyase is the enzyme that converts Hgo to Hg2+!
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) and heavy metals.
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.
4.
5.
6.
7.
Enzyme-SH(active) + Hg2+
Enzyme-S-Hg+(inactive) + GSH
GS-Hg+ + GSH
2 GSH + OH.
GSSG + NADH + H+
Enzyme-S-Hg+(inactive) + H+
Enzyme-SH (active)+ GS-Hg+
GS-Hg-SG(excreted form) + H+
GSSG + H20
2 GSH + NAD+
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!
The Importance of Glutathione (GSH) Levels
1. GSH serves as a frontline reducing agent keeping all our
enzymes protected from oxidation.
2. GSH serves as a “natural chelator” for excretion of many
heavy metals including Hg, Pb, Cd, etc.
3. GSH is attached to many water insoluble toxicants by
glutathione-S-transferase (GST) allowing them to become
water soluble and excretable.
4. GSH can react with certain yeast, fungal toxins (e.g.
gliatoxin) decreasing their activity.
5. GSH prevents viral infections by binding to the viral
surface preventing cell penetration. The influenza and HIV
virus are two that are susceptible to GSH inhibition.
6. GSH conversion to GSSG controls apoptosis.
INHIBITION OF INFLUENZA INFECTION BY GLUTATHIONE
JIYANG CAI,* YAN CHEN,* SHAGUNA SETH,† SATORU FURUKAWA,‡ RICHARD W. COMPANS,† and DEAN P. JONES*
*Department of Biochemistry, †Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA; and ‡Nutri-Quest,
Inc., Chesterfield, MO, USA
(Received 27 August 2002; Revised 23 December 2002; Accepted 9 January 2003)
Abstract—Infection by RNA virus induces oxidative stress in host cells. Accumulating
evidence suggests that cellular redox status plays an important role in regulating viral
replication and infectivity. In this study, experiments were performed to determine
whether the thiol antioxidant glutathione (GSH) blocked influenza viral infection in
cultures of Madin-Darby canine kidney cells or human small airway epithelial cells.
Protection against production of active virus particles was observed at a low (0.05– 0.1)
multiplicity of infection (MOI). GSH inhibited expression of viral matrix protein
and inhibited virally induced caspase activation and Fas upregulation. In BALB/c
mice, inclusion of GSH in the drinking water decreased viral titer in both lung and
trachea homogenates 4 d after intranasal inoculation with a mouse-adapted influenza
strain A/X-31. Together, the data suggest that the thiol antioxidant GSH has an antiinfluenza activity in vitro and in vivo. Oxidative stress or other conditions that
deplete GSH in the epithelium of the oral, nasal, and upper airway may, therefore,
enhance susceptibility to influenza infection. © 2003 Elsevier Science Inc.
Most likely even the new Swine or Avian influenza types.
Molecular Mechanism of Decreased Glutathione Content in Human
Immunodeficiency Virus Type 1 Tat-transgenic Mice.
Jinah Choi, Rui-Ming Liu, Ramendra K. Kundu, Frank Sangiorgi, Weicheng Wu, Robert Maxson, and Henry Jay Forman.
Human immunodeficiency virus (HIV) progressively
depletes GSH content in humans. Although the accumulated evidence
suggests a role of decreased GSH in the pathogenesis of HIV, significant controversy
remains concerning the mechanism of GSH depletion, especially in regard to envisioning
appropriate therapeutic strategies to help compensate for such decreased antioxidant
capacity.
Tat, a transactivator encoded by HIV, is sufficient to cause GSH depletion in
vitro and is implicated in AIDS-associated Kaposi's sarcoma and B cell lymphoma. In
this study, we report a decrease in GSH biosynthesis with Tat, using HIV-1 Tat transgenic
(Tat+) mice. A significant decline in the total intracellular GSH content in liver and
erythrocytes of Tat+ mice was accompanied by decreased γ-glutamylcysteine synthetase
regulatory subunit mRNA and protein content, which resulted in an increased sensitivity of
γ-glutamylcysteine synthetase to feedback inhibition by GSH. Further study revealed a
significant reduction in the activity of GSH synthetase in liver of Tat+ mice, which was
linearly associated with their GSH content.
Therefore, Tat appears to decrease GSH in vivo, at least
partially, through modulation of GSH biosynthetic enzymes.
Source: J Biol Chem, 2000, 275 (5), 3693-3698.
URL Accessed: 12/5/2008, http://www.jbc.org/cgi/content/abstract/275/5/3693.
This research implies that oxidative stress, i.e. low GSH levels must be induced
for effective HIV replication to occur and that low GSH levels must be a risk
factor for HIV infection.
Glutathione deficiency is associated with impaired
survival in HIV disease.
Herzenberg, LA, De Rosa, SC, Dubs, JG, Roederer, M, Anderson, MT, Ela, SW, Deresinski, SC, Herzenberg, LA.
Department of Genetics, Stanford University Medical School, CA ,USA.
Glutathione (GSH), a cysteine-containing tripeptide, is essential for the
viability and function of virtually all cells. In vitro studies showing that
low GSH levels both promote HIV expression and impair T cell
function suggested a link between GSH depletion and HIV disease
progression.
Clinical studies presented here directly demonstrate that low GSH levels predict poor
survival in otherwise indistinguishable HIV-infected subjects. Specifically, we show that
GSH deficiency in CD4 T cells from such subjects is associated with markedly decreased
survival 2-3 years after baseline data collection (Kaplan-Meier and logistic regression
analyses, P < 0.0001 for both analyses). This finding, supported by evidence demonstrating
that oral administration of the GSH prodrug N-acetylcysteine replenishes GSH in these
subjects and suggesting that N-acetylcysteine administration can improve their survival,
establishes GSH deficiency as a key determinant of survival in HIV disease.
Further, it argues strongly that the unnecessary or excessive
use of acetaminophen, alcohol, or other drugs known to deplete
GSH should be avoided by HIV-infected individuals.
Source: Proc Natl Acad Sci USA, 1997, 94 (5), 1967-72.
URL Accessed: 12/5/2008, http://www.ncbi.nlm.nih.gov/pubmed/9050888?dopt=Abstract.
Glutathione inhibits HIV replication by acting
at late stages of the virus life cycle.
Palamara, AT, Perno, CF, Aquaro, S, Buè, MC, Dini, L, Garaci, E.
Department of Experimental Medicine and Biochemical Sciences, University of Rome, Italy.
We investigated the effect of glutathione on the replication of human
immunodeficiency virus (HIV) in chronically infected macrophages, a known
reservoir of the virus in the body.
We found that exogenous GSH strongly suppresses the
production of p24gag protein as well as the virus infectivity. This is
related to a dramatic decrease in both budding and release of virus particles from chronically infected
cells (either macrophages or lymphocytes), together with a selective decrease in the expression of gp120,
the major envelope glycoprotein, rich in intrachain disulfide
bonds and thus potentially sensitive to the effect of a reducing
agent such as GSH.
Overall data suggest that GSH can interfere with late stages of virus
replication. This would be in agreement with data obtained in cells exposed to
herpesvirus type 1 (a DNA virus) or to Sendai (an RNA virus), showing that the
suppression of virus replication by GSH is related to the selective inhibition of
envelope glycoproteins.
These results suggest a potential role of GSH in combination
with other antivirals in the treatment of virus-related diseases.
AIDS Res Hum Retroviruses, 1996,12 (16), 1537-41. URL Accessed: 03/14/2009, http://www.ncbi.nlm.nih.gov/pubmed/8911579.
The –SH terminal to GSH structure inserts into the disulfide (V-S-S-V) of the viral (V)
coat protein as follows: GSH + V-S-S-V
GS-S-V + HS-V
Evidence for antiviral activity of glutathione: in vitro inhibition of
herpes simplex virus type 1 replication.
Palamara, AT, Perno, CF, Ciriolo, MR, Dini, L, Balestra, E, D'Agostini, C,
Di Francesco, P, Favalli, C, Rotilio, G, Garaci, E.
Department of Experimental Medicine and Biochemical Sciences, University of Rome, Italy.
The role of glutathione (GSH) in the in vitro infection and replication of human herpes simplex
virus type 1 (HSV-1) was investigated. Intracellular endogenous GSH levels
dramatically decreased in the first 24 h after virus adsorption, starting
immediately after virus challenge. The addition of exogenous GSH was not only
able to restore its intracellular levels almost up to those found in uninfected
cells, but also to inhibit > 99% the replication of HSV-1. This inhibition was
concentration-dependent, not related to toxic effects on host cells and also maintained if the exogenous
GSH was added as late as 24 h after virus challenge, i.e. when virus infection was fully established.
Electron microscopic examination of HSV-1-infected cells showed that GSH dramatically reduced
the number of extracellular and intracytoplasmic virus particles, whereas some complete nucleocapsids
were still detected within the nuclei of GSH-treated cells. Consistent with this observation, immunoblot
analysis showed that the expression of HSV-1-glycoprotein B, crucial for the release and the infectivity
of virus particles, was significantly decreased.
Data suggest that exogenous GSH inhibits the replication of HSV-1 by
interfering with very late stages of the virus life cycle, without affecting cellular
metabolism.
Source: Antiviral Res, 1995, 27 (3), 237-53.
URL Accessed: 12/5/2008,
http://www.ncbi.nlm.nih.gov/pubmed/8540746?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryP
anel.Pubmed_Discovery_RA&linkpos=3&log$=relatedarticles&logdbfrom=pubmed.
Relationship Between Plasma Glutathione Levels and Cardiovascular
Disease in a Defined Population ;The Hisayama Study. Haruki Shimizu et al.
Stroke. 2004;35:2072
Background and Purpose— Glutathione (GSH) appears to
have marked antioxidant
activities and therefore may prevent cardiovascular disease (CVD). However, there are
very few reports on this subject. In a community-based case–control study, we tested the hypothesis that low
levels of plasma GSH are closely associated with CVD and its clinical types.
Methods— The association between fasting plasma total GSH (tGSH) levels and CVD were assessed using
conditional logistic regression analysis among 134 CVD cases and 435 age- and sex-matched healthy control
subjects.
Results— Mean tGSH concentrations were lower in all CVD cases than in the control subjects (3.06 versus
3.71 µmol/L; P=0.0001). Among the CVD types, both the cerebral infarction cases (2.98 versus 3.59 µmol/L;
P=0.001) and cerebral hemorrhage cases (2.51 versus 3.43 µmol/L; P=0.0027) had significantly lower tGSH
levels than the corresponding control groups had. The same tendency was observed for cases of subarachnoid
hemorrhage (3.45 versus 3.83 µmol/L; P=0.36) and myocardial infarction (3.65 versus 3.77 µmol/L; P=0.69),
but these differences were not statistically significant. After adjustment for other confounding factors, the risk
of CVD was significantly lower in the third (adjusted odds ratio, 041; 95% CI, 0.21 to 0.77) and the fourth
quartiles (adjusted odds ratio, 0.25; 95% CI, 0.12 to 0.51) than in the first. This association was most prominent
in patients with lacunar infarction or cerebral hemorrhage.
Conclusions— These
findings suggest that reduced plasma tGSH levels are a risk
factor for CVD, especially for cerebral small vessel disease.
Hepatitis C virus core protein inhibits mitochondrial electron
transport and increases reactive oxygen species (ROS) production.
M. Korenaga, T. Wang, Y. Li, LA. Showalter, T. Chan, J. Sun, SA. Weinman. Center for Hepatitis Research, Department of
Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, USA.
Hepatitis C infection causes a state of chronic oxidative stress,
which may contribute to fibrosis and carcinogenesis in the liver.
Previous studies have shown that expression of the HCV core protein in hepatoma
cells depolarized mitochondria and increased reactive oxygen species (ROS)
production, but the mechanisms of these effects are unknown.
In this study we examined the properties of liver mitochondria from transgenic mice
expressing HCV core protein, and from normal liver mitochondria incubated with
recombinant core protein. Liver mitochondria from transgenic mice expressing the HCV
proteins core, E1 and E2 demonstrated oxidation of the glutathione pool and a decrease in
NADPH content. In addition, there was reduced activity of electron transport complex I, and
increased ROS production from complex I substrates. There were no abnormalities observed
in complex II or complex III function. Incubation of control mitochondria in vitro with
recombinant core protein also caused glutathione oxidation, selective complex I inhibition,
and increased ROS production. Proteinase K digestion of either transgenic mitochondria or
control mitochondria incubated with core protein showed that core protein associates strongly
with mitochondria, remains associated with the outer membrane, and is not taken up across
the outer membrane. Core protein also increased Ca(2+) uptake into isolated mitochondria.
These results suggest that interaction of core protein with
mitochondria and subsequent oxidation of the glutathione pool and
complex I inhibition may be an important cause of the oxidative stress
seen in chronic hepatitis C.
Source: J Biol Chem, 2005, 280, 37481-8. URL Accessed: 12/5/2008,
http://www.mitochondrial.net/showabstract.php?pmid=16150732&redirect=yes&terms=reduced+glutathione+in+virus.
CONCLUSIONS
• GLUTATHIONE EXPERIMENTS INDICATE THAT GSH IS
IMPORTANT IN BOTH PREVENTING AND ELIMINATING VIRAL
INFECTIONS.
•IT APPEARS AS IF THE –SH GROUP IS PARAMOUNT IN
DISRUPTING THE DITHIOL (-S-S) BONDS OF VIRAL COAT
PROTEIN IMPEDING FURTHER REPLICATION AND SPREAD OF
THE VIRAL INFECTION.
•IT HAS BEEN HYPOTHESIZED THAT GLUTATHIONE-BOUND
TO VIRAL PROTEINS ENHANCES THE IMMUNE RESPONSE TO
VIRAL INFECTIONS.
•LOW BODY GSH LEVELS SEEM TO BE A MAJOR RISK FACTOR
FOR VIRAL INFECTIONS, THIS IS IMPORTANT WITH THE
CURRENT CONCERN ABOUT THE SWINE FLU.
•TAKING ANTIOXIDANTS TO ELEVATE BODY GLUTATHIONE
LEVELS SEEMS TO BE AN IMPORTANT APPROACH.
Apoptosis, programed 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.
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
CONVERSION OF GSH TO GSSG PRECEDES CELL DEATH IN CULTURED
FIBROBASTIC CELLS
GSSG
% DEAD 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 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
THERE ARE SEVERAL ITEMS THAT LEAD TO
ABNORMAL OXIDATIVE STRESS: OR LOWER
REDUCED GLUTATHIONE AND ELEVATED
GSSG LEVELS.
1.
2.
3.
4.
5.
TOXICITIES
INFECTIONS
INADEQUATE DIETS (LOW CYSTEINE)
AGING
LACK OF WARMTH
CONCEPT: WE NEED TO DIRECTLY
TREAT OXIDATIVE STRESS BY:
1. REDUCING THE PRODUCTION OF FREE
RADICALS OR SCAVENGING THEM TO
SALVAGE GSH. (ANTIOXIDANTS IN DIET,
REMOVE TOXINS)
2. INCREASE PRODUCTION OF GLUTATHIONE
BY PROVIDING PRO-GLUTATHIONE
NUTRIENTS (e.g CYSTEINE) AND
REMOVING ANY TOXICANTS (e.g. HEAVY
METALS) THAT PREVENT GSH SYNTHESIS.
3. 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 and are rapidly cleared from the body.
They are not efficient at removing hydroxyl radicals that are
located inside of cells or in the mitochondria because of the
rapid excretion and the fact they are excluded from these
sites due to their chemistry.
• Toxin generated reactive oxygen species (ROSs) in the
body are located intracellular or in hydrophobic locations.
• The new antioxidants are needed that enter intracellular
areas. Entering these hydrophobic regions places the new
antioxidants nearer the produced free radicals and increases
the time spent in the body enhancing the scavenging of
newly produced free radicals.
• Therefore, efficacious 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
SH
HS
Free radical scavenging sites
SH
HS
Potent scavengers of hydroxyl radicals in lipophilic areas.
N1N2bis(2-mercaptoethyl)isophthamide
A New Antioxidant Called OSR#1
Pyridine Analog
Comparative ORAC Scores
μmoleTE/100g
OSR#1
192,400
Aςai
18,500
Dark Chocolate
13,120
Pomegranates
3,307
Blueberries
2,400
Garlic
1,939
1.
2.
3.
4.
5.
Cranberries
1,750
Spinach
1,260
Broccoli Florets
890
Kiwi Fruit
610
6.
7.
ORAC, oxygen radical absorbance capacity test, is a measure of
a compound’s ability to prevent oxidation of Trolox (a vit-E
analog) by ROSs (reactive oxygen species).
This means OSR would preserve vitamin-E in cells.
The HORAC, hydroxyl radical absorbance capacity test, score
for OSR is 299,000/100g. This is a measure of a compound’s
ability to prevent oxidation of Trolox by hydroxyl free radicals.
Therefore, OSR is one of the most potent antioxidants ever
tested ranking with clove oil and other essential oils, however
OSR is without toxicity.
Pharmacokinetics studies show that OSR peaks in plasma and
all organs tested, including the brain, 2 hours after ingestion. At
24 hours post-ingestion about 4 to 12% of OSR remains in the
organs indicating an effective excretion occurs.
The plasma half-life of OSR is 6-7 hours.
The hydrophobic nature of OSR allows it to penetrate cell
membranes and the blood-brain barrier where OSR can
scavenge ROSs helping salvage glutathione and protect against
free radical type damage.
TOXICITY TESTING BY ORAL
DELIVERY
•A commercial toxicology laboratory has confirmed
that the new antioxidant has an LD50 greater than
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 certified laboratory.
•These compounds are dietary antioxidants and are not
FDA approved to treat any illness or disease.
OSR: GSH and Thiol Data in ASD
Peach colored samples hemolyzed- disregard
8 yo wm ASD
9 yo wf ASD gd
recovery
9 yo wf ASD Severe
11 yo wm ASD
Baseline
Week 4
Week 12
Baseline
Week 4
Week 12
Baseline
Week 4
Week 12
Baseline
Week 4
Week 12
Total GSH/GSSG
40.3
53.6
87.1
42.9
37.5
87.7
24.8
32.3
64.5
14.8
22.1
28.6
Free GSH/GSSG
15.7
18.0
24.3
13.5
8.2
26.2
8.7
14.1
29.5
5.3
6.9
12.2
Glu-Cys
2.1
2.4
3.4
3.6
3.3
4.0
2.2
3.0
3.9
2.5
2.9
3.2
Cys-Gly
37.9
38.1
33.3
41.2
36.8
46.9
35.0
35.6
34.0
51.7
42.4
35.8
Cysteine
200.4
212.2
201.9
170.2
166.8
169.1
240.2
231.3
260.0
237.1
250.5
185.8
Homocys
4.6
5.5
5.3
5.7
5.1
5.0
5.2
5.9
6.3
7.9
8.4
9.2
Methionine
14.8
15.4
16.4
20.7
22.7
26.0
22.1
22.6
26.3
22.2
19.4
30.9
OSR: GSH and Thiol Data Seniors
Peach colored samples hemolyzed- disregard
72 yo wm
Baseline
71 yo wf
Week 4
Week 12
Baseline
73 yo wf
Week 4
Week 12
Baseline
Week 4
Week 12
Total GSH/GSSG
11.4
16.9
48.8
17.2
36.2
28.7
15.8
42.8
69.6
Free GSH/GSSG
3.5
5.3
17.0
8.9
12.1
15.6
8.0
17.3
25.4
Glu-Cys
3.2
3.3
3.6
2.9
2.8
4.0
1.8
3.2
4.1
Cys-Gly
63.0
59.1
61.2
45.0
51.4
48.0
39.8
41.9
51.5
Cysteine
344.2
255.4
317.9
304.7
243.6
290.0
288.2
253.7
324.2
Homocys
21.2
13.9
12.8
9.7
9.3
9.1
11.4
12.6
16.1
Methionine
20.5
28.3
31.2
15.4
17.2
25.4
21.1
23.1
33.7
HUMAN STUDIES: Effect of OSR on Glutathione-S-transferase (GST) levels (ng/ml)
GST
1
Time (months)
0
2
Patient #
1
L
L
0.48
2
L
L
0.48
3
L
0.46
0.43
4
L
L
0.53
5
L
L
0.43
6
L
L
0.37
7
L
L
0.32
8
L
0.58
0.43
9
L
L
0.63
10
L
L
0.43
GST activities increased in every patient. Detection levels were 0.4 for normals to 3.1
for a high level for GST.
CONCLUSIONS
• A NON-TOXIC, LIPID SOLUBLE, FREE
RADICAL SCAVENGING ANTIOXIDANT HAS
BEEN DEVELOPED AND FOUND TO BE
WITHOUT DETECTABLE TOXICITY.
• THIS ANTIOXIDANT EFFECTIVELY
SCAVENGES HYDROXYL RADICALS.
• THIS ANTIOXIDANT IS EFFECTIVE IN
HELPING MAINTAIN A HEALTHY
GLUTATHIONE LEVEL.
• A HEALTHY GLUTATHIONE LEVEL IS
IMPORTANT FOR HEALTH.
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
Hg VAPORS
FROM DENTAL
AMALGAM
THE FDA HAS
STEADFASTLY
REFUSED TO
TEST THEM
FOR SAFETY!
Amalgam is 50%
Mercury, inches from
your brain and
olfactory tissues.
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. “Hijacking Science Example”
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!
Mercury in saliva and feces after removal of amalgam fillings.
Björkman L, et al. Toxicol Appl Pharmacol. 1997 May;144(1):156-62. Department of Basic Oral Sciences,
Karolinska Institutet, Stockholm, Sweden.
The toxicological consequences of exposure to mercury (Hg) from dental amalgam
fillings is a matter of debate in several countries. The purpose of this study was to
obtain data on Hg concentrations in saliva and feces before and after removal of dental
amalgam fillings. In addition Hg concentrations in urine, blood, and plasma were
determined. Ten subjects had all amalgam fillings removed at one dental session.
Before removal, the median Hg concentration in feces was more than 10 times
higher than in samples from an amalgam free reference group consisting of 10
individuals (2.7 vs 0.23 mumol Hg/kg dry weight, p < 0.001). A considerable
increase of the Hg concentration in feces 2 days after amalgam removal (median 280
mumol Hg/kg dry weight) was followed by a significant decrease. Sixty days after
removal the median Hg concentration was still slightly higher than in samples
from the reference group. In plasma, the median Hg concentration was 4 nmol/liter at
baseline. Two days after removal the median Hg concentration in plasma was increased
to 5 nmol/liter and declined subsequently to 1.3 nmol/liter by Day 60. In saliva, there
was an exponential decline in the Hg concentration during the first 2 weeks after
amalgam removal (t 1/2 = 1.8 days). It was concluded that amalgam fillings are a
significant source of Hg in saliva and feces. Hg levels in all media decrease
considerably after amalgam removal. The uptake of amalgam mercury in the GI tract in
Human exposure to mercury and silver released from
dental amalgam restorations.
Skare, I and Engqvist, A. Arch Environ Health. 1994 Sep-Oct;49(5):384-94. National
Institute of Occupational Health Stockholm, Sweden.
In 35 healthy individuals, the number of amalgam surfaces was related to the emission
rate of mercury into the oral cavity and to the excretion rate of mercury by urine. Oral
emission ranged up to 125 micrograms Hg/24 h, and urinary excretions ranged from
0.4 to 19 micrograms Hg/24 h. In 10 cases, urinary and fecal excretions of mercury
and silver were also measured. Fecal excretions ranged from 1 to 190
micrograms Hg/24 h and from 4 to 97 micrograms Ag/24 h. Except for urinary
silver excretion, a high interplay between the variables was exhibited. The worst-case
individual showed a fecal mercury excretion amounting to 100 times the mean intake of
total Hg from a normal Swedish diet. With regard to a Swedish middle-age
individual, the systemic uptake of mercury from amalgam was, on average,
predicted to be 12 micrograms Hg/24 h.
• Maternal amalgam dental fillings as the source of mercury
exposure in developing fetus and newborn. Journal of Exposure Science and
•
•
Environmental Epidemiology (2008) 18, 326–331.
Lubica Palkovicovaa, Monika Ursinyovaa, Vlasta Masanovaa, Zhiwei Yub and Irva Hertz-Picciottob
Dental amalgam is a mercury-based filling containing approximately 50% of metallic mercury (Hg0).
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 substudy 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 mcg/l (range 0.14–2.9 g/l) and 0.80 mcg/l (range 0.15–2.54 mcg/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 mcg/l
in cord blood). A strong positive correlation between maternal and cord blood Hg levels was found
(=0.79; P<0.001). Levels of Hg in the cord blood were significantly associated with
the number of maternal amalgam fillings (=0.46, P<0.001) and with the number of years
since the last filling (=- 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.
Irreversible color vision losses in patients with chronic mercury
vapor intoxication
CLÁUDIA FEITOSA-SANTANAa1a2 c1, MIRELLA T.S. BARBONIa1a2, NESTOR N. OIWAa1a2, GALINA V.
PARAMEIa3, ANA LUISA A.C. SIMÕESa2, MARCELO F. DA COSTAa1a2, LUIZ CARLOS L. SILVEIRAa4a5
and DORA F. VENTURAa1a2 Visual Neuroscience (2008), 25:487-491
This longitudinal study addresses the reversibility of color vision losses in subjects
who had been occupationally exposed to mercury vapor. Color discrimination was assessed
in 20 Hg-exposed patients (mean age = 42.4 ± 6.5 years; 6 females and 14 males) with exposure to Hg vapor
during 10.5 ± 5.3 years and away from the work place (relative to 2002) for 6.8 ± 4.2 years. During the Hg
exposure or up to one year after ceasing it, mean urinary Hg concentration was 47 ± 35.4 μg/g creatinine.
There was no information on Hg urinary concentration at the time of the first tests, in 2002 (Ventura et al.,
2005), but at the time of the follow-up tests, in 2005, this value was 1.4 ± 1.4 μg/g creatinine for patients
compared with 0.5 ± 0.5 μg/g creatinine for controls (different group from the one in Ventura et al. (2005)).
Color vision was monocularly assessed using the Cambridge Colour Test (CCT). Hg-exposed patients had
significantly worse color discrimination (p < 0.02) than controls, as evaluated by the size of MacAdam's
color discrimination ellipses and color discrimination thresholds along protan, deutan, and tritan confusion
axes. There were no significant differences between the results of the study in Ventura et al. (2005) and in the
present follow-up measurements, in 2005, except for worsening of the tritan thresholds in the best eye in
2005. Both chromatic systems, blue-yellow and red-green, were affected in the first evaluation (Ventura et
al., 2005) and remained impaired in the follow-up testing, in 2005. These findings indicate that
following a long-term occupational exposure to Hg vapor, even several years away
from the source of intoxication, color vision impairment remains irreversible.
ELEVATED MERCURY IN IDIOPATHIC
DILATED CARDIOMYOPATHY (IDCM).
WHERE DOES THE Hg COME FROM?
LEVELS ng/g
Hg
Controls
8.0
IDCM
178,400
Sb
1.5
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.
Le Transport Axonal – Un Process
Essentiel à la Survie des Neurones
Dendrite
Axon
Membrane
Bound
Organelle
Dynien
Microtubule
Kinesin
HgEDTA entraîne des anomalies au niveau de
l’intéraction [32P]8N3GTP-ß-tubuline, caractéristique de
la maladie d’Alzheimer
Autoradiogramme du [32P]8N3GTP Photo Labellisée
Sujets Sains (C) & Sujets atteints de l’Alzheimer (AD)
Brain Hippocampus Homogenates
La répartition de la ß-tubuline est anormale pour les
malades atteints de l’Alzheimer (Brain Homogenates)
NORMALS
NORMALS
NORMALS
ALZHEIMERS
ANTIBODY DETECTION OF BETA-TUBULIN
EDTA empêche le Cd, Cu & Zn mais pas le Hg.
Inhibition de [32P]8N3GTP ‘Photolabeling’ de la ß-tubuline dans le cerveau.
EFFET D’EXTRACTIONS SUCCESSIVES DE
SOLUTIONS D’AMALGAMES SUR LA VIABILITÉ
DE LA TUBULINE (DU CERVEAU)
120
100
80
60
40
20
Hours of Amalgam Soak
to
12
0
96
96
to
72
72
48
to
48
24
to
24
to
12
to
12
8
8
4
to
4
2
to
2
1
to
1
to
0
tr
ol
0
co
n
%
Active
Degenerating Neurons into Neurofibillary Tangles by Treatment with
Nanomolar Levels of Hg2+. Leong et al. NeuroReports 2001,12 (4):733737.
MERCURY, AND ONLY
MERCURY COULD CAUSE THE
FORMATION OF NFTs, THE
MAJOR DIAGNOSTIC
HALLMARK OF ALZHEIMER’S
DISEASE!
Alzheimer's Metal Concentrations in Plasma and
Cerebrospinal Fluid in Patients with Disease. Dement Geriatr
Cogn Disord. 2008 May 5;25(6):508-515. 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.
•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. In July 2009 the FDA finally
evaluated the safety of dental amalgam and found
them safe for use in all ages and levels of health
despite the overwhelming studies showing toxicity!
Blood mercury levels rising among U.S. women.
Dr. Dan Laks,
UCLA August 09. A study involving more than 6,000 American women suggests that
blood levels of mercury are accumulating over time, with a big rise noted over the past
decade. Using data from the U.S. Centers for Disease Control and Prevention's
National Health and Nutrition Examination Survey (NHANES), a researcher from the
University of California, Los Angeles, found that while inorganic mercury was detected
in the blood of 2 percent of women aged 18 to 49 in the 1999-2000 NHANES survey,
that level rose to 30 percent of women by 2005-2006. "My study found compelling
evidence that inorganic mercury deposition within the human body is a cumulative
process, increasing with age and overall in the population over time," study author and
neuroscience researcher Dan R. Laks said in an UCLA news release. "My findings also
suggest a rise in risks for disease associated with mercury over time.“
According to the news release, chronic mercury exposure has been linked in studies to a
higher risk for autism, mental impairment and neurodegenerative disorders such as
Alzheimer's disease. Laks also found a connection between levels of the pituitary
hormone lutropin and chronic mercury exposure, which he said might help explain
mercury's link to neurodegenerative disease. Inorganic mercury can also accumulate in
the brain and stay there for years, according to the news release. “these results suggest
that chronic mercury exposure has reached a critical level where inorganic mercury
deposition within the human body is accumulating over time," Laks said. "It is logical
to assume that the risks of associated neurodevelopmental and neurodegenerative
diseases will rise as well."
EPIDEMIOLOGICAL STUDIES
NO AGENCY OF THE US GOVERNMENT HAS
EVER COMMISSIONED ANY SIGNIFICANT
EPIDEMIOLOGICAL STUDY ON AUTISM AND
VACCINATIONS BY ANY MAJOR AMERICAN
UNIVERSITY.
ALL SUCH STUDIES HAVE BEEN DONE BY
FOREIGN RESEARCHERS AND FUNDED BY
THE CDC.
Autism Risks From 5 Sequential Studies by
Verstraten et al. of CDC
Study1
7.62
(1999)
Study2
Study3
Study4
Indicates thimerosal is causal
for autism.
2.48
1.69
Study5
Conflicts with other CDC
accepted studies from
Europe!
Simpsonwood Meeting
1.52
(2001)
1.00*
(2005)
*i.e., no increased risk of autism compared to low exposure
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
1.
In USA rate was 1/150 or 67/10,000!
2.
Outpatients added in 1995.
3.
Large Copenhagen Clinic added in1992.
4.
Autism classification changed in 1994.
5.
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 Olmsted finds:
1. Very little, if any, autism in the unvaccinated Amish!
2. 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).
CONCLUSIONS
THE REFUSAL OF THE CDC AND OTHER
APPROPRIATE GOVERNMENT HEALTH
AGENCIES TO SUPPORT THE EPIDEMILOGICAL
EVALUATION OF UNVACCINATED CHILDREN
VERSUS VACCINATED CHILDREN FOR
NEUROLOGICAL ILLNESSES BY USA BASED
UNIVERSITIES IS SYMPTOMATIC OF
COVERING UP A SEVERE WRONG DOING BY
ADMINISTRATORS OF THESE VERY SAME
AGENCIES.