PRESENTS: A Tidal Wave of Terror: Thimerosal in Vaccines Boyd Haley, PdD Professor of Chemistry,...

PRESENTS

A Tidal Wave of Terror Thimerosal in Vaccines

Boyd Haley PdDProfessor of Chemistry University of Kentucky

This vaccine webinar series is provided as a community service by Homefirst Natural Pharm

Source wwwhomefirstcom

wwwmedicalvoicesorg

TOXICITEacute DU MERCURE ET SA RELATION AUX MALADIES

NEUROLOGIQUES

DR BOYD E HALEY

PROFESSEUR ET PREacuteSIDENT DU DEacutePARTEMENT DE CHIMIE

UNIVERSITEacute DU KENTUCKY

WHAT CAUSED THE USA AUTISM EPIDEMICbullIT IS NOT CAUSED BY GENETICS

bullIT IS LIKELY A GENETIC SUSCEPTIBILITY TO AN ENVIRONMENTAL TOXICANT

bullTHE TOXICANT HAD TO INCREASE IN ALL 50 STATES AT APPROXIMATELY THE SAME TIME (1988-90)

bullEXPOSURE HAS TO OCCUR BEFORE AGE 2

bullTHE TOXICANT HAS TO EFFECT BOYS MUCH MORE THAN GIRLS (ONLY MERCURY IS KNOWN TO DO THIS)

bullANY SUGGESTED TOXICANT HAS TO EXPLAIN THE MULTIPLE CELLULAR AND BIOCHEMICAL ABNORMALITIES OBSERVED CLINICALLY IN AUTISTICS

bullONLY THE THIMEROSAL EXPOSURE FROM THE CDC MANDATED VACCINE PROGRAM FITS THIS CRITERIA

bull

Important Observations1 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 YEAR EVALUATED ASD10000(ADDM) HEP-B (CDC DATA)

1992 2000 67 8 1994 2002 74 27 1996 2004 gt100 82 2000 2008

Thimerosal removed() from infant vaccines in 2003 ADDM (Autismamp Developmental Disabilities Monitoring network CDCrsquos Morbidity and Mortality Weekly Report) Hep-B introduced in 1991 with 25mcgs thimerosal Hep-B rates were from National Immunization Survey

FACTSbullHepatitis B vaccine to newborn baby boys more than triples the risk of ASD Annals of EpidemiologybullInfant male primates who received one dose of the Hepatitis-B were far more likely to display developmental delays than unvaccinated controls NeurotoxicologybullBoys 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 ChemistrybullChildren 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 AUTISMCM 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 651ndash680 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 US 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 US probability samples obtained from National Health Interview Survey 1997ndash2002 datasets Logistic regression modeling was used to estimate the effect of neonatal hepatitis B vaccination on ASD risk among boys age 3ndash17 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 294 greater odds for ASD (Nz31 of 7486 OR Z 294 p Z 003 95 CI Z 110 790) compared to later- or unvaccinated boys Non-Hispanic white boys were 61 less likely to have ASD (ORZ039 pZ004 95 CIZ016 094) relative to non-white boysCONCLUSION Findings suggest that US 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 EA Gottshall RY Appl Microbiol 1967 May15(3)590-3

Pertussis vaccines preserved with 001 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 (001)-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 vaccinePMID 6035051 [PubMed - indexed for MEDLINE]

Le thimeacuterosal est composeacute drsquoacide thiosalicylique et drsquo eacutethyl 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

bull Between 1969-75 13 cases were treated 10 died Mercury analysis of organs ranged from 65 to 2700 times normal levels This appears to be from 9 to 48 topical applications of 01 thimerosal applications NOTE These children were most likely on antibiotics Consider the effect on their immune system

bull ldquoParadoxically (in another study) 3 infants exposed postnatally (Iraq Methyl-Hg by ingestion) did not exhibit signs or symptoms though their blood levels were

gt1000ppb and one was gt1500ppbrdquo No antibiotics involved Blood levels are not a measure of toxicity

bull CONCLUSION IN 1977 ldquoOrganic 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 forgottenrdquo 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

bull Pregnant rabbits were injected subcutaneous with [203Hg]-thimerosal

bull From hour 1 post injection to hour 6 the cpm of 203Hg in the blood decreased from 100000 to less than 25000 cpm or over 75

bull 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)

bull Yet the IOMCDCAAP 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 3601737 2002

THE BIG MISTAKEbull 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

bull The EPA ldquosafe levelrdquo was based on mercury exposure from eating fish and whale meat

bull 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

0

50

100

150

200

85 86 87 88 89 90 91 92 93 94 95 96 97 98

0

5

10

15

20

Californiaautismprevalence(cases per 10000)

Vaccinemercuryexposure(micrograms)

Year of birth

Cumulative mercury(1)

exposures throughchildhood vaccines in 19-35 month olds surveyed

Californias reportedrates of autismby year of birth

(1) Includes DPT haemophilus influenza B and hepatitis B exposures weighted by survey year compliance

Year of survey 87 88 89 90 91 92 93 94 95 96 97 98 99 00

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 ProcedureCadmium Mercury amp Lead J of Toxicology amp Environmental Health 4763 1978

1 ldquothe administration of an essentially no response level (LD1) of a mercury salt together with a 120 of the LD1 of a lead salt killed all of the animalsrdquo ldquoGenerally 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 memberrdquo

2 Conclusion Mixing borderline toxic levels of two toxic metals (Pb2+ amp Hg2+) makes an extremely toxic solution

Time (hr) After Treatment

0 5 10 15 20 25 30

Neu

ron

Surv

ival

( In

itial

Num

ber)

0

20

40

60

80

100

120

Control

50 nM thimerosal

500 nM Al(OH)3

175 microg Neomycinml

50 nM Thimerosal500 nM Al(OH)3

50 nM Thimerosal175 microg Neomycinml



AluminumNeomycinTestosterone Effects

+ TESTOSTERONE

TOXICITEacuteS SYNERGEacuteTIQUES

50 NANOMOLAR TESTOSTERONE

DR MARK LOVELL

COLLABORATOR


0 5 10 15 20 25 30

Neu

ron

Su

rviv

al

( I

nit

ial

Nu

mb

er)

20

40

60

80

100

120

Control

50 nM thimerosal

50 nM thimerosal+10 nM HgCl2

50 nM thimerosal+ 25 nM HgCl2

10 nM HgCl2

25 nM HgCl2

LE Hg ET LE THIMEacuteROSAL MONTRENT DES TOXICITEacuteS ADDITIVES

TAUX NANOMOLAIRES ESTIMEacuteS DE THIMEacuteROSAL (POUR NOURISSONS) APREgraveS VACCINATION VALEURS EXPRIMEacuteES EN Kg 16 ( sang sain) 50 OU 75 ACCEgraveS DU VOLUME SUPPOSEacute 1 kg = 1 litre en volume

Hg Hg 125 125 g g 50 50 g g 675 675 gg1kg(22)1kg(22) 8484125125391391 33533550050015621562 453453676676210621062kg(44)2kg(44) 42426262196196 167167250250781781 226226338338105310533kg(66)3kg(66) 28284242130130 111111166166520520 1511512262267017015kg (11)5kg (11) 171726267878 6767100100312312 919113613642142110kg(22)10kg(22) 8812123939 34345050156156 4545686821021015kg(33)15kg(33) 55882626 23233434104104 31314646140140NOTE 1 nM thimerosal inhibits the enzyme methionine NOTE 1 nM thimerosal inhibits the enzyme methionine

synthetase and phagocytosissynthetase 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 Jan10 2006

bull 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

bull ldquoThe estrogenic effects were associated with a reduction of mercury content of the anterior pituitary gland and medial hypothalmus suggesting a protective estrogenic effectrdquo

Gender-selective toxicity of thimerosalDonald 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 384ndash768 mgkg 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 differencesr 2008 Elsevier GmbH All rights reserved

EacuteMISSION GAZEUSE DU MERCURE Agrave PARTIR DrsquoUN AMALGAME DENTAIRE

bull Source www uninformed consentcom

bull David Kennedyrsquos IAOMT tape

BOYS

GIRLS

J Woods et al Environmental Health Perspectives (2007) 11510 1527-1531

From a study funded by NIH done on orphans in Lisbon Portugal which concluded amalgams were safe for use in children

bull The previous slide shows that prolonged exposure to mercury vapor decreases the childrsquos 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

bull The observation is consistent with testosterone causing retention of mercury

bull This is consistent with the well known toxic effects of mercury on kidneys

bull 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 EacuteLEVEacute DE MERCURE SOUS CARDIOMYOPATHIE DILATATIVE

IDIOPATHIQUE (CMDI)

QUELLE EST LA SOURCE DE MERCURE

LEVELS ngg Hg Sb

Controls 80 15

IDCM 178400 19260Frustaci et al J of American College of Cardiology 33 (6) 1578 1999 Controls were patients with valvular or ischemic heart disease Question is lsquowhere does this mercury come fromrsquo Athletic youth die of IDCM

TAUX DE MERCURE DANS LES CHEVEUX (de naissance) POUR DES PATIENTS AUTISTES ET SAINS

0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94

Non-autisticMean=379

n=34

Data from Amy Holmes Mark Blaxill amp Boyd Haley Int J Toxicology v22 in press 2003

AMALGAM COUNT

LOW

HIGH

TAUX DE MERCURE DANS LES CHEVEUX (de naissance) EN FUNCTION DES AMALGAMES POUR LES SUJETS ATTEINTS DE LA MALADIE DrsquoALZHEIMER ET LES SUJETS SAINS

0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)

Number of amalgamsControl autistic ratio

4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control

Data from A Holmes M Blaxill amp B Haley Int J of Toxicology v221-9 2003

CONTRASTE ENTRE LE TAUX DE Hg DANS LES CHEVEUX (de naissance) ET LE TAUX DE Hg DANS LE CORPS

bull Les enfants autistes ont un taux de Hg beaucoup plus bas dans leur cheveux de naissance

bull De nombreux physiciens ont rapporteacute que les enfants autistes preacutesentaient un taux plus eacuteleveacute de Hg dans le corps (par rapport aux enfants sains)

bull Lrsquoexplication la plus simple serait ducirct agrave la susceptibiliteacute geacuteneacutetique de retenir le mercure

bull Il existe eacutegalement une diffeacuterence eacutevidente entre Genre (Hommes amp Femmes) Ceci peut ecirctre expliqueacute par les effets de la testosteacuterone sur la toxiciteacute-T

CONCLUSIONS IMPORTANTES

bull IL EXISTE DONC UN CLASSE DE POPULATION QUI NE PEUT PAS EFFICACEMENT EacuteLIMINER LE MERCURE CES PERSONNES SONT PAR CONSEacuteQUENT SOUMISES Agrave DE PLUS GRANDS RISQUES DrsquoEXPOSITION AU MERCURE PAR RAPPORT AU RESTE DE LA POPULATION

bull ILS POURRAIENT EcircTRE DES PORTEURS DE LrsquoAPO-E4 DES PERSONNES PREacuteSENTANT UNE DEFFICIENCE DE MEacuteTALLOTHIONINE UNE DIMINUTION DE GSH OU ENCORE DES ANOMALIES GEacuteNEacuteTIQUES

bull EST CE QUE CECI RESTE VALIDE POUR LA MALADIE DrsquoALZHEIMER ET POUR DrsquoAUTRES MALADIES NEUROLOGIQUES

IMPORTANTES CONCLUSION

bull 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

bull THESE MAY BE APO-E4 CARRIERS OR METALLOTHIONINE DEFICIENT GSH DEPLETED OR OTHER GENETIC DIFFERENCES

bull DOES THIS HOLD ALSO FOR AD AND OTHER NEUROLOGICAL DISEASES

Mercury Effects on the Immune Systembull 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

bull 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)384-932005) 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

NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin

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

High Hg2+ Pb2+ Cd2+ and arsenic affinity

WHAT WOULD REPLACEMENT OF Mo BY Hg ON MOLYBDOPTERIN DO

1 Inhibit the enzyme sulfite oxidase leading to decreased sulfate levels and higher toxic sulfite levels

2 Cause a depletion of Mo

3 Cause a more rapid breakdown of Molybdopterin to neopterin

4 Decrease the removal of toxins like tylenol which require sulfation for removal

5 Inhibit other pathways that require sulfation and increase sulfite sensitivity Sulfite decreases mylenation of white matter in the CNS

CONCLUSIONS

bullSULFITE INDUCED IMPROPER MYLENATION OF THE CNS LEADS TO SEIZURESbullDEMYLENATION IS OBSERVED IN MANY NEUROLOGICAL ILLNESSES INCLUDING MULTIPLE SCLEROSIS AND AUTISM bullANYTHING (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 ILLNESSESbullINDIVIDUALS 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 mutationsJames SJ Cutler P Melnyk S et al Metabolic markers of increased oxidative stress and methylation capacity in children with autism Am J Clin Nutr 2004801611ndash1617

Ischiropoulos H Beckman JS Oxidative stress and nitration in neurodegeneration Cause effect or association J Clin Invest

2003111163ndash169

Muravchick S Levy RJ Clinical implications of mitochondrial dysfunction Anesthesiology 2006105819ndash837

Kern JK Jones AM Evidence of toxicity oxidative stress and neuronal insult in autism J Toxicol Environ Health B Crit Rev 20069485ndash499

Deth R Muratore C Benzercry J et al How environmental and genetic factors combine to cause autism A redoxmethylation hypothesis Neurotoxicology 200829190ndash201

GLUTATHIONE amp OXIDATIVE STRESS

The effect of most toxicants and infections on humans are

1most likely to occur in individuals who are already suffering from oxidative stress

2induce oxidative stress in the process of causing the medical symptoms they express

3reduced or prevented by various mechanisms if the body can maintain a healthy redox status

HOW TO DETECT AND EVALUATE LEVEL OF OXIDATIVE STRESS

bullA BLOOD GLUTATHIONE TEST IS THE MOST DIRECT MEASURE OF OXIDATIVE STRESSbullOXIDIZED DNA BASES (8-OH-deoxyGUANOSINE) AND OXIDIZED LIPID FRAGMENTS IN URINE ARE ALSO RELIABLEbullA URINARY PORPHYRIN PROFILE CAN HELP IDENTIFY POSSIBLE TOXINSbullURINARY NEOPTERIN LEVELS SEEM TO CORRELATE ALSO

bullOne of the main sources of free radicals are damaged toxic or dysfunctional mitochondrial which may result from toxic damage

bullGlutathione (GSH) is the major compound that scavenges hydroxyl free radicals and protects the cell from oxidative damage

REACTIVE OXYGEN SPECIES (ROSs)bull Superoxide Anion O2 + e- O2

-

bullHydrogen Peroxide O2- HO2

(hydroperoxyl radical) 2HO2

H2O2 + O2

bullHydroxyl Radical O2- + H2O2O2 + HO- + HO (Haber-Weiss)

Fe2+ + H2O2 Fe3+ + HO- + HO (Fenton)The hydroxyl radical is the most damagingNATURAL REMOVAL OF ROSs

SOD or Superoxide Dismutase Catalyzed Reaction2O2

- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)

Catalyase Catalyzed Reaction 2H2O2 2H2O + O2

Peroxidase Catalyzed Reaction H2O2 + AH2 2H2O + AldquoArdquo could be glutathione (GSH) with glutathione peroxidaseCatalyase is the enzyme that converts Hgo to Hg2+

Structures and General Chemistry of GlutathioneGlutathione (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 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+

6 2 GSH + OH GSSG + H20

7 GSSG + NADH + H+ 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) Levels1 GSH serves as a frontline reducing agent keeping all our

enzymes protected from oxidation

2 GSH serves as a ldquonatural chelatorrdquo 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 (eg 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 SETHdagger SATORU FURUKAWADagger RICHARD W COMPANSdagger and DEAN P JONESDepartment of Biochemistry daggerDepartment of Microbiology and Immunology Emory University School of Medicine Atlanta GA USA and DaggerNutri-Quest Inc Chesterfield MO USA(Received 27 August 2002 Revised 23 December 2002 Accepted 9 January 2003)

AbstractmdashInfection 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 (005ndash 01) multiplicity of infection (MOI) GSH inhibited expression of viral matrix protein and inhibited virally induced caspase activation and Fas upregulation In BALBc 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 AX-31 Together the data suggest that the thiol antioxidant GSH has an anti-influenza 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 copy 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 Kaposis 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) 3693-3698URL Accessed 1252008 httpwwwjbcorgcgicontentabstract27553693

This research implies that oxidative stress ie 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 lt 00001 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) 1967-72URL Accessed 1252008 httpwwwncbinlmnihgovpubmed9050888dopt=Abstract

Glutathione inhibits HIV replication by acting at late stages of the virus life cycle

Palamara AT Perno CF Aquaro S Buegrave 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 199612 (16) 1537-41 URL Accessed 03142009 httpwwwncbinlmnihgovpubmed8911579

The ndashSH 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 DAgostini 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 gt 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 ie 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 1252008httpwwwncbinlmnihgovpubmed8540746ordinalpos=1ampitool=EntrezSystem2PEntrezPubmedPubmed_ResultsPanelPubmed_DiscoveryPanelPubmed_Discovery_RAamplinkpos=3amplog$=relatedarticlesamplogdbfrom=pubmed

Relationship Between Plasma Glutathione Levels and Cardiovascular Disease in a Defined Population The Hisayama Study Haruki Shimizu et al

Stroke 2004352072

Background and Purposemdash 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 casendashcontrol study we tested the hypothesis that low levels of plasma GSH are closely associated with CVD and its clinical types

Methodsmdash 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

Resultsmdash Mean tGSH concentrations were lower in all CVD cases than in the control subjects (306 versus 371 micromolL P=00001) Among the CVD types both the cerebral infarction cases (298 versus 359 micromolL P=0001) and cerebral hemorrhage cases (251 versus 343 micromolL P=00027) had significantly lower tGSH levels than the corresponding control groups had The same tendency was observed for cases of subarachnoid hemorrhage (345 versus 383 micromolL P=036) and myocardial infarction (365 versus 377 micromolL P=069) 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 021 to 077) and the fourth quartiles (adjusted odds ratio 025 95 CI 012 to 051) than in the first This association was most prominent in patients with lacunar infarction or cerebral hemorrhage

Conclusionsmdash 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 CSource J Biol Chem 2005 280 37481-8 URL Accessed 1252008 httpwwwmitochondrialnetshowabstractphppmid=16150732ampredirect=yesampterms=reduced+glutathione+in+virus

CONCLUSIONSbull GLUTATHIONE EXPERIMENTS INDICATE THAT GSH IS IMPORTANT IN BOTH PREVENTING AND ELIMINATING VIRAL INFECTIONS

bullIT APPEARS AS IF THE ndashSH GROUP IS PARAMOUNT IN DISRUPTING THE DITHIOL (-S-S) BONDS OF VIRAL COAT PROTEIN IMPEDING FURTHER REPLICATION AND SPREAD OF THE VIRAL INFECTION

bullIT HAS BEEN HYPOTHESIZED THAT GLUTATHIONE-BOUND TO VIRAL PROTEINS ENHANCES THE IMMUNE RESPONSE TO VIRAL INFECTIONS

bullLOW BODY GSH LEVELS SEEM TO BE A MAJOR RISK FACTOR FOR VIRAL INFECTIONS THIS IS IMPORTANT WITH THE CURRENT CONCERN ABOUT THE SWINE FLU

bullTAKING 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

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


CONVERSION OF GSH TO GSSG PRECEDES CELL DEATH IN CULTURED FIBROBASTIC CELLS

GSSG

DEAD CELLS


INCREASED DNA DAMAGE WITH INCREASED OXIDATIVE STRESS IN REGRESSING MAMMARY CELLS

THERE ARE SEVERAL ITEMS THAT LEAD TO ABNORMAL OXIDATIVE STRESS OR LOWER

REDUCED GLUTATHIONE AND ELEVATED GSSG LEVELS

1TOXICITIES

2INFECTIONS

3INADEQUATE DIETS (LOW CYSTEINE)

4AGING

5LACK 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 (eg CYSTEINE) AND REMOVING ANY TOXICANTS (eg HEAVY METALS) THAT PREVENT GSH SYNTHESIS

3 PREVENT AND REVERSE THE DAMAGE CAUSED BY OXIDATIVE STRESS FACTORS

New Antioxidant Partitioning Conceptbull 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

bull Toxin generated reactive oxygen species (ROSs) in the body are located intracellular or in hydrophobic locations

bull 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

bull Therefore efficacious antioxidants need to be both effective in the ORAC test (oxygen radical absorbance capacity test) and hydrophobic

O O

NH NH

SH SH

NO O

NH NH

SH SH

New Hydrophobic Antioxidant Agents

N1N2bis(2-mercaptoethyl)isophthamide Pyridine Analog

A New Antioxidant Called OSR1

Potent scavengers of hydroxyl radicals in lipophilic areas

Free radical scavenging sites

1 ORAC oxygen radical absorbance capacity test is a measure of a compoundrsquos ability to prevent oxidation of Trolox (a vit-E analog) by ROSs (reactive oxygen species)

2 This means OSR would preserve vitamin-E in cells3 The HORAC hydroxyl radical absorbance capacity test score

for OSR is 299000100g This is a measure of a compoundrsquos ability to prevent oxidation of Trolox by hydroxyl free radicals

4 Therefore OSR is one of the most potent antioxidants ever tested ranking with clove oil and other essential oils however OSR is without toxicity

5 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

6 The plasma half-life of OSR is 6-7 hours7 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

bullA commercial toxicology laboratory has confirmed that the new antioxidant has an LD50 greater than 5gramskg body weight when given orally the highest testing level This is equivalent to a 100 lb person taking 227grams

Nor did mice given 10gkg body weight for 28 straight days demonstrate any toxic effects

bullThe compounds are not mutagenic as determined by a FDA certified laboratory

bullThese 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 Severe

9 yo wf ASD gd recovery 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 GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309

OSR GSH and Thiol Data Seniors Peach colored samples hemolyzed- disregard

72 yo wm 71 yo wf 73 yo wf

Baseline Week 4 Week 12 Baseline Week 4 Week 12 Baseline Week 4 Week 12

Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337

HUMAN STUDIES Effect of OSR on Glutathione-S-transferase (GST) levels (ngml)

GSTTime (months) 0 1 2Patient

1 L L 0482 L L 0483 L 046 0434 L L 0535 L L 0436 L L 0377 L L 0328 L 058 0439 L L 06310 L L 043

GST activities increased in every patient Detection levels were 04 for normals to 31 for a high level for GST

CONCLUSIONSbull A NON-TOXIC LIPID SOLUBLE FREE

RADICAL SCAVENGING ANTIOXIDANT HAS BEEN DEVELOPED AND FOUND TO BE WITHOUT DETECTABLE TOXICITY

bull THIS ANTIOXIDANT EFFECTIVELY SCAVENGES HYDROXYL RADICALS

bull THIS ANTIOXIDANT IS EFFECTIVE IN HELPING MAINTAIN A HEALTHY GLUTATHIONE LEVEL

bull A HEALTHY GLUTATHIONE LEVEL IS IMPORTANT FOR HEALTH

bull From www uninformed concentcom


IN SPITE OF THE OBVIOUS EMISSION OF Hg VAPORS FROM DENTAL AMALGAM THE FDA HAS STEADFASTLY REFUSED TO TEST THEM FOR SAFETY

Visualization of Mercury Vapor Escaping from an Aged Dental Amalgam

Amalgam is 50 Mercury inches from your brain and olfactory tissues

Mercury from Dental Amalgam1 Pro-amalgam ADA spokespersons ldquoestimaterdquo that

about 003 mcg mercury are emitted from a single amalgam per day Estimate that it would take several hundred amalgams to provide a toxic exposure ldquoHijacking Science Examplerdquo

2 A new IAOMT study shows that different amalgam types emit more mercury and that a single spill (very small amalgam) emits between 40 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 fillingsBjoumlrkman L et al Toxicol Appl Pharmacol 1997 May144(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 (27 vs 023 mumol Hgkg dry weight p lt 0001) A considerable increase of the Hg concentration in feces 2 days after amalgam removal (median 280 mumol Hgkg 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 nmolliter at baseline Two days after removal the median Hg concentration in plasma was increased to 5 nmolliter and declined subsequently to 13 nmolliter by Day 60 In saliva there was an exponential decline in the Hg concentration during the first 2 weeks after amalgam removal (t 12 = 18 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 conjunction with removal of amalgam fillings seems to be low

Human exposure to mercury and silver released from dental amalgam restorations

Skare I and Engqvist A Arch Environ Health 1994 Sep-Oct49(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 Hg24 h and urinary excretions ranged from 04 to 19 micrograms Hg24 h In 10 cases urinary and fecal excretions of mercury

and silver were also measured Fecal excretions ranged from 1 to 190 micrograms Hg24 h and from 4 to 97 micrograms Ag24 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 Hg24 h

bull Maternal amalgam dental fillings as the source of mercury exposure in developing fetus and newborn Journal of Exposure Science and Environmental Epidemiology (2008) 18 326ndash331

bull Lubica Palkovicovaa Monika Ursinyovaa Vlasta Masanovaa Zhiwei Yub and Irva Hertz-Picciottob

bull 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 Hg0 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 motherndashchild 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 063 mcgl (range 014ndash29 gl) and 080 mcgl (range 015ndash254 mcgl) 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 58 mcgl in cord blood) A strong positive correlation between maternal and cord blood Hg levels was found

(=079 Plt0001) Levels of Hg in the cord blood were significantly associated with the number of maternal amalgam fillings (=046 Plt0001) and with the number of years since the last filling (=- 037 Plt0001) 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

CLAacuteUDIA FEITOSA-SANTANAa1a2 c1 MIRELLA TS BARBONIa1a2 NESTOR N OIWAa1a2 GALINA V PARAMEIa3 ANA LUISA AC SIMOtildeESa2 MARCELO F DA COSTAa1a2 LUIZ CARLOS L SILVEIRAa4a5 and DORA F VENTURAa1a2 Visual Neuroscience (2008) 25487-491

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 = 424 plusmn 65 years 6 females and 14 males) with exposure to Hg vapor during 105 plusmn 53 years and away from the work place (relative to 2002) for 68 plusmn 42 years During the Hg exposure or up to one year after ceasing it mean urinary Hg concentration was 47 plusmn 354 μgg 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 14 plusmn 14 μgg creatinine for patients compared with 05 plusmn 05 μgg 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 lt 002) than controls as evaluated by the size of MacAdams 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 ngg Hg SbControls 80 15IDCM 178400 19260Frustaci 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 HASNrsquoT NIH REQUESTED PROPOSALS FOR RESEARCH TO STUDY THISTHIS 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 ndash Un Process Essentiel agrave la Survie des Neurones

Dendrite

Microtubule

MembraneBound Organelle

DynienAxon

Kinesin

HgEDTA entraicircne des anomalies au niveau de lrsquointeacuteraction [32P]8N3GTP-szlig-tubuline caracteacuteristique de la maladie drsquoAlzheimer

Autoradiogramme du [32P]8N3GTP Photo LabelliseacuteeSujets Sains (C) amp Sujets atteints de lrsquoAlzheimer (AD)

Brain Hippocampus Homogenates

La reacutepartition de la szlig-tubuline est anormale pour les malades atteints de lrsquoAlzheimer (Brain Homogenates)

NORMALSNORMALSNORMALS ALZHEIMERSANTIBODY DETECTION OF BETA-TUBULIN

EDTA empecircche le Cd Cu amp Zn mais pas le HgInhibition de [32P]8N3GTP lsquoPhotolabelingrsquo de la szlig-tubuline dans le cerveau

EFFET DrsquoEXTRACTIONS SUCCESSIVES DE SOLUTIONS DrsquoAMALGAMES SUR LA VIABILITEacute

DE LA TUBULINE (DU CERVEAU)

0

20

40

60

80

100

120

Hours of Amalgam Soak

Active

Degenerating Neurons into Neurofibillary Tangles by Treatment with Nanomolar Levels of Hg2+ Leong et al NeuroReports 200112 (4)733-737

MERCURY AND ONLY MERCURY COULD CAUSE THE FORMATION OF NFTs THE MAJOR DIAGNOSTIC HALLMARK OF ALZHEIMERrsquoS DISEASE

Alzheimers Metal Concentrations in Plasma and Cerebrospinal Fluid in Patients with Disease Dement Geriatr Cogn Disord 2008 May 525(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 Alzheimers 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 lt 0001) and AD + vasc (p lt= 0013) than in controls In CSF however the concentrations of vanadium manganese rubidium antimony cesium and lead were significantly lower among subjects with AD (p lt= 0010) and AD + vasc (p lt= 0047) than in controls Strong positive correlations were noted between plasma Cs versus CSF Cs in subjects with AD (r(s) = 050 p lt 0001) and AD + vasc (r(s) = 068

p lt 0001) Conclusion Besides the raised plasma mercury concentrations no consistent metal pattern in plasma or CSF was observed in patients with AD

bullMercury and only mercury can mimic the abnormal biochemistry observed in Alzheimerrsquos 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

bullAmalgams are only inches from the brain and the olfactory nerves and constantly release mercury vapor

bullYet 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 US women Dr Dan Laks UCLA August 09 A study involving more than 6000 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 US Centers for Disease Control and Preventions 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 timeldquoAccording 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 Alzheimers disease Laks also found a connection between levels of the pituitary hormone lutropin and chronic mercury exposure which he said might help explain mercurys link to neurodegenerative disease Inorganic mercury can also accumulate in the brain and stay there for years according to the news release ldquothese 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

Evidence of Harm

Autism Risks From 5 Sequential Studies by Verstraten et al of CDC

Study1 Study2 Study3 Study4 Study5 762(1999)

248

169152(2001) 100

(2005) ie 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 10 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 ldquolostrdquo by the CDC

Go to Safemindsorg to read the FOIA material on the Verstraten studies

Simpsonwood Meeting

Conflicts with other CDC accepted studies from Europe

Indicates thimerosal is causal for autism

1 In USA rate was 1150 or 6710000

2 Outpatients added in 1995

3 Large Copenhagen Clinic added in1992

4 Autism classification changed in 1994

5 Thimerosal removed from vaccine

DANISH STUDY

Conclusion exposure to a potent neurotoxin thimerosal prevents autism Nonsense

bullThe 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 AlaskabullThese studies are quite unbelievable if one looks at the content in detail The major question to the CDC and AAP is why havenrsquot the Danes Swedes and English replaced thimerosal in their vaccines if it is proven as these studies suggest that thimerosal prevents autism

bullPerhaps the medical establishments in these countries are more concerned about infant health than ours

Other Considerationsbull In England between 1970-1980 about 147 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

bull The UPI series on autism by Dan Olmsted finds1 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 35000 children

bull 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)

CONCLUSIONSTHE 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

Slide 1

TOXICITEacute DU MERCURE ET SA RELATION AUX MALADIES NEUROLOGIQUES

WHAT CAUSED THE USA AUTISM EPIDEMIC

Important Observations

Slide 5

Slide 6

Slide 7

Le thimeacuterosal est composeacute drsquoacide thiosalicylique et drsquo eacutethyl de mercure une substance toxique bien connue



THE BIG MISTAKE

Slide 12

SYNERGISTIC EFFECTS OF HEAVY METALS IS QUITE COMPLEX AND CAN GREATLY ENHANCE THE TOXICTY OF MERCURY

Slide 14

Slide 15


Estradiol Reduces Cumulative Mercury and Associated Disturbances in the Hypothalamus-Pituitary Axis of Ovariectomized Rats Oliveria et al Ecotoxicol Environ Safety Jan10 2006

Slide 18


Slide 20

Slide 21

TAUX EacuteLEVEacute DE MERCURE SOUS CARDIOMYOPATHIE DILATATIVE IDIOPATHIQUE (CMDI) QUELLE EST LA SOURCE DE MERCURE

Slide 23






Mercury Effects on the Immune System


Slide 31


CONCLUSIONS

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



One of the main sources of free radicals are damaged toxic or dysfunctional mitochondrial which may result from toxic damage

REACTIVE OXYGEN SPECIES (ROSs)

Structures and General Chemistry of Glutathione

The Importance of Glutathione (GSH) Levels

Slide 41

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

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 inhibits HIV replication by acting at late stages of the virus life cycle Palamara AT Perno CF Aquaro S Buegrave MC Dini L Garaci E Department of Experimental Medicine and Biochemical Sciences University of Rome Italy

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 DAgostini C Di Francesco P Favalli C Rotilio G Garaci E Department of Experimental Medicine and Biochemical Sciences University of Rome Italy

Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53


New Antioxidant Partitioning Concept

Slide 56

Slide 57


OSR GSH and Thiol Data in ASD Peach colored samples hemolyzed- disregard


Slide 61

Slide 62


Mercury from Dental Amalgam

Slide 65

Slide 66

Slide 67

Slide 68

ELEVATED MERCURY IN IDIOPATHIC DILATED CARDIOMYOPATHY (IDCM) WHERE DOES THE Hg COME FROM



Autoradiogramme du [32P]8N3GTP Photo Labelliseacutee Sujets Sains (C) amp Sujets atteints de lrsquoAlzheimer (AD) Brain Hippocampus Homogenates


EDTA empecircche le Cd Cu amp Zn mais pas le Hg Inhibition de [32P]8N3GTP lsquoPhotolabelingrsquo de la szlig-tubuline dans le cerveau

EFFET DrsquoEXTRACTIONS SUCCESSIVES DE SOLUTIONS DrsquoAMALGAMES SUR LA VIABILITEacute DE LA TUBULINE (DU CERVEAU)

Slide 76

Slide 77

Slide 78

Slide 79



Slide 82

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

Other Considerations

Slide 85

TOXICITEacute DU MERCURE ET SA RELATION AUX MALADIES

NEUROLOGIQUES

DR BOYD E HALEY

PROFESSEUR ET PREacuteSIDENT DU DEacutePARTEMENT DE CHIMIE

UNIVERSITEacute DU KENTUCKY








bull








1992 2000 67 8 1994 2002 74 27 1996 2004 gt100 82 2000 2008


























0

50

100

150

200

85 86 87 88 89 90 91 92 93 94 95 96 97 98

0

5

10

15

20



Year of birth





Year of survey 87 88 89 90 91 92 93 94 95 96 97 98 99 00







0 5 10 15 20 25 30

Neu

ron

Surv

ival

( In

itial

Num

ber)

0

20

40

60

80

100

120

Control

50 nM thimerosal

500 nM Al(OH)3







+ TESTOSTERONE



DR MARK LOVELL

COLLABORATOR


0 5 10 15 20 25 30

Neu

ron

Su

rviv

al

( I

nit

ial

Nu

mb

er)

20

40

60

80

100

120

Control

50 nM thimerosal



10 nM HgCl2

25 nM HgCl2





INFANT WEIGHT











BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85








bull








1992 2000 67 8 1994 2002 74 27 1996 2004 gt100 82 2000 2008


























0

50

100

150

200

85 86 87 88 89 90 91 92 93 94 95 96 97 98

0

5

10

15

20



Year of birth





Year of survey 87 88 89 90 91 92 93 94 95 96 97 98 99 00







0 5 10 15 20 25 30

Neu

ron

Surv

ival

( In

itial

Num

ber)

0

20

40

60

80

100

120

Control

50 nM thimerosal

500 nM Al(OH)3







+ TESTOSTERONE



DR MARK LOVELL

COLLABORATOR


0 5 10 15 20 25 30

Neu

ron

Su

rviv

al

( I

nit

ial

Nu

mb

er)

20

40

60

80

100

120

Control

50 nM thimerosal



10 nM HgCl2

25 nM HgCl2





INFANT WEIGHT











BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85








1992 2000 67 8 1994 2002 74 27 1996 2004 gt100 82 2000 2008


























0

50

100

150

200

85 86 87 88 89 90 91 92 93 94 95 96 97 98

0

5

10

15

20



Year of birth





Year of survey 87 88 89 90 91 92 93 94 95 96 97 98 99 00







0 5 10 15 20 25 30

Neu

ron

Surv

ival

( In

itial

Num

ber)

0

20

40

60

80

100

120

Control

50 nM thimerosal

500 nM Al(OH)3







+ TESTOSTERONE



DR MARK LOVELL

COLLABORATOR


0 5 10 15 20 25 30

Neu

ron

Su

rviv

al

( I

nit

ial

Nu

mb

er)

20

40

60

80

100

120

Control

50 nM thimerosal



10 nM HgCl2

25 nM HgCl2





INFANT WEIGHT











BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85
























0

50

100

150

200

85 86 87 88 89 90 91 92 93 94 95 96 97 98

0

5

10

15

20



Year of birth





Year of survey 87 88 89 90 91 92 93 94 95 96 97 98 99 00







0 5 10 15 20 25 30

Neu

ron

Surv

ival

( In

itial

Num

ber)

0

20

40

60

80

100

120

Control

50 nM thimerosal

500 nM Al(OH)3







+ TESTOSTERONE



DR MARK LOVELL

COLLABORATOR


0 5 10 15 20 25 30

Neu

ron

Su

rviv

al

( I

nit

ial

Nu

mb

er)

20

40

60

80

100

120

Control

50 nM thimerosal



10 nM HgCl2

25 nM HgCl2





INFANT WEIGHT











BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85







0 5 10 15 20 25 30

Neu

ron

Surv

ival

( In

itial

Num

ber)

0

20

40

60

80

100

120

Control

50 nM thimerosal

500 nM Al(OH)3







+ TESTOSTERONE



DR MARK LOVELL

COLLABORATOR


0 5 10 15 20 25 30

Neu

ron

Su

rviv

al

( I

nit

ial

Nu

mb

er)

20

40

60

80

100

120

Control

50 nM thimerosal



10 nM HgCl2

25 nM HgCl2





INFANT WEIGHT











BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85


0 5 10 15 20 25 30

Neu

ron

Su

rviv

al

( I

nit

ial

Nu

mb

er)

20

40

60

80

100

120

Control

50 nM thimerosal



10 nM HgCl2

25 nM HgCl2





INFANT WEIGHT











BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85




INFANT WEIGHT











BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85










BOYS

GIRLS








IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85






IDIOPATHIQUE (CMDI)


LEVELS ngg Hg Sb

Controls 80 15



0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85


0

2

4

6

8

10

12

14

16

18

20

Hair Hg level(ppm)

Female

Male

AutisticMean=047

n=94


n=34


AMALGAM COUNT

LOW

HIGH


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85


0

2

4

6

8

10

12

14

0-3

Hair Hg level(mcgg)


4-5 6-7 8-9 gt10264 693 670 632 1791

N 15 22 29 30 43

Autistic

Control


























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85

























NH

NNH2

O

NH

NH

O

S

S

Mo

O

O

OP

O-

OO

-

Molybdopterin









CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85







CONCLUSIONS




2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85



2003111163ndash169














-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85











-



H2O2 + O2




- + 2H+ H2O2 + O2 (keeps O2- lt10-11M)






















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85




















































Stroke 2004352072






















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85


















GSSG

DEAD CELLS





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85





1TOXICITIES

2INFECTIONS


4AGING

5LACK OF WARMTH










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85










O O

NH NH

SH SH

NO O

NH NH

SH SH






















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85

















Total GSHGSSG 403 536 871 429 375 877 248 323 645 148 221 286

Free GSHGSSG 157 180 243 135 82 262 87 141 295 53 69 122

Glu-Cys 21 24 34 36 33 40 22 30 39 25 29 32

Cys-Gly 379 381 333 412 368 469 350 356 340 517 424 358

Cysteine 2004 2122 2019 1702 1668 1691 2402 2313 2600 2371 2505 1858

Homocys 46 55 53 57 51 50 52 59 63 79 84 92

Methionine 148 154 164 207 227 260 221 226 263 222 194 309




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85




Total GSHGSSG 114 169 488 172 362 287 158 428 696

Free GSHGSSG 35 53 170 89 121 156 80 173 254

Glu-Cys 32 33 36 29 28 40 18 32 41

Cys-Gly 630 591 612 450 514 480 398 419 515

Cysteine 3442 2554 3179 3047 2436 2900 2882 2537 3242

Homocys 212 139 128 97 93 91 114 126 161

Methionine 205 283 312 154 172 254 211 231 337





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85





































Dendrite

Microtubule


DynienAxon

Kinesin









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85









0

20

40

60

80

100

120


Active













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85













UNIVERSITY


THE CDC

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85

Evidence of Harm



248

169152(2001) 100




Simpsonwood Meeting








DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85






DANISH STUDY














AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85













AGENCIES

Slide 1




Slide 5

Slide 6

Slide 7




THE BIG MISTAKE

Slide 12


Slide 14

Slide 15



Slide 18


Slide 20

Slide 21


Slide 23








Slide 31


CONCLUSIONS








Slide 41





Slide 46


Slide 48


Slide 50

Slide 51

Slide 52

Slide 53



Slide 56

Slide 57




Slide 61

Slide 62



Slide 65

Slide 66

Slide 67

Slide 68








Slide 76

Slide 77

Slide 78

Slide 79



Slide 82



Slide 85

PRESENTS: A Tidal Wave of Terror: Thimerosal in Vaccines Boyd Haley, PdD Professor of Chemistry,...

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Transcript of PRESENTS: A Tidal Wave of Terror: Thimerosal in Vaccines Boyd Haley, PdD Professor of Chemistry,...