Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
September 20, 2009
Peer-reviewed findings
announced in 2009 describe an increased rate of autism-spectrum
disorders (triple) among boys who as neonates had received HepB
vaccination, which originally contained thimerosal (1,2). Similarly and
previously, the Stony Brook medical school researchers had reported
special education rates were nine times higher among boys who, early in
life, had received HepB vaccinations containing thimerosal (3).
These two sets of findings are consistent (i) with outcomes in a number
of other studies, and (ii) with the CDC's original findings (1999)
wherein early-life vaccinations which included thimerosal were
associated with autism, PDD/NOS, tics, language problems, and sleep
disorders (eg, 4-7). In contrast, the 2009 findings are inconsistent
with widely touted epidemiological studies that may not have had the
power to reveal subgroups with increased susceptibility (8-10).
Augmenting concern are facts found in CDC documents obtained by FOIA.
For instance, one CDC-investigator's email about their 1999 findings
stated that making the autism-thimerosal association "go away" was not
easy. Ultimately, however, the CDC team led by Thomas Verstraeten was
able to dilute their own findings and did so by using large data-sets
from HMOs wherein autism and other developmental disorders were
under-reported. A study based upon the diluted-data findings was
published by a trade-journal called "Pediatrics". This history is
delineated in David Kirby's Evidence of Harm... (2; see also 5).
Why some children more than others are susceptible to adverse effects
from vaccinations remains an important issue. Genetic and non-genetic
factors are implicated. In other words, for any given child, increased
susceptibility can be acquired and/or genetic. For instance, having one
or more pro-inflammatory alleles of an immune-related gene may heighten
the infant's or toddler's immune-system's reaction to vaccine
ingredients (reviewed in 11). Alternatively, some children are known to
have weak alleles in genes related to detoxification (eg, 12).
Hypersensitivity to thimerosal has long been known, and glutathione
status and glutathione pathways are implicated (eg, 13-14).
Among the non-genetic reasons for why a child can have increased
susceptibility, the vaccinating of sick or recently sick children
remains problematic because an illness utilizes and may incline towards
depletion of a child's reserves of glutathione (eg, 15-18), which helps
detoxify mercury and other toxic metals (19). Ironically, giving
Tylenol aka acetaminophen aka paracetemol increases utilization and
potentiates depletion of glutathione (20).
When co-authors of the initial mercury/autism paper (21) and colleagues
met with CBER personnel in their Bethesda facility (2000), I stated my
concerns regarding the vaccinating of sick or recently sick children.
CBER's then acting-director William Egan, M.D., responded by explaining
that NOT vaccinating sick children had long been the official
recommendation. However, so as to increase rates of vaccine coverage,
that recommendation was changed and now stands as encouraging the
vaccinating of sick children. In my opinion, this policy change has
exacerbated the tendency of small subgroups of children to develop
lastingly adverse traits in response to vaccinations, especially among
children with pro-inflammatory and/or weak-detox alleles, especially in
susceptible children given Tylenol.
As previously cited, transcripts of the CDC's Simpsonwood conference
with pharmaceutical companies make clear that highly placed individuals
of the CDC and and their colleagues representing companies that profit
from vaccines and vaccinations knew by the year 2000 that thimerosal
injections induced significant adverse effects in some children. This
decade-old knowledge is consistent with the findings described by Stony
Brook's Goodman and Gallagher (1,3). Given this damning track-record
for early-life thimerosal injections, a question looms large: Why do
government agencies continue to encourage the injection of thimerosal
during vaccinations?
Towards an answer:
Since Verstraeten et al's intitial findings about thimerosal's adverse
effects (CDC 1999) and despite similar findings (eg, 1,3) amid growing
evidence of thimerosal's pathological mechanisms (eg, 14, 22-25),
vaccinologists and regulatory agency personnel, and others (eg,
executives within the AAP and AMA) seem to have allowed themselves to
accept as Sacred Truth epidemiological findings which have been
described as not having sufficient design or power so as to identify
small but numerically important subgroups of children with increased
likelihood for adverse reactions (8-9). Indeed, declarations about
thimerosal's lack of harm are not rooted in science and are based upon
a deliberate ignoring of data which demonstrate thimerosal's adverse
effects.
Often in scientific papers, prior findings not consistent with one
another and conclusions that differ are mentioned. Contrary findings
are presented and fairly summarized. In contrast, circa 2009, we have
an ongoing situation wherein vaccination policies are no longer based
upon the full range of peer-reviewed findings available to
vaccinologists, physicians, and members of the too influential,
pharmaceutical company's virtual subsidiary known as the Advisory
Committee on Immunization Practices (ACIP), whose purpose seems that of
promoting vaccinations regardless of evidence of adverse effects --
while deliberately ignoring that evidence.
As news reports and vaccine package inserts make clear, many and
perhaps most flu and H1N1 vaccines will contain aluminum, thimerosal,
and/or squalene. Each of these ingredients has been linked with
neurodenegeneration (26-27) or with the induction of rheumatioid
processes (28-29) and developmental disabilities (1-3). We are
reminded of Alice in Wonderland, wherein logic and reason were turned
upside down and inside out. Ignoring adverse effects of thimerosal,
aluminum, and squalene is not a sound basis for vaccination policies
and their enforcement.
An historical insight rings true. In 1855 a journal article stated that
"vaccination benefited only doctors as it produced a sicklier
population" (30; see also 31-32).
References:
1. Hepatitis B triple series vaccine and
developmental disability in US children aged 1-9
years
Gallagher C, Goodman M. Toxicol Environ Chem 2008 90(5):997-1008.
{free online}
http://fourteenstudies.org/pdf/hep_b.pdf
2. Evidence of Harm
David Kirby
http://www.evidenceofharm.com
3. Hepatitis B vaccination of male neonates
and autism
[conference abstract as published]
CM Gallagher, MS Goodman, Graduate Program in Public
Health, Stony Brook University Medical Center, Stony Brook, NY
Annals of Epidemiology, p659
Vol. 19, No. 9 Abstracts (ACE) September 2009: 651–680
4. Autism, mercury, other toxic metals,
& glutathione
Teresa Binstock, Aug 12, 2009
http://www.ravenintellections.com/gre/autism-toxic-metals-glutathione.htm
5. Simpsonwood
Chapter II: 1999-2000
http://www.putchildrenfirst.org/chapter2.html
6. CDC 1999 findings
summarized
Cheri Jacobus, Sallie Bernard
http://www.cherab.org/news/JointStatement.html
7. There's Mercury in
Vaccines?
Chapter I: pre-1999
http://www.putchildrenfirst.org/chapter1.html
8. Fighting the Autism-Vaccine
War
By Bernadine Healy, M.D. [former director of NIH]
http://health.usnews.com/articles/health/brain-and-behavior/2008/04/10/fighting-the-autism-vaccine-war.html
9. The Vaccines-Autism War: Détente Needed
- Heart to Heart
By Bernadine Healy, M.D. [former director of NIH]
Apr 14, 2009
http://health.usnews.com/blogs/heart-to-heart/2009/04/14/the-vaccines-autism-war-dtente-needed.html
10. Duane Alexander. M.D., NICHD
director
Quoted in: NIH Agency Head: Vaccine-Autism Research is "Legitimate"
- by David Kirby
http://www.huffingtonpost.com/david-kirby/nih-agency-head-vaccine-a_b_170034.html
11. Vaccination policy lags behind vaccine
science
by Teresa Binstock December 9, 2007
http://ravenintellections.typepad.com/
12. Metabolic endophenotype and related
genotypes are associated with oxidative stress in children with
autism
James SJ et al. Am J Med Genet B Neuropsychiatr Genet. 2006
141B(8):947-56.
{free online}
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2610366&blobtype=pdf
13. Homozygous gene deletions of the
glutathione S-transferases M1 and T1 are associated with thimerosal
sensitization
Westphal GA et al. Int Arch Occup Environ Health. 2000
Aug;73(6):384-8.
14. Inhibition of the human erythrocytic
glutathione-S-transferase T1 (GST T1) by thimerosal
Muller M et al. Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81.
15. The effects of sulfur amino acid intake
on immune function in humans
Grimble RF. J Nutr. 2006 Jun;136(6 Suppl):1660S-1665S.
{free online}
http://jn.nutrition.org/cgi/content/full/136/6/1660S
16. Glutathione levels in mental and
physical illness
Cohen M et al. AMA Arch Neurol Psychiatry. 1956 Dec;76(6):630-4.
17. Glutathione, cysteine, and ascorbate
concentrations in clinically ill dogs and cats
Viviano KR et al. J Vet Intern Med. 2009 Mar-Apr;23(2):250-7.
BACKGROUND: Oxidative stress plays a role in the pathogenesis of many
systemic diseases. Hospitalized human patients are glutathione,
cysteine, and ascorbate deficient, and antioxidant depletion has been
correlated with poor clinical outcome. To date little is known about
antioxidant concentrations in hospitalized veterinary patients. The
purpose of this study was to determine whether ascorbate, cysteine, or
glutathione depletion is present in ill dogs and cats compared with
healthy controls. HYPOTHESIS: Clinically ill dogs and cats would be
antioxidant depleted, and depletion would correlate with illness
severity and clinical outcome. ANIMALS: Clinically ill client-owned
dogs (n = 61) and cats (n = 37), healthy control dogs (n = 37) and cats
(n = 33). METHODS: Prospective, observational, case control study.
Erythrocyte reduced glutathione, plasma cysteine, and plasma ascorbate
were quantified using high-performance liquid chromatography. RESULTS:
Clinically ill dogs had significantly lower erythrocyte glutathione
concentrations (1.22 mM, range 0.55-3.61) compared with controls (1.91
mM, range 0.87-3.51; P = .0004), and glutathione depletion correlated
with both illness severity (P = .038) and mortality (P = .010). Cats
had higher ascorbate concentrations when ill (10.65 microM, range
1.13-25.26) compared with controls (3.68 microM, range 0.36-13.57; P =
.0009). CONCLUSIONS AND CLINICAL IMPORTANCE: Clinically ill dogs had
decreased erythrocyte glutathione concentrations, which could be a
marker of illness severity and prognostic of a poor outcome. Clinically
ill cats had an unexpectedly high plasma ascorbate, which could
represent a unique species response to oxidative stress.
18. Glutathione metabolism in
sepsis
Biolo G et al. Crit Care Med. 2007 Sep;35(9 Suppl):S591-5.
...Glutathione synthesis can be impaired by cysteine depletion,
protein-energy malnutrition, hyperglycemia, glucocorticoid at
pharmacologic doses, and decreased secretion of anterior pituitary
hormones (growth hormones, thyrotropin, gonadotropins), as often
observed in prolonged critical illness.
19. Cysteine metabolism and metal
toxicity
Quig D. Altern Med Rev. 1998 Aug;3(4):262-70.
{free online}
http://www.thorne.com/altmedrev/.fulltext/3/4/262.pdf
Chronic, low level exposure to toxic metals is an increasing global
problem. The symptoms associated with the slow accumulation of toxic
metals are multiple and rather nondescript, and overt expression of
toxic effects may not appear until later in life. The
sulfhydryl-reactive metals (mercury, cadmium, lead, arsenic) are
particularly insidious and can affect a vast array of biochemical and
nutritional processes. The primary mechanisms by which the
sulfhydryl-reactive metals elicit their toxic effects are summarized.
The pro-oxidative effects of the metals are compounded by the fact that
the metals also inhibit antioxidative enzymes and deplete intracellular
glutathione...
20. Glutathione, glutathione-dependent
enzymes and antioxidant status in erythrocytes from children treated
with high-dose paracetamol
[paracetamol = acetaminophen = Tylenol]
Kozer E et al. Br J Clin Pharmacol. 2003 Mar;55(3):234-40.
{free online}
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1884208&blobtype=pdf
AIM: To investigate glutathione and antioxidant status changes in
erythrocytes from febrile children receiving repeated supratherapeutic
paracetamol doses. METHODS: Fifty-one children aged 2 months to 10
years participated in the study. Three groups were studied: group 1 (n
= 24) included afebrile children who did not receive paracetamol; and
groups 2 (n = 13) and 3 (n = 14) included children who had fever above
38.5 degrees C for more than 72 h. Patients in group 2 received
paracetamol at a dose of 50 +/- 15 (30-75) mg kg(-1) day(-1) and those
in group 3 received paracetamol above the recommended therapeutic dose,
ie 107 28 (80-180) mg kg(-1) day(-1). A blood sample was taken for the
measurement of liver transaminases, gammaglutamil transferase (GGT),
reduced glutathione (GSH), glutathione reductase (GR), glutathione
peroxidase (GPX), glutathione S-transferase (GST), superoxide dismutase
(SOD) and antioxidant status. RESULTS: Aspartate aminotransferase
activity in group 3 was higher than in the other groups (P = 0.027).
GSH, SOD and antioxidant status were significantly lower in group 3
compared with groups 1 and 2 (mean differences: for GSH 3.41 micromol
gHb(-1), 95% confidence interval (CI) 2.10-4.72, and 2.15 micromol
gHb(-1), 95% CI 0.65-3.65, respectively; for SOD 856 U min(-1) gHb(-1),
95% CI 397-1316, and 556 U min(-1) gHb(-1), 95% CI 30-1082,
respectively; and for antioxidant status 0.83 mmol l(-1) plasma, 95% CI
0.30-1.36, and 0.63 mmol l(-1) plasma, 95% CI 0.02-1.24, respectively).
GR activity was significantly lower in groups 3 and 2 in comparison
with group 1 (mean differences 3.44 U min(-1) gHb(-1), 95% CI
0.63-6.25, and 5.64 U min(-1) gHb(-1), 95% CI 2.90-8.38, respectively).
Using multiple regression analysis, paracetamol dose was found to be
the only independent variable affecting GR, GST and SOD activities (P =
0.007, 0.003 and 0.008, respectively). CONCLUSIONS: In febrile
children, treatment with repeated supratherapeutic doses of paracetamol
is associated with reduced antioxidant status and erythrocyte
glutathione concentrations. These significant changes may indicate an
increased risk for hepatotoxicity and liver damage.
21. Autism: a novel form of mercury
poisoning
Bernard S et al. Med Hypotheses. 2001 Apr;56(4):462-71.
22. Activation of methionine synthase by
insulin-like growth factor-1 and dopamine: a target for
neurodevelopmental toxins and thimerosal
Waly M et al. Mol Psychiatry. 2004 Apr;9(4):358-70.
23. Thimerosal neurotoxicity is associated
with glutathione depletion: protection with glutathione
precursors
James SJ et al. Neurotoxicology. 2005 Jan;26(1):1-8.
24. Cellular and mitochondrial glutathione
redox imbalance in lymphoblastoid cells derived from children with
autism
James SJ et al. FASEB J. 2009 Aug;23(8):2374-83.
25. Thimerosal induces neuronal cell
apoptosis by causing cytochrome c and apoptosis-inducing factor release
from mitochondria
Yel L et al. Int J Mol Med. 2005 Dec;16(6):971-7.
26. Some aspects of astroglial functions
and aluminum implications for neurodegeneration
Aremu DA, Meshitsuka S. Brain Res Rev. 2006 Aug 30;52(1):193-200.
27. Nanomolar aluminum induces
pro-inflammatory and pro-apoptotic gene expression in human brain
cells in primary culture
Lukiw WJ et al. J Inorg Biochem. 2005 Sep;99(9):1895-8.
28. [squalene]
Vaccine A: The Covert Government Experiment
That's Killing Our Soldiers--And Why GI's Are Only The First
Victims
Gary Matsumoto, 2004.
http://www.amazon.com/Vaccine-Government-Experiment-Killing-Soldiers/dp/046504400X
29. Squalene & Gulf War
illnesses (GWI)
http://www.rense.com/general87/mill.htm
30. p3 in: Hygeist or Medical Reformer, 1955. As presented on p34 of:
Bodily Matters: The anti-vaccination movement in England, 1853-1907.
Nadja Durbach, 2005; Duke University Press.
31. .Delay in
diphtheria, pertussis, tetanus vaccination is associated with a reduced
risk of childhood asthma
McDonald KL et al. J Allergy Clin Immunol 2008;121:626-31.
32. Polymerase chain reaction detection of
the hemagglutinin gene from an attenuated measles vaccine strain in the
peripheral mononuclear cells of children with autoimmune
hepatitis
Kawashima H et al. Arch Virol. 1996;141(5):877-84.
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