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
reported special education rates were nine
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
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
had the power to reveal subgroups with increased susceptibility (8-10).
Augmenting concern are facts found in CDC documents obtained by FOIA.
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
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),
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
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
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
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
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
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).
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.
2. Evidence of Harm
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
Chapter II: 1999-2000
6. CDC 1999 findings summarized
Cheri Jacobus, Sallie Bernard
There's Mercury in Vaccines?
Chapter I: pre-1999
8. Fighting the Autism-Vaccine War
By Bernadine Healy, M.D. [former director of NIH]
9. The Vaccines-Autism War: Détente Needed - Heart to Heart
By Bernadine Healy, M.D. [former director of NIH]
Apr 14, 2009
10. Duane Alexander. M.D., NICHD director
Quoted in: NIH Agency Head: Vaccine-Autism Research is "Legitimate"
- by David Kirby
11. Vaccination policy lags behind vaccine science
by Teresa Binstock December 9, 2007
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
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
Grimble RF. J Nutr. 2006 Jun;136(6 Suppl):1660S-1665S.
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.
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
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.
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
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.
Vaccine A: The Covert Government Experiment That's Killing Our
Soldiers--And Why GI's Are Only The First Victims
Gary Matsumoto, 2004.
29. Squalene & Gulf War illnesses (GWI)
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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