Teresa
Binstock
Researcher in Developmental & Behavioral Neuroanatomy
October 01, 2009
Boyd E. Haley, Ph.D., is Professor
Emeritus of chemistry and has published important studies about mercury
(eg, 1-3). One of his team's finding documented that a major phenomenon
in Alzheimer's-like pathologies could be induced by physiologically
occurring levels of mercury (1).
A recent essay is titled "Aluminum in vaccination-associated cognitive
decline, motor neuron disease, autism" (4). That essay prompted an
insightful comment from Dr. Haley, wherein he reports that
vaccine-levels of aluminum exacerbate the pathologic potential of
vaccinal thimerosal:
Dr. Haley explained, "Note that aluminum alone does not cause the
abnormal biochemistry and production of neurofibillary tangles as does
mercury (and only mercury) due to the specific interaction of mercury
at specific sulfhydryl sites in specific enzymes/proteins known to be
affected dramatically in Alzheimer’s disease. However, in our studies
on neurons in culture we found that aluminum at levels found in
vaccines dramatically enhanced the toxicity of thimerosal and mercury
cation thereby decreasing the level of mercury required to have the
toxic effects."
Importantly, some vaccines including many flu shots still contain
thimerosal, and many contain one or another of the aluminum compounds
used as adjuvants. Thus we repeat: aluminum at levels present in
vaccines increases the toxicity of thimerosal, which is ~49.6%
ethylmercury by weight. Thus when an infant, toddler, or pregnant woman
is injected with a vaccine or a combination of vaccines containing
aluminum compounds and thimerosal, the likelihood of adverse effects is
increased.
Perhaps we should ask, Why care?
Many media reports assure us that no evidence links thimerosal with
neurologic harm. For instance, Melissa Healy of the Los Angeles Times
expresses a popular notion by writing, "Many argue that environmental
exposures -- in particular, to preservatives used in certain vaccines
-- are a key factor in the development of autism. But a wide range of
comprehensive investigations has failed to find such a link." (5)
Unfortunately, Melissa Healy's glib statement is misleading.
However, at least three major studies have found thimerosal injections
to be associated with developmental disabilities including autism. Two
researchers at Stony Brook medical school found that male infants
injected with thimerosal via hepatitis B vaccinations (a) were nine
times as likely to be enrolled in special education services, and (b)
were three times as likely to have autism -- when compared with male
infants who had not been so vaccinated (6-7). Importantly, these
findings are consistent with the original CDC study (Verstraeten et al
1999) wherein early live thimerosal injections were associated with
autism, PDD, language problems, sleep disorders, and tics (reviewed in
8).
Furthermore, other peer-reviewed studies have documented some of the
mechanisms by which aluminum and mercury induce pathologies seen as
neurodeneneration (eg, 10-14, 15-17).
Noteworthy: in a recently published study, researchers dared mention
that "The demonstrated neurotoxicity of aluminum hydroxide and its
relative ubiquity as an adjuvant suggest that greater scrutiny by the
scientific community is warranted." (14)
Similarly, "Although Thimerosal has been recently removed from most
children's vaccines, it is still present in flu vaccines given to
pregnant women, the elderly, and to children in developing countries."
(17)
Needless to say, I and others are perplexed. Why do most vaccinologists
and many health officials proclaim the safety of vaccines containing
aluminum compounds and/or thimerosal? Why do reporters such as Melissa
Healy and spokespersons for the CDC and FDA turn our attention away
from peer-reviewed studies demonstrating adverse effects from aluminum
and thimerosal?
Why must myriad children and their families live with adverse effects
of vaccinations whose ingredients cause neurodegeneration and
developmental disabilities?
References:
1. Mercury vapor inhalation inhibits
binding of GTP to tubulin in rat brain: similarity to a molecular
lesion in Alzheimer diseased brain
Pendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL.
Neurotoxicology. 1997;18(2):315-24.
Hg2+ interacts with brain tubulin and disassembles microtubules that
maintain neurite structure. Since it is well known that Hg vapor (Hg0)
is continuously released from "silver" amalgam tooth fillings and is
absorbed into brain, rats were exposed to Hg0 4h/day for 0, 2, 7, 14
and 28 d at 250 or 300 micrograms Hg/m3 air, concentrations present in
mouth air of some humans with many amalgam fillings. Average rat brain
Hg concentrations increased significantly (11-47 fold) with duration of
Hg0 exposure. By 14 d Hg0 exposure, photoaffinity labelling on the
beta-subunit of the tubulin dimer with [alpha 32P] 8N3 GTP in brain
homogenates was decreased 41-74%, upon analysis of SDS-PAGE
autoradiograms. The identical neurochemical lesion of similar or
greater magnitude is evident in Alzheimer brain homogenates from
approximately 80% of patients, when compared to human age-matched
neurological controls. Total tubulin protein levels remained relatively
unchanged between Hg0 exposed rat brains and controls, and between
Alzheimer brains and controls. Since the rate of tubulin polymerization
is dependent upon binding of GTP to tubulin dimers, we conclude that
chronic inhalation of low-level Hg0 can inhibit polymerization of brain
tubulin essential for formation of microtubules.
2. Reduced levels of mercury in first baby
haircuts of autistic children
Holmes AS, Blaxill MF, Haley BE.
Int J Toxicol. 2003 Jul-Aug;22(4):277-85.
Reported rates of autism have increased sharply in the United States
and the United Kingdom. One possible factor underlying these increases
is increased exposure to mercury through thimerosal-containing
vaccines, but vaccine exposures need to be evaluated in the context of
cumulative exposures during gestation and early infancy. Differential
rates of postnatal mercury elimination may explain why similar
gestational and infant exposures produce variable neurological effects.
First baby haircut samples were obtained from 94 children diagnosed
with autism using Diagnostic and Statistical Manual of Mental
Disorders, 4th edition (DSM IV) criteria and 45 age- and gender-matched
controls. Information on diet, dental amalgam fillings, vaccine
history, Rho D immunoglobulin administration, and autism symptom
severity was collected through a maternal survey questionnaire and
clinical observation. Hair mercury levels in the autistic group were
0.47 ppm versus 3.63 ppm in controls, a significant difference. The
mothers in the autistic group had significantly higher levels of
mercury exposure through Rho D immunoglobulin injections and amalgam
fillings than control mothers. Within the autistic group, hair mercury
levels varied significantly across mildly, moderately, and severely
autistic children, with mean group levels of 0.79, 0.46, and 0.21 ppm,
respectively. Hair mercury levels among controls were significantly
correlated with the number of the mothers' amalgam fillings and their
fish consumption as well as exposure to mercury through childhood
vaccines, correlations that were absent in the autistic group. Hair
excretion patterns among autistic infants were significantly reduced
relative to control. These data cast doubt on the efficacy of
traditional hair analysis as a measure of total mercury exposure in a
subset of the population. In light of the biological plausibility of
mercury's role in neurodevelopmental disorders, the present study
provides further insight into one possible mechanism by which early
mercury exposures could increase the risk of autism.
3. Mercury toxicity presenting as chronic
fatigue, memory impairment and depression: diagnosis, treatment,
susceptibility, and outcomes in a New Zealand general practice setting
(1994-2006)
Wojcik DP, Godfrey ME, Christie D, Haley BE.
Neuro Endocrinol Lett. 2006 Aug;27(4):415-23.
In a group of 465 patients diagnosed as having chronic mercury toxicity
(CMT), 32.3% had severe fatigue, 88.8% had memory loss, and 27.5% had
depression. A significant correlation was found between CMT and the
Apo-lipoprotein E4 genotype (p=0.001). An investigation into an
additional 864 consecutively seen general practice patients, resulted
in 30.3% having evidence consistent with CMT, and once again a
significant correlation was found with the APO-E4 genotype (p=0.001).
Removal of amalgam mercury fillings when combined with appropriate
treatment resulted in a significant symptom reduction (p<0.001) to
levels reported by healthy subjects.
4. Aluminum
in vaccination-associated cognitive decline, motor neuron disease,
autism
Teresa Binstock; Sept 28, 2009
5. Autism's genetic roots examined in new
government-funded study
Melissa Healy, Los Angeles Times
September 30, 2009
http://latimesblogs.latimes.com/booster_shots/2009/09/autisms-genetic-roots-probed-by-new-governmentfunded-study.html
6. 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
7. Hepatitis B vaccination of male neonates
and autism
CM Gallagher, MS Goodman
Annals of Epidemiology
Vol. 19, No. 9 ABSTRACTS (ACE)
September 2009: p. 659
Stony Brook University Medical Center, NY
PURPOSE: Universal newborn immunization with hepatitis B vaccine was
recommended in 1991; however, safety findings are mixed. The Vaccine
Safety Datalink Workgroup reported no association between hepatitis B
vaccination at birth and febrile episodes or neurological adverse
events. Other studies found positive associations between hepatitis B
vaccination and ear infection, pharyngitis, and chronic arthritis; as
well as receipt of early intervention/special education services (EIS);
in probability samples of
U.S. children. Children with autistic spectrum disorder (ASD) comprise
a growing caseload for EIS. We evaluated the association between
hepatitis B vaccination of male neonates and parental report of ASD.
METHODS: This cross-sectional study used U.S. probability samples
obtained from National Health Interview Survey 1997–2002 datasets.
Logistic regression modeling was used to estimate the effect of
neonatal hepatitis B vaccination on ASDrisk amongboys age 3–17 years
with shot records, adjusted for race, maternal education, and
two-parent household.
RESULTS:Boyswho received the hepatitis B vaccine during the first month
of life had 2.94 greater odds for ASD (nZ31 of 7,486; OR Z 2.94; p Z
0.03; 95% CI Z 1.10, 7.90) compared to later- or unvaccinated boys.
Non-Hispanicwhite boys were 61% less likely to have ASD(ORZ0.39;
pZ0.04; 95% CIZ0.16, 0.94) relative to non-white boys.
CONCLUSION: Findings suggest that U.S. male neonates vaccinated with
hepatitis B vaccine had a 3-fold greater risk of ASD; risk was greatest
for non-white boys.
8. [Synopsis & review]
Blockbuster primate Study Shows Significant
Harm from One Birth Dose of a Mercury-containing
Vaccine
By Mark Blaxill; Sept 30, 2009
http://tinyurl.com/y9dvzae
9. Blood-brain barrier flux of aluminum,
manganese, iron and other metals suspected to contribute to
metal-induced neurodegeneration
Yokel RA.
J Alzheimers Dis. 2006 Nov;10(2-3):223-53.
10: Aluminum complexing enhances amyloid
beta protein penetration of blood-brain barrier
Banks WA et al.
Brain Res. 2006 Oct 20;1116(1):215-21.
11: Some aspects of astroglial functions
and aluminum implications for neurodegeneration
Aremu DA, Meshitsuka S.
Brain Res Rev. 2006 Aug 30;52(1):193-200.
12: 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.
13. Long-term persistence of
vaccine-derived aluminum hydroxide is associated with chronic cognitive
dysfunction
Maryline Couette et al.
Journal of Inorganic Biochemistry (2009) in press
14. Aluminum hydroxide injections lead to
motor deficits and motor neuron degeneration
Christopher A. Shaw; Michael S. Petrik.
Journal of Inorganic Biochemistry (2009) in press
15. Biochemical and molecular basis of
thimerosal-induced apoptosis in T cells: a major role of mitochondrial
pathway
Makani S et al.
Genes Immun. 2002 Aug;3(5):270-8.
{free online}
http://www.nature.com/gene/journal/v3/n5/abs/6363854a.html
16. 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.
17. Thimerosal neurotoxicity is associated
with glutathione depletion: protection with glutathione
precursors
James SJ et al.
Neurotoxicology. 2005 Jan;26(1):1-8.
Thimerosol is an antiseptic containing 49.5% ethyl mercury that has
been used for years as a preservative in many infant vaccines and in
flu vaccines. Environmental methyl mercury has been shown to be highly
neurotoxic, especially to the developing brain. Because mercury has a
high affinity for thiol (sulfhydryl (-SH)) groups, the thiol-containing
antioxidant, glutathione (GSH), provides the major intracellular
defense against mercury-induced neurotoxicity. Cultured neuroblastoma
cells were found to have lower levels of GSH and increased sensitivity
to thimerosol toxicity compared to glioblastoma cells that have higher
basal levels of intracellular GSH. Thimerosal-induced cytotoxicity was
associated with depletion of intracellular GSH in both cell lines.
Pretreatment with 100 microM glutathione ethyl ester or
N-acetylcysteine (NAC), but not methionine, resulted in a significant
increase in intracellular GSH in both cell types. Further, pretreatment
of the cells with glutathione ethyl ester or NAC prevented cytotoxicity
with exposure to 15 microM Thimerosal. Although Thimerosal has been
recently removed from most children's vaccines, it is still present in
flu vaccines given to pregnant women, the elderly, and to children in
developing countries. The potential protective effect of GSH or NAC
against mercury toxicity warrants further research as possible adjunct
therapy to individuals still receiving Thimerosal-containing
vaccinations.
Contact Teresa
Binstock by email
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