Is there some reason that you could not even link to as much
as the abstract of the study you are referencing, Mr. Editor, Costner? So that
tells me as well that likely you did not even read the study, yourself. You
just based what you claimed to off the two articles in itself. Would I be
correct? That’s right; you never even as much as read the study you are
promoting.
What is actually hilarious is the fact that you obviously do
not even realize it, that in fact that your said study actually in fact
directly supports the ASD/ vaccine connection. The reason you do are oblivious
to that fact and do not realize that, is based in the fact that you have failed
to study any of the unbiased non CDC connected scientific studies, to begin
with. Your pathetic presentation of this Molecular Psychiatry study, with the
additional claim that it debunks the vaccine connection, amounts to just
another expose of your own misunderstanding of the science. In the
further promotion of such said incorrect and unjustified claims on your
part; you are thus in that effort only promoting further baseless
conclusions. Conclusions that not only show a large amount of lack of critical
thinking on your part, but as well a major degree of intellectual
dishonesty. And you want to accuse others of promoting, “Quackery”?
That is more than a bit hypocritical, coming from the obvious head Quack, such
as yourself.
What I am as well referring to of course are all the studies
on this page right here, that of course as said; you conveniently
ignored.
The Vaccine Damage – Science
Here is a copy of your said study, the one you failed to
provide a link to in your blog page.
Molecular Psychiatry advance online publication 11 September
2012; doi: 10.1038/mp.2012.126
Predicting the diagnosis of autism spectrum disorder using
gene pathway analysis
E Skafidas1, R Testa2,3, D Zantomio4, G Chana5, I P Everall5
and C Pantelis2,5
See if you can actually follow the science, Costner; and
make the obvious connections??? Clueless yet?
J Neurodev Disord. 2011 Jun;3(2):132-43. Epub 2011 Mar 5.
Glutathione pathway gene variation and risk of autism
spectrum disorders.
Bowers K, Li Q, Bressler J, Avramopoulos D, Newschaffer C,
Fallin MD.
Source: Department of Epidemiology, Johns Hopkins Bloomberg
School of Public Health, 615 N. Wolfe St. room W6509, Baltimore, MD, 21205,
USA.
Abstract
Despite evidence that autism is highly heritable with
estimates of 15 or more genes involved, few studies have directly examined
associations of multiple gene interactions. Since inability to effectively
combat oxidative stress has been suggested as a mechanism of autism, we
examined genetic variation 42 genes (308 single-nucleotide polymorphisms
(SNPs)) related to glutathione, the most important antioxidant in the brain,
for both marginal association and multi-gene interaction among 318 case-parent
trios from The Autism Genetic Resource Exchange. Models of multi-SNP
interactions were estimated using the trio Logic Regression method. A three-SNP
joint effect was observed for genotype combinations of SNPs in glutaredoxin,
glutaredoxin 3 (GLRX3), and cystathione gamma lyase (CTH); OR?=?3.78, 95% CI:
2.36, 6.04. Marginal associations were observed for four genes including two
involved in the three-way interaction: CTH, alcohol dehydrogenase 5,
gamma-glutamylcysteine synthetase, catalytic subunit and GLRX3. These results
suggest that variation in genes involved in counterbalancing oxidative stress
may contribute to autism, though replication is necessary.
Autism and Glutathione
Article description
Recent research indicates that Autism is related to immune,
neurologic, and inflammation issues that are triggered by a genetic disposition
to be sensitive to certain pollutants, toxins, food additives and so on. Strong
evidence relates the lack of cellular glutathione (the major anti-inflammatory
agent) and Autism.
Excerpts:
Originally it was thought that autism was mainly from the
brain, we now find that there are three components of autism. They are the
brain, immune system, the intestinal track. It's not uncommon that these
children have intestinal disorders—maybe they are constipated or have certain
food sensitivities that irritate their stomachs. Autism is now being related as
a immune, neurological, and inflammatory disorder. Being that glutathione is
the major anti inflammatory agent, inflammation very well can be the component
associated with low glutathione in Autism.
It has been discovered that there are vulnerable genes that
in combination with the right environmental triggers do not allow the child to
stay healthy. Is this an outgrowth of increased pollution and toxins in our
food and air? If the child has a genetic disposition, then under the right
environmental factors (or shall we say unhealthy factors) autism appears. These
genetic variants are called Polymorphisms. When theses genes are affected they
disturb fundamental pathways in the body and the end result of autism is
chronic inflammation through out the brain, digestive and the immune system.
The good news is that inflammation is treatable. In the studies that have been
done the correlation between low glutathione levels and autism is staggering.
Dr. Daria suggests that you simply google “autism and low glutathione” and
you'll find many references to attest to this fact.
Jill James PhD. at the Arkansas Children’s Hospital
Research Institute where she is the director of the Metabolic Genomics Austin
Lab and also she is the professor for pediatrics at the same institute.
In an article published in New Science of Health Sept of 09
page 75, she states that “children with Autism do not make as much of a
compound called glutathione as nero-typical children do. Glutathione is the
cells most abundant antioxidant and is critical for removing toxins. If cells
lack sufficient antioxidants they experience oxidative stress which is often
found with chronic inflammation.”
The mitochondria use oxygen to help make ATP, but if the
cell is deficient in glutathione the cell senses this and diminishes the
production of ATP which will diminish the functioning of that cell—whatever its
purpose.
In American Journal of Medical Genetics in 2006 Jill James
found that common genes variants that support glutathione pathways may be
associated with Autism risks. Jill James says “We also plan to look at
mitochondria dysfunctions. Since mitochondria are the powerhouses of the cells,
this is also the place where the most free radicals are that play a role in
oxidative stress are produced. If the electron transport chain in a
mitochondria is faulty and you are not effectively making ATP. You’ll
produce more free radicals to deplete your glutathione.”
For children with Autism we have to help them control their
diet, the environmental toxins and do what we can to boost glutathione.
Diet generally means gluten and or casein free. It's based
on the theory that children with autism are more likely to have allergies to
gluten (the protein in wheat, oats, barley and rye) and casein (the protein in
milk). Unfortunately most children with these allergies are drawn to foods with
gluten—especially junk foods-- and foods with casein in them, making a change
challenging for some families. If you google “King Diet,” you'll find a diet
for parasite sufferers. Ironically it's an anti-inflammatory diet and will work
wonders with inflammation. It's a three stage diet with Stage I being devoid of
any milk or casein products. For the most part Stage II can be employed for
Autism minus the casein products. Later on, one can be advanced to Stage
III (again minus the casein unless casein is not a problem.) The other
advantage is that this diet is rich in foods that contribute to the cellular
production of glutathione.
Whereas most children under age 20 have enough glutathione,
those with Autism have a problem with the mitochondria that uses up too much
glutathione and they simply don't have enough glutathione.
In summary, inflammation plays an important role in Autism
and glutathione is the major anti inflammatory agent and anti toxin agent in
the cellular mechanism. Genetically there is a predisposition for certain
children to be subject to certain environmental/food toxins which cause the
mitochondria to produce more free radicals than normal which in turn uses up
the cellular glutathione resulting in insufficient production of ATP.
There is a strong correlation between children with Autism and the lack of
glutathione. It makes sense to do whatever can be done to boost cellular levels
of glutathione.
Evidence of oxidative damage and inflammation associated
with low glutathione redox status in the autism brain http://www.ncbi.nlm.nih.gov/pubmed/22781167
Citation: Translational Psychiatry (2012) 2, e134;
doi:10.1038/tp.2012.61
Published online 10 July 2012
Abstract
Despite increasing evidence of oxidative stress in the
pathophysiology of autism, most studies have not evaluated biomarkers within
specific brain regions, and the functional consequences of oxidative stress
remain relatively understudied. We examined frozen samples from the cerebellum
and temporal cortex (Brodmann area 22 (BA22)) from individuals with autism and
unaffected controls (n=15 and n=12 per group, respectively). Biomarkers of
oxidative stress, including reduced glutathione (GSH), oxidized glutathione
(GSSG) and glutathione redox/antioxidant capacity (GSH/GSSG), were measured.
Biomarkers of oxidative protein damage (3-nitrotyrosine; 3-NT) and oxidative
DNA damage (8-oxo-deoxyguanosine; 8-oxo-dG) were also assessed. Functional
indicators of oxidative stress included relative levels of 3-chlorotyrosine
(3-CT), an established biomarker of a chronic inflammatory response, and
aconitase activity, a biomarker of mitochondrial superoxide production.
Consistent with previous studies on plasma and immune cells, GSH and GSH/GSSG
were significantly decreased in both autism cerebellum (P<0.01) and BA22 (P<0.01).
There was a significant increase in 3-NT in the autism cerebellum and BA22
(P<0.01). Similarly, 8-oxo-dG was significantly increased in autism
cerebellum and BA22 (P<0.01 and P=0.01, respectively), and was inversely
correlated with GSH/GSSG in the cerebellum (P<0.01). There was a significant
increase in 3-CT levels in both brain regions (P<0.01), whereas aconitase
activity was significantly decreased in autism cerebellum (P<0.01), and was
negatively correlated with GSH/GSSG (P=0.01). Together, these results indicate
that decreased GSH/GSSG redox/antioxidant capacity and increased oxidative
stress in the autism brain may have functional consequence in terms of a
chronic inflammatory response, increased mitochondrial superoxide production,
and oxidative protein and DNA damage.
Another recent study, to be published later this year, was
conducted by Dr. Jill James of the Autism Speaks' Autism Treatment
Network. It relates to the mother’s inability to produce sufficient
levels of a chemical called Glutathione. The chemical is essential in fighting
toxic metals in the body. Several studies have already established that high
levels of toxic metals in children are strongly correlated with the severity of
Autism, Adams said. According to Adams, the glutathione study shows that low
levels of Glutathione, coupled with high production levels of another chemical,
homocysteine, greatly increase the chances of a woman having a child with
Autism. Among ? Autism moms? in the study, 41 percent of them carried this
chemical abnormality.
Introduction
Clinical findings in autism and relevance of dysfunctional
calcium signaling in
Abnormal Biomedical Findings in Autism – SUMMARY
Reduced cerebral blood flow and cerebral edema in autism
Results of several studies have shown abnormal platelet
reactivity and altered blood flow in children with autism. Following these
findings it has been suggested that platelet and vascular endothelium
activation could be one of the contributing factors to the development and
clinical manifestations of the disorder (16908745). Relative to this the
following case reports are of particular interest, both describing cases of
inflammation of brain blood vessels resulting in loss of language and emergence
of symptoms of autism. In both cases administration of nicardipine lead to
recovery of language and behaviour (1373338, 11008286).
PET and SPECT scans in autistic children show a decreased
cerebral blood floow in some regions of the brain (12077922, 10960047, 7790938)
and cerebral water content was found to be raised in brain grey matter in
children with autism (16924017). A model has been suggested in which the
observed gray matter abnormality could be inflammatory (see
Immunity-Inflammation section below). This finding of cerebral edema at the
same time offered an alternative explanation for enlarged brain size in autism,
which up to then had been hypothesized to be due to lack ‘pruning’ of neurons
during development.
Abnormality of the immune function and chronic inflammation
in autism
Results of numerous studies point to an abnormality of the
immune function in autism, as well as active, ongoing inflammation in the GI
tract, the brain and the cerebrospinal fluid (CSF).
A recent study by Vargas et al (15546155) investigated the
presence of immune activation in postmortem brain specimens and CFS from
subjects with autism. The authors found active neuroinflammation in multiple
areas of the brain, for example in the cerebral cortex and white matter, and in
the cerebellum. A marked migroglial and astroglial activation was also found,
as well as the presence of an altered cytokine pattern, with macrophage
chemoattractant protein (MCP)-1 and tumor growth factor-beta1 (TGF-beta1) being
the most prevalent cytokines. There was also an accumulation of macrophages and
monocytes, and a marked absence of lymphocytes and antibodies, pointing toward
an innate neuroimmune activation with the absence of adaptive immune system/T
cell activation in the brain. In addition, an enhanced proinflammatory cytokine
profile was observed in the CSF, including once more a marked increase in
MCP-1. These observations resemble findings in other neurological disorders in
which elevations in cytokine levels is associated with the pathogenesis of
neuroinflammation, neurotoxicity and neuronal injury and subsequent behavioural
and cognitive impairments, for example HIV-associated dementia and multiple
sclerosis (15288500, 11282546, 16875710, 9852582). Animal experiments
illustrate that, during early pre and postnatal development, inflammatory
cytokine challenge can induce various psychological, behavioral and cognitive impairments
(17804539, 16147952, 9852582). At the same time the expression of many
cytokines, including MCP-1, in neurons and glial cells seems to be upregulated
by increased intracellular calcium triggered by membrane depolarisation
(11102468, 10943723).
Another investigation into inflammatory markers in the brain
tissue of patients with autisms revealed significantly increased levels of
several proinflammatory cytokines (TNF-alpha, IL-6 and GM-CSF, IFN-gamma,
IL-8). The Th1/Th2 ratio was also significantly increased in ASD patients,
suggesting that localized brain inflammation and autoimmune disorder may be
involved in the pathogenesis of ASD (19157572).
Various serological findings further confirm the presence of
immune system dysregulation and active inflammation in autism - raised levels
of proinflammatory cytokines have often been observed in blood of patients with
autism, with significant increases of IFN-gamma, IL-6 and TNF-alpha. These
results are followed by findings of decreased peripheral lymphocyte numbers,
incomplete or partial T cell activation following stimulation, decreased NK
cells activity, dysregulated apoptosis mechanisms, imbalances of serum
immunoglobulin levels, increased numbers of monocytes and abnormal T helper
cell (Th1/Th2) ratio, with a Th2 predominance, and without the compensatory
increase in the regulatory cytokine IL-10 (16698940, 16360218). It is of
interest to note that, following increased levels of TGF-beta1 in brain
specimen as observed by Vargas et al, this cytokine was found to be
significantly lower in the blood of adult patients with autism compared to
controls (17030376).
Another relevant observation is the elevation of
cerebrospinal fluid levels of TNF-alpha compared to its serum levels in
subjects with autism. The observed ratio of 53.7:1 is significantly higher than
the elevations reported for other pathological states for which cerebrospinal
fluid and serum tumor necrosis factor-alpha levels have been simultaneously
measured (17560496).
Central Role of Voltage Gated Calcium Channels
and Intercellular Calcium Homeostasis in Autism
[Although this below study again looks at a lot of variable
aspects to ASD, and in that as well they seem to not ever address the potential
vaccine connection; one thing is clear, the information actually does not
exonerate vaccines, but indirectly again points right to that likely
possibility].
part 2:
Dysregulating Factors:
Genetic Factors – page 2
In addition, autism has been link to some genetic mutations
and polymorphisms that raise
suceptibility to oxidative stress (see Oxidative_Stress).
Toxic Agents
Of special interest might be the findings of a series of
murine studies pointing to links
between viral infections and absorbtion and tissue/organ
distribution of
environmental toxins, in the light of reports indicating
impaired detoxification and
accumulation in the body of environmental toxins in ASD
individuals (see Infectious
_Agents)
In addition to effects of mercury on neuronal cells, of
equal interest are the findings of its negative effects in immune responses.
Dysturbances of calcium homeostasis induced by lowlevel chronic exposure to
mercury is suggested to be one of the mechanisms behind immune dysfunction and
tendency towards development of chronic disease following viral infection
[9653674, 8952707]. Both organic and inorganic mercury have been observed to
screw immune responses and induce autoimmunity in mice, with mouse strains that
are genetically suceptible to autoimmunity showing most pronuonced
developmental disturbances following exposure to ethylmercury [17084957,
15184908] (see also Viruses/Bacteria).
Dendritic cells, crucial for the first-line response of the
immune system towards external pathogens, have recently demonstrated particular
sensitivity to changes in calcium levels as induced by ethylmercury-containing
perservative thimerosal [16835063] (see Immunity/Inflammation). The tendency of
increased persistence of virus with methylmercury exposure may turn out to be
of particular relevance in autism, as this toxin has been observed in a murine
model to change viral myocarditis in a direction compatible with the
development of chronic
inflammatory disease. Amongst other markers significantly
raised levels of calcium and decreased levels of zinc were recorded in the
inflamed heart [11314973, 8682094].
The continuous application of heavy metals lead and mercury
in vivo resulted in their accumulation in brain cells and the occurrence of
delayed toxic effects in rat fetuses. It was shown that when methylmercury is
applied at non-toxic concentrations it becomes neurotoxic under pro-oxidative
conditions. Lead and mercury induce glial cell reactivity, a hallmark of brain
inflammation and increase the expression of the amyloid precursor protein.
Mercury also
stimulates the formation of insoluble beta-amyloid, which
plays a crucial role in the pathogenesis of AD and causes oxidative stress and
neurotoxicity in vitro. Based on their results and reviews of previous findings
authors suggest that those heavy metals may contribute to the etiology of
neurodegenerative diseases [16898674] (see Related Disorders)
[AND THUS IF MERCURY (THIMEROSAL), CAN CAUSE THAT OUTCOME;
THEN CLEARLY SO CAN SUCH AS A NEUROLOGICAL TOXIN, KNOWN AS AN ALUMINUM VACCINE
ADJUVANT!]
J Toxicol Environ Health B Crit Rev. 2006
Nov-Dec;9(6):485-99.
Evidence of toxicity, oxidative stress, and neuronal insult
in autism.
Glutathione
Increasing intracellular glutathione levels has been shown
to:
Read more:
Glutathione and Autism
J Toxicol Environ Health B Crit Rev. 2006
Nov-Dec;9(6):485-99.
Evidence of toxicity, oxidative stress, and neuronal insult
in autism.
Subcellular compartmentalization of glutathione:
Correlations with parameters of oxidative stress related to genotoxicity
Glutathione Articles/Studies - ASD (Autism Spectrum
Disorders)
Health Concerns and Low Glutathione Levels, (more endless
studies connecting low glutathione and detoxification, to ASD)
56 studies in Pubmed in relation to glutathione depletion
and ASD
J Neurol Sci. 2009 May 15;280(1-2):101-8. Epub 2008 Sep 25.
Biomarkers of environmental toxicity and susceptibility in
autism.
Molecular Psychiatry 14, 968-975 (October 2009) |
doi:10.1038/mp.2008.54
Genetic variants in AVPR1A linked to autism predict amygdala
activation and personality traits in healthy humansAVPR1A genetic variation,
amygdala reactivity and personality.
Abstract
In mammals, the neuropeptide vasopressin is a key molecule
for complex emotional and social behaviors. Two microsatellite polymorphisms,
RS1 and RS3, near the promoter of AVPR1A, encoding the receptor subtype most
heavily implicated in behavior regulation, have been linked to autism and
behavioral traits. However, the impact of these variants on human brain
function is unknown. Here we show that human amygdala function is strongly
associated with genetic variation in AVPR1A. Using an imaging genetics approach
in a sample of 121 volunteers studied with an emotional face-matching paradigm,
we found that differential activation of amygdala is observed in carriers of
risk alleles for RS3 and RS1. Alleles in RS1 previously reported to be
significantly over- and under transmitted to autistic probands showed opposing
effects on amygdala activation. Furthermore, we show functional difference in
human brain between short and long repeat lengths that mirror findings recently
obtained in a corresponding variant in voles. Our results indicate a neural
mechanism mediating genetic risk for autism through an impact on amygdala
signaling and provide a rationale for exploring therapeutic strategies aimed at
abnormal amygdala function in this disorder.
Get it, yet? You should!
Again do not forget about THIS science, that you should have included in the combined information assessment, as to the proper conclusion regarding that said Molecular Psychiatry so called genetics study!
The Vaccine Damage – Science
