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.
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
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.
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
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.
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].
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).
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
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  (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  (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.
Increasing intracellular glutathione levels has been shown to:
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.
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