Wednesday, September 26, 2012

Reply to: Does the National Vaccine Injury Compensation Program Protect Vaccine Manufacturers?

Does the National Vaccine Injury Compensation Program Protect Vaccine Manufacturers?

This is the reply that was sent to the above linked to, and opposing blog. However, as always editor no identity Costner, will never publish; as it again contains to much truth.

Your claim that pharmaceutical companies can be sued; is entirely false, Mr. Editor. In most any court you can file a lawsuit for almost anything; however that does not mean that the plaintiff can actually be successfully sued. If you know anything about the courts legal system; you would realize that a precedence was set by the Bruesewitz case. Meaning that any such cases that follow it if they are filed, will strongly be influenced by and determined by any previous precedence in a similar case that has been set. So, quite obviously if with the clearly good merits that the Bruesewitz case had, they were not successful; then there is little to no chance that any other such case filed will have any better luck. Those types of cases against the vaccine manufacturer, are clearly preempted by the existence of the NCVIA. So, in reality and at this point, no parent of a vaccine damaged child is going to ever again pursue the avenue that the Bruesewitz family did against such as Wyeth. Common sense should tell you that Mr. Editor. That family spent over a decade chasing that claim and came up with no compensation. If you call that justice, then something is way wrong with you.

In reality here you are being flat out intellectually dishonest, to yet claim that a vaccine maker can be sued for anything, ever. They are quite obviously. immune to any lawsuits of any kind from a parent of a vaccine damaged child. 

BRUESEWITZ ET AL. v. WYETH FKA WYETH, INC.,ET AL.

Excerpt:

Held: The NCVIA preempts all design-defect claims  against vaccine manufacturers brought by plaintiffs seeking compensation for injury
or death caused by a vaccine’s side effects.  Pp. 7–19.



NVIC Cites "Betrayal" of Consumers by U.S. Supreme Court Decision Giving Total Liability Shield to Big Pharma

Excerpt: Hannah Bruesewitz was brain injured by DPT vaccine as a child but she was denied compensation by the U.S. Court of Claims, which administers the federal vaccine injury compensation program created by the 1986 Act that has turned away two out of three plaintiffs. Her attorneys then sued in civil court, providing evidence that Wyeth-Lederle had the technology to produce a less reactive, purified pertussis vaccine but declined to do so.

“The U.S. Supreme Court has removed all financial incentive for multi-national pharmaceutical corporations, which enjoy a $20 billion dollar business, to make vaccines as safe as they can be,” said Fisher. “This is a sad day for all Americans forced by law to use dozens of doses of vaccines or be barred from school or health insurance or employment. The only leverage left to American consumers to ensure that vaccines with the fewest health risks are produced is to oppose vaccine mandates and work to defend vaccine exemptions in all public health laws.”


The Latest in Atrocious Supreme Court Decisions - Only 2 Justices Stand Up for Your Rights...

Vaccination Profiteers Gang Up on Hannah Bruesewitz - In Supreme Court

Excerpt: The Court took the Bruesewitz case to determine whether 18-year-old Hannah, disabled by injuries she received from Wyeth’s diphtheria, tetanus and pertussis (DPT) vaccine at 6-months-old in 1992, has the right to bring a lawsuit against Wyeth after the Vaccine Court, set up by the 1986 National Childhood Vaccine Injury Act, refused compensation even though she will require life-long care and her vaccine was traced to a lot that had 65 adverse reactions including two deaths, 39 emergency room visits, and 6 hospitalizations.


No Pharma Liability? No Vaccine Mandates, March 3, 2011

YOUR CHILDS DEATH WILL BE A COINCIDENCE AND NO ONE IS LIABLE

Global vaccine market now exceeds $20B
http://www.healthcarefinancenews.com/news/global-vaccine-market-now-exceeds-20b

--------------

I wish to address one other matter as well, and will be directly.

This involves some replies by character name on that blog, Dakota James, and is on again this mindless and dimwitted blog page right here. One mans obsession with me for now since the summer of 2010, and some now over 80 blog pages of personal attack, on me.

Is Lowell Hubbs' "Vacfacts.info" Anti-Vaccination Website Gone?
http://vaccineconspiracytheorist.blogspot.com/2012/08/is-lowell-hubbs-vacfactsinfo-anti.html

This is a copy of the statement and claims made in so called Dakota James reply on that said page.

Dakota James, September 24, 2012 9:29 PM

It looks like Lowell is having some landlord issues:

https://www.facebook.com/lowell.hubbs/posts/4578538663244?notif_t=feed_comment 

https://www.facebook.com/lowell.hubbs/posts/4578600224783?notif_t=feed_comment 

And for more reassurance of his sickening obsession with children, he went as far as to list LS Magazine as his employer!

FYI, you must be logged into Facebook to view his "Info" page:

http://www.facebook.com/lowell.hubbs/info

Ref: Wikipedia article of the 2004 Child Pornography raids listing LS Magazine as a manufacturer and distributor of child porn media:

http://en.wikipedia.org/wiki/2004_Ukrainian_child_pornography_raids

-------------

This is the reply I made and as well quite obviously will never be published, in my defense, and nor in the defense of myself personally.

Your claim that pharmaceutical companies can be sued; is entirely false, Mr. Editor. In most any court you can file a lawsuit for almost anything; however that does not mean that the plaintiff can actually be successfully sued. If you know anything about the courts legal system; you would realize that a precedence was set by the Bruesewitz case. Meaning that any such cases that follow it if they are filed, will strongly be influenced by and determined by any previous precedence in a similar case that has been set. So, quite obviously if with the clearly good merits that the Bruesewitz case had, they were not successful; then there is little to no chance that any other such case filed will have any better luck. Those types of cases against the vaccine manufacturer, are clearly preempted by the existence of the NCVIA. So, in reality and at this point, no parent of a vaccine damaged child is going to ever again pursue the avenue that the Bruesewitz family did against such as Wyeth. Common sense should tell you that Mr. Editor. That family spent over a decade chasing that claim and came up with no compensation. If you call that justice, then something is way wrong with you.

In reality here you are being flat out intellectually dishonest, to yet claim that a vaccine maker can be sued for anything, ever. They are quite obviously. immune to any lawsuits of any kind from a parent of a vaccine damaged child. 

BRUESEWITZ ET AL. v. WYETH FKA WYETH, INC.,ET AL.

Excerpt:

Held: The NCVIA preempts all design-defect claims  against vaccine manufacturers brought by plaintiffs seeking compensation for injury
or death caused by a vaccine’s side effects.  Pp. 7–19.



NVIC Cites "Betrayal" of Consumers by U.S. Supreme Court Decision Giving Total Liability Shield to Big Pharma

Excerpt: Hannah Bruesewitz was brain injured by DPT vaccine as a child but she was denied compensation by the U.S. Court of Claims, which administers the federal vaccine injury compensation program created by the 1986 Act that has turned away two out of three plaintiffs. Her attorneys then sued in civil court, providing evidence that Wyeth-Lederle had the technology to produce a less reactive, purified pertussis vaccine but declined to do so.

“The U.S. Supreme Court has removed all financial incentive for multi-national pharmaceutical corporations, which enjoy a $20 billion dollar business, to make vaccines as safe as they can be,” said Fisher. “This is a sad day for all Americans forced by law to use dozens of doses of vaccines or be barred from school or health insurance or employment. The only leverage left to American consumers to ensure that vaccines with the fewest health risks are produced is to oppose vaccine mandates and work to defend vaccine exemptions in all public health laws.”


The Latest in Atrocious Supreme Court Decisions - Only 2 Justices Stand Up for Your Rights...

Vaccination Profiteers Gang Up on Hannah Bruesewitz - In Supreme Court

Excerpt: The Court took the Bruesewitz case to determine whether 18-year-old Hannah, disabled by injuries she received from Wyeth’s diphtheria, tetanus and pertussis (DPT) vaccine at 6-months-old in 1992, has the right to bring a lawsuit against Wyeth after the Vaccine Court, set up by the 1986 National Childhood Vaccine Injury Act, refused compensation even though she will require life-long care and her vaccine was traced to a lot that had 65 adverse reactions including two deaths, 39 emergency room visits, and 6 hospitalizations.


No Pharma Liability? No Vaccine Mandates, March 3, 2011

YOUR CHILDS DEATH WILL BE A COINCIDENCE AND NO ONE IS LIABLE

Global vaccine market now exceeds $20B
http://www.healthcarefinancenews.com/news/global-vaccine-market-now-exceeds-20b



Friday, September 14, 2012

Reply to: Genetic Test For Autism Developed By Australian Scientists: HuffPo

 Genetic Test For Autism Developed By Australian Scientists: HuffPo

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

Sunday, September 02, 2012

Reply to: The Vaccine Song

The Vaccine Song

This is a far more honest and appropriate video regarding the vaccine truth situation, editor Costner. Take a look. THIS video is far better than yours!!!!

Animated Video Showing a Typical Conversation Between a Mother and her Doctor Regarding Autistic Child



VacFacts.info

The Vaccine Damage - Science




More Information:


Thimerosal - MSDS - (Material Safety Data Sheet) A flu vaccine ingredient unless you ask for a single dose vial.

Mother Explains Vaccine Injury, Deteriorating Health, Autism, and Why Not To Vaccinate

Autistic Child Fully Recovered with Biomedical Treatment for Autism - Holly Riley

Autism Is A Medical Problem And There Is Proven, Effective Medical Treatment - Dr. Stoller, MD


C’mon Sheeple! Just Hand Your Kids Over to the Doctors.

Doctor in his indoctrinated ignorance attempts to give child 14 vaccines in one day, and when the mother refuses he threatens to all child protective services, ranting ignoranmtly, "your going to kill your child".

http://gaia-health.com/gaia-blog/2012-08-02/cmon-sheeple-just-hand-your-kids-over-to-the-doctors/

CDC Schedules
http://www.cdc.gov/vaccines/schedules/

Vaccine Ingredients
http://www.novaccine.com/vaccine-ingredients/
http://www.informedchoice.info/cocktail.html

Vaccine Package Inserts
http://www.vaccinesafety.edu/package_inserts.htm

Aluminium in vaccines can cause serious polio-like damage, damage motorneuron cells and cause brain damage – possibly leading to Alzheimer’s and other forms of dementia and increasing the risk in children of Autistic Spectrum
Disorders.

From the Transcripts of the US Vaccines and Related Biological Advisory Committee Meeting (VRBAC) and Scientific Papers

The Experts admitted Ignorance


ASD and Aluminum Toxicity

Brain Res. 2006 Oct 20;1116(1):215-21. Epub 2006 Aug 30.
Aluminum complexing enhances amyloid beta protein penetration of blood-brain barrier.
Banks WA, Niehoff ML, Drago D, Zatta P.

Source:GRECC, Veterans Affairs Medical Center-St. Louis and Saint Louis University School of Medicine, Division of Geriatrics, Department of Internal Medicine, WAB, 915 N. Grand Blvd, St. Louis, MO 63106, USA.

Abstract
A significant co-morbidity of Alzheimer's disease and cerebrovascular impairment suggests that cerebrovascular dysregulation is an important feature of dementia. Amyloid beta protein (Abeta), a relevant risk factor in Alzheimer's disease, has neurotoxic properties and is thought to play a critical role in the cognitive impairments. Previously, we demonstrated that the 42mer of Abeta (Abeta42) complexed with aluminum (Al-Abeta42) is much more cytotoxic than non-complexed Abeta42. The level of Abeta in the brain is a balance between synthesis, degradation, and fluxes across the blood-brain barrier (BBB). In the present paper, we determined whether complexing with aluminum affected the ability of radioactively iodinated Abeta to cross the in vivo BBB. We found that the rates of uptake of Al-Abeta42 and Abeta42 were similar, but that Al-Abeta42 was sequestered by brain endothelial cells much less than Abeta42 and so more readily entered the parenchymal space of the brain. Al-Abeta42 also had a longer half-life in blood and had increased permeation at the striatum and thalamus. Brain-to-blood transport was similar for Al-Abeta42 and Abeta42. In conclusion, complexing with aluminum affects some aspects of blood-to-brain permeability so that Al-Abeta42 would have more ready access to brain cells than Abeta42.


--------------------

J Cell Biochem. 2004 Dec 15;93(6):1267-71.
Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria.
Murakami K, Yoshino M.

Source
Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.


Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria


------------------------
  
Mult Scler. 2006 Oct;12(5):533-40.
Elevated urinary excretion of aluminium and iron in multiple sclerosis.
Exley C, Mamutse G, Korchazhkina O, Pye E, Strekopytov S, Polwart A, Hawkins C.

Source:Birchall Centre for Inorganic Chemistry and Materials Science, Lennard-Jones Laboratories, Keele University, Staffordshire, UK. c.exley@chem.keele.ac.uk

Abstract
Multiple sclerosis (MS) is a chronic, immune-mediated, demyelinating disease of the central nervous system of as yet unknown aetiology. A consensus of opinion has suggested that the disorder is the result of an interplay between environmental factors and susceptibility genes. We have used a battery of analytical techniques to determine if the urinary excretion of i) markers of oxidative damage; ii) iron and iii) the environmental toxin aluminium and its antagonist, silicon, are altered in relapsing-remitting (RRMS) and secondary progressive MS (SPMS). Urinary concentrations of oxidative biomarkers, MDA and TBARS, were not found to be useful indicators of inflammatory disease in MS. However, urinary concentrations of another potential marker for inflammation and oxidative stress, iron, were significantly increased in SPMS (P<0.01) and insignificantly increased in RRMS (P>0.05). Urinary concentrations of aluminium were also significantly increased in RRMS (P<0.001) and SPMS (P <0.05) such that the levels of aluminium excretion in the former were similar to those observed in individuals undergoing metal chelation therapy. The excretion of silicon was lower in MS and significantly so in SPMS (P<0.05). Increased excretion of iron in urine supported a role for iron dysmetabolism in MS. Levels of urinary aluminium excretion similar to those seen in aluminium intoxication suggested that aluminium may be a hitherto unrecognized environmental factor associated with the aetiology of MS. If aluminium is involved in MS then an increased dietary intake of its natural antagonist, silicon, might be a therapeutic option.


J Cell Biochem. 2004 Dec 15;93(6):1267-71.
Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria.
Murakami K, Yoshino M.

Source
Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.


Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria


J Inorg Biochem. 2007 Sep;101(9):1275-84. Epub 2007 Jun 12.
An aluminum-based rat model for Alzheimer's disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration.
Walton JR.

Source: Australian Institute for Biomedical Research, Sydney, NSW, Australia.

Abstract
In Alzheimer's disease (AD), oxidative damage leads to the formation of amyloid plaques while low PP2A activity results in hyperphosphorylated tau that polymerizes to form neurofibrillary tangles. We probed these early events, using brain tissue from a rat model for AD that develops memory deterioration and AD-like behaviors in old age after chronically ingesting 1.6 mg aluminum/kg bodyweight/day, equivalent to the high end of the human dietary aluminum range. A control group consumed 0.4 mg aluminum/kg/day. We stained brain sections from the cognitively-damaged rats for evidence of amyloid plaques, neurofibrillary tangles, aluminum, oxidative damage, and hyperphosphorylated tau. PP2A activity levels measured 238.71+/-17.56 pmol P(i)/microg protein and 580.67+/-111.70 pmol P(i)/microg protein (p<0.05) in neocortical/limbic homogenates prepared from cognitively-damaged and control rat brains, respectively. Thus, PP2A activity in cognitively-damaged brains was 41% of control value. Staining results showed: (1) aluminum-loading occurs in some aged rat neurons as in some aged human neurons; (2) aluminum-loading in rat neurons is accompanied by oxidative damage, hyperphosphorylated tau, neuropil threads, and granulovacuolar degeneration; and (3) amyloid plaques and neurofibrillary tangles were absent from all rat brain sections examined. Known species difference can reasonably explain why plaques and tangles are unable to form in brains of genetically-normal rats despite developing the same pathological changes that lead to their formation in human brain. As neuronal aluminum can account for early stages of plaque and tangle formation in an animal model for AD, neuronal aluminum could also initiate plaque and tangle formation in humans with AD.


KURODA, Y. and KAWAHARA, M. Aggregation of Amyloid  -Protein and Its Neurotoxicity: Enhancement by
Aluminum and Other Metals.

Brain Res Bull. 2001 May 15;55(2):211-7.
Effects of aluminum on the neurotoxicity of primary cultured neurons and on the aggregation of beta-amyloid protein.
Kawahara M, Kato M, Kuroda Y.


-----------------

Toxicol In Vitro. 2007 Feb;21(1):16-24. Epub 2006 Aug 5.
Aluminum toxicity triggers the nuclear translocation of HIF-1alpha and promotes anaerobiosis in hepatocytes.
Mailloux RJ, Appanna VD.

Source:Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ont., Canada P3E 2C6.

Excerpted: HPLC analyses confirmed increased glycolytic ATP production in Al-exposed hepatocytes. These findings reveal the ability of Al to create a hypoxic environment that promotes the translocation of HIF-1alpha to the nucleus and stimulates the anaerobic metabolism of D-glucose.

-----------------

J Trace Elem Med Biol. 2001;15(2-3):139-41.
Inhibitory effect of aluminum on dopamine beta-hydroxylase from bovine adrenal gland.

Excerpt: Aluminum is a well known neurotoxic agent that is overaccumulated in the substantia nigra of patients affected by Parkinson's disease as well as in certain cerebral areas of other neurodegenerative pathologies such as Alzheimer's disease. Although the role of aluminum in neurodegenerative diseases is yet to be clearly understood, the metal ion is known to substantially alter the activity of several key enzymes in the central nervous system.

The potential implications of aluminum in the etiopathogenesis of neurological disorders are discussed.


-------------

[Toxic effects of aluminum on human embryonic cerebral neurocytes in vitro studies].
Huang G, Kang J, Zhang W, Liu L, Yu M, Mei M, Dong Y.

Excerpt: CONCLUSIONS:
The growth, development and function of human embryonic cerebral neurocytes was inhibited in the high Al group. The neurotoxicity of Al may be caused by lipid peroxidation and the damage of cell membrane.


--------------

J Inorg Biochem. 2003 Sep 15;97(1):132-42.
Aluminium-induced impairment of Ca2+ modulatory action on GABA transport in brain cortex nerve terminals.
Cordeiro JM, Silva VS, Oliveira CR, Gonçalves PP.

Source:Centre for Environmental and Marine Studies, Department of Biology, University of Aveiro, 3810-193 Aveiro, Portugal.

Excerpt: In conclusion, aluminium-induced relief of Ca(2+) modulatory action on GABA transporter may contribute significantly to modify GABAergic signalling during neurotoxic events in response to aluminium exposure.


---------------

J Biochem Mol Toxicol. 2006;20(4):198-208.
Aluminum toxicity elicits a dysfunctional TCA cycle and succinate accumulation in hepatocytes.
Mailloux RJ, Hamel R, Appanna VD.

Source:Department of Chemistry and Biochemistry, Laurentian University, Sudbury, Ontario, Canada, P3E 2C6.

In conclusion, these results suggest that Al toxicity promotes a dysfunctional TCA cycle and impedes ATP production, events that may contribute to various Al-induced abnormalities.


---------------

Aluminum modulates brain amyloidosis through oxidative stress in APP transgenic mice.
Praticò D, Uryu K, Sung S, Tang S, Trojanowski JQ, Lee VM.

Source: Center for Experimental Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Excerpt: These results indicate that dietary Al can modulate in vivo AD-like amyloidosis in Tg2576 by increasing brain oxidative stress.

Toxicol Ind Health. 2006 Feb;22(1):39-46.
Possible peripheral markers for chronic aluminium toxicity in Wistar rats.
Kaur A, Gill KD.

Source:Department of Biochemistry, Post Graduate Institute of Medical Education and Research, Chandigarh, India.

Abstract

This investigation gives detailed analysis of peripheral marker enzymes as well as neurobehavioral tests following chronic aluminium (Al) exposure (10 mg/kg b.w. for 12 weeks intragastrically). We observed a significant decrease in the levels of serum cholinesterase after toxicity. The enzymatic activity of cytochrome oxidase (CO), the terminal enzyme of the electron transport chain, was significantly diminished and that of glucose-6-phosphate dehydrogenase (G-6-PD) was significantly enhanced. Neuromuscular co-ordination was assessed using motor and memory function tests. Deficits were observed suggesting a probable model for chronic Al neurotoxicity.


--------------------------------

J Cell Biochem. 2004 Dec 15;93(6):1267-71.
Aluminum decreases the glutathione regeneration by the inhibition of NADP-isocitrate dehydrogenase in mitochondria.
Murakami K, Yoshino M.


Source:Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.

Abstract
Effect of aluminum on the NADPH supply and glutathione regeneration in mitochondria was analyzed. Reduced glutathione acted as a principal scavenger of reactive oxygen species in mitochondria. Aluminum inhibited the regeneration of glutathione from the oxidized form, and the effect was due to the inhibition of NADP-isocitrate dehydrogenase the only enzyme supplying NADPH in mitochondria. In cytosol, aluminum inhibited the glutathione regeneration dependent on NADPH supply by malic enzyme and NADP-isocitrate dehydrogenase, but did not affect the glucose 6-phosphate dehydrogenase dependent glutathione formation. Aluminum can cause oxidative damage on cellular biological processes by inhibiting glutathione regeneration through the inhibition of NADPH supply in mitochondria, but only a little inhibitory effect on the glutathione generation in cytosol.


--------------------------------

J Enzyme Inhib Med Chem. 2004 Aug;19(4):317-25.

The effect of cations on the amidase activity of human tissue kallikrein: 1-linear competitive inhibition by sodium, potassium, calcium and magnesium. 2-linear mixed inhibition by aluminium.
De Sousa MO, Santoro MM, De Souza Figueiredo AF.

Source:Departamento de Análises Clínicas e Toxicológicas, Faculdade de Farmácia, Universidade Federal de Minas Gerais, C. P. 689, 30123-970 Belo Horizonte, MG, Brazil.

Excerpt: Aluminium is not a physiological cation, but is a known neurotoxicant for animals and humans. The neurotoxic actions of aluminium may relate to neuro-degenerative diseases.


Proc Soc Exp Biol Med. 2000 Apr;223(4):397-402.
Aluminum increases levels of beta-amyloid and ubiquitin in neuroblastoma but not in glioma cells.

Excerpted: These data suggest that one of the mechanisms by which Al may play a role in AD is by promoting the formation of Abeta and ubiquitin in neurons.


------------------

The MMR vaccine is made by use of aborted fetal tissue; more specifically, MRC-5 and WI-38.

Computational Detection of Homologous Recombination Hotspots in X-Chromosome Autism-Associated Genes

Vaccine Ingredients:

Here is a little more information, and a list of vaccines that have been made with human diploid cells, (shocking).

Vaccines, Abortion, & Fetal Tissue

"Designer" Cells as Substrates, (What the FDA clearly knows)
for the Manufacture of Viral Vaccines

How would THIS be possible, if all the vaccines are actually purified during that said step process? What has actually been improved since the days of SV-40 contasmination in the polio vaccines? Not much, it surely does not appear to be/

Gardasil Vaccine Found to be Contaminated
SEPTEMBER 10, 2011

Gardasil victim found to have HPV DNA in her blood 2 Years Post-Vaccination
13 different vaccine vials – 13 different lots of Gardasil from around the world tested
Results – 100% contamination with HPV Recombinant DNA.


Contaminated Gardasil Vaccine May Be Infectious – Potentially Causing Millions More to Become Sick via Blood Transference – Merck Doctor Admits Contaminant Does Not Belong in the Vaccine

Gardasil Vaccine rDNA Introduced at Coroner’s Inquest

Bombshell Interview Reveals DNA Fragments Discovered 6 Months After Vaccination, (Gardasil)

Science 14 February 1975:
Vol. 187 no. 4176 pp. 522-523
DOI: 10.1126/science.187.4176.522

Phage in Live Virus Vaccines: Are They Harmful to People?

And since 1975, do you think anything has changed to correct that situation? The answer is clearly, no.

Autism Epidemic, Is Foreign DNA in MMR II Vaccine Responsible? CBCD Suggests CDC Study Microcompetition Theory

The Center for the Biology of Chronic Disease (CBCD) believes that the cause of the epidemic is the foreign DNA in the MMR II vaccine.


Foreign DNA Fragments Cause Major Diseases

Vaccine Contamination Pig Virus DNA Found in Rotarix April 7, 2010

Corrupted Rotavirus Vaccine Contains Pig Virus (Part 1 of 6)
http://www.youtube.com/watch?v=d2tqttvy9ig



Saturday, September 01, 2012

Reply to: Is the Age of the Father a Risk Factor For Autism?

Is the Age of the Father a Risk Factor For Autism?           

                          

You know what alias no identity Costner? Your study is so dumb, I am not even going to waste the time to address it. Do you really think that is what has caused the 1 in 88 autistic number that the CDC up until 2008 study found. I pity you if you had to figure out the causation of anything actually at all difficult. You know, you aren't biased at all are you, looking for something, any half baked study; anything other than VACCINES.

Well, I have something for you that is far more relevant to the actual reality autism spectrum situation. My study is far better and MORE realistic than your throwing mud cakes at the wall and and hoping one out of twenty will stick. Here it is. But first of all to set the focus correctly, you know of all the aluminum adjuvant studies I have that show the mechanism of the vaccine aluminum adjuvants causing over activation of the brains microglia and resulting chronic brain inflammation for some of those children, maybe far more than we know. In many of the Pubmed studies they state that the understanding of how aluminum adjuvants work say is a poorly understood. However in other many of those studies one that is clearly understood is that aluminum adjuvants produce a great deal of inflammation, in the process of stimulating the immune system to go on high alert to recognize a so called killed/attenuated form of vaccine antigen. And what else would that tend to cause? Autoimmune conditions, allergies, asthma; the body turning on itself the immune system to dysregulated to know better, or as to what is what. No connection to ASD, right? No proof ever, vaccines do not cause autism, all the CDC funded epidemiological studies on one vaccine and one ingredient prove.

 I just happened to get sent this study and find it more than a bit interesting and troubling. Several of the vaccines given today have been made with aborted fetal cell tissue. I will as well show you, more like prove to you; that none of these vaccines can actually be purified by the step processes they have set forth. Quite obviously, and quite obviously as well the FDA is aware of that fact,

 This particular study is as well another big strike against several of the currently made vaccines that are made by used of aborted fetal cells. Although the study article doesn't makes reference per say to human diploid cells, it rather refers to human DNA residuals. That to me would be the same thing, or derived from the same thing. Human diploid cells of course can only come from and typically one thing, aborted fetal tissue. The MMR vaccine is made by use of aborted fetal tissue; more specifically, MRC-5 and WI-38. I would ack you WHY the FDA and CDC have not paid more attention to this; instead of making the false and blanket claim that there are no aborted fetal cells in those vaccines.

Take a look. 

Excerpt from the abstract:

Results: The average human DNA fragment length in rubella vaccine was 220 base pairs. Out of 1145 hotspots in the X-chromosome, 25 hotspots are located in 5 of 15 X-chromosome AAGs, between the transcription start and end sites. These genes are NLGN3 and NLGN4X (neuroligins involved in synapse formation), AFF2 and IL1RAPL1 (involved in X-linked mental retardation), and GRPR (gastrin releasing peptide receptor).

Conclusions: Autism-associated genes in the X-chromosome contain multiple regions where potential insertion of short, non-host homologous DNA can occur. With new knowledge due to the human genome project, particularly in regards to SNPs and epigenetics, further work must be done to understand the implications of integrated residual human DNA to the etiology of autism.
The said study:


There is also shown in the study what they call a Changepoint analysis for US(DOE) and CA(DDS) Autistic Disorder, Fig. 1. You can see the what appear to be direct increases in ASD after the use of vaccines containing human DNA residuals.

The study is said to be only a hypothesis, but none the less comes up with some very significant findings not only in relation to autism, but as well in what would be clear resulting in potential adverse effects on health as well.

The said study:

Computational Detection of Homologous Recombination Hotspots in X-Chromosome Autism-Associated Genes

Vaccine Ingredients:

Here is a little more information, and a list of vaccines that have been made with human diploid cells, (shocking).

Vaccines, Abortion, & Fetal Tissue

The CDC would have us believe that vaccines go through a step process of purification.

With what we have more recently seen since the days that SV- 40 was known of as a contaminant in the polio vaccine, there has been as well ongoing issues since with such as so called pig virus DNA in Rotarix, and HPV DNA found in such as Gardasil, that DNA is said to be or have been firmly locked onto the aluminum adjuvent. (Two articles exist on this vactruth site which discuss that issue as well).

Then we can add this information below as well and piece it together as a conclusion in fact that vaccine makers hav NOT been able to purify these vacines anywhere nearly as well as they would have us believe they are.

The whole picture leaves remaining as to these kinds of vaccines, a showing as to the facts in reality of there being something far less remaining than a picture of proven and unquestioned safety.

Gardasil Vaccine Found to be Contaminated

Related Video

Vaccine Contamination: Pig Virus DNA Found in Rotarix

So, quite obviously you can see that those so called purification steps used to so called purify vaccines, and of what they at the FDA already knows should not and can not be in them in relation to causation of chronic disorders and illness, is at times still in the vaccines, and clearly as well has been connected in relation to some serious problems. Of course then has arrived from them the FDA, a complete denial that there is any issue nor evidence of any problem.

Officially they have told us that even though aborted fetal tissue is used to make vaccines, that no cells remain in the vaccine after the manufacturing process. Yet how then and do they list diploid cells, and human albumin, in and on the vaccine ingredient list; but they still say there are none in there?

And here below you can as well see it stated by the FDA that they have been clearly aware of some of the significant risks of foreign DNA contamination left in vaccines. They do not a solution, and they know they don't

Computational Detection of Homologous Recombination Hotspots in X-Chromosome Autism-Associated Genes

Vaccine Ingredients:

Here is a little more information, and a list of vaccines that have been made with human diploid cells, (shocking).

Vaccines, Abortion, & Fetal Tissue

Here is another problem.

Science 14 February 1975:
Vol. 187 no. 4176 pp. 522-523
DOI: 10.1126/science.187.4176.522

Phage in Live Virus Vaccines: Are They Harmful to People?

And another problem with vaccine contamination.

Deadly Mycoplasma in Vaccines - Garth Nicolson_ microbiologist

Chronic Diseases: Who's killing us, and how?

(If you think Mr. Nicholson may be unqualified, I suggest checking out his extensive bio listing under this video).


These are all the publications he has written, or been involved with writing.

The Institute for Molecular Medicine

Project Day Lily

By:Garth L. Nicolson, Ph.D and Nancy L. Nicolson, Ph.D.

Project Day Lily chronicles the events surrounding the "Gulf War Syndrome” suffered by over 150,000 veterans (and tens of thousands dead) without proper acknowledgment or treatment to keep secret the origin of their illnesses. Were our Armed Forces exposed to chemical and biological toxins that were supplied, in part, by a sinister network of rogue bureaucrats, intelligence operatives and scientists? This is the story of how one of these biological agents was found by two American scientists as part of a massive testing program and how various academic and government employees did everything in their power to keep this information secret.


"Safe, and effective"! Never any reason to question anything, right?

Go to the previous titled pages for an example of the said aluminum adjuvant studies. it is clearly not only one ingredient nor just one vaccine in the causation of vaccine induced ASD/autism. The information available as to biomedical treatment and as to the many recoveries from ASD as well show this fact to be true. it is not a one size fits all, as to those recoveries.