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

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".

CDC Schedules

Vaccine Ingredients

Vaccine Package Inserts

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

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.

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.

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.

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.

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.

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.

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.


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.

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)

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