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The latest scandal to hit the CDC is explosive: what appears to be a deliberate cover-up of damning scientific data.
Thimerosal, a controversial mercury compound used as a preservative in certain vaccines, was removed from all vaccines in Denmark in 1992. A subsequent Danish study showed a marked decline in autism rates following the removal of thimerosal, indicating a clear link between mercury in vaccines and the development of autism.
Documents obtained by the Coalition for Mercury-free Drugs (CoMeD) through the Freedom of Information Act (FOIA) suggest that officials at the US Centers for Disease Control and Prevention were fully aware of the Danish data, yet published an article about the study in the journal Pediatrics which excluded this information, manipulated the data to misrepresent the decline as an increase, and propagated the erroneous conclusion that thimerosal in vaccines does not cause autism.
Even the CDC admits, on its own website, that flu shot immunity is at best temporary. Why the shot does not confer the kind of immunity provided by other vaccines is not explained, but it presumably has to do with the changing nature of the flu virus. What is also not explained is why the CDC may recommend exactly the same shot two years in a row,
A subsequent Danish study showed a marked decline in autism rates following the removal of thimerosal,
Originally posted by predator0187
I do not care how they put it, but the studies speak for themselves.
I "The discontinuation of thimerosal-containing vaccines in Denmark in 1992 was followed by an increase in the incidence of autism." -from the study cited in the op's source
Originally posted by predator0187 I do not care how they put it, but the studies speak for themselves.
Autistic children have abnormalities in their immune systems and unusual constellations of proteins in their blood that may be an indicator of the disorder, UC Davis researchers said Thursday.
Two groups of researchers from the MIND Institute at UC Davis reported that autistic children have a dysfunctional immune system, giving them an abnormal response to pathogens and other agents in the environment.
Of 4,000 proteins examined, for instance, 500 occurred at different levels in the two groups. "None of the proteins absolutely diagnose autism," he said, but the group is confident that it can identify a panel of perhaps 100 that will be indicative of the disease with a very high level of confidence.
Hope for early autism diagnosis
Researchers in Italy are reporting discovery of abnormal proteins in the saliva of autism patients that could eventually provide a clue for the molecular basis of this severe developmental disorder and could be used as a biomarker for a subgroup of patients with autism spectrum disorders (ASD).
Science Daily: Toward A Long-Sought Saliva Test For Autism
"Genetic factors play a major role [in ASD] and include chromosomal abnormalities (in about 10% of patients) or mutations in single genes (probably less than 5%) involved in synaptic development," the researchers explain. "However, according to a general way of thinking, it has been proposed that a few strong acting genes or, alternatively, many weak genes work together to cause autism susceptibility." Given the complex genetics of ASD explaining the biochemical-biological causes of ASD and developing a test have remained a major research challenge.
Scientists have been searching for biomarkers, such as abnormal proteins, present in the bodily fluids of individuals with ASD for many years. The discovery of such a biomarker would provide the means to accurately diagnose ASD, allow support for patients and carers to be provided in a more effective and timely manner. It could also allow the patient's response to treatment to be monitored with greater precision.
They found that at least one of four protein fragments, the salivary peptides statherin, histatin 1 and acidic proline-rich proteins, in 19 of the children from the ASD group had significantly lower levels of phosphorylation. Phosphorylation is a key biochemical process that activates proteins. "Phosphorylation of salivary peptides involves a Golgi casein kinase [enzyme] common to many organs and tissues, CNS included, whose expression seems to be synchronized during foetal development," the researchers explain.
Abnormal salivary proteins found in autism
New electrophysiological data reveal that the continuity of the rhythmical oscillation in membrane potential generated by inferior olive neurons requires the formation of neuronal assemblies by the connexin36 protein that mediates electrical synapses and promotes neuronal synchrony.
Welsh JP, Ahn ES, Placantonakis DG. Int J Dev Neurosci. 2005 Apr-May;23(2-3):253-63.
Is Autism due to brain desynchronization?
A limited number of reports have demonstrated abnormalities involving the glutamate and gamma amino butyric acid systems in blood and platelets of subjects with autism.
Fatemi SH et al. Biol Psychiatry. 2002 Oct 15;52(8):805-10.
Glutamic acid decarboxylase 65 and 67 kDa proteins are reduced in autistic parietal and cerebellar cortices
Abnormalities in the protein or mRNA levels of several additional molecules in the glutamate system were identified on further analysis, including glutamate receptor binding proteins.
Purcell AE et al. Neurology. 2001 Nov 13;57(9):1618-28.
Postmortem brain abnormalities of the glutamate neurotransmitter system in autism
Autism is a common neurodevelopmental disorder of complex genetic etiology. Rett syndrome, an X-linked dominant disorder caused by MECP2 mutations, and Angelman syndrome, an imprinted disorder caused by maternal 15q11-q13 or UBE3A deficiency, have phenotypic and genetic overlap with autism.
Samaco RC, Hogart A, LaSalle JM Hum Mol Genet. 2005 Feb 15;14(4):483-92.
Epigenetic overlap in autism-spectrum neurodevelopmental disorders: MECP2 deficiency causes reduced expression of UBE3A and GABRB3
Recent studies have implicated a number of membrane-associated proteins, including the signaling pair neuroligin and beta-neurexin, in synapse formation, suggesting that they govern the ratio of inhibitory and excitatory synapses on CNS neurons. These findings, together with data indicating that the genes encoding neuroligin and PSD95 are altered in autism patients, suggest that a molecular understanding of complex neurological diseases is within reach.
Cline H. Curr Biol. 2005 Mar 29;15(6):R203-5.
Synaptogenesis: a balancing act between excitation and inhibition
This mutation leads to a premature stop codon in the middle of the sequence of the normal protein and is thought to suppress the transmembrane domain and sequences important for the dimerization of neuroligins that are required for proper cell-cell interaction through binding to beta-neurexins.
Laumonnier F et al. Am J Hum Genet. 2004 Mar;74(3):552-7.
X-linked mental retardation and autism are associated with a mutation in the NLGN4 gene, a member of the neuroligin family
Neuropathological studies have demonstrated that a number of disease states, ranging from schizophrenia to autism spectrum disorders, display abnormal dendritic spine morphology or numbers. Moreover, recent genetic studies have identified mutations in numerous genes that encode synaptic proteins, leading to suggestions that these proteins may contribute to aberrant spine plasticity that, in part, underlie the pathophysiology of these disorders.
Srivastava DP, Woolfrey KM, Penzes P J Vis Exp. 2011;(53):13.
Analysis of dendritic spine morphology in cultured CNS neurons
The autism spectrum disorder tuberous sclerosis complex (TSC) is caused by mutations in the Tsc1 or Tsc2 genes, whose protein products form a heterodimeric complex that negatively regulates mammalian target of rapamycin-dependent protein translation.
Bateup HS et al. Neurosci. 2011 Jun 15;31(24):202-7.
Loss of Tsc1 In Vivo Impairs Hippocampal mGluR-LTD and Increases Excitatory Synaptic Function