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The reason for the rapid rise of autism in the United States that began
in the 1990s is a mystery. Although individuals probably have a genetic
predisposition to develop autism, researchers suspect that one or more
environmental triggers are also needed. One of those triggers might be
the battery of vaccinations that young children receive.

Using regression analysis and controlling for family income and ethnicity, the
relationship between the proportion children who received the recommended vaccines by age 2 years and the prevalence of autism (AUT) or speech or language impairment (SLI) in each U.S. state from 2001 and 2007 was determined.

A positive and statistically significant relationship was found: The higher the proportion of children receiving
recommended vaccinations, the higher was the prevalence of AUT or SLI. A 1% increase in vaccination was associated with an additional 680 children having AUT or SLI. Neither parental behavior nor access to care affected the results, since vaccination proportions were not significantly related (statistically) to any other disability or to the number of pediatricians in a U.S. state. The results suggest that although mercury has been removed from many vaccines, other culprits may link vaccines to autism. Further study into the relationship between vaccines and autism is warranted.

For more information about the Links Between Vaccination and Autism visit these pages.

• The USA is remarkable in that we now have the highest rate and number of vaccines given the earliest to infants and now have one of the highest rates of infant mortality in the Western nations as well as the highest rate of autism by far.
• In spite of our high level of science and technology in biomedicine we still claim that all of the illnesses given above have “no known cause”——but common sense and a basic understanding of biological science tells us the causes cannot be purely genetic and that a toxic exposure is required, and it is scientifically logical the mercury compounds in our vaccines are the primary cause for early infant death and autism.
• Due to the involvement of the CDC in the vaccine program it is critical that an unbiased group be formed to look at the both the toxic effects of our vaccines and other questions concerning the efficacy of the CDC vaccine program (remember the mumps epidemic where about 85% of those infected were also vaccinated?). The CDC administrators cannot play a controlling role in this evaluation of the vaccine program.
• The autism epidemic started soon after the CDC mandated vaccine program was implemented and it is a good question to ask our health authorities “if the CDC vaccine program prevents significant amounts of infant death from infectious diseases then what are USA infants dying of that place the USA at such a disastrous position in comparison to other progressive countries?”
• It is critical to have an independent research group do an epidemiological study of the rate of autism of non-vaccinated children versus vaccinated children. The CDC has refused to do this and has instead employed foreign researchers to do studies on foreign data bases where the exposure to mercury from vaccines was much later and much lower and where the autism rate was also commensurately lower. This scientifically illogical stand by CDC administrators has greatly damaged the entire reputation of the CDC, especially since two of the foreign epidemiologists who were involved and paid by the CDC are now facing criminal charges.
• Note that autism and other autism spectrum disorders affect boys much more than girls—and it is documented science that mercury and organic mercury compounds are more toxic to the male species. Most toxins show little gender difference.
• I could go on much longer but brevity may be best to focus on the issue that the USA health agencies are more and more losing the faith of the American people and seem unable to solve the problems leading to the causation and prevention of the “modern man illnesses”. This failure is most likely because modern medicine does not want to consider that these illnesses are primarily caused by toxic exposures generated by pharmaceutical based toxins delivered by physicians and dentists. It is the failure of modern medicine to comprehend the toxicity of low level exposures to heavy metals that leads to damaging of our most susceptible citizens, our infants and elderly.

Boyd E. Haley, PhD
Professor Emeritus

University of Kentucky
Chemistry Department
2430 Palumbo Drive, Suite 140
Lexington, KY 40509-1117

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Dr. Wakefield has always recommended single antigen vaccines. He hypothesized that the three live viruses given together in the MMR vaccine are the source of potential problems in at least SOME children.

Learn more: http://www.cent4dent.com/html/mercury_issues/vaccines.html
Read the whole article: http://drtenpenny.com/Wakefield_Inquisitioners_Have_their_day.aspx

Findings were published online in Nature Neuroscience on January 10.

TSC causes benign tumors throughout the body, including the brain. But patients with TSC may have autism, epilepsy or intellectual disabilities even in the absence of these growths. Now, researchers led by Mustafa Sahin, MD, PhD, of Children’s Department of Neurology, provide evidence that mutations in one of the TSC’s causative genes, known as TSC2, prevent growing nerve fibers (axons) from finding their proper destinations in the developing brain.

Studying a well-characterized axon route — between the eye’s retina and the visual area of the brain — Sahin and colleagues showed that when mouse neurons were deficient in TSC2, their axons failed to land in the right places. Further investigation showed that the axons’ tips, known as “growth cones,” did not respond to navigation cues from a group of molecules called ephrins. “Normally ephrins cause growth cones to collapse in neurons, but in tuberous sclerosis the axons don’t heed these repulsive cues, so keep growing,” says Sahin, the study’s senior investigator.

Additional experiments indicated that the loss of responsiveness to ephrin signals resulted from activation of a molecular pathway called mTOR, whose activity increased when neurons were deficient in TSC2. Axon tracing in the mice showed that many axons originating in the retina were not mapping to the expected part of the brain.

Although the study looked only at retinal connections to the brain, the researchers believe their findings may have general relevance for the organization of the developing brain. Scientists speculate that in autism, wiring may be abnormal in the areas of the brain involved in social cognition.
“People have started to look at autism as a developmental disconnection syndrome — there are either too many connections or too few connections between different parts of the brain,” says Sahin. “In the mouse models, we’re seeing an exuberance of connections, consistent with the idea that autism may involve a sensory overload, and/or a lack of filtering of information.”

Sahin hopes that the brain’s miswiring can be corrected by drugs targeting the molecular pathways that cause it. The mTOR pathway is emerging as central to various kinds of axon abnormalities, and drugs inhibiting mTOR has already been approved by the FDA. For example, one mTOR inhibitor, rapamycin, is currently used mainly to prevent organ rejection in transplant patients, and Sahin plans to launch a clinical trial of a rapamycin-like drug in approximately 50 patients with TSC later this year, to see if the drug improves neurocognition, autism and seizures.

In 2008, Sahin and colleagues published related research in Genes & Development showing that when TSC1 and TSC2 are inactivated, brain cells grow more than one axon — an abnormal configuration that exacerbates abnormal brain connectivity. The mTOR pathway was, again, shown to be involved, and when it was inhibited with rapamycin, neurons grew normally, sprouting just one axon.

Supporting the mouse data, a study by Sahin and his colleague Simon Warfield, PhD, in the Computational Radiology Laboratory at Children’s, examined the brains of 10 patients with TSC, 7 of whom also had autism or developmental delay, and 6 unaffected controls. Using an advanced kind of MRI imaging called diffusion tensor imaging, they documented disorganized and structurally abnormal tracts of axons in the TSC group, particularly in the visual and social cognition areas of the brain (see image). The axons also were poorly myelinated — their fatty coating, which helps axons conduct electrical signals, was compromised. (In other studies, done in collaboration with David Kwiatkowski at Brigham and Women’s Hospital, giving rapamycin normalized myelination in mice.)

Sahin has also been studying additional genes previously found to be deleted or duplicated in patients with autism, and finding that deletion of some of them causes neurons to produce multiple axons — an abnormality that, again, appears to be reversed with rapamycin.

“Many of the genes implicated in autism may possibly converge on a few common pathways controlling the wiring of nerve cells,” says Sahin. “Rare genetic disorders like TSC are providing us with vital clues about brain mechanisms leading to autism spectrum disorders. Understanding the neurobiology of these disorders is likely to lead to new treatment options not only for TSC patients, but also for patients with other neurodevelopmental diseases caused by defective myelination and connectivity, such as autism, epilepsy and intellectual disability.”

The current study was funded by grants from the National Institutes of Health, the John Merck Scholars Fund, Tuberous Sclerosis Alliance, the Manton Foundation, the Children’s Hospital Boston Translational Research Program, and the Children’s Hospital Boston Mental Retardation and Developmental Disabilities Research Center.

Duyu Nie was first author on the paper. Coauthors were Duyu Nie, Alessia Di Nardo, Juliette M Han, Hasani Baharanyi, Ioannis Kramvis, and ThanhThao Huynh, all of the F.M. Kirby Neurobiology Center and Department of Neurology, Children’s Hospital Boston; Sandra Dabora of Brigham and Women’s Hospital; Simone Codeluppi and Elena B Pasquale of the Burnham Institute for Medical Research, and University of California San Diego; and Pier Paolo Pandolfi of Beth Israel Deaconess Cancer Center.

For more info, look at the Mercury and Autism pages of My Website.

Visit our website: www.cent4dent.com for more information about the links between vaccination and autism.

Abstract

This study examined whether acquisition of neonatal reflexes and sensorimotor skills in newborn rhesus macaques (Macaca mulatta) is influenced by receipt of the single neonatal dose of Hepatitis B (HB) vaccine containing the preservative thimerosal (Th). HB vaccine containing a standardized weight-adjusted Th dose was administered to male macaques within 24 hours of birth (n = 13). Unexposed animals received saline placebo (n = 4) or no injection (n = 3). Infants were raised identically and tested daily for acquisition of 9 survival, motor, and sensorimotor reflexes by a blinded observer. In exposed animals there was a significant delay in the acquisition of three survival reflexes: root, snout and suck, compared with unexposed animals. No neonatal responses were significantly delayed in unexposed animals compared with exposed. Gestational age (GA) and birth weight were not significantly correlated. Cox regression models were used to evaluate the main effects and interactions of exposure with birth weight and GA as independent predictors and time-invariant covariates. Significant main effects remained for exposure on root and suck when controlling for GA and birth weight such that exposed animals were relatively delayed in time-to-criterion. There was a significant effect of GA on visual follow far when controlling for exposure such that increasing GA was associated with shorter time-to-criterion. Interaction models indicated that while there were no main effects of GA or birth weight on root, suck or snout reflexes there were various interactions between exposure, GA, and birth weight such that inclusion of the relevant interaction terms significantly improved model fit. This, in turn, indicated important influences of birth weight and/or GA on the effect of exposure which, in general, operated in a way that lower birth weight and/or lower GA exacerbated the detrimental effect of vaccine exposure. This primate model provides a possible means of assessing adverse neurodevelopmental outcomes from neonatal Th-containing HB vaccine exposure, particularly in infants of lower GA or low birth weight. The mechanism of these effects and the requirements for Th is not known and requires further study.

This information presented for educational purposes by The Centre for Dentistry at Haddon, Haddon Heights, NJ. For further information about vaccines and autism please

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Laura Hewitsona, c, , , Lisa A. Housera, Carol Stottc, Gene Sackettb, Jaime L. Tomkoa, David Atwoodd, Lisa Blued, E. Railey Whited and Andrew J. Wakefieldc

a Department of Obstetrics and Gynecology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213
b Washington National Primate Research Center, University of Washington, Seattle, WA 98195
cThoughtful House Center for Children, Austin, TX, 78746
dDepartment of Chemistry, University of Kentucky, Lexington, KY 40506