Guess the number of comments @ NJ.COM on "Autism continues to climb, with NJ rates now the highest"

[proverbialwisdom]

19. Please review that more carefully, you've misinterpreted an admittedly rushed post.

Just discovered that Andrew W. Zimmerman, MD (previously affiliated with Johns Hopkins University) is currently a member of the Dept. of Neurology, MassGeneral Hospital for Children Lurie Center for Autism, see http://www.massgeneral.org/neurology/doctors/doctor.aspx?id=18782 .

Zimmerman AW is the author of 89 publications on PUBMED, see http://www.ncbi.nlm.nih.gov/pubmed/?term=Zimmerman%20AW%5Bauth%5D , including the following case history written with Dr. Jon Poling, MD, PhD, the parent of a child with autism, see http://hannahcenter.org/page30.html.

It's outrageous to trust an assessment of their work by a crank oncologist with an agenda, Gorski. You're being punked.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536523/

J Child Neurol. Author manuscript; available in PMC Sep 15, 2008.

Published in final edited form as:
J Child Neurol. Feb 2006; 21(2): 170–172.
doi: 10.2310/7010.2006.00032
PMCID: PMC2536523
NIHMSID: NIHMS48754

Developmental Regression and Mitochondrial Dysfunction in a Child With Autism

Jon S. Poling, MD, PhD, Richard E. Frye, MD, PhD, John Shoffner, MD, and Andrew W. Zimmerman, MD

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Discussion:

To our knowledge, this is the first description of an autistic child with mitochondrial dysfunction, growth failure, and abnormal muscle histopathology without seizures or a defined chromosomal abnormality. This patient exemplifies important questions about mitochondrial function in autism and developmental regression. It is unclear whether mitochondrial dysfunction results from a primary genetic abnormality, atypical development of essential metabolic pathways, or secondary inhibition of oxidative phosphorylation by other factors. If such dysfunction is present at the time of infections and immunizations in young children, the added oxidative stresses from immune activation on cellular energy metabolism are likely to be especially critical for the central nervous system, which is highly dependent on mitochondrial function. Young children who have dysfunctional cellular energy metabolism therefore might be more prone to undergo autistic regression between 18 and 30 months of age if they also have infections or immunizations at the same time. Although patterns of regression can be genetically and prenatally determined,9 it is possible that underlying mitochondrial dysfunction can either exacerbate or affect the severity of regression. Abnormalities of oxidative phosphorylation can be developmental and age related and can normalize with time.10

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http://www.scribd.com/doc/115393658/Andrew-Zimmerman

Andrew Zimmerman / Poling v HHS Exhibit 3

Published by Heather Rhodes White

In a second case Zimmerman was called to give his expert report on was Poling v. HHS. He revised his testimony, which was in complete contradiction from Cedillo v. HHS. His report to the Special Masters;

“The cause for regressive encephalopathy in Hannah (Poling) at age 19 months was underlying mitochondrial dysfunction, exacerbated by vaccine-induced fever and immune stimulation that exceeded metabolic energy reserves. This acute expenditure of metabolic reserves led to permanent irreversible brain injury. Thus, if not for this event, Hannah may have led a normal full productive life. Presently, I predict Hannah will have a normal lifespan but with significant lifelong disability."

Fiction fits here: http://www.democraticunderground.com/1014767639