Vaccines/Autism - 65% of ASD Kids Have Mitichondrial Disorder

From: "Clifford G. Miller"

April 2008

Please circulate - latest research below.  The US vaccines-to-autism case of Hannah Poling is not new or rare.

At an American Academy of Neurology meeting last Sunday it was revealed in a recent research paper "
Oxidative Phosphorylation (OXPHOS) Defects in Children with Autistic Spectrum Disorders " (see abstract below) that 65% of children with Austistic Spectrum Disorders assessed were found to have mitochondrial disorder (MtD) and so were always at risk of autism caused by one or more vaccines.

Write to your political representatives. Keep asking them "what are you doing about this for child health safety and all children" and keep writing and keep asking.  If you are in the UK, it's easier with  Ask all your relatives and friends to write to their political representatives.

The new figures from the AAN meeting correlate with 68% of regressive autism cases following MMR being found to have measles virus RNA in their cerebro spinal fluid (CSF).  This was found using sensitive molecular laboratory detection methods.   But bear in mind the problem is caused by vaccines in general and not just MMR, as the Hannah Poling case shows.

Looks like the UK's The Sunday Times, and its editor John Witherow have a lot of explaining to do with all their attacks on Andrew Wakefield now turning out to be false.  Phone and write to Witherow (see address below) and ask him what he is going to do about this, ask him when he is going to resign

Here are contact details for The Sunday Times editor, John Witherow:-

John Witherow Esq
The Sunday Times
1 Pennington Street
London E1 9XN

Main - Tel: 020 7782 5000 Fax: 020 7782 5658
Here is the abstract of the AAN paper, courtesy of Professor Jeff Bradstreet of Thoughtful House, Austin, Texas:-
"Oxidative Phosphorylation (OXPHOS) Defects in Children with Autistic Spectrum Disorders  

John Shoffner, Lauren C. Hyams, Genevieve N. Langley, Atlanta, GA

OBJECTIVE: To retrospectively survey patients with autistic spectrum disorders that were evaluated clinically for mitochondrial disease and to assess the clinical and laboratory features of this group of patients. BACKGROUND: Autism is a developmental disorder characterized by disturbance in language, perception and socialization. A variety of biochemical, anatomical and neuroradiographical studies imply a disturbance of brain energy metabolism in autistic patients. Recent studies confirmed the previously reported high frequency of biochemical markers of mitochondrial dysfunction, namely hyperlactacidemia and increased lactate/pyruvate ratio, in a significant fraction of 210 autistic patients. (J Autism Dev Disord, 2006. 36:1137) Although rare, Mecp2 mutations can produce autistic features and the mouse model has significant mitochondrial defects. (Mol Cell Biol, 2006. 26: 5033) Additional genetic defects associated with mitochondrial dysfunction include inverted 15q11-13 duplication (Complex III defect) (Ann Neurol, 2003,53,801), A3243G mutation (mitochondrial transfer RNALeucine(UUR) gene, mtDNA depletion(J Pediatr, 2004,144,81), G8363A mutation (mitochondrial transfer RNALysine gene. (J Child Neurol, 2000,15,357). DESIGN/METHODS: Retrospective analysis of 37 children with autistic spectrum disorders. Clinical, biochemical, metabolic, and genetic data is assessed. RESULTS: Twenty four children (65%) had skeletal muscle OXPHOS defects: Complex I (16), Complex I and Complex III (5), Complex III (1), Complex I and Complex IV (2). Thirteen (35%) had normal skeletal muscle OXPHOS enzyme activities for Complexes I-IV. Clinical, metabolic, protein chemistry, and sequencing of coding regions of the mitochondrial DNA will be reported. CONCLUSIONS/RELEVANCE: Most children with autistic spectrum disorders do not have recognizable abnormalities on a broad range of imaging, metabolic and genetic studies. However, a subset of patients do harbor significant defects in oxidative phosphorylation function. Complex I abnormalities are the most frequently encountered defect. Recognition of these children is important for understanding how genes that produce autistic spectrum disorders impact mitochondrial function. Supported by: Horizon Molecular Medicine.
Category - Neurogenetics and Gene Therapy
SubCategory - Other

Sunday, April 13, 2008 2:45 PM

Platform Session: Integrated Neuroscience: Autism (2:00 PM-3:15 PM)
Annual Meeting American Academy of Neurology