Autism-Mitochondria Connection?
The Hannah Poling case calls attention to the need
for more research on metabolism in autism
On March 6, 2008, Jon and Terry Poling announced that a Department of Health and Human Services panel awarded an undisclosed sum to their daughter, Hannah, as compensation for injury possibly caused by a vaccine-mediated aggravation of an underlying metabolic dysfunction. As a result, the words "mitochondria" and "metabolic dysfunction" became part of the lexicon of the autism community.
The Polings reported that Hannah ran a high fever and began to regress in language and motor ability after a round of vaccinations at 19 months. As part of subsequent neurological evaluations, it was discovered that Hannah had a mitochondrial disorder, which may have been aggravated by the vaccines, resulting in brain damage and features of Autism Spectrum Disorder (ASD). Previously, although there had been some evidence of a role for mitochondria in autism, it had not been a major focus of autism research.
Mitochondria are unique cellular structures that play a central role in metabolism. Because they are a cell's energy producers, damage to mitochondria can have dire consequences when energy is insufficient to maintain typical cellular functions. Mitochondria contain their own DNA, much of which encodes instructions for making proteins that convert simple sugars and oxygen into ATP – the energy cells need to function. As the brain places great demands on a body's energy resources, dysfunctional mitochondria often result in cognitive and motor control deficits.
The Polings' announcement received extensive media coverage and reinvigorated the scientific search for metabolic underpinnings of ASD. In conjunction with the United Mitochondrial Disease Foundation (www.umdf.org), the National Institutes of Health sponsored a symposium on mitochondria and autism in late June 2008. At the meeting, scientists, clinicians and public stakeholders gathered to discuss the co-incidence of ASD and mitochondrial dysfunction or disorders, and the need for improving methods of their diagnosis. Based on the reaction to the meeting, the role of metabolic dysfunction in autism will remain a hot topic of research for 2009 and beyond.
The Polings reported that Hannah ran a high fever and began to regress in language and motor ability after a round of vaccinations at 19 months. As part of subsequent neurological evaluations, it was discovered that Hannah had a mitochondrial disorder, which may have been aggravated by the vaccines, resulting in brain damage and features of Autism Spectrum Disorder (ASD). Previously, although there had been some evidence of a role for mitochondria in autism, it had not been a major focus of autism research.
Mitochondria are unique cellular structures that play a central role in metabolism. Because they are a cell's energy producers, damage to mitochondria can have dire consequences when energy is insufficient to maintain typical cellular functions. Mitochondria contain their own DNA, much of which encodes instructions for making proteins that convert simple sugars and oxygen into ATP – the energy cells need to function. As the brain places great demands on a body's energy resources, dysfunctional mitochondria often result in cognitive and motor control deficits.
The Polings' announcement received extensive media coverage and reinvigorated the scientific search for metabolic underpinnings of ASD. In conjunction with the United Mitochondrial Disease Foundation (www.umdf.org), the National Institutes of Health sponsored a symposium on mitochondria and autism in late June 2008. At the meeting, scientists, clinicians and public stakeholders gathered to discuss the co-incidence of ASD and mitochondrial dysfunction or disorders, and the need for improving methods of their diagnosis. Based on the reaction to the meeting, the role of metabolic dysfunction in autism will remain a hot topic of research for 2009 and beyond.
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