Parents of Hannah Poling: Differing Explanations for Daughter's Autism?

At the center of the government's controversial decision to award compensation to the family of Hannah Poling is whether vaccination caused the child's mitochondrial disorder (and associated autism) or whether vaccination aggravated her underlying mitochondrial condition (which then manifested clinically as autism). In the NYT, the child's mother, Terry Poling (who is a nurse and lawyer), was quoted as stating that the government "chose to believe" the latter explanation; but she added, "We don’t know that [Hannah] had an underlying disorder."

Terry Poling's implication that vaccination may have caused her child's mitochondrial disorder is rebutted, however, by the 2006 case report of Hannah in the Journal of Child Neurology. Curiously enough, the lead author for this case report was Terry's husband and Hannah's father, neurologist Jon Poling. In the report, Poling implied that immunization aggravated his daughter's underlying mitochondrial disorder, which resulted in her partially reversible autistic regression at the age of 19 months.

If such [mitochondrial] 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, 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.

Poling and his coauthors concluded, "There is a need for reliable laboratory markers to detect abnormalities of mitochondrial function, which will then facilitate further clinical investigations in this subgroup of children with autism [italics added]."