This study, recently published in January 2014, links mitochondrial abnormalities in a subset of individuals with autism with impaired ability to manage oxidative stress:
Oxidative Stress Induces Mitochondrial Dysfunction in a Subset of Autism Lymphoblastoid Cell Lines in a Well-Matched Case Control Cohort
Shannon Rose, Richard E. Frye*, John Slattery, Rebecca Wynne, Marie Tippett, Oleksandra Pavliv,
Stepan Melnyk, S. Jill James
My impressions of the study:
This study shows that children with autism spectrum disorder (ASD) have a lower tolerance to oxidative stress than their non-ASD peers.
In contrast to children who are not on the spectrum, the mitochondria of children with autism have a reduced capacity to handle reactive oxygen species, or free radicals. Free radicals, from oxidative environmental toxins, are damaging to cellular and chromosomal material and can lead to cell death. Damage from reactive oxygen species in vulnerable individuals may contribute to developmental delays and immune system dysfunction in children with autism.
The study demonstrates that a subgroup, consisting of over 30% of individuals with autism, exhibit mitochondrial abnormalities making them more susceptible to oxidative damage from free radicals than their peers.
Children who were not on the autism spectrum exhibited mitochondria with a greater capacity to neutralize free radicals when exposed to higher concentrations of reactive oxygen species.
The findings of this study support the concept that ASD is caused by a combination of both genetic and environmental factors. As a clinician using biomedical interventions for ASD, this study highlights the importance of managing environmental pro-oxidative toxins, mitochondrial support, and ensuring optimal glutathione levels to neutralize oxidative stress.