Autism Spectrum Disorder Research
SAN DIEGO, April 4-Researchers have discovered that autistic children have a severely abnormal metabolic profile that suggests an increased vulnerability to oxidative stress.
This factor might eventually be used as a test to support the purely behavioral empiric approach for diagnosis, reported S. Jill James, PhD, of the Arkansas Children's Hospital Research Institute.
In a preliminary study presented at a meeting of the American Society for Nutritional Sciences over the weekend, she also identified a significantly increased presence of three genetic polymorphisms that her group believes may raise the risk of childhood autism.
The Arkansas researchers measured plasma levels of the major intracellular antioxidant glutathione and its metabolic precursors in 95 autistic children and 75 children without autism. They found that glutathione levels as well as the ratio of reduced to oxidized glutathione (the redox ratio) were significantly decreased in the autistic children.
This finding, they said, indicates the presence of oxidative stress, which occurs when the antioxidant system fails to counteract the generation of free radicals. Because free radicals can damage sensitive cells in the brain, gastrointestinal tract, and immune system, the researchers pointed out, they may contribute to the neurologic, gastrointestinal, and immunologic pathology that occurs in autistic children.
The researchers then studied 360 autistic children and 205 youngsters without the disorder in an effort to identify genetic polymorphism's that could directly or indirectly affect metabolic pathways and induce oxidative stress.
They found that three polymorphism's (the catecho-O-methyltransferase gene, the transcobalamin II gene, and the glutathione-S-transferase M1 gene) were significantly elevated in the autistic subjects.
These genetic polymorphisms are prevalent in the general population and do not cause autism. However, she said, specific combinations of these and additional genetic factors could promote chronic metabolic imbalance in children and thus increase the risk of autism.
The next step, Dr. James said, is to determine whether the metabolic profile discovered by the research team could be used as a diagnostic test for autism.
It would also be important, she added, to determine whether the abnormal profile is present in high-risk children, such as toddler siblings of autistic children and toddlers with developmental delays.
This factor might eventually be used as a test to support the purely behavioral empiric approach for diagnosis, reported S. Jill James, PhD, of the Arkansas Children's Hospital Research Institute.
In a preliminary study presented at a meeting of the American Society for Nutritional Sciences over the weekend, she also identified a significantly increased presence of three genetic polymorphisms that her group believes may raise the risk of childhood autism.
The Arkansas researchers measured plasma levels of the major intracellular antioxidant glutathione and its metabolic precursors in 95 autistic children and 75 children without autism. They found that glutathione levels as well as the ratio of reduced to oxidized glutathione (the redox ratio) were significantly decreased in the autistic children.
This finding, they said, indicates the presence of oxidative stress, which occurs when the antioxidant system fails to counteract the generation of free radicals. Because free radicals can damage sensitive cells in the brain, gastrointestinal tract, and immune system, the researchers pointed out, they may contribute to the neurologic, gastrointestinal, and immunologic pathology that occurs in autistic children.
The researchers then studied 360 autistic children and 205 youngsters without the disorder in an effort to identify genetic polymorphism's that could directly or indirectly affect metabolic pathways and induce oxidative stress.
They found that three polymorphism's (the catecho-O-methyltransferase gene, the transcobalamin II gene, and the glutathione-S-transferase M1 gene) were significantly elevated in the autistic subjects.
These genetic polymorphisms are prevalent in the general population and do not cause autism. However, she said, specific combinations of these and additional genetic factors could promote chronic metabolic imbalance in children and thus increase the risk of autism.
The next step, Dr. James said, is to determine whether the metabolic profile discovered by the research team could be used as a diagnostic test for autism.
It would also be important, she added, to determine whether the abnormal profile is present in high-risk children, such as toddler siblings of autistic children and toddlers with developmental delays.
posted by kevin at 9:10 AM
