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Glutathion waarden sterk verlaagd bij autistische
kinderen.*
Uit onderzoek blijkt dat glutathion waarden in autistische
kinderen duidelijk lager zijn als bij normale kinderen. Hierdoor ontstaat meer
vrije radicalen schade in de hersenen, het spijsverterings- en het
immuunsysteem. De genen die deze oxidatieschade veroorzeken bleken bij
autistische kinderen geen duidelijk verschil te hebben dan bij gewone kinderen.
Vermoedelijk is een andere genetische aanleg mede verantwoordelijk.voor autisme.
Autistic children's abnormal
metabolic profile findings
Linked to increased oxidative
stress and a deficit in antioxidant capacity
Chronic biochemical imbalance
is often a primary factor in the development of many complex diseases but a
possible metabolic basis for autism has not been well explored. Now Arkansas
Children's Hospital Research Institute researchers report for the first time
that children with autism have a severely abnormal metabolic profile indicating
increased vulnerability to oxidative stress. The scientists also identified a
significant increase in the frequency of several genetic polymorphisms that they
believe may increase the risk of autism in specific combinations yet to be
determined.
Dr. S. Jill James, Professor
of Pediatrics at the University of Arkansas for Medical Sciences College of
Medicine, presented the study Saturday, April 2, at the American Society for
Nutritional Sciences scientific sessions at Experimental Biology 2005 in San
Diego.
Autism is a neurodevelopment
disorder characterized by impairment in social interactions, limited language
acquisition, repetitive behaviors, and restricted interests. Usually diagnosed
before the age of three, the disorder appears to have increased tenfold over the
last 15 years, now affecting more than 30 of every 10,000 children in the United
States. Although both genetic and environmental factors are believed to
contribute to the development of autism, no firm causal evidence exists. And
with no available physiological or biochemical markers, diagnosis currently is
made entirely on a behavioral basis.
Dr. James and colleagues
measured plasma levels of the major intracellular antioxidant glutathione and
its metabolic precursors in 95 autistic children and 75 children without autism.
Glutathione levels (and also the ratio of reduced to oxidized glutathione or
redox ratio) were significantly decreased in the autistic children, indicating
presence of a significant level of oxidative stress. Oxidative stress occurs
when the antioxidant system fails to counteract the generation or exposure to
free radicals. Unopposed free radicals can damage sensitive cells in the brain,
the gastrointestinal tract, and the immune system, and the researchers believe
they may contribute to the neurological, gastrointestinal and immunologic
pathology that occurs in autistic children.
Working with a larger number
of autistic (360) and non-autistic controls (205), the researchers then looked
at common polymorphisms in genes that could directly or indirectly affect these
metabolic pathways and induce oxidative stress. Three (the
catecho-O-methyltransferase gene, the transcobalamin II gene, and the
glutathione-S-transferase M1 gene) were found to be significantly elevated in
the autistic children. These genes are prevalent in the general population, says
Dr. James, and clearly do not "cause" autism. However, she and her
colleagues believe specific combinations of these and additional genetic changes
could promote the chronic metabolic imbalance seen in the children and thus
increase the risk of the disorder.
The next step, says Dr. James,
is to determine whether the metabolic profile discovered by the researchers
could be used as a diagnostic test for autism to support the purely behavioral
diagnosis currently in use. It also would be important, she says, to determine
whether the abnormal profile is present in high-risk children, such as toddler
siblings of autistic children and/or toddlers with developmental delays.
Dr. James' coauthors are Dr. Stephan Melnyk and Ms. Stefanie Jernigan in her Biochemical Genetics Laboratory at Arkansas Children's Hospital Research Institute and The University of Arkansas for Medical Sciences. (Mei 2005)