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closeThe conclusion is seriously misleading.
Posted by richfrye on 13 Jul 2011 at 03:00 GMT
The premise of this paper is excellent on the surface. It is very important to know the prevalence of inborn errors of metabolism in non-syndromic autism. Unfortunately these investigators have only screened for very rare inborn errors of metabolism and have not measured the most common biomarkers for the most common inborn errors of metabolism found in children with ASD, mitochondrial disorders. Indeed, blood lactate, pyruvate, carnitine and other mitochondrial biomarkers that have been shown to be abnormal in children with autism with a higher rate than typically developing controls were not measured in this paper. In addition, the laboratory testing was not reported to be collected in any standardized manner, such as first morning fasting, leading to variability in the measurements.
In our recent meta-analysis (Rossignol and Frye, Mol Psych, 2011; http://www.nature.com/mp/... ) we reviewed the many well done studies that have examined the prevalence of mitochondrial disease and biomarkers of mitochondrial dysfunction in the autism population. We found that, overall, 5% of children with autism have a classically defined mitochondrial disease and that up to 30% of children with autism have biomarkers of mitochondrial dysfunction.
So why did these researchers not confirm the findings of the many previous studies on mitochondrial disorders in autism? Simple, they did not measure biomarkers of mitochondrial disease.
Despite the fact that these researchers did not measure the basic biomarkers of mitochondrial disease, the most prevalent inborn error of metabolism in autism, they claim that the prevalence of inborn errors of metabolism in autism in equal to the general population. The conclusion is seriously misleading.