Nutritional and Metabolic Status of Children With Autism vs. Neurotypical Children, and the Association With Autism Severity

James B Adams; Tapan Audhya; Sharon McDonough-Means; Robert A Rubin; David Quig; Elizabeth Geis; Eva Gehn; Melissa Loresto; Jessica Mitchell; Sharon Atwood; Suzanne Barnhouse; Wondra Lee

Disclosures

Nutr Metab. 2011;8(41) 

In This Article

Conclusions

Many significant differences (p < 0.001) were observed in the autism group compared to the neurotypical group, including low levels of biotin, plasma glutathione, RBC SAM, plasma uridine, plasma ATP, RBC NADH, RBC NADPH, plasma sulfate (free and total), and plasma tryptophan; and high levels of oxidative stress markers and plasma glutamate. Decreased ATP may be a contributing factor to decreased sulfate and decreased SAM/methylation. Decreased NADPH may be a cause of the increased oxidation of glutathione. This study replicated previous findings of very low lithium in children with ASD, but the p-value was only 0.006 (possibly significant). There were also many marginal differences, and many possible differences, but a larger study is needed to confirm the validity of those observations. Overall, it appears that children with autism do have many abnormalities in their nutritional and metabolic status. The underlying causal relationships of these abnormalities are not yet well understood. An important issue in the clinical care of ASD children is that most vitamins, minerals, and plasma amino acids were within the reference range, but other biomarkers (oxidative stress, methylation, sulfation) were very abnormal, suggesting that those other biomarkers can be important guides for treatment.

The regression analysis found that some vitamins, minerals, amino acids, and (to a lesser extent) other biomarkers are significantly associated with variations in the severity of autism, with vitamins being especially important.

We hypothesize that support for these nutritional and metabolic problems by increasing nutrient intake may reduce the symptoms and co-morbidities that are associated with autism. These nutritional and metabolic dysfunctions may be related to the etiology of autism. Certainly much more research is needed to investigate these hypotheses.

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