Autism Linked to Lower Levels of Distinct Gut Bacteria
Children with autism appear to have distinctly different levels of intestinal flora, which may increase their vulnerability to pathogenic bacteria and perhaps play a role in autism pathogenesis, new research suggests.
In a small study, investigators at Arizona State University in Tempe found that autistic children had significantly fewer types of 3 critical types of gut bacteria compared with normal control individuals.
“Most notably, we also discovered that the genera Prevotella, Coprococcus, and unclassified Veillonellaceae were significantly reduced in autistic children,” the researchers stated.
GI Disorders Common
Gastrointestinal (GI) disorders are frequent in children with autism, and many researchers believe there may be a link between autism and abnormalities in gut microbial functions.
Another study also recently published in PLoS One and reported by Medscape Medical News showed that a subset of children with autism have increased immune reactivity to gluten that is unrelated to celiac disease.
They found that the participants with autism had a lower diversity of gut microbiomes compared with healthy control individuals — specifically, lower levels of Prevotella, Coprococcus, and Veillonellaceae. The 3 genera represent important groups of carbohydrate-degrading or fermenting microbes.
Such bacteria could be critical for healthy microbial-gut interactions or play a supportive role for a wide network of different microorganisms in the gut. The latter would explain the decreased diversity observed in autistic samples.
Prevotella was the most conspicuously reduced among the autistic patients in this study.
Prevotella is believed to play a key role in the composition of the human gut microbiome and is common in normal children with more diverse and robust microbial communities.
It is not totally clear whether the observed differences in the gut microbiome are specific to autism or if they are associated with GI symptoms in general.
PLoS One. Published online July 3, 2013. Full article
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