Study finds no significant causal link between gut microbiome and autism

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The hypothesis that gut health influences autism has been overturned by a new Australian study. Based on the analysis of microflora in children, the study indicates that rather than playing a causal role, these microbiome differences are the result of restricted diets associated with autism.

Our understanding of the gut-brain connection and the role our microbiome plays in a host of health issues is growing rapidly. Along with autism, obesity, inflammatory bowel disease, autoimmune disease, and depression have all been linked to what goes on in our gut. Generally, a more diverse microbiome has been linked to better health.

A correlation between autism and alterations in our microbiota has been confirmed by animal and human studies. A study in mice has shown that alterations in the microbiome promote autism-like behaviors, and clinical trials using fecal transplants have been used to “treat” or minimize autism by improving the gut microbiome.

Of course, gastrointestinal (GI) symptoms such as constipation, diarrhea, and abdominal pain are common in children with autism. Studies suggest that about 40 percent of children with autism experience gastrointestinal symptoms, which are usually linked to abnormal behavior and social interactions.

But is this difference in gut microflora a factor leading to autism, or is autism causing the microbial changes?

The recent Australian study, published in the journal Cell, decided to answer this question.

The researchers collected stool samples from 247 children aged 2 to 17, 99 of whom were diagnosed with autism. The children belonged to the Australian Autism Biobank and the Queensland Twin Adolescent Brain Project. Metagenomic sequencing was used to analyze the stool samples, providing a more accurate description of the composition of the microbiome compared to previous methods. The study also controlled for many variables such as age, gender, dietary data, and stool consistency, which the authors say were not properly addressed in previous “low power” studies. Detailed psychometric tests (including social communication difficulties, restricted interests, and sensory sensitivity) and human genotyping data were also included.

The analysis showed almost no direct association between the diagnosis of autism and the gut microbiome. Only one of the 600 bacterial species analyzed was associated with a diagnosis of autism, while a strong correlation was identified between gut bacteria and factors such as age and the quality and diversity of the diet.

The results indicate that repetitive and restricted interests and sensory sensitivity, which are hallmarks of autism, lead to more difficult eating. This restricted diet is what then leads to a less diverse microbiome and more watery stools. In other words, the characteristics of autism contribute to differences in the microbiome, not the other way around.

“Our results are consistent with an upstream role of ASD-related behaviors and food preferences on the gut microbiome and contradict claims that the microbiome has a major (or causal) role in ASD,” the authors explain.

The researchers also note that the findings are at odds with interventions that propose to “treat” autism by targeting the microbiome, such as potentially dangerous fecal transplants, and indicate that caution should be exercised in the use of autism. Unproven restrictive diets in autistic children. Instead, the study highlights the need to help families improve the quality and diversity of diets, improving microbiome diversity and health outcomes.

“What this study shows is that the microbiome per se is by no means a cause of why the brain develops differently and why children develop autism,” said the author of the study and research strategy director at Autism CRC, Professor Andrew Whitehouse, in an interview with ABC News Australia. “But what he also invites us to do is help promote a healthy and balanced diet in children so that they get all the nutritional benefits possible that can help promote their development.”

The research article is published in the journal Cell.

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