There has been much speculation that the community of bacteria living within the gut – often called the microbiome – could also be different amongst people on the autism spectrum than the broader population. This has led some researchers and clinicians to invest that gut bacteria could cause autism.
But our latest research, published today within the journal Cell, turns this theory on its head.
Rather than differences in gut bacteria influencing brain development, our research suggests changes in gut bacteria are driven by restricted diets, or “picky eating”.
Restricted diets are more common amongst children with autism due to their sensory sensitivities and restricted and repetitive interests. Some can have strong preferences for a select few foods, while others find some flavours, smells or textures unpleasant or off-putting.
What’s the idea?
You can have heard claims the microbiome is expounded to autism: it can have a “causal” role, or microbiome “therapies” can alter autistic behaviours.
Interest within the autism gut microbiome first got here from observations people on the autism spectrum usually tend to experience gut problems, similar to constipation and diarrhoea.
Further studies looked as if it would suggest children on the autism spectrum had different mixtures of bacteria living of their gut.
These intriguing relationships inspired studies of mice and rats, a few of which indicated the microbiome may cause differences in behaviour.
But the thrill has been misguided.
Assessing the evidence
Weighing up all of the findings, the evidence linking the microbiome to autism is highly inconsistent and lots of studies have significant problems with their scientific design.
There are also problems in relating mouse studies to humans, because autism doesn’t exist in mice.
Despite the uncertainty within the science, the hype across the microbiome and autism has continued to collect momentum.
Out of this momentum emerged speculative therapies claiming to support children with autism by altering the microbiome, including faecal microbiota transfers and eating regimen therapies.
These “therapies” were long on hope but short on evidence for efficacy and safety, and are available with their very own risks and substantial costs.
What our study did
We worked with the Australian Autism Biobankwhich incorporates extensive clinical and biological data from children on the autism spectrum and their families, in addition to the Queensland Twin Adolescent Brain Project.
We compared microbial DNA from stool samples of 99 children on the autism spectrum to 2 groups of non-autistic children: 51 of their siblings and 97 unrelated children.
We also checked out clinical, family and lifestyle information, including in regards to the child’s eating regimen, for a comprehensive, broad have a look at aspects that will contribute to the their microbiome.
What we found
We found no evidence for a relationship between autism and measures of the microbiome as an entire, or with microbiome diversity.
Only one bacterial species out of greater than 600 showed an association with autism. We found no evidence for other bacterial groups which have previously been reported in autism (for instance, ).
Instead, we found children on the autism spectrum were more more likely to be “picky eaters” – consistent with reports from earlier studies – and this was related to particular traits related to autism, similar to restricted interests and sensory sensitivity.
We also found pickier eaters tended to have a less diverse microbiome, and runnier (more diarrhoea-like) stool. We’ve also known for a while children on the autism spectrum usually tend to have gastrointestinal issues similar to constipation, diarrhoea and abdominal pain.
The genetic information told an identical story: autism and restricted interests corresponded to a less-diverse eating regimen, but circuitously with the microbiome.
These genetic data are critical, because they rule out other environmental aspects that will have influenced the findings.
Overall, our results didn’t support the favored view that gut microbes cause autism.
What we propose as a substitute is strikingly easy: autism-related traits and preferences are related to less-diverse eating regimen, resulting in a less-diverse microbiome and runnier stool.
What do our findings mean?
Our findings have necessary implications for the autism community.
First, microbiome interventions for autism, similar to faecal microbiota transplants, needs to be viewed with caution. Our findings suggest they’re unlikely to be effective and may do more harm than good.
Our study also draws attention to the importance of eating regimen for youngsters on the autism spectrum. Poor eating regimen in children and young people is a major public health concern in Australiawith necessary implications for his or her well-being, development and health conditions similar to obesity.
We must do more to support families at mealtimes, specifically for families with autistic children, somewhat than resorting to fad “therapies” that will do more harm than good.