Molecular Characterisation of Gastrointestinal Microbiota of Children With Autism (With and Without Gastrointestinal Dysfunction) and Their Neurotypical Siblings.

2 Oct

The possibility that gastrointestinal problems are linked–either causally or a comorbid condition–with autism is a topic of much discussion. Some of this focus results from the failed “leaky-gut” theory of autism causation and the also failed idea that the MMR vaccine causes the “leaky-gut”. Recently groups have started to look at the bacteria in the feces or intestines of autistics. From Wikipedia:

The human body, consisting of about 10 trillion cells, carries about ten times as many microorganisms in the intestines. The metabolic activities performed by these bacteria resemble those of an organ, leading some to liken gut bacteria to a “forgotten” organ. It is estimated that these gut flora have around 100 times as many genes in aggregate as there are in the human genome.

One recent study claimed to find a difference in intestinal bacteria between autistics and non-autistics with gastrointestinal disease. In specific, they claimed that

These findings elevate this little-recognized bacterium to the forefront by demonstrating that Sutterella is a major component of the microbiota in over half of children with autism and gastrointestinal dysfunction (AUT-GI) and is absent in children with only gastrointestinal dysfunction (Control-GI) evaluated in this study.

The authors were careful in their conclusions, mentioning that this finding might shed light on the “extent to which Sutterella may contribute to the pathogenesis of GI disturbances in children with autism”. Note this is different than saying that this sheds light on the origins of autism. This point was missed in some discussions of the study, I’ll point out.

It is odd in that study that Sutterella was not found in the non-autistics in that it has been found in non-autistics previously.

As happens too frequently, one study is followed by another which seems to claim the opposite. The study out recently, Molecular Characterisation of Gastrointestinal Microbiota of Children With Autism (With and Without Gastrointestinal Dysfunction) and Their Neurotypical Siblings, doesn’t find differences between autistics and non-autistics with GI complaints. In this study, the controls were neurotypical siblings of the same autistics. This is good choice as the siblings “share a similar environment”. Here is the abstract:

Many children with autism spectrum disorders (ASDs) suffer from gastrointestinal problems such as diarrhoea, constipation and abdominal pain. This has stimulated investigations into possible abnormalities of intestinal microbiota in autistic patients. Therefore, we designed this study to identify differences (and/or similarities) in the microbiota of children with autism (without gastrointestinal dysfunction: n = 23; with gastrointestinal dysfunction: n = 28) and their neurotypical siblings (n = 53) who share a similar environment using bacterial tag-encoded FLX amplicon pyrosequencing. Regardless of the diagnosis and sociodemographic characteristics, overall, Firmicutes (70%), Bacteroidetes (20%) and Proteobacteria (4%) were the most dominant phyla in samples. Results did not indicate clinically meaningful differences between groups. The data do not support the hypothesis that the gastrointestinal microbiota of children with ASD plays a role in the symptomatology of ASD. Other explanations for the gastrointestinal dysfunction in this population should be considered including elevated anxiety and self-restricted diets.

Emphasis added.

Note that this study claims to discuss the role of microbiota in the symptomology of ASD, not just GI disease in autistics.

There are multiple reasons why a direct comparison of the two studies is not precise, but the general idea is the there, especially to the lay public: one study says there autistics have a specific gut bacteria profile, another says there isn’t. And, so, we will see more studies.

In case you are wondering–do either of these studies have anything to do with Andrew Wakefield’s ideas of measles virus being involved with autism? The answer is clearly no. Unfortunately, many who promote the vaccine-causation link will jump on any study of the digestive system as somehow related to Mr. Wakefield’s hypotheses. Sad, but true.

By Matt Carey


3 Responses to “Molecular Characterisation of Gastrointestinal Microbiota of Children With Autism (With and Without Gastrointestinal Dysfunction) and Their Neurotypical Siblings.”

  1. Goldy October 2, 2012 at 02:54 #

    Clostridia bacterium seems to be receiving a lot of attention these days (ABC 4 Corners Program) Children from Somalia have higher rates of autism when they come to America with a diet higher in sugar and refined carbs. This encourages ear and other infections and and it has been found that particularly after antibiotic use – clostridia bacterium overgrowth becomes a problem and the propionic acid produced causes autistic symptoms in some children.. Vancomycin will kill this bacterium and autism symptoms improved but the spores remain and reinfection is inevitable. However there was a vast improvement when the children were put on probitoics and fermented foods. Worth a lot more studies.

  2. rgross7 October 2, 2012 at 06:21 #

    Thank you, Matt. Your summary is clear and precise.

  3. futuredave5Dave October 2, 2012 at 10:21 #

    It seems to me the cause and effect can become indistinct. My son has low stomach acid, for example, and many of the common symptoms that go with it. The low acid, all by itself, seems like it would change the composition of bacteria.

    Similarly, I would think that people who take lots of medicines and vitamins have different ecosystems in their stomach. One you have a different set of bacteria, I suspect the odds increase that you will take even more vitamins, medicines, and so on.

    Low stomach acid is statistically linked to other problems that seem unrelated. I have heard, for example, that cancer and arthritis are more common in people with low stomach acid. Even if true, though, I don’t know how you could test causation.

    I am surprised, to an extent, that it could be tested at all. My son’s diet is very distinct from mine. If he had a typical sibling, I doubt the sibling would want the same diet my son wants.

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