Gut bacterial diversity and autism

Let's face it, those who regularly read this blog probably knew that I was always going to be interested in the paper published by Dae-Wook Kang and colleagues* (open-access) discussing the gut microbiome and autism.

Holding it in @ Wikipedia  

For quite a while now I've been going on (and on and on) about how those trillions of wee beasties which call us home might be doing so much more than just helping to digest our food and producing the odd vitamin or two.

Indeed it's come to the point that questions have started to be asked about whether gut bacteria might not just shape or influence behaviour (see here) but indeed whether our very psychological development might be linked to what goes on in the deepest, darkest recesses of our bowels: psychobacteriomics anyone?

Appreciating that such work still needs to go some before we proclaim that social development for example, is linked to gut bacteria (it was a study of mice** after all) and put quite a few psychologist-theorists out of business, there is nevertheless a growing tide of research highlighting how important the symbiotic relationship between bacteria and human might be. Just call me Dax.

The Kang paper has, as one might expect, already received some media attention (see here). Indeed, the authorship list also includes a favourite autism researcher of mine - Prof. Jim Adams - who aside from publishing that pretty good gold-standard RCT of vitamin supplementation for autism a while back (see here), has himself already dabbled in the science of gut bacteria and autism as per other articles*** (open-access).

• In the latest study, the name of the game was stool analysis; said stools provided by 20 children diagnosed with an autism spectrum disorder (ASD) and 20 age- and sex-matched aysmptomatic control kids. DNA was extracted from the stools (what a lovely job that must have been!) and analysed to discern what bacteria and families of bacteria were present across the two groups. If you really want more information about 16S rDNA sequencing method used in the Kang study, I've got another post scheduled soon on more gut microbiomics in chronic fatigue syndrome (CFS) which gives a little more information on the science.
• The results: well, after some fancy analysis based on the various groupings of bacteria and the "microbial richness and diversity" present between the groups, one of the main conclusions was that the control asymptomatic group "harbored more diverse gut microbiota than the autistic group did". 
• When they looked at the presence of gastrointestinal (GI) issues related to cases of autism there was some hint of an effect too on gut bacterial diversity but it appeared that the severity of autism was a more important factor to potentially account for the microbial differences detected.
• The authors note findings of: "significantly lower abundances of the genera Prevotella, Coprococcus, and unclassified Veillonellaceae in autistic samples". Not being an expert on the various types of bacteria which colonise our gut, I can't necessarily suggest anything more than what the authors noted about the link between some of these bacterial families and things like the digestion of carbohydrate-rich foods. Interesting though that the name Brent Williams appears in the paper text and his 'carbs and dysbiosis' work in autism (see here). 
• The authors conclude that the reduced microbial diversity and specific differences across the groups should be further investigated taking into account issues like dietary effects (see here) and the 'cross-talk' between bacteria and other biological functions.

OK you can perhaps appreciate that this was a relatively small study based on the participant numbers included. That and the fact that unlike the hunt for autism-related genes and genetic mutations (yep, lots of them potentially) when we talk about the gut microbiome, we are 'generally' (see here) talking about a dynamic system influenced by all manner of environmental effects not just the food we eat (see here). Kinda more like the methylome me thinks. That gut bacteria might also only be one part of the 'triad' of issues (pathogenic gut bacteria, gut hyperpermeability / leaky gut, immune response) which seem to be discussed with autism and the gut in mind is also worthwhile remembering.

But on the positive side of things, the Kang paper represents a lot of hard work and is yet another brick in the autism research wall suggesting that we should be looking more 'whole-body' when it comes to cases and phenotypes. Of particular note is the suggestion that behavioural symptom severity might trump GI symptom presentation as being 'correlated' to gut microbiome diversity. The authors do qualify this assertion by suggesting that "autism-related GI disorders may be linked to a unique shift in microbial balance", part of which they detected in their study. Whether or not this statement ties into those Stephen Walker 'distinctive features' bowel findings reported recently (see here) is perhaps further source for speculation and investigation.

To close Franz Ferdinand and Take Me Out.

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* Kang D-W. et al. Reduced Incidence of Prevotella and Other Fermenters in Intestinal Microflora of Autistic Children. PLoS ONE 8(7): 2013; e68322. doi:10.1371/journal.pone.0068322

** Desbonnet L. et al. Microbiota is essential for social development in the mouse. Molecular Psychiatry. 2013. doi: 10.1038/mp.2013.65

*** Adams JB. et al. Gastrointestinal flora and gastrointestinal status in children with autism -- comparisons to typical children and correlation with autism severity. BMC Gastroenterology 2011, 11:22 doi:10.1186/1471-230X-11-22

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Kang D-W (2013). Reduced Incidence of Prevotella and Other Fermenters in Intestinal Microflora of Autistic Children PLoS ONE DOI: 10.1371/journal.pone.0068322