Carbs and dysbiosis in autism reloaded

I have had a day to reflect upon the new paper by Brent Williams and colleagues published in PLoS ONE on carbohydrate digestion and dysbiosis in autism covered in my last post. I am still of the opinion that this is a 'game-changer' to borrow a phrase; not so much in the concepts it discusses which many have been talking about for quite a few years, but the fact that it is all bundled into a smart peer-reviewed package so perhaps making the research more 'accessible' to those working at the sharp end.

A few further details from the Williams paper are also noteworthy based on my very, very limited knowledge of the techniques used:

• This was a study looking at 'bacterial community composition' in intestinal biopsies taken from the ileum and cecum. This is a new way of looking at the world of gut bacteria outside of the analysis of 'number twos' ('free fecal material' as the authors put it) more traditionally seen in autism research. It is however a more invasive way of looking at things also. I suppose it gives a more real-time picture of what is going on in various sections of the gut assuming that like human communities before the onset of globalisation, different ethnicities inhabit different parts of our tiny rock.
• Decreased mRNA (messenger RNA) expression for dissacharidases and hexose transporters was a feature of the autism group analysis. In other words, the source material for enzymes such as sucrase isomaltase, maltase glucoamylase and lactase was not quite what it should have been in the ileal biopsies; nearly 75% of participants had combined deficiencies in all three enzymes. Quite a nice summary of the various hexose transporters can be found here. Two transporters were looked at in the study: sodium-dependent glucose cotransporter (SGLT1) and glucose transporter 2 (GLUT2). Two-thirds of the autism group were found to show deficiencies in both. Two-thirds of the autism study group had mRNA deficiencies in all 5 genes.
• The 'ratio' measurements undertaken on bacterial communities pointed to some interesting findings. Decreasing Bacteriodetes and increasing Firmicutes or Proteobacteria were the main findings for the autism group, taking into consideration the different biopsy areas analysed. Further analysis of the Firmicutes directed the authors to Clostridiales which further directed them to specifics: Lachnospiraceae and Ruminococcaceae as being predominant. Lachnospiraceae has been linked to the introduction of high grain diets - at least if you are a beef cow. They also suggested that probiotic use might interfere with the bacterial ratios identified (included in a Table S5 just in case you want to see more).

There is an awful lot of information in this paper and unless you happen to be a molecular biologist with a combined degree in microbiology and enzymology, it is a struggle to get all that information out. I don't doubt that as this paper percolates through the various autism communities (lay and research) more details will emerge related to the findings and their significance. 

Whilst trying to remain as dispassionate and objective as possible on all things autism research, I still can't help raise a smile at seeing this work and the thought that something really did change following its publication.