The gut microbiota and ME/CFS

Continuing a common theme of gut bacteria on this blog, most recently with autism in mind, my attention today turns to a paper by Frémont and colleagues* looking at the gut microbiota in cases of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS).

Cross my palm @ Wikipedia 

This is not the first time that those trillions of bacterial masters of ours have cropped up on this blog with CFS/ME in mind as per my recent post on yuck factor 10 and the fecal microbiota transplant (FMT) with CFS/ME in mind (see here).

Frémont et al utilised the most commonly used tool of the bacteriologists trade, high-throughput 16S rRNA gene sequencing (see here for an overview** and here for some issues with the method), to classify bacteria derived from a lovely sample medium - stool samples - provided by 43 participants diagnosed with ME/CFS compared with 36 asymptomatic controls.

They reported a few interesting things.

• Because samples were provided by both Belgian and Norwegian participants (both ME/CFS and control groups), the authors reported differences in the type of bacteria between the different country samples. I'm guessing that quite a lot of this variation has to do with environmental factors such as food preferences and the like as per what other studies have shown. We also know for example that what you eat can have a fairly important effect on what bacteria you have in your gut (see here).
• "Norwegians showed higher percentages of specific Firmicutes populations" when looked at as a whole in comparison to the Belgian samples.
• When comparing Norwegian CFS/ME participants with their fellow asymptomatic country-people "patients presented increased proportions of Lactonifactor and Alistipes, as well as a decrease in several Firmicutes populations". Readers who clicked on the link for more information about Alistipes might recognise the name carried by a particular species, A. finegoldii named in honour of one Sydney Finegold, a regular on the autism-gut bacteria research scene. 
• "In Belgian subjects the patient/control separation was less pronounced, however some abnormalities observed in Norwegian patients were also found in Belgian patients". Not too much more to add there aside from the suggestion that searching for diagnosis-wide biomarkers for a heterogeneous condition like CFS/ME perhaps suffers from the same methodological ills as has been talked about with the autisms in mind (see here). That and the whole brain CFS/ME vs gut CFS/ME subgroup discussions that I've had on this blog. 

Appreciating that this was a relatively small scale study in terms of participant numbers, I'm intrigued by this study and its results. Heterogeneity in presentation and all the myriad of other factors which can and do affect gut bacteria are important interfering factors in any kind of research in this area. Indeed if one compares the gut microbiome with some of the other -omes such as the genome or epigenome, one starts to appreciate the similar issues involved in building up a picture of the underlying pathology behind a condition like CFS/ME in terms of no one gene or epigenetic factor probably working in isolation covering all cases. So it is probably true for the gut microbiome too.

That being said, unlike genes and to a lesser extent the epigenome, where differences are identified in the various phylum/class/order/family/genus/species of bacteria present potentially even in just subgroups of the condition, one would assume that some corrective intervention could be put in place which might, just might, affect the presentation of symptoms. Indeed the authors speculate on "treatments based on gut microbiota modulation (antibiotics, pre and probiotics supplementation)" which brings me to the paper by Groeger and colleagues**** and back to the original paper by Borody and colleagues***** and indeed outside of CFS/ME, that interesting case study on antibiotics and autism which I discussed recently (see here) [no medical advice is given or intended].

To close, Muscial Youth and a blast from the 80s past.

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* Frémont M. et al. High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients. Anaerobe. 2013 Jun 19. pii: S1075-9964(13)00092-9. doi: 10.1016/j.anaerobe.2013.06.002.

** Trichopoulou A. et al. Disparities in food habits across Europe. Proceedings of the Nutrition Society. 2002; 61, 553–558.

*** Větrovský T. & Baldrian P. The Variability of the 16S rRNA Gene in Bacterial Genomes and Its Consequences for Bacterial Community Analyses. PLoS ONE. 2013; 8(2): e57923. doi:10.1371/journal.pone.0057923

**** Groeger D. et al. Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut. Gut Microbes. 2013 Jun 21;4(4).

***** Borody TJ. et al. The GI microbiome and its role in Chronic Fatigue Syndrome: A summary of bacteriotherapy. Journal of the Australasian College of Nutritional and Environmental Medicine. 2012; 31: 3-8.

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Frémont M, Coomans D, Massart S, & De Meirleir K (2013). High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients. Anaerobe PMID: 23791918