The Gut Microbiota and ME/CFS

A paper out in the journal Anaerobe explores the potential role of our commensal bacteria and the development and progression of chronic fatigue syndrome, also known as myalgic encephalomyelitis.[1]

Developing a theme started in part by the Australian scientist Thomas Borody and colleagues[2] in which they utilised the method of faecal transplant therapy and identified that 70% of the patients responded initially and after a prolonged follow up period ((15-20 years) found that 58% had a sustained response, suggesting that the relationship between bacteria in the digestive tract and symptoms of CFIDS may have a credible mechanism for intervention.

Frémont et al in the more recent study explored the bacteria and then classified them (using 16S rRNA gene sequencing techniques) after collecting stool samples from 43 participants diagnosed with ME/CFS compared with 36 asymptomatic controls.

In their paper they describe some interesting discoveries:

• Regional variations were noted in the stool samples between those collected from Norwegians and those from Belgium’s. It is well understood that variations in bacterial compositions are reflected in geographic and food differences.
• In effect the Norwegian cohort had more “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”.
• “In Belgian subjects the patient/control separation was less pronounced, however some abnormalities observed in Norwegian patients were also found in Belgian patients”.

In effect a state of dysbiosis was determined to exist in the target groups suggesting that modification of the bacterial communities may represent a point of intervention and or causation.

One particular bacterium found in the digestive tracts of humans has also been linked to effects on human function outside of the gastrointestinal tract.[3] In this paper the well known authors assessed the impact of oral administration of B. infantis 35624, for 6‒8 weeks on inflammatory bio marker and plasma cytokine levels in patients with ulcerative colitis (UC) (n = 22), chronic fatigue syndrome (CFS) (n = 48) and psoriasis (n = 26) in three separate randomized, double-blind, placebo-controlled interventions.

Their results demonstrate the ability of this microbe to reduce systemic pro-inflammatory bio markers in both gastrointestinal and non-gastrointestinal conditions. In conclusion, these data show that the immunomodulatory effects of the microbiota in humans are not limited to the mucosal immune system but extend to the systemic immune system.

Comments

The role of the microbiota in the development and or prolongation of inflammation driven conditions is becoming well recognised, if not yet fully understood. The implication that food and bacterial manipulators may present a more profound and safer modifier of these triggers than drugs is finding increasing stability in the scientific community, who are catching up with the clinical appreciation of dysbiosis and suitable interventions to resolve it.

In perhaps one of the most interesting cross overs the relationship between the historical bacterial component in mitochondria and the microbiome sits the multi protein trigger known as the inflammasome – as more natural agents are identified in terms of their ability to modify inflammasome activation it is likely that we will see a new set of treatments being developed that may provide better outcomes that those achieved without the recognition of this connection.

References