Joaquim Fernández Solà
Professor of Medicine at the University of Barcelona and coordinator of the Central Sensitisation Unit at the Hospital Clínic de Barcelona.
The two studies are novel and of high scientific interest, and have a high methodological quality, with the use of metabolomic and metagenomic techniques. They are published in a journal specialised in the microbiome, with high scientific impact.
These studies corroborate the line of research initiated some five years ago on the role of the microbiota in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). However, these studies are more systematised, carried out on larger samples and with better methodology than the previous ones. They not only make it possible to establish pathogenic correlations between the microbiota and CFS/ME, but also to determine the role of certain mediators, such as intestinal butyrate biosynthesis and the abundance of Faecalibacterium prausnitzii. They also profile specific microbiota phenotypes for increased fatigue intensity and for newly diagnosed versus long-standing CFS/ME subgroups.
These articles provide biomarkers that may be useful for assessing gastrointestinal involvement in CFS/ME patients. However, as the authors themselves state in the limitations of the studies, these are not diagnostic markers of disease, but of the process of gastrointestinal dysfunction. Nor do they immediately assume that they can act directly on the microbiota and improve the symptoms of CFS/ME. We are still in the early stages of scientific understanding of the microbiota and its mediating role in multiple diseases, including CFS/ME.
CFS/ME is a complex disease of neuroinflammatory pathogenesis with systemic repercussions. The microbiota interrelates with the brain in this disease, modulating intestinal reactivity to food and external factors and triggering local inflammatory reactions, with potential systemic repercussions. The more we know about the microbiota in CFS/ME, the better we will understand what happens in gut dysfunction in this disease. However, we must not forget that the main site where this dysfunction mainly occurs is in the central nervous system. What happens in the gut may only be secondary to the central nervous system alteration in the brain-gut axis.