![]() The aim of this review is to explore and discuss the current state of knowledge on the interplay between ME/CFS and the microbiome ( Table 1), to identify potential diagnostic or interventional approaches ( Table 2) and finally to describe areas where further research is needed. Increasing recognition of the gut-brain axis in general further motivates closer inspection of this possibility. Juxtaposing the relevance of the immune system in pathogenesis and etiology of ME/CFS ( 10) with the role of the microbiome in the early development of an ongoing influence on the immune system ( 11) supports our idea of an interplay between ME/CFS and the microbiome. The role of the microbiome in ME/CFS has been discussed more and more over the past years, as many patients suffer from gastrointestinal symptoms and there is a very frequent comorbidity with irritable bowel syndrome (IBS) ( 8) and inflammatory bowel disease (IBD) ( 9). The evolution of DNA-sequencing methods with reduced costs, reduction of sequencing errors, higher throughput and third generation sequencing has advanced insight into the microbiome ( 6, 7). It is an area which is rapidly expanding due to its complexity and manifold implications in health and disease ( 4, 5). The gut microbiome in contrast has gained much scientific and public attention over the last decade in different research fields. While there is evidence for several pathophysiological abnormalities including the neurological, immunological, infectious, mitochondrial and endocrine system, the underlying etiology and sequence of events remain unknown ( 3). Myalgic Encephalomyelitis (ME), also known as Chronic Fatigue Syndrome (CFS), is a neglected, serious debilitating disease with no proven diagnostic marker and specific therapy ( 1, 2). The therapeutic potential of fecal microbiota transfer and of targeted dietary interventions should be systematically evaluated. Activity levels, bedridden hours and disease progression should be compared to antibiotic exposure, drug intakes and alterations in the composition of the microbiota. As causality remains unclear, we recommend longitudinal studies. An association between the gut microbiome and the disease ME/CFS is plausible. Further larger studies are needed, above all to clarify whether D-lactic acidosis and early-life antibiotic use may be part of ME/CFS etiology and what role changes in the tryptophan metabolism might play. Considering the gut-brain axis we strongly suspect that the microbiome may contribute to neurocognitive impairments of ME/CFS patients. Beyond increasing gut permeability and bacterial translocation, specific dysbiosis may modify fermentation products, affecting peripheral mitochondria. We review options for microbiome manipulation in ME/CFS patients including probiotic and dietary interventions as well as fecal microbiota transplantations. Main proposed pathomechanisms include gut dysbiosis, altered gut-brain axis activity, increased gut permeability with concomitant bacterial translocation and reduced levels of short-chain-fatty acids, D-lactic acidosis, an abnormal tryptophan metabolism and low activity of the kynurenine pathway. ![]() Based on the literature we hypothesize that antibiotic use throughout life favours an intestinal microbiota composition which might be a risk factor for ME/CFS. We iteratively selected and elaborated on key theories about a correlation between microbiome state and ME/CFS pathology, developing further hypotheses. ![]() Here we review the current state of knowledge on the interplay between ME/CFS and the microbiome, to identify potential diagnostic or interventional approaches, and propose areas where further research is needed. The gut microbiome gained much attention in the last decade with manifold implications in health and disease. Despite evidence for neurological, immunological, infectious, muscular and endocrine pathophysiological abnormalities, the etiology and a clear pathophysiology remains unclear. Myalgic encephalomyelitis (ME) or Chronic Fatigue Syndrome (CFS) is a neglected, debilitating multi-systemic disease without diagnostic marker or therapy. ![]()
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