The microbiota-gut-brain axis in myalgic encephalomyelitis/chronic fatigue syndrome: a narrative review of an emerging field.
El-Sehrawy, Amr Ali Mohamed Abdelgawwad, Ayoub, Ibtihal Ibrahim, Uthirapathy, Subasini et al. · European journal of translational myology · 2025 · DOI
Quick Summary
This review examines how bacteria in your gut may be connected to ME/CFS symptoms like fatigue and brain fog. Researchers looked at studies from 1995 to 2025 about how gut bacteria communicate with the brain and immune system. The review suggests that fixing imbalances in gut bacteria might help treat ME/CFS, though more research is needed to confirm this.
Why It Matters
Understanding the gut-brain connection in ME/CFS could identify new treatment targets beyond symptom management. This emerging research area offers potential for personalized interventions such as targeted probiotics or dietary modifications, which may help improve fatigue, cognitive function, and overall quality of life.
Observed Findings
Alterations in gut microbial composition are documented in ME/CFS patients compared to healthy controls
Gut dysbiosis may impair intestinal barrier function and increase systemic immune activation
Dysbiosis correlates with ME/CFS symptoms including fatigue and cognitive dysfunction
Multiple mechanistic pathways link the microbiota-gut-brain axis to systemic manifestations of ME/CFS
Inferred Conclusions
The microbiota-gut-brain axis represents a significant pathophysiological mechanism in ME/CFS
Targeted interventions correcting dysbiosis may offer therapeutic benefit for ME/CFS management
Further research integrating microbiota composition, immune markers, and neurological function is warranted
Personalized microbiota-targeted approaches could enhance clinical outcomes and quality of life in ME/CFS
Remaining Questions
Which specific bacterial taxa or microbial patterns are most relevant to ME/CFS pathogenesis, and do these differ across patient subgroups?
What This Study Does Not Prove
This review does not prove that dysbiosis causes ME/CFS, only that an association exists. The findings do not establish that correcting gut bacteria will treat ME/CFS, nor do they replace the need for clinical trials testing specific microbiota-targeted therapies. Additionally, the review does not determine whether dysbiosis is a primary driver or a secondary consequence of ME/CFS.