“Who wants to live like this? We can’t even take a shower, much less clean our house…after 17 days confined to bed, not even able to take a bath, much less function at all… where is the quality of life and what is the purpose?”
– ‘Linda’, woman with chronic fatigue syndrome
Always tired. Continually in pain. Unable to maintain a normal career and relationships. These are common threads among people with a condition called chronic fatigue syndrome (CFS), otherwise known as myalgic encephalomyelitis (ME), characterized by excessive fatigue that can’t be attributed to an underlying medical condition. People with the condition may experience symptoms ranging from headaches, memory and cognitive problems, and unexplained pain to digestive disturbances—but the black hole of fatigue is paramount. It gets worse with physical or mental activity, and doesn’t get better with rest.
Many individuals with ME/CFS say a huge challenge is getting the condition diagnosed—a process that involves ruling out a host of other health problems. In medical research, a biomarker of this condition has so far been elusive.
Now, a promising line of research is exploring whether a biomarker for ME/CFS might be found in the gut microbiota. A 2017 study adds to previous research that has scientists inching closer to the urgently needed biological parameter that would aid diagnosis of this mystifying disease.
In the study, Dr. W. Ian Lipkin and colleagues from Columbia University compared a group of people with ME/CFS with healthy individuals. Some in the ME/CFS group also had a diagnosis of irritable bowel syndrome (IBS)—a functional gastrointestinal disorder—and others did not.
Circulating immune cells did not end up distinguishing one group from another. But the gut microbiota did—and a main finding from the study was that people with ME/CFS who also had IBS looked different, gut microbiota wise, from those with ME/CFS without IBS. The top biomarkers of ME/CFS with IBS were an increased abundance of Alistipes and decreased Faecalibacterium in the gut, compared to healthy controls; on the other hand, increased Bacteroides abundance along with a specific decrease in the species Bacteroides vulgatus seemed to indicate ME/CFS without IBS.
From the bacterial profiles alone, researchers were able to predict the three different groups with impressive accuracy: people without ME/CFS, people with ME/CFS alone, and people with ME/CFS and IBS. In addition, researchers also found that the markers of ME/CFS in general—regardless of IBS—included a decrease in certain bacterial metabolic pathways in the gut.
Researchers also found an intriguing correlation between the severity of certain symptoms—pain, fatigue, and reduced motivation—and the abundance of various bacteria and metabolic pathways in the people with ME/CFS.
The work indicates that gut bacterial dysbiosis specific to ME/CFS could be difficult to separate from the dysbiosis typical of IBS—another disorder for which a biomarker is so far elusive. Senior author Dr. W. Ian Lipkin notes the interesting overlap between the two conditions: “Much like IBS, ME/CFS may involve a breakdown in the bidirectional communication between the brain and the gut mediated by bacteria, their metabolites, and the molecules they influence,” he says.
While the study ultimately doesn’t shed light on the underlying cause of ME/CFS, it provides evidence of gut microbiota dysbiosis in ME/CFS, along with hope for finding an eventual biomarker—most promisingly, in gut microbiota composition or bacterial metabolic pathways. Research teams still have a long way to go, but the biomarker they hope to find will mark a turning point for patients with this mysterious disease.
Giloteaux L, Goodrich JK, Walters WA, et al. Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome. 2016; 4:30.
Nagy-Szakal D, Williams BL, Mishra N, et al. Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome. 2017; 5:44.