Idiopathic diseases are frustrating to patients and physicians. With little information as to the cause or triggers, these maladies often get dismissed as much less debilitating than what the patient is presenting or psychosomatic in nature. For instance, physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to incapacitating fatigue that isn't alleviated by rest. Moreover, there are no known triggers, and diagnosis requires lengthy tests administered by an expert.
Now, researchers at Cornell University have discovered the first biological markers for chronic fatigue in gut bacteria and inflammatory microbial agents in the blood. In the new study, the Cornell team was able to correctly diagnose myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83% of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.
“Our work demonstrates that the gut bacterial microbiome in ME/CFS patients isn't normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” explained senior study author Maureen Hanson, Ph.D., professor in the department of molecular biology and genetics at Cornell University. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”
The findings from this study were published recently in Microbiome in an article entitled “Reduced Diversity and Altered Composition of the Gut Microbiome in Individuals with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.”
The investigators recruited 48 people diagnosed with ME/CFS and 39 healthy controls to provide stool and blood samples. Furthermore, they sequenced regions of microbial DNA from the stool samples to identify different types of bacteria. Overall, the diversity of types of bacteria was significantly reduced, and there were fewer bacterial species known to be anti-inflammatory in ME/CFS patients compared with healthy people, an observation also seen in people with Crohn's disease and ulcerative colitis.
“We profiled gut microbial diversity by sequencing 16S ribosomal ribonucleic acid (rRNA) genes from stool as well as inflammatory markers from serum for cases (n = 48) and controls (n = 39),” the authors wrote. “We also examined a set of inflammatory markers in blood: C-reactive protein (CRP), intestinal fatty acid-binding protein (I-FABP), lipopolysaccharide (LPS), LPS-binding protein (LBP), and soluble CD14 (sCD14).”
Interestingly, the researchers discovered specific markers of inflammation in the blood, likely due to a permeable gut from intestinal problems that allow bacteria to enter the blood. Bacteria in the blood will trigger an immune response, which could worsen symptoms.
“We observed that bacterial diversity was decreased in the ME/CFS specimens compared to controls, in particular, a reduction in the relative abundance and diversity of members belonging to the Firmicutes phylum,” the authors penned. “In the patient cohort, we find less diversity as well as increases in specific species often reported to be pro-inflammatory species and reduction in species frequently described as anti-inflammatory. …Our results indicate dysbiosis [microbial imbalance] of the gut microbiota in this disease and further suggest an increased incidence of microbial translocation, which may play a role in inflammatory symptoms in ME/CFS.”
“In the future, we could see this technique as a complement to other noninvasive diagnoses, but if we have a better idea of what is going on with these gut microbes and patients, maybe clinicians could consider changing diets, using prebiotics such as dietary fibers or probiotics to help treat the disease,” concluded lead study author Ludovic Giloteaux, Ph.D., a postdoctoral researcher in Dr. Hanson’s laboratory.