Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndromeOriginal paper
Karen Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease, four years before the first published case study.
Read MoreWhat was studied?
This study asked whether myalgic encephalomyelitis, or chronic fatigue syndrome (ME/CFS), is linked to an altered gut microbiome and to signs of bacteria leaking into the blood. Researchers sequenced the V4 region of the 16S rRNA gene from stool to profile gut bacteria. They also measured five blood markers of microbial translocation and inflammation. The markers were C-reactive protein, intestinal fatty acid-binding protein (I-FABP), lipopolysaccharide (LPS), LPS-binding protein (LBP), and soluble CD14 (sCD14). A machine learning model then tried to separate patients from controls.
Who was studied?
The cohort was 48 adults with ME/CFS and 39 healthy controls in the United States. Patients met the Fukuda diagnostic criteria and were established patients of an ME/CFS specialist. The groups were similar in age and sex, and controls came from the same geographic area. Of the 48 patients, 34 reported gastrointestinal problems such as constipation or diarrhea, versus 7 of the controls. Stool was collected at home, and blood plasma was assayed for the translocation markers.
What were the most important findings?
ME/CFS patients showed reduced gut bacterial diversity and elevated blood markers of microbial translocation. Median plasma LPS was 119.43 pg/mL in patients versus 74.74 pg/mL in controls (p less than 0.0005). Plasma sCD14 and LBP were also significantly higher in patients (both p less than 0.0005). Stool samples had lower richness and evenness, including a Chao1 of 2363 versus 2918 (p equals 0.002). The Firmicutes phylum fell (35 versus 46 percent) while Proteobacteria rose, driven by a twofold increase in Enterobacteriaceae. Faecalibacterium and Bifidobacterium, described as anti-inflammatory, were reduced. A model using genus-level taxa plus blood markers classified subjects with 82.93 percent cross-validation accuracy.
What are the greatest implications of this study?
The results point to gut dysbiosis and increased microbial translocation in ME/CFS, which may drive inflammatory symptoms. Loss of anti-inflammatory bacteria alongside more pro-inflammatory taxa fits a pro-inflammatory gut environment. The combined microbiome and blood-marker model suggests a possible non-invasive aid to diagnosis. The authors note the cohort is small and a larger study is needed before clinical use. Because this is cross-sectional, it cannot show whether dysbiosis causes ME/CFS or results from it.