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Gut bacteria provide clues to ME/CFS

Maureen Hanson: Gut bacteria abnormality refutes the ridiculous concept that the disease is psychological

Cornell researchers report they have identified novel biological markers of ME/CFS in gut bacteria and inflammatory microbial agents in the blood.

In the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.

The researchers noted that gastrointestinal disturbances are commonly reported in cases of ME/CFS.

Taken together, our results suggest an ongoing damage to the gut mucosa, leading to increased microbial translocation in ME/CFS, which in turn could alter antimicrobial regulators and disregulate the innate immune system.

Elaborating further, Maureen Hanson, the study’s senior author, noted in the Cornell Chronicle: “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.”

Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.

The Cornell team sequenced regions of microbial DNA from stool samples to identify different types of bacteria. Overall, they found that the diversity of types of bacteria in patients was greatly 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.

The authors noted: “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.

“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.”

 

To read the study abstract, please toggle the panel below.

Abstract:Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome
Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome

Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley and Maureen R. Hanson
Microbiome 20164:30 | DOI: 10.1186/s40168-016-0171-4© | The Author(s). 2016
Received: 29 February 2016 Accepted: 11 May 2016 Published: 23 June 2016

Abstract
Background
Gastrointestinal disturbances are among symptoms commonly reported by individuals diagnosed with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). However, whether ME/CFS is associated with an altered microbiome has remained uncertain.

Here, 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). 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).

Results
We observed elevated levels of some blood markers for microbial translocation in ME/CFS patients; levels of LPS, LBP, and sCD14 were elevated in ME/CFS subjects. Levels of LBP correlated with LPS and sCD14 and LPS levels correlated with sCD14.

Through deep sequencing of bacterial rRNA markers, we identified differences between the gut microbiomes of healthy individuals and patients with ME/CFS. 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.

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. Using a machine learning approach trained on the data obtained from 16S rRNA and inflammatory markers, individuals were classified correctly as ME/CFS with a cross-validation accuracy of 82.93 %.

Conclusions
Our results indicate dysbiosis 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.

 

Findings could lead to new non-invasive diagnosis of ME/CFS

In the Cornell Chronicle article, Ludovic Giloteaux said the technique used in the study could be used 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”.

Interestingly, the researchers also discovered specific markers of inflammation in the blood, likely due to a leaky gut from intestinal problems that allow bacteria to enter the blood, which could yield further clues.

“Bacteria in the blood will trigger an immune response, which could worsen symptoms,” said Giloteaux.

The research did not determine whether the altered gut microbiome was a cause or a whether it was a consequence of disease.

Gastrointestinal symptoms in 92% of ME/CFS patients

Though underappreciated, the link between ME/CFS and gastrointestinal symptoms is well documented. In a very recent comprehensive review of the current evidence, Navaneetharaja et al. (2016) proposed that the intestinal microbiota and in particular members of the virome are a source of the “infectious” trigger of ME/CFS.

Such an approach has the potential to identify disease biomarkers and influence therapeutics, providing much-needed approaches in preventing and managing a disease desperately in need of confronting.

One study found that 92% of ME/CFS patients have co-existent irritable bowel syndrome. Additionally, significantly higher levels of Enterococcus and Streptococcus and lower levels of Bifidobacteria bacterial species has been reported in ME/CFS patients with 77% of them having some form of bacterial overgrowth.

High D-lactic acid linked to cognitive and neurological impairment

Other studies have reported altered gut microbiota in ME/CFS patients.

Using culture-based methods, Sheedy et al. (2009) found higher levels of D-lactic acid-producing Enterococcus and Streptococcus spp. in ME/CFS patients, which he linked to symptoms of cognitive dysfunction and neurological impairment in patients presented with D-lactic acidosis.

In the study, of 108 CFS patients and 177 controls, a significant increase of Gram positive facultative anaerobic faecal microorganisms was found.

Analysis of exometabolic profiles of Enterococcus faecalis and Streptococcus sanguinis showed that these organisms produced significantly more lactic acid from C-labeled glucose, than the Gram negative Escherichia coli.

Further, both E. faecalis and S. sanguinis secrete more D-lactic acid than E. coli.

Another study finds reduced diversity of Firmicutes bacteria

More recently, M Frémont et al. (2013) found differences in gut microbiota composition in a gene sequencing study of Norwegian and Belgian patients.

In the study, of 43 ME/CFS patients and 36 healthy controls, bacterial DNA was extracted from stool samples, PCR amplification was performed on 16S rRNA gene regions, and PCR amplicons were sequenced using a Roche FLX 454 sequencer.

Norwegian patients showed higher percentages of specific Firmicutes populations (Roseburia, Holdemania) and lower proportions of most Bacteroidetes genera.

FEATURE PHOTO: Gut Bacteria by NIAID

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Written by Russell Logan

Russell Logan worked as a magazine publisher and editor until forced into early retirement through ill health with ME. He has battled with moderate to severe ME for 25 years. He now lives in Noosaville, Australia.

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