Ha, I should have learned by now to not just read the abstract. I was a bit concerned that the abstract didn't actually say whether the butyrate producing bacteria and the butyrate levels were up or down. Here's the relevant section:
Consistent alterations in the abundance of butyrate-metabolism-related bacteria were observed:F. prausnitzii and B. uniformis were found in lower relative abundance in FM patients, while higher relative abundance was observed for Intestinimonas butyriciproducens, Flavonifractor plautii, Butyricoccus desmolans, Eisenbergiella tayi and Eisenbergiella massiliensis.
To explore the possible metabolic effect of these alterations, a targeted metabolite approach was used to measure the serum concentrations of butyric acid, isobutyric acid, propionic acid and lactic acid.
Serum levels of butyric acid in FM patients (n=73) were higher compared to unrelated controls (n=46, p=0.005), while levels of propionic acid were lower (p=0.006) and a trend towards lower levels of isobutyric acid was also observed (p=0.056). No significant differences in the serum levels of lactic acid was observed (Figure 4B). Multivariate analysis showed a significant between-group difference (Pillai’s Trace, F=8.97, p<0.0001).
So FM patients actually had higher levels of butyric acid in their serum, with just a trend to lower levels of isobutyric acid. And levels of butyrate-metabolism-related bacteria were a bit all over the place at the species level. And there was no difference in the fibre-intake between the FM cohort and the controls.
As usual, it seems that it's complicated...
When considering the nineteen specific species identified as significantly differentially abundant between FM patients and unrelated control participants, there was a broad range in how well- characterised these species were. Those species putatively depleted (lower in relative abundance) in FM were relatively well-characterised and included Faecalibacterium prausnitzii, Bacteroides uniformis, Prevotella copri and Blautia faecis.
Faecalibacterium prausnitzii is one of the most abundant and well-studied butyrate producing bacteria in the human gut [46]. This species has been reported to be depleted in multiple intestinal diseases and was therefore suggested as a potential marker for gut disorders. Within the gut, F. prausnitzii has been reported to exert anti- nociceptive as well as anti-inflammatory effects [58,79] and to enhance the intestinal barrier function [46]. Similar to our observations, F. prausnitzii was also reported to be depleted in patients with CFS [61].
Bacteroides uniformis, is one of several species which have recently been reported as having altered relative abundance in patients with inflammatory arthritis, along with H. parainfluenza,P. copri and others [96]. B. uniformis and H. parainfluenza were detected in synovial tissues of osteoarthritic joints, whereas P. copri and H. parainfluenza were detected in rheumatoid arthritis synovial fluid. P. copri is thought to mediate inflammatory response via Th17 activation [37,43], and was also shown to induce arthritis in an animal model of arthritis-prone mice [51]. In this study, these species were found in lower abundance in FM patients. Although FM is often considered to be a rheumatologic disease, it seems that at least some species previously found at higher abundance in inflammatory rheumatic diseases are depleted in FM.
In contrast to the depletion of butyrate producers F. prausnitzii and B. uniformis in FM patients, we observed significant higher relative abundance of a number of other known intestinal butyrate producers: Intestinimonas butyriciproducens, Flavonifractor plautii, Butyricoccus desmolans,Eisenbergiella tayi and the recently identified Eisenbergiella massiliensis . Alterations in butyrate and propionate metabolizing species were further supported by alterations in serum levels of these short chain fatty acids. Coherent with this putative shift in the butyrate producing community of FM patients, Parabacteroides merdae was also significantly higher in relative abundance in FM patients.
Recently, P. merdae has been reported by Olson et al. to be one of two key mediators of the anti-epileptic effect of the ketogenic diet [64]: in a mouse model, ketogenic diet can drive an increase in the abundance of P. merdae, which in turn, by regulation of amino acid γ-glutamylation leads to an increase in hippocampal γ-aminobutyric acid (GABA)/glutamate ratio. The increase in the inhibitory to excitatory neurotransmitter ratio in the brain is thought to protect against seizures. The second key mediator species of the ketogenic diet effect on seizures reported by Olson et al. was Akkermansia muciniphila, which in our cohort was also found at higher abundance in FM patients, although this observation did not reach statistical significance (p=0.042, Benjamini-Hochberg FDR=0.27).
It's interesting stuff, although clearly early days.
The study looks to have been well done as far as a quick skim by someone unqualified to judge can tell. Canadian researchers. Perhaps worth encouraging them.
