A couple of recent studies indicate a link between fibromyalgia (FM) and gut bacteria. Whether this is a causative association or not remains unclear, but certainly these preliminary observations may pave the way for further studies elucidating the pathophysiology of FM.
The first study entitled: ‘Altered microbiome composition in individuals with fibromyalgia’ describes significant differences in several bacterial taxa in FM patients versus healthy controls. As per Amir Minerbi, the first author of this study, from the McGill University Health Centre, Montreal, QC, Canada, “this is the first demonstration of gut microbiome alteration in nonvisceral pain”. Approximately 20 different species of bacteria were found in either greater or lesser quantities in the microbiomes of FM patients.
Species putatively depleted in FM were relatively well characterised and included F. prausnitzii, B. uniformis, P. copri, and Blautia faecis.
B. uniformis is one of several species that have recently been reported as having altered relative abundance in patients with inflammatory arthritis. B. uniformisis detected in synovial tissues of osteoarthritic joints, whereas P. copri is detected in rheumatoid arthritis synovial fluid.
Of note, Clostridium scindens and B. desmolans, two bacterial species capable of converting cortisol to androgens by 20α-hydroxysteroid dehydrogenase activity were found in higher abundance in FM patients. Interestingly, abnormal regulation of hypothalamic-pituitary-adrenal axis has been reported in FM patients, although the direction of dysregulation remains controversial.
The study also reports a decrease in the abundance of several members of the Lachnospiraceae family, the bacteria involved in butyric acid production. Butyrate, the conjugate base of butyric acid, is produced by a small number of bacteria, including several Eubacterium species.
The authors of this study also detected a significant increase in the serum levels of glutamate in fibromyalgia patients. Also, the abundance of bacteria from Bifidobacterium and Lactobacillus genera (involved in the transformation of glutamate into GABA) was reduced in the FM group. This might contribute to the elevated systemic levels of glutamate.
Interestingly, the authors discuss that “in the presence of excess of glutamate, as observed here, the pain inhibition by GABA might be suppressed in female patients by this E2 (17β-estradiol)-specific regulation. This might partly explain the increased prevalence of FM in the female population”.
Of note, the fourth study investigates in fact the relationship between the reduced diversity in the microbiome and chronic widespread musculoskeletal pain. The chronic widespread musculoskeletal pain (CWP), affecting some 5–15% of the general population, forms part of the fibromyalgia syndrome that includes fatigue and sleep disturbance in addition to CWP.
Coprococcus comes is one of the most important butyrate-producing bacteria. Butyric acid produced by C. comes and other gut commensals exhibits remarkable anti-inflammatory effects in the gut. The authors of this study discuss that a high-fat diet may cause a decrease of Coprococcus species abundance in the gut. Of note, people with CWP are known to have on average a diet higher in fat. Thus, a high-fat diet may promote the decrease of Coprococcus and other anti-inflammatory species that “in turn results in a low-grade inflammation, supporting the development of CWP”.
A bit of History
Fibromyalgia was first described in the early 1800s as a condition called “muscular rheumatism.” The symptoms were stiffness, aches, pains, tiredness, and difficulty sleeping. A MD in Scotland first described the tender points of fibromyalgia in the early 1820s.
Eighty years later, the term “fibrositis” was first used. Because inflammation (swelling) was thought to be a cause of the pain, the ending “itis” was given. In 1976, the name of the condition was changed to “fibromyalgia.” Swelling in the body was no longer believed to be the cause of pain.
A Bit of Pathophysiology & Pathogenesis
Fibromyalgia’s pathogenesis has not been elucidated but may include sympathetic dysautonomia as an explanation to the multiplicity of FM symptoms including its main complaint, widespread pain. Thus, FM may represent a sympathetically maintained neuropathic pain syndrome, and the reports about a small nerve fiber pathology in FM may reinforce this mechanism.
Apparently, further studies are needed to confirm the link, described here, between fibromyalgia and gut bacteria. Whether, and how, some of the above-mentioned pathophysiology pathways and mechanisms are involved remains to be determined.