Plasma cytokine concentrations do not distinguish ME/CFS groups
Immune profiling (Additional file 1: Table S4A) was performed to test for alterations in the ME/CFS and IBS subgroups. No significant findings were obtained after adjusting for multiple comparisons of all 61 cytokines. However, prior to adjustment, TNF-α was increased in the ME/CFS cases compared to the controls (Additional file 1: Table S4B) and plasma levels of leptin, CSF-2, CXCL-8, and TNF-α were higher in the ME/CFS + IBS patients than the controls (Additional file 1: Table S4B). The ME/CFS patients without IBS had a pre-adjustment trend toward increased TNF-α compared to controls.
Unsupervised hierarchical clustering was used to visualize the variation in plasma cytokine levels between the total ME/CFS, ME/CFS + IBS, ME/CFS without IBS, and controls. Although the clusters did distinguish a range of cytokine profiles in individuals (ranging from high to low cytokine profiles), there was no distinct clustering observed between disease groups (Additional file 2: Figure S2).
- Levels of distinct intestinal bacterial species—Faecalibacterium, Roseburia, Dorea, Coprococcus, Clostridium, Ruminococcus, Coprobacillus—were strongly associated with ME/CFS; their combined relative abundance appears to predict if someone has the illness.
- Increased abundance of the Alistipes group of bacteria, and decreased Faecalibacterium were the top biomarkers of ME/CFS with IBS.
- Enrichment in the pathway for vitamin B6 biosynthesis and salvage (i.e. recycling B6) was the strongest predictor of ME/CFS, regardless of whether or not patients had IBS. Vitamin B6 helps the body use and store both proteins and carbohydrate, as well as help form the haemoglobin that carries oxygen round the body. There is some evidence B6 is low in patients, but this could be down to changes in the body rather than in gut bacteria.
- No changes were observed in immune markers which may reflect the lack of participants who had been ill for a short time; earlier research suggests immune changes may only be evident when comparing short and long duration cases
Great blog post!
Fecal transplants. People have tried it both orally and anally. Here is the story of one person who has had success using the enema version:Yes, that's me! I'm already wondering how to experiment with this. Anybody got ideas?
I know a teenager who got diagnosed with abnormaly long colon and whose only symptom was constipation. I just don't buy it, there must be and underlying cause for that symptom of hersI found some B.S. with out the I part : "ME/CFS and its underlying pathology or the emotional response to illness in these individuals may predispose ME/ CFS sufferers to IBS."
Oh S***. Literally and figuratively. IBS is a very poorly defined disorder to begin with. I spent 15 years with this diagnosis ( at large university research group) Despite having a a dx of possible tethered cord syndrome ( from the neurosurgeon who defined the pathophysiology of thus disorder!!! ) and a long, redundant, tortuous colon. Just by 'luck' ( if you can call it that) I developed solitary rectal ulcer syndrome - my colon was telescoping. This is difficult to diagnose , as on colonoscopy the bowel is filled with air and the telescoping is not occurring.
A long redundant colon has been considered an incidental finding, but I found one article where researchers felt it was the result of a malrotation/ malattachment phenomenon. This is important, as there can be abnormal bands of soft tissue that can be present and hold the colon in an abnormal position.
So, how many of us have been diagnosed with a long,redundant colon ?
it is not benign and incidental, especially when the neurology takes a hit.