Dr Jose Montoya, Live Webcast from Stanford, Jan 18th 7PM PST

Among other things, Tofacitinib is used to treat Inflammatory Bowel Disease.

One cause of IBD are changes in the intestinal microbiota.


Changes in the composition of the intestinal microbiota are an important environmental factor in the development of IBD. Detrimental changes in the intestinal microbiota induce an inappropriate (uncontrolled) immune response that results in damage to the intestinal epithelium. Breaches in this critical barrier (the intestinal epithelium) allow further infiltration of microbiota that, in turn, elicit further immune responses. IBD is a multifactorial disease that is nonetheless driven in part by an exaggerated immune response to gut microbiota that causes defects in epithelial barrier function
https://en.m.wikipedia.org/wiki/Inflammatory_bowel_disease

There have been a couple of papers showing altered composition of the gut microbiota in ME/CFS.

There is a history of IBD in my family, so it's tempting for me to wonder if some chronic alteration of the gut microbiome, and the resulting immune response, could be the engine driving ME/CFS.
 
I wonder if he knows about filgotinib then, by the looks of it a way more accurate jak-inhibitor. The gist I get from this theory is that changes in intestinal microbiota cause inflammation, which causes an exaggerated immune response, which keeps the intestinal microbiota screwy. A jak-inhibitor would take out the inflammation and the immune response would then perhaps be gone? Allowing things to get back to normal?
 
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