Just a comment or two and a question re: the hypothetical… .
Great, the attention and the focus on specific neurology research related to CFS! However, I think it’s way early to get excited about this; AND the research is on rats with broad presumptions about human CFS (when only ~50%-? of 'rat findings' apply to humans). Also, by his own admission, there are so many ancillary neuronal areas (receptors) that could simulate similar conditions to CFS… . And isn't he really drawing a line between auto-immune and
anti-inflammatory affects; this part seems unclear to his focus?
As a PWC +/- 30 years, trying a whole bunch of related medical this and that, and studying more research than I would wish on an enemy,
and still declining, my own resultant opinion as a cause leans towards over-stress inducing processes not unlike the mechanisms described in the discussion but with differences in biochemistry… . To wit,
From the interview:
…Even mast cells have these receptors that basically look for things that look kind of like a virus or look kind of like a bacteria and they become activated when they discover something that seems sort of foreign. They start pumping out these immune modulators, which then are detected by the vagus nerve and cause a sickness response... .
So, I would pose the question if he thinks over productions of adrenaline/norephinephrin might fit his research model and could possible
look kind of like a virus or look kind of like a bacteria... and cause similar results…?
If so, this kind of research might be appended towards satisfying the bifurcating schools of pathogen mediated CFS vs stress induced immune dysfunction (ala HPA up-regulation affecting this doc's referenced mast or glia affects).