I think I´ve got a fairly detailed description of the problem in my head now (although being detailed doesn´t necessarily mean that it´s right). I will try to write it up so that it makes sense sometime later in the week, and then we can compare notes.
Cool, thanks for the pointer. I see someone has been paying attention to Dr. Younger (re microglia and LDN). I´m glad that he´s going to be there at the meeting in August, as it´s all part of the same puzzle.
Thanks, I think it´s a good idea, but it´s hard to know where best to put it - think I´ll write it as a blog, but they disappear quite fast. I already have benefited from that kind of treatment, as I´m a patient of KDM (who I´m sure has a similar theory, and in fact my ideas have built on what I know of his ideas about the gut and ME), but hopefully it will convince some of those who have never considered the gut as the cause to look into treatments for the gut.
I think large increases in extracellular ATP may be linked to Naviaux's Cell Danger Response. To be honest though that's about as far as my knowledge goes, i'm sure someone with more knowledge on the subject will put me right!
I don't have more knowledge on the subject, but that was my thought too. Osler's Web mentioned deformed RBCs as causing our low SED rates and I saw somewhere (Health Rising?) that shear stress from the RBC deformities cause ATP release. I think if you plop normal cells into our overly ATP'd plasma it sets off their CDR. On the flip side, our cells act normal in control plasma in vitro, but that isn't the same as sending RBCs careening around a vascular system.
If this were actually the case then they would be describing a mechanism. The cause would be what was causing the RBC deformity in the first place.
In response to some of the comments on neuro-inflammation.
I know microglia have p2x & p2y receptors. I was wondering if microglia p2x signalling could translate to peripheral purigenic signalling CDR and cause the hypometabolism. I don't even know if that's possible. But we don't see really neuro-inflammation per se, so the whole thing is even more confusing. We see what should be neuro-inflammation in the Japanese study and in the consistent rCBF finding in the brainstem. But then, not anything consistently remarkable in the cerebral spinal fluid.
And we all feel like we have neuroinflammation! Makes me wonder if the microglia have a state other than M1/M2 that activates the CDR but not the production of cytokines, chemokines and other stuff the churn out.
If there is a genetic tendency towards ME then I may of found my pathway,there maybe many other pathways
If missing foxc1 (still waiting for results) this has an effect on many other genes but I’ve picked out the ones that seem relevant hsp70 and foxo1a
EBV also lowers foxo1a further