A.B. said: How difficult is it to isolate the factor that's responsible? Can we look forward to a paper on this in next year?



Sounds like the proverbial smoking gun! Click to expand...

ash0787 said: I think someone said that ron was already working on it, might be possible to figure out using metabolomics ?

cant imagine its going to be easy. Click to expand...

ash0787 said: I think this rules out the argument that a metabolic process within the cells is broken though and the cells are shutting down to prevent damage ( one of the triggers suggested in the dauer state hypothesis ) Click to expand...

Cheesus said: if the two things have the same cause, this would suggest it is something more broadly harmful than an autoantibody. Lipopolysaccharide?



Or perhaps mitochondrial dysfunction has a broad effect across a number of different cell-types...? Click to expand...

taniaaust1 said: what the implications then have been to those we have donated blood too? Click to expand...

Bear in mind that Fluge and Mella already presented (probably) all of this in Norwegian: translated, here . As reported on by Cort in this article , stemming from this PR thread I imagine (i.e. speculate that) their dysfunction measure could have been direct measurements of cellular metabolism, like the methods used by the group that found elevated ATP production. Or, during the conference, Jon D. Kaiser MD mentioned Agilent's 'Seahorse' equipment ( their site with informative videos and diagrams ), which seems to be an off the shelf solution for measuring oxygen consumption rate (and acidity) from a tiny (single) layer of sampled cells, in real time (to assess glycolosis rate, etc).So something like that, no need for Ron's magical new single cell exercise endurance testing gizmo (although that sounds more awesome). This comes from one of the panels which had a video steam up on OMF Facebook page and I made notes on here Ron was also talking there (I think) about 'fractionalising' blood, to hone in on the problematic blood factor (i.e. repeatedly filtering out, separating, half the remaining types of stuff and retesting it's effect, etc). And quite possibly he (and Mella/Fluge) are already into something like this...It would be, and see Cort's last tweet (within "one year" hype):Depending on what kind of factor it turns out to be (if they are right), and Ron also conceded it could be something missing, at this point, then a metabolomics blood test, or even narrower metabolite test, might well be sufficient. But if it's an antibody, or illusive chemical signal, I don't now.I'm not so sure. no cell exists in isolation, the metabolic substrates are mostly shared via blood. And anything attacking/impacting the mitochondria directly might trigger it into some level of cell defense mode, certainly there is a shift away from aerobic mitochondrial OxPhos and that's quite likely to be self imposed to some extent.I think there was someone at the conference pushing for the word "inflammation" to be included in (a name for) CFS/ME? But not acute inflammation, presumably, some more subtle mix of altered cytokines, other signaling molecules, various metabolite balances and immune cell balances and activation states... And then (I'm not sure if there's) overlap with (blood borne) oxidative stress...?Maybe. Maybe the blooming and death debris of blood borne bacteria that aren't as rare as we thought, or LPS via translocation from gut.Immune cells are supposed to use their mitochondria very differently to most other cells, less so for energy, but don't know if that would make them less sensitive to reduced capacity. And other, as yet poorly understood signalling/sensing functions might still be in play...?Myis that the problem won't be infectious in that way, in that a particular blood component (e.g. plasma) might introduce a CFS-like blood borne stress on the recipient, but it would be transient, or immediately diluted away. Red blood cells alone are surely unlikely to cause additional issue (beyond the general "controversy" over efficacy of transfusions ). I don't know if, don't think that, B-cells, for example, are transfused at all (the ones wiped out by Rituximab, with some success). Any that got through would presumably be mopped up by the recipient's immune system. I don't think you can transfer any known auto-immune diseases, for example...