Nature-Translational Psychiatry: Different protein expression in saliva of people with/ without CFS.

[M Paine]

I'm not qualified to ask these questions, so if I'm totally off course, please be polite.

Is downregulation of NADH a metabolic adaptation to reduce the generation of ROS in order to prevent what the body believes is further damage? Why does this persist so long, and what finally stops it (if it stops at all)? Is there something like a glyoxalate cycle in humans which is used as compensatory/alternate pathway when downregulation of NADH (hypometabolism) is required/initiated?

Accepting that NADH is in effect, upregulated... your thoughts on the role of ROS seem to be shared with the authors of the the Nature paper just released (Index markers of chronic fatigue syndrome with dysfunction of TCA and urea cycles) which also looked at some of these Metabolic processes. In specific, aconitase activity.

They wrote:

"Aconitase includes a 4Fe–4S cluster and is vulnerable to oxidative stress. In addition to the previous study, the findings that CFS patients who were recruited from the same hospital as the present study showed higher oxidative stress relative to healthy controls [34] supports the hypothesis that the predominant reduction of isocitrate may result from the inactivation of aconitase via chronic oxidative stress"