Just so people trying to follow along don't become confused - transferrin isn't made in the bone marrow its made in the liver, I think everyone is just speculating whether this alleged observation of ME/CFS reflects their own situation.
Did he cover something that unites LC ? well he said that the two diseases appear to be separate but could be 'looping around' in some cases, possibly what he means there is the dysfunction of the endothelial cells, or the changes to fibronectin which he says perpetuates the CDR in some sort of feedback loop ( but the change in fibronectin has to be initiated by several other stages by the sounds of it ). He did say however that some people with LC that have neurological issues also exhibit some of the markers that he found, does that mean that those people also or alternatively have CFS ? its hard to say because we don't have biomarker for long covid either and we have to assume they did the patient selection correctly and the people had many symptoms not consistent with ME/CFS but also something beyond just 'damage' caused by the virus. That might be what he was getting at though in terms of something that 'unites' the two, and that would be my guess.
With some of these markers I wonder if the effects could be disproportionate to the magnitude of the deviation from normal, or alternatively if mixing a few people who were misdiagnosed or didn't have true ME/CFS into the studies could have made the results seem insignificant ( because the deviation isn't large e.g. 75 vs 100 ).
