Apologies in advance for my very limited understanding of the principles underlying the below science. After recently relapsing following a 15 year remission, I've spent the past few weeks catching up on research and reading about the great work of Dr. Davis, Dr. Naviaux, and Dr. Fluge/Dr. Mella. In doing so, I keep trying to reconcile the idea that there is "something in the serum", which is causing a cell danger response with Fluge and Mella's findings related to likely autoimmunity and endothelial dysfunction. My question is could autoimmune endothelial dysfunction be the trigger that leads to the cell danger response? Perhaps endothelial dysfunction results in a lack for oxygen (see Fluge/Mella patent involving Imdur), which triggers the cell danger response and resulting metabolic problems. Further, could "the something in serum" be an intentional signal sent to protect tissue from a endothelial dysfunction induced by a low oxygen state? Assuming this were the case, perhaps PEM represents the body doubling down on the signal in the serum when exercise further reduces oxygen levels.