Hey guy, So we know from the great research in Norway that a big driver of our disease is that pryruvate dehdrogenase is inhibited. This nearly shuts down glycolysis and then there is not enough acetyl-CoA the go into the Krebs i believe. In a nut shell this results in a big lack of ATP and we all know what that does to us. My question to you is does anyone have any remote idea why the heck this enzyme is shut down!??? I know too much NADH will shut it down when there is plenty of it in supply but I think thats not the case because I've heard NADH is low in us and it's way, way too simply. Does the mTOR gene expression maybe have something to do with this. I know it's a hard question but I'm dying to hear your thoughts.