I am afraid the treatment regime pushed by Patterson is utter bs, I hope I am wrong obviously.
Apart from that, I believe endothelitis, capillary leakage and straight up destruction (petechiae) of blood vessels is a key driver of this disease, so he is looking in the right direction, downstrean pathology of this is very obvious: tissue hypoxia, mitochondrial dysfunction, etc.
It would also make sense from the high eds phenotype prevalance perspective, as people with these phenotypes "start the game with an already taxed system", especially when it comes to bloodvessels ...