I could be wrong, but I believe naloxone isn't really orally bioavailable. Most of the very limited research focuses on low dose naltrexone (LDN) instead, naltr

I could be wrong, but I believe naloxone isn't really orally bioavailable. Most of the very limited research focuses on low dose naltrexone (LDN) instead, naltrexone being another opioid receptor antagonist with paradoxical properties, namely analgesic and anti-inflammatory properties, at low dosages. There could be a link here, although it is tenuous and purely lay speculation. ER stress is discussed in the article: >Both S1 and the people with ME/CFS had biochemical signatures of ER stress in their muscles, and treating S1’s cells in a dish with a drug that blocks ER stress lowered WASF3 levels and restored mitochondrial function. On the flipside, using toxins to artificially induce ER stress in cultured cells or in mice caused a rise in WASF3 levels, Hwang says. LDN has been found to be quite effective in alleviating ER stress specifically in the epithelial barrier in IBD [0], rather than the ER stress - WASF3 levels being investigated in muscle cells in the above article. Certainly worth investigating. And, as noted in the article, the WASF3 angle is merely one potential pathway of the disorder. [0] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5845217/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5845217/ >Low dose Naltrexone induced clinical improvement in 74.5%, and remission in 25.5% of patients. Naltrexone improved wound healing and reduced ER stress induced by Tunicamycin, lipopolysaccharide or bacteria in epithelial barriers.