Hello everyone, Im new here so Ill briefly introduce myself. Im a retired aeronautical structural stress engineer (hence my nom de plume). My daughter was diagnosed two years ago with ME/CFS and Ive devoted the intervening time to studying the condition. Ive studied all the big names associated with the disease, but did not discover the work of the good Rich van Konynenburg until a couple of months back, sadly. Quite a revelation! This posting is a draft submission for peer review. I have not included any references at this stage. So here we are, the three Ps, predisposition, precipitation and perpetuation, the first and last of which are well understood and described. So what leads to the final precipitation of the condition? Ive dug out some very interesting stuff on the conditions that obtain prior to precipitation in a quest to answer my ongoing question as to why PWCs all have (very similar) gut dysbiosis. Stress seemed to be the most common link, so my Google Stress gut flora gave me the answer, though not the expected one. All hits were about IBS, not CFS. Well, well It turns out that stress destabilises glutathione, the HPA axis and of course, cortisol. This plays havoc with the gut flora. Question answered. However, it also indicated that PWIBS (sorry about the jargon) suffer the same physiological conditions as obtain in post-precipitation (i.e. chronic) ME/CFS. So far then: Many PWCs also have IBS but not all PWIBSs have precipitated into the CFS state although the pathologies are very similar if not identical. It must be a matter of degree, then, if both conditions display loss of toxic protection from glutathione depletion, and H2S poisoning from the gut flora. So- If we turn the degree up a couple of notches until CFS precipitates, what changed? Well, the toxic load of course. From then on, as is well documented, the condition is self-perpetuating. Its said that what turns it on will turn it off. Efforts to supplement d-ribose to turn on ATP production meet with very limited success. The much more successful efforts to re-start the methylation cycle nevertheless do not produce a universal cure. Should we not therefore start by addressing the toxic load? That is, after all, where I believe we came in. If Ive screwed up somewhere on this, start shooting now! If I havent, then I suggest that selenium, NAC, MSM and ALA are the necessary starting agents though please DONT TRY THIS AT HOME! Dosages and phasing (if necessary) need to be determined by one much more knowledgeable than I.