And there are others in your subgroup. But there are others in my subgroup, too, who just don't find any correlation between stress and our disease (other than that having a chronic disease causes a certain amount of stress--which doesn't make this a stress-related disease; and this disease in particular makes certain kinds of stress harder to deal with, especially if there's any adrenalin involved--which still doesn't make this a stress-related disease). And studying the stress connection in your subgroup at this point in time will reinforce negative stereotypes and stymatizing myths, even if that wasn't intended, even if linked to a real biomarker. The psychobabble crowd will either ignore the biomarker or make an ad hoc fallacy incorporating it into their model (like they have done with cytokines). And it still doesn't explain why their background reads like most of it was written by William Reeves, James Jones, or Samuel Harvey. edit: background sounding like it was written by Reeves, etc. was probably an overreaction on my part, due to higher expectations given Klimas and Fletcher's names on the study and given that I don't normally read psychology studies other than those related to CFS, and particularly given the politicized environment surrounding ME/CFS at the current time (and that a huge part of that politicization is the fraudulent idea that stress and maladaptive coping, such as focusing on symptoms [or even on "normal bodily processes" erroneously believed to be symptoms] and believing one has a serious debilitating physiological disease which should be treated with rest/pacing, cause the disease instead of an organic disease process). The paper did leave a lot to be desired as far as explaining what the disease was (which, in my opinion, should be done at every opportunity--although possibly they had a better chance of being published without), and as far as being careful to define what they meant by terms which have standard uses in CFS (standard uses which were established by the Wessely crowd) but which this study was using differently. The focus on excacerbation via stress was understandable given that they were specifically talking about those patients who have a worse response to stress (patients who do exist), but this was still a little confusing to me given the points that 1) they were also talking about a group who doesn't respond to CBT (if you can't remediate it through psychotherapy, it's doubtful that psychosis played any significant role, even in an exacerbatory role) and 2) they were talking about a biomarker they tied to a viral infection (also doubtful that stress plays a role, even in an exacerbatory function).