With CFS there are no established biomarkers for CFS (repeat CPET was thought to be one, but the recent MS study didn't replicate the earlier findings). .
I'm not usually on the forum these days but this statement you made stands out.
Which study are you referring to? I'm genuinely curious as I collect these articles.
Because if it is
this 2017 one, what it shows is that in MS patients, MS subjects were able to reproduce their cardiometabolic parameters from one day to the next whereas ME/CFS patients were not able to. The conclusions from this study were:
On day 2, both CFS and MS had significantly reduced max workload compared to HC. On day 2, significant differences were apparent in WL between CFS and CFS HC (93 ± 37 W, 132 ± 42 W, P<0·042). CFS workload decreased on day 2, alongside a decrease in HR but with an increase in V˙O2 (ml kg min-1 ). This was in comparison with an increase in WL, HR and V˙O2 for CFS HC. MS demonstrated a decreased WL compared to MS HC on both days of the study (D1 81 ± 30 W, 116 ±30 W; D2 84 ± 29 W, 118 ± 36 W); however, patients with MS were able to achieve a higher WL on day 2 alongside MS HC.
"These results suggest that exercise exhibits a different physiological response in MS and CFS/ME, demonstrating repeated cardiovascular exercise testing as a valid measure for differentiating between fatigue conditions."
Note that the way they designated the healthy controls in this study could be confusing -- HC refers to healthy controls with CFS HC meaning controls matched to those with CFS and MS HC referring to healthy controls matched to MS. It adds to the 5 published studies from 4 independent research groups showing that 2-day CPET measures are not replicable in ME/CFS patients although the exact cardiometabolic measure (V02 max vs. max work load vs. workload at anaerobic threshold vs. VO2 at anaerobic threshold) and the degree of drop from the first day to the 2nd might be different. There are also results from 2 other groups which are similar but unpublished.
In fact, another review paper just came out recently -- not about ME/CFS - but verifying the small degree of difference between 2 different CPETs in healthy people and other conditions. And in 2015
there was a paper on sarcoidosis -- again unrelated to ME/CFS - showing that repeated CPET was not useful as the results did not differ much from one day to the next.
In terms of what is being talked about generally, I trained at the university where the "biopsychosocial" model of health originated in the 1970s -- and so, coincidentally, did 5 of well-known ME/CFS clinicians/ researchers in the US -- so it permeated the years I spent there, even 3 decades later. (Anyone who can name that school without looking it up gets a gold star!) And yet all of us who are in this field and trained there do not view ME/CFS as a psychiatric, psychological, or psychosomatic condition. (By the way, if the word psychosomatic is used "loosely" to get at interactions among these 3 different realms, why is it we rarely see congestive heart failure or rheumatoid arthritis, etc. termed as "psychosomatic" conditions?)
The model itself is not wrong but it's a matter of what is emphasized where, when, how, and why. For instance, many medical conditions could benefit from stress reduction or illness coping skills but we would not treat heart disease, chronic lung disease, cancer, or stroke without any medications. And these patients would feel justifiably incensed if doctors and researchers only focused on the "psycho" and "social" aspects to the exclusion or downplaying of the "bio". Why is it that psycho or social aspects are always the ones emphasized just because we don't know enough about the bio of a any condition?
That's what has happened in ME/CFS of the last few decades and it's only starting to turn the tide a bit now due to the efforts of many, many people around the world. If you are not familiar with the history of ME/CFS, please consider learning more about it -- one source, although it only goes up to the mid- 1990s, is
Hilary Johnson's Osler's Web.