Disappointing to see. They did not account for lack of blinding and subjective outcomes as a limitation. Same with all the other issues with the PACE trial.
I also wonder how they ended up with a short-term effect of 6.93 points on the Chalder Fatigue Scale (CFQ), because the Cochrane review...
Reminds me of that Cochrane review on exercise for chronic low back pain. There were like 270 trials already and new ones kept coming so the authors couldn't keep up and review them all. In total there were like 400 trials on this topic! This obviously has nothing to do with science.
Exercise...
Thanks, I haven't looked at this in depth, but noticed this in the introduction:
Doesn't the score you calculated then mainly reflect the (arbitrary?) weights you gave to the categorical variables 'minor', 'moderate', 'major'?
For example, I don't see why the gap between minor and moderate is...
Interesting study.
Suspect it's mainly due to not having a control group.
When looking up Vasopressin, it seems that it is difficult to measure due to low levels and a short half life. The main finding of this paper was that 82% of patients did not have detectable levels of Vasopressin...
Thanks very much, means a lot coming from you. Your posts and analysis really help me in understanding complex studies. Also thanks for highlighting the empty spaces - fixed it.
Not familiar with this: is it a measure of how well datapoints have clustered into separate groups?
EDIT: and do the most left points corresponded to M9 (degradation of ubiquitinated proteins) and M20 (synaptic function)?
Haven't read these studies but noticed that most found substantially higher estimates than 18% for Long Covid. It's mainly the Xie 2024 Veterans Affairs study that is dragging the estimate down because it had almost half a million participants.
What kind of antibody theory are you thinking of then for this distinction to matter, the FcγRI hypothesis by Jo?
In the later section we also focus on CD20, CD38 and immunoadsorption trials, so these would affect all antibodies.
Autoantibodies are just antibodies that target one of your own proteins, rather than a pathogen. So think it's also correct to just say 'antibody theory'.
Yes but with negative results there will never be 100% certainty that a hypothesis is refuted so suspect that some group will not give up on...
We just published our review of the most interesting ME/CFS studies of 2025 and shared it in this thread:
2025: looking back on a year of ME/CFS research | Science for ME
We've published our review of the most interesting ME/CFS studies in 2025. Feels like it was a fruitful year where we made some modest progress, mostly because of DecodeME. interested in hearing what others think and if perhaps we missed an important paper.
Here's the link to the full blog...
Good point. This recent PNAS paper argues that the cells likely still exist but have been reprogrammed epigenetically.
Epigenetic silencing of selected hypothalamic neuropeptides in narcolepsy with cataplexy | PNAS
So if that's the case, the question would be: what could be doing something...
Also think this has the potential to be an important finding. Was anyone besides Cort able to watch the presentation?
Suppose there is this major depletion of CRH neurons: wouldn't this be visible on brain scans or is the region too small to be picked up by the tiny brain scan studies that we...
For the other mutations listed in the table, the patients were heterozygous so they had only this mutation only once. Suspect that most diseases that they associate with these mutations are recessive: they only manifest if people have two of these mutations without normal back up copy.
So not...
Am confused because if these identified mutations are truly pathogenic, they would be a major finding and tell us something important about common misdiagnosis of ME/CFS pathology.
But looking up mutations for the first gene, KCNJ18, shows that are "seldom pathogenic" as this paper concludes...
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