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They included '6 studies', 4 of which are papers from the PACE trial (I wonder if they fully realise this is the same study/trial?), one is the GETSET study and one is the review of patient surveys by Keith Geraghty.

You posted about age of onset. I was wondering if you have data on actual age at the time of the survey and if the cohort from the Netherlands was younger than that of other countries?

I wonder if increased leptin and fatty acid-binding proteins (FABPs) are simply due to ME/CFS patients having relatively more fat. Patients and controls have a similar BMI but the composition of their body mass might be different: more fat and less muscle for ME/CFS patients?

Thanks for checking! I hope will see more studies like this that test large amounts of data and make it all available online. It offers so much more possibilities for us (and other researchers) to check particular results and compare them to other studies. Making data available online is a...

There is the group of Sanne Nijhof and Elise van de Putte who developed FITNET, an online and quite assertive form of CBT. It aims at full recovery, includes graded activity and is similar to the CBT version of Bleijenberg and Knoop. Their team works at the WKZ in Utrecht which is probably the...

Could you explain this a bit more? I think it might be hard to tell if improvements are due to exercising or the improvement that made exercising possible in the first place.

Complement C3 has come up in a couple of studies before, for example this one: Complement Component C1q as a Potential Diagnostic Tool for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Subtyping - PubMed

Also see no good solution. I kept them in, hence why there are two datapoints for, leptin or for 'Fatty acid-binding protein, adipocyte'. For example, if there are two rows for leptin in the Hoel dataset and 1 in the Germain dataset, it would duplicate the latter and have 2 rows for leptin in...

The fold changes are not symmetric around 1. It's a ratio of the abundance of the ME/CFS group versus controls. So if the ME/CFS group had higher values, the ratio could be somewhere between 1 and infinity. If the ME/CFS group had lower values it would be somewhere between 0 and 1. That...

I used an inner join with as key 'TargetFullName'. It's possible that some proteins were lost because their name wasn't identical in both datasets. EDIT: perhaps we should just use the one that gives the highest amounts of rows?

Attempt to highlight some proteins that were increased in both datasets (leptin appears twice because it was measured twice in the Hoel study):

Had a go using this method but I'm far from the best coder so might have made a mistake. I got a relatively weak correlation of 0.33. In the Hoel et al. dataset there were 845 observations with an adjusted p-value below 0.05 and after an inner join with the Germain et al. dataset there were 672...

Perhaps we could first filter based on small p-values in the Norwegian study and then compare how the fold changes of these proteins relate to those the Hanson study.

Was looking at how the results of this Norwegian study (Hoel et al. 2025) could be compared to the aptamers study from the Hanson group (Germain et al. 2021) but ran into a problem of not having a good effect size to compare. The fold change simply gives a ratio of the abundance of the protein...

The fact that age and BMI have a large influence on leptin levels, doesn't necessarily exclude that ME/CFS has an additional effect on top of those factors I suppose (it does probably mean that matching of groups is really important). It's notable that it keeps coming back in different studies...

For what it is worth Leptin was also increased in ME/CFS patients in this group. Here's my own plot of the raw data (I used Aptname seq.2575.5) The authors do note that much of the variance in leptin was explained by BMI and sex:

One of the interesting things is that Jos Van Der Meer supported the findings from Visser/Van Campen for example on tilt table testing and cerebral blood flow and that he was critical of the insurance physicians who dismissed the symptoms and disability of ME/CFS patients.

Would it be useful to get an overview of findings on interferon-gamma in ME/CFS research? It seems to have come up quite a few times. Or would these results not matter too much because the theory only assumes local increases of cytokines?

Currently the hypothesis seems quite flexible with lots of connections not yet filled in yet. I wonder if there are any tests, observations or experiments that would not fit or refute the hypothesis? Also interested in the sentence about intravenous immunoglobulin because quite a lot of...

Would be good to have a reference for this. Anorexia nervosa probably has a high female predominance and depression and anxiety also affect about 2 times more females then men if I recall correctly.