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Yeah, not really a surprise, the way he romanticized his descriptions and case studies, things that were hard to confirm by others, it already gave the impression that there were many embellishments.

The researchers have a Dutch grant for ME/CFS research: https://www.zonmw.nl/nl/artikel/blog-een-behandeling-op-maat-met-immuunhandtekeningen-voor-mecvs Don't quite understand why this also showed an interferon difference between groups, given that it was mainly meant as a control condition.

Not really, because the co-occurrence of concepts is probably based on the text of the manuscript, not on the actual data. Suppose that several studies found a slight increase in metabolite X, but do not mention it anywhere in their paper, it's only visible in the supplementary data: would the...

Not far, think I didn't manage to do the FINEMAP.

The statistical tests used age as a covariate, but suspect that the data points shown do not take this into account. The HC group had a mean age of 31, and the LC group of 51. They also don't give much info about how the patients were selected. Suspect the study was done on patients in...

This isn't the first time that we've seen questionable papers from this group. See: Comparing DNA Methylation Landscapes in Peripheral Blood from [ME/CFS] and Long COVID Patients, 2025, Peppercorn et al | Page 4 | Science for ME

The raw data of the experiments, for example, in CSV format. A big problem I see is that almost all studies misrepresent their data in the abstract and text (to make it look like a bigger deal than it is or to promote the authors' favoured theory). So I think machine learning/AI/network...

Seems like a useful commentary. If I understand correctly: - The groups are independent; this wasn't a longitudinal study following the same people over time - Although there were differences between groups, they were relatively modest and still within normal limits - The difference might be...

Thanks for trying this. I gave up because my coding skills are rather amateurish. There was also the issue that I wouldn't be entirely sure if it worked or if I had misapplied it somehow. I was hoping that either researchers would use this in future publications (e.g. the official DecodeME...

Thanks. If I understand correctly, though, your network analysis is based on mentions in abstracts and the text of a publication and not on the actual data of studies?

8/13 trials were from China.

Was curious what would happen if ME/CFS patients got interferon treatment. Would it make their fatigue/malaise even worse, would it have less effect, or, if this pathway is involved in ME/CFS pathology, might it help correct it or induce inhibitory pathways? Found this 1993 report on...

Yes would be interested. Had plans to write blog posts about the history of ME/CFS (there seems to be a lot of myths about it), but never got to it. Perhaps somewhere in the future.

Same situation here.

Looks like a complex analysis that must have been lots of work (kudos to the authors)! But I have my doubts about how relevant the results are. In my view, it's mainly the comparison with controls that matters, while this study seems to have focused on correlations with SNPs and metabolites...

I suppose their combinatorial analysis can be useful to get new or clearer findings, but in this case, it seems to have made things more complicated and muddled. Their disease signatures map to 2,311 genes, while humans only have approximately 20.000-25.000 protein-coding genes.

The paper writes: But on X someone commented: "There is already a known autoimmune disease of the CNS, where autoantibodies directed against AQP4 its named Neuro Myelitis Optica (NMO) The autoantibodies were discovered in 2006/07." "The AQP4 autoantibodies causes extensive and severe...

Yes, so these are probably too important to be defective in ME/CFS; otherwise, we would see other abnormalities in patients. So it should likely be something more specific to this pathway that is defective in ME/CFS, and if DecodeME results are to be believed, might be more on the brain than...

Yes, that's also the explanation I was thinking of: that the sickness behavior pathway involves proteins that are too important elsewhere in the body, so that mutations aren't viable. But that begs the question of why we don't see clear immune dysfunction elsewhere in ME/CFS and why DecodeME...

These seem like the main results: Self-reported activity was the strongest predictor but there was no relationship between objectively measured activity and fatigue changes: Some also suspect that the effect can be explained by people with depression improving with CBT, but not LC. This also...