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Ok but still a bit strange to see an opinion piece like this that isn't based on a new study or news fact by people who have little expertise in ME/CFS research. Perhaps it was in response to the news articles about Maeve's inquest and the publication got delayed?

This is disappointing to see. None of the 4 authors have actually done much research on ME/CFS so I do not understand why they are commissioned to write a controversial piece like this. Perhaps some lobbying went on behind the scenes or is there someone at the BMJ who is entirely on Garner's line?

On the other hand: the AUC is measured against current diagnostic practices of ME/CFS which may not be very precise anyway in terms of pathology. Suppose only a small subgroup has pathology involving synaptic function, then the maximum AUC score would be quite low. So perhaps what matters most...

Interesting point. Not speaking from expertise or experience but I would think these networks are sufficiently complex so that it still means quite a lot if multiple genes from a pathway are highlighted. I suppose that having an abnormal result for one gene highlights the pathways it is...

Thanks. I think you might get better results if you don't mention ME/CFS and just ask it if there are any patterns in these genes that were found to be abnormal. Otherwise it will try to connect it to popular memes in ME/CFS research such as inflammation, mitochondrial dysfunction etc. I tried...

Excellen thanks @forestglip ! On Twitter the first author Sai Zhang also briefly mentioned that they are working on the part of how the ME/CFS genes correlated with self-reported ME/CFS in the UK Biobank.

Yes suspect that the cohorts were simply too different. Half of the pneunomia cohort was above 70 years, compared to roughly a third for COVID-19 and only a sixth for Influenza.

I think this is the main finding of the paper but wonder if it may simply be a longer-term consequence of less extreme deconditioning. For example that the longer you remain inactive the more type 1 fibers are affected relative to others. The bed rest was a short period of extreme inactivity...

Yes, a bit. The main caveat is that past literature was mainly about head-up tilt table testing which usually show higher heart rate increases upon standing than this (NASA) lean test. In this study only 4 out of 112 had abnormal tests, including one with a heart rate increase > 30 bpm and 2...

Some more references: Bias caused by reliance on patient-reported outcome measures in non-blinded randomized trials: an in-depth look at exercise therapy for chronic fatigue syndrome: Fatigue: Biomedicine, Health & Behavior: Vol 8, No 4 Assessment of the scientific rigour of randomized...

I think Leptin (LEP in figure 2B) is also showing up again, as in the study by Beentjes et al?

The lifelines cohort is very valuable. I wonder if they could retrospectively try to make the definition of ME/CFS more stringent to get something below 1% prevalence. They could for example make the CDC symptom inventory items for PEM, unrefreshing sleep and concentration problems mandatory...

I suspect the ME/CFS prevalence in this cohort was largely based on the CDC symptom inventory. This Wiki for the Lifelines project provides some more information: https://wiki.lifelines.nl/doku.php?id=cfs_diagnostic_score https://wiki.lifelines.nl/doku.php?id=fatigue_cdc

The supplementary material states: So I suppose we have to wait until that other manuscript is published until we know more how the Fukuda criteria were assessed (my guess is through questionnaires rather than a medical examination). The paper itself does not comment on the remarkable high...

The authors clarify that they could not distinguish between genetics and shared environments. For most disorders the recurrence risk ratio was similar for first or second degree relatives and the authors argue that this suggests that the recurrent was likely not due to a shared environment...

If I understand the data correctly, having one (or more) first-degree relatives with ME/CFS makes it 2.23 times more likely that you have ME/CFS compared to the general population (which includes those with first-degree relatives with ME/CFS).

They said they evaluated the Fukuda criteria yet 4.7% of the more than 150.000 people in the cohort had ME/CFS (Table 1)? That seems an unreasonably high estimate.

I suspect it is this study: Familial coaggregation and shared familiality of functional and internalizing disorders in the Lifelines cohort, 2025, Bos et al | Science for ME

Thanks for tagging me. Interesting that cerebral blood flow and small fiber neuropathy showed no significant differences. The sample size was really small though. Almost as if the added the conclusions of a different paper, it doesn't match what the study actually found.

Interesting study. Sad that the concordance between the different ME/CFS pieces information in the UK biobank is so low. For example: 2,312 (0.46% of the 0.5 million biobank participants) self-reported a clinical diagnosis of CFS (C1). But of these, 28% also reported 'good' or 'excellent'...