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I'm not aware of any examples where that has happened. Just hundreds of papers going nowhere. all of which is true. But none of it takes us any closer to getting answers about this illness. I'm afraid I've lost patience after 30 years and I want researchers to raise their game. They've been...

I appreciate the problem, but this approach has got us nowhere in decades, and I'm not sure that things will ever change. We need better science to make progress ,otherwise the list of weak biomarker claims will just grow. I've been ill for over thirty years and am desperate for real progress...

I would love to see researchers come together to agree standards for ME/CFS biomarker research. This might include minimum sample sizes, including a validation cohort, at least one disease control group and being clear on the degree of biomarker overlap between patients and others. We've seen...

@Jonathan Edwards PS the Andrew German/Maureen Hanson single cell RNA sequencing study also highlighted monocytes, I believe.

That's an interesting point. I had assumed that the vaccine was intended to stop EBV ever infecting; if it merely delays it, it would lead to more mono, so presumably more ME/CFS. And still people would get MS, just delayed. That big EBV/military study showed that EBV was a necessary step for MS...

Summary of a long post: Do the cases selected in the study appear to be severe enough to qualify for ME/CFS? For S-ME/CFS yes, but this seems less plausible for the ME/CFS group. The previous post argued that the SF36 questions and thresholds used in this study would pull in those who hadn't...

I'm concerned that assessment of "substantial reduction in activities" has included those too mild to have ME/CFS, which would weaken the study if it is the case. The authors used thresholds and scales validated in an earlier study that compared accuracy of CFS cases vs negative controls, which...

So good to see this published. The field would be stronger if we had more work like this.

I'm working from memory, which is never a good idea for me. But I'm fairly sure that the 2022 study captured severity measures, so if they wanted to define severe ME/CFS , they had better ways of doing it. I'm sure this was discussed at length on the thread for the original paper

this is new to me, and interesting. Having two age peaks is very unusual for diseases, and the examples are clustered, applying mostly to some cancers (mostly pretty young and pretty old) and quite a few autoimmune diseases (where there's more variation in the age of peak onset).

That's an incredibly helpful perspective, thank you.

This is really interesting approach, and I'm looking forward to seeing what you come up with. Just one question: are gene expression levels normally distributed? I thought they weren't, and if not, are Z scores appropriate? Thought I'd toss that in, but I am seriously out of my depth.

It's out there somewhere – not definitely published, but try this paper (1st 17 K questionnaireresponders ) https://pubmed.ncbi.nlm.nih.gov/37881452/

It's great to have some data on this,but the NIHS survey is highly questionable because if you ask a general audience if they have an ME/CFS diagnosis, you get an implausibly high prevalence rate (1.7% here - probably <<0.5% is true with a diagnosis). Luis Nacul did a follow up study on a Canada...

I'm not even beginning to keep up, but how is it possible to have more than twice as many double-refined signatures as cases?

There is quite a lot of evidence that severity of illness is important in the risk of ME/CFS post infection: 1. The Dubbo study (EBV, Q fever and Ross River Virus, RRV) found that the severity of initial infection was the only predictor of CFS at 6 months. 2. Peter White found that days of bed...

I certainly am, thanks. Unfortunately, there is precious little reliable data (and often no data at all) on rates of mono in different countries. We probably have better data in the UK than anywhere else, and it's not brilliant here

Is this cultural or geographical, relating to the prevalence of mono? But there is good evidence that mono is more common in teens, and as we know mono is a trigger for ME/CFS, it seems logical that higher rates of mono are linked to higher rates of ME/CFS in teens. But people may also be more...

That's fantastic. Thanks to you and to them.

Good to know ;-). I thought we also needed people studying the biological role of its protein product. It's great that a research team are focusing on a key finding from DecodeME. Do you know how the geneticists will be approaching this e.g. looking at gene expression or how its genetics varies...