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In his large study of glandular fever, Peter White found that days of bedrest was a predictor of developing CFS. Bedrest is most obviously a marker of severity of illness, though Peter, White. chose to interpret it as a sign that excessive resting was a risk factor.

From a recent review on LC: The impact of vaccination on long COVID symptoms in people who had already developed long COVID differs among patients, with 16.7% of patients experiencing a relief of symptoms, 21.4% experiencing a worsening of symptoms and the remainder experiencing unchanged...

Joshua was working in Chris Ponting’s group, and his PhD was jointly funded by Action for. ME and the office of the Scottish chief medical officer. Kudos to Joshua and all involved. (With a nod to the company that did a lot of sequencing of Tcell receptors genes, Systems Biology Laboratory,).

If I’ve understood right, using best practice mathematical and immunological methods, Joshua did find a single genetic difference that was significant in Uk Biobank: for males with ME/CFS within the gene PDE10A. He also helpfully ruled out a number of other findings. This is what our field...

Thank you, I’m glad the issue will be clearly raised. Like many others, I’ve achieved that short term gain under the encouragement of a therapist, which ended in long term loss.

I know you and Adrian do, but unless the research group absolutely locks in subjective outcome measures to use only in blinded trials, I think the sf-36 is not a suitable measure. We'll just end up down the same rabbit hole as before.

Thanks. I would much prefer objective measures. but does the research group understand the prolem of using subjective outcomes in non-blinded trials?

It would be helpful to know the purpose of using the sf-36 scale. and apologies if this is posted earlier, I haven't been able to read the whole thread.

SF-36 Physical Function subscale I actually think the SF 36 scale provides the best available self-report measure of physical function (I'm not keen on the rest of it). It is quick to complete and can be done online and by thousands of people without access to special kit. Plus, it's widely...

I’m not sure that such hypothesising based on a large number of generic symptoms gets us anywhere useful. It’s easy to fit just about any narrative to any broad collection of symptoms. We need hard biomedical evidence to identify causes. And I suspect it’s more productive to go from evidence...

edited I feel I and others with severe ME have a lot to offer ME research projects. At no point in my illness could I have ever done 4 hours, but I have been able to contribute to DecodeME, and do sometimes have different perspective and expertise from others with more energy. We need full...

@FMMM1 The approach uses combinations of features (in this case between three and 5 SNPs) to create “disease signatures“ that identify a subgroup of patients. It’s very different from traditional GWAS, which look at the difference between individual SNPs for the entire group. You could see it...

Key section from the published paper. There are a number of limitations with this study discussed above, and a larger, more detailed longitudinal patient dataset is likely to significantly improve the results. For this reason, we aim to replicate and extend the results from this UK Biobank...

The full paper has now been peer-reviewed and published (open access). Genetic risk factors for ME/CFS identified using combinatorial analysis Abstract Background Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating chronic disease that lacks known pathogenesis...

The approach of the Edinburgh Genetics Centre of Excellence and aim of DecodeME is the first find genetic clues pointing to the causes of ME. Then go looking for researchers to bring their relevant expertise to pursue those clues. Apart from anything else, actually having evidence that a...

Has this been published yet? It would be good to have more detail. E.g. anything over 3 months to recovery I woulc call a relapse. But I am pleased they are finally reporting data. I'd also be interested to see the severity of people who volunteer for CPETs - how representative are they of PwME?

Despite being in the field for at leat a decade, CPET researchers are still failing to collect and publish harms data. That is as unacceptable for biomedical research as it is for psychosocial research.

I think this is the first specific study looking at ethnic differences, which is is a very important area. but I'm not sure how much we can conclude from these results. It's a very small study, and we don't know if patients of different ethnicities are equally representative of their ethnic groups.

The Jason 1999 community prevalence study was based on just 32 CFS cases: 0.42% prevalence with an overall 95% confidence range of 0.29%-0.56%. The confidence intervals for male and female prevalence separately will be even wider than this so that the sex ratio can tell us nothing reliable. I...

[Re my comment about GWAS and the 'role' of IL-10 in rheumatoid arthritis and other autoimmune diseases] Oh dear, I can clearly no longer rely on my memory to accurately recall stuff like this! Thanks for pointing out my error. I should have referrd more broadly to the iL-23 pathway, where...