Search results

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...

those are all good points. I'm not at all wedded to Norway or any particular country. The big advantage Norway does have is a well respected health and health data collection system. This would make it faster and cheaper to set up any study, but the most important thing is to get reliable data...

I agree that the priority is finding core mechanisms and I understand the scepticism over genetic studies But people have been following hypotheses for mechanisms for decades and we've got nowhere. Genetic studies are different because any DNA differences are causal, so provide better clues...

2. Getting serious about epidemiology We need to kneel down the epidemiological findings to date on prevalence and incidence (onset). Personally, I think Norway might be the ideal place for this because of its comprehensive health system and quality of health reporting (many cohorts, e.g...

Here are my two suggestions. 1. Prospective study: infectious mononucleosis (and Covid?) As suggested above. Think of this as Dubbo 2, recruiting people at the point of diagnosis with glandular fever/infectious mononucleosis. Then follow-up detailed follow-up for two years, checking people's...

As for any other rare variant whole genome/exome study, the aim is to find mutations with a big effect, usually affecting the protein normally made by the gene. That then provides a massive clue as to the underlying biology: 1. It could point to the biology in rare cases, tiny sub-groups of ME...

Agreed. Can you say how that would work? I've been tracking this in studies for decades and have never seen good evidence for anything much below 80%. Could you explain more? I think the Bakkens study had over 5,800 cases, taken from a retrospective analysis of the entire Norwegian health...

DecodeME is banking half of every DNA sample so that a future whole genome sequencing study can be done that will pick up these rare mutations. And I agree, spending some of the hypothetical buddies on this would be a smart move. I agree and include prospective studies of glandular fever etc in...

No, really: @Veronica Ashenhurst is a poet with severe ME. Her poem “Redefining Her” was chosen as a finalist in Health Affairs’ poetry contest. It’s a “found poem,” meaning that text from another source is used to create poetic meaning. Specifically, in writing the poem, Veronica restricted...

Thanks :) To be fair to the authors, they used an omics approach as a broad sweep (given how little we know), as a way of identifying areas to worth pursuing. The discussion section says: "our analysis discovered upregulation of chemokine/cytokine pathway genes in patientderived monocytes as...