DecodeME - UK ME/CFS DNA study underway

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Michael VanElzakker said:
A GWAS study is something that, all things being equal, should be done. But all things aren't equal and I am not sure it's the very best use of $4million, given all of the clues screaming 'environmental factors.'
This seems to assume that funding a GWAS for ME is depriving other ME researchers from getting funding. But there is no fixed pot for ME research and no reason to think that this will reduce anyone else’s chances of getting funding for ME research. In the long run the results of the GWAS will likely lead to much more, and more useful, ME research being funded, and in the short term I’m not sure if it will have much effect – although I hope it may convince more researchers that it is worthwhile applying to the MRC and NIHR for funding for biomedical ME studies. GWAS is either worth doing or it’s not, and I think we’re all agreed that it will be useful, and it is very good news that it has been funded.
 
Totally agree that funding this study is
  • not likely to be taking away funding that would have gone to other useful biomedical investigations of ME/CFS.
  • important as a foundation study - even if it identifies no genes increasing vulnerability, that is useful information.
Also, substantial funding currently goes to tiny genetic studies and other biomedical studies based on theories built on the belief that there are specific genetic causes (e.g. the Griffith TRP channelopathy idea). DecodeME might rule out or confirm these ideas, helping to reduce the amount of time and research funding spent on dead-ends.
 
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UK Funding for Major Genetics ME Study

Two of the UK’s largest public funding agencies announced this week that they would provide £3.2 million (around $4 million at current rates) for a study that will analyze genetic material from as many as 20,000 people to search for underlying causes of myalgic encephalomyelitis. The Medical Research Council and the National Institute for Health Research are providing, respectively, £1.8 million and £1.4 million to support the project, called DecodeME.
https://www.virology.ws/2020/06/25/...ics-project-my-letter-to-codes-investigators/
 
I'm wondering if anyone could direct me to previous discussions about what a "null result" might mean for the study. I cannot find what I'm looking for through the forum search. I remember such discussion, possibly last year.
 
I would like to know how a GWAS can assist in separating the multiple diseases which are by many thought to be grouped under the ME/CFS label.

When GWAS results are dicussed, what is usually shown is a Manhattan plot. When that plot shows many different gene associations, the usual interpretation given appears to be that there are many genes that each confer a small increase in disease risk and that the disease in question must be very complex.

But what if the disease in question is actually several diseases which aren't as complex and don't have that many involved genes? Is there a way to figure out if certain combinations of genes tend to appear together, indicating perhaps the existence of multiple diseases? Are there other ways to separate such subgroups in a GWAS?
 
I would like to know how a GWAS can assist in separating the multiple diseases which are by many thought to be grouped under the ME/CFS label.

When GWAS results are dicussed, what is usually shown is a Manhattan plot. When that plot shows many different gene associations, the usual interpretation given appears to be that there are many genes that each confer a small increase in disease risk and that the disease in question must be very complex.

But what if the disease in question is actually several diseases which aren't as complex and don't have that many involved genes? Is there a way to figure out if certain combinations of genes tend to appear together, indicating perhaps the existence of multiple diseases? Are there other ways to separate such subgroups in a GWAS?
Not qualified to answer ... but I'm going to have an unqualified guess anyway. Suppose the ME/CFS cohort ended up showing distinctions from healthy controls, but in two or three different areas, possibly overlapping, possibly not. With such a large cohort might that be possible. If so, that would presumably be enlightening.
 
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I would like to know how a GWAS can assist in separating the multiple diseases which are by many thought to be grouped under the ME/CFS label.

When GWAS results are dicussed, what is usually shown is a Manhattan plot. When that plot shows many different gene associations, the usual interpretation given appears to be that there are many genes that each confer a small increase in disease risk and that the disease in question must be very complex.

I haven't even mastered long division yet, which might give you some indication of my grasp of the subject! – but there are many ways to interrogate and interpret data already, and in three or four years' time machine learning will presumably have gone through another exponential expansion in capability. Add to that the fact that other diseases are being studied in the same way, with really strong potential to provide – eventually – additional filters?
 
But what if the disease in question is actually several diseases which aren't as complex and don't have that many involved genes? Is there a way to figure out if certain combinations of genes tend to appear together, indicating perhaps the existence of multiple diseases? Are there other ways to separate such subgroups in a GWAS?

I'm obviously not a geneticist, but I know there are ways to interrogate multi-parameter data from individuals to find subgroups. You might show the results in a chart that looks a bit like a tree (a dendrogram) - with groups with certain similarities branching off. I imagine you'd have to carefully work out which genes to focus on.

tree chart.png
 
"Chronic fatigue syndrome sufferers hope for breakthrough as they fight for recognition", https://inews.co.uk/news/long-reads/chronic-fatigue-syndrome-cfs-decodeme-genetic-research-456045

In 1970, two psychiatrists, Colin McEvedy and Bill Beard, published a report that declared the illness was “mass hysteria”, citing as evidence the fact that many who fell ill were young women.

Neither man had seen a patient.
Nice to see that in a mainstream news article.
 
"Chronic fatigue syndrome sufferers hope for breakthrough as they fight for recognition", https://inews.co.uk/news/long-reads/chronic-fatigue-syndrome-cfs-decodeme-genetic-research-456045
Chronic fatigue syndrome sufferers hope for breakthrough as they fight for recognition
DecodeMe
Sorry to bring up the name thing again (it was bound to happen sometime), but there is a lot of emphasis on 'chronic fatigue syndrome' and minor recognition of ME in these articles and in this one the name of the project ie ' DecodeME' appears to be being misunderstood as 'Decode me'.
 
Sorry to bring up the name thing again (it was bound to happen sometime), but there is a lot of emphasis on 'chronic fatigue syndrome' and minor recognition of ME in these articles
I would have loved it if the project was able to use ME throughout, with no mention of CFS. However, given the situation that we are in at the moment in the UK and globally, we need to use both ME and CFS because not all potential participants will have been diagnosed with, or identify themselves as, ME patients. Therefore we use both ME and CFS in communications to reach as many people as possible, to give us the best chance to recruit sufficient participants.

in this one the name of the project ie ' DecodeME' appears to be being misunderstood as 'Decode me'.
I didn't get that from this article, could you highlight the parts were you think this is the case?
 
Sorry to bring up the name thing again (it was bound to happen sometime), but there is a lot of emphasis on 'chronic fatigue syndrome' and minor recognition of ME in these articles and in this one the name of the project ie ' DecodeME' appears to be being misunderstood as 'Decode me'

True, but I'm inclined to think the most important thing right now is the story. If any of the influential people or organisations who're currently listening actually stay engaged, perhaps that's the time to approach this? The vast majority won't, and so it's arguably a waste of time trying to debate it with them.
 
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