The Netherlands - €28.5 million ME/CFS research program - ZonMW funding awards announced April 2023

Also, as with all these sorts of posts. If you're well enough to leave a comment and possibly retweet that would be hugely helpful. The algorithm pushes up posts that are liked, but exponentially more if they're retweeted or commented on.

 

Post copied and reply moved from the news from the Netherlands thread.

There was a short update on the ZonMw ME/CFS program. Sjaak de Gouw will be the new chair of the program.
https://www.zonmw.nl/nl/nieuws/mecv...uwe-richtlijn-mecvs-en-1e-projecten-van-start

 

Lots and lots of lip service is what I'm reading on that page and the pages it links to, with nothing tangible to back it up. I hope Sjaak de Gouw can do a full reversal to the agreed methods of selecting programs for funding, but I'm very skeptical.

 

Do we have on these forums a thread which outlines all the different groups in which the BPS cabal is organized? And if not, where would be the appropriate place to start one? I've noticed the same people organize in different structures, the Oslo group, COFFI and at least one other. I think it might be helpful to keep documentation who's affiliated to what group as there might be a lot of overlap.

It might make it easier to spot conflicts of interest.

 

No, we don't have such a thread. If I started one I think I would be inclined to put it here, https://www.s4me.info/forums/psychosomatic-news-me-cfs-and-long-covid.27/

 

https://mecentraal.wordpress.com/2024/02/15/en-de-uitslagen-zijn/

Don't think you can get a bigger middlefinger as ZonMw and Rosmalen/ME/CFS Lines consortium.

 

Post copied and subsequent posts moved from
Genetic Risk Factors of ME/CFS: A Critical Review. Joshua J Dibble, Simon J McGrath, Chris P Ponting. 2020

During the ZonMw conference on the Dutch ME/CFS research program yesterday, one researcher said that they estimated the heritability of ME/CFS in the Lifelines cohort at 43% [34-51] - findings that are still to be published.

 

Interesting. A caveat would be though whether the Lifelines cohort identifies ME/CFS accurately or not, and I believe there are doubts about that.

 

I wonder what that is based on. These things usually require something like monozygotic versus dizygotic twin studies.

If heritability was 40% I would have expected some risk loci to have shown up on the smaller screens done so far, although there might be reasons why not.

 

The researcher mentioned above was Martje Bos, who is a ME/CFS patient herself and is studying ME/CFS in relation to other functional syndromes such as IBS and fibromyalgia.

Another researcher, Cindy Boer said that she is leading a new major collaboration: ‘Genetic epidemiology of ME/CFS’ that has 30.000 people with ME/CFS and several hundred thousand without ME/CFS. [EDIT: I corrected this sentence and changed with to without: see the following post by MESci]

When someone asked if their study is not too similar to DecodeME she responded that there have been talks talked with the DecodeME team but that higher sample sizes around 40.000 will be needed and that therefore collaboration is necessary. She also said it is important to validate the results that will come out of DecodeME in other cohorts.

 

I think you've erroneously repeated 'ME/CFS' here. Should it be something else?

 

Apologies, the last one should have been 'without ME/CFS'.

 

The genetic Lifelines project description funded by ZonMW also states that "Getting ME/CFS is possibly 48-56% determined by a person's genetic (DNA) background. This has not been researched extensively until now, even though it is known that genetic research can be used to determine the cause of ME/CFS. The aim of this project is to investigate which genetic (DNA) variations are involved in ME/CFS in order to discover the genes and biological cause(s) of ME/CFS."

Does anybody have any idea where those numbers come from?

https://projecten.zonmw.nl/nl/project/mecvs-genetica-onderzoek-naar-de-biologische-oorzaak

 

So presumably they are doing another genome screen like DecodeME, but yes, the question is where the genetic component calculation comes from.

I thin there may have been a twin analysis in the US from a huge cohort about five years back but I heard no more about that and it seemed that the definition of the cohort might be pretty loose.

 

This is good news, and exactly what we need. With GWAS studies, size makes a big difference, and it’s fairly easy to combine the results of different studies to get more robust results. Separately, it’s also important to validate/replicate findings from one study in a separate, independent cohort.

As Chris Ponting said in the recent excellent piece on Channel 4, this kind of work is 20 years behind other diseases, but it’s good that things are getting going now.

That is very high, and as @Jonathan Edwards says, if it were this high, you’d expect some genetic findings by now.

I think planning for DecodeME estimated heritability at around 10%, based on previous studies, which I think included this one using data from Utah
https://pubmed.ncbi.nam.nih.gov/21619629/

When all the data for DecodeME is ready and has been analysed, it will be possible to an estimate for hereditability, which should then be the best estimate we have.

 

I gather there are ways of doing this on genomic data that are not based on related individuals. There's one way that exploits linkage disequilibrium ( the property of a causal SNP to drag other nearby SNPs along with it just based on proximity), and the correlation of the chi squared value for each SNP with the linkage disequilibrium score for each SNP gives a measure of heritability.

From the paper [this thread concerns:] link:
Genetic Risk Factors of ME/CFS: A Critical Review. Joshua J Dibble, Simon J McGrath, Chris P Ponting. 2020

They report quite a range of heritability results - I'm not sure how they're calculated but the large estimate from the US insurance data is surely not a twin study, maybe it's just based on a correlation between parents and offspring. Maybe you would expect some degree of confounding from lifestyle that could lead to a higher estimate? Would be good to look at these studies a bit closer.

Happy to defer to those perhaps more knowledgeable about this @Simon M ?

 

From what I understood, the lifelines estimate was based on how prevalent ME/CFS was among relatives of ME/CFS patients.

 

I remember a large US insurance study from a few years back - not sure if it wsa this one - but it had a low sex ratio and CFS incidence was highest in the over 60s, making that study look suspect.

 

The Lifelines ME/CFS cohort was based on Fukuda criteria, (Rosmalen) in Groningen. Patients got reimbursed for the 4.4 million by the government. New database in line with Decode ME, with that 4.4 million budget.

 

Yes i.e. you'd need to see the methodology.
Interesting to see the responses (above) to the claimed figure {43% [34-51]} - thanks.

EDIT - note - moved from another thread - discussion & comments from Simon McGrath - claimed genetic figure seems too high - DecodeME assumed 10% genetic contribution