I wonder if the reason is that if you provided (free) genetic data then a lot of people (who do not have ME/CFS) may be inclined to apply to participate in the study.
Yes, Sir Humphrey and the survey comes to mind - you can get any answer you want --- if you don't care ---
EDIT - should have added this:
"Dr. Bruce Levin, a professor of biostatistics at Columbia University and an expert in clinical trial design, said, “To let participants know that...
Failure of the Government Officials on the project board i.e. overseeing the project (it was paid for by the UK Government - civil servants lead the project oversight board). Of course, they should have been advised by the "scientists/academics" - lead Peter White Queen Mary University of...
Obviously checkout Jonathan's comments above. My impression is that this looks OK -
1. Research Strategy
MRC expert group led to GWAS +ve ---- funding research which cannot possibly tell us anything [unblinded & subjective outcome indicators AKA questionnaires]* -ve.
2. Building capacity and...
Don't know much but yes there's a danger that the last Minister's agenda/interests aren't supported by the next incumbent/Minister. The APPG is the obvious route to challenge lack of progress/implementation. E.g. if there's evidence that health trusts are not following the NICE guideline then...
Yea I assume that's why folks like Brian Hughes highlight that unblinded studies, with subjective outcome criteria (questionnaires), are unreliable. I think Jonathan Edwards highlighted the placebo effect in his evidence to the PACE guideline review.
So basically they're telling you this...
I think I should have mentioned that a gene being "upregulated" basically means that it's making more of whatever protein it codes for. Basically, without checking, it's an MRNA that controls the gene ---telling it to make more/less of the protein. If you've an illness then upregulating the gene...
I agree fully - where's the evidence to support the statement?
A thought occurs that Jose Montoya (before he exited stage) gave a presentation in which he talked about patients having walked the Rockies (mountains) and similar fetes ---. So maybe, in the way that a camel is a horse designed by...
10 out of 17 would appear to be a very high proportion. You'd need to think of the inclusion criteria, i.e. basis the 17 were selected, of course.
Interesting to see what the increase was (e.g. clearly distinguishing patients from activity matched controls ---) and whether it's a potential...
Surely there can't be many people who could keep pace (no pun intended) with this lot --- spin and spread misinformation to hide the truth... covers it pretty accurately. Surely he should be pointing out the strategies they've used and telling the ill/those representing them to keep up/learn...
To have a chance we need studies like GWAS [Chris Ponting]
Sadly I have to agree although Fluge and Mella's rituximab trial showed that ME/CFS is
not a B-cell autoimmune disease, or
B-cell autoimmune cases are rare.
I actually think we haven't applied techniques, like GWAS, which have been...
Haven't read it but where do the antibodies come from - people who have been infected?
If the antibodies work then that might be useful in treating those who are at risk of serious illness --- those who are hospitalised,---
We certainly are in the early days of finding out ---- my understanding is very limited but long lived plasma cells do produce antibodies and are presumably capable of producing autoantibodies/autoimmunity. I'm open to the idea that autoimmunity may explain some cases of ME/CFS - but there's no...
Given that Trudie Chalder "is a Professor of Cognitive Behavioural Psychotherapy*" you'd expect some evidence to support this statement--- OK I'm showing my lack of knowledge --- presumably asking for supporting evidence means that "you don't understand" or some such.
Presumably if you started...
"Many of the genes identified are linked to the key cellular mechanisms hypothesized to underpin ME/CFS, including vulnerabilities to --- autoimmune development. Well, since rituximab failed that statement ("--vulnerabilities to --- autoimmune development--") would be a bit surprising - i.e. if...
I haven't read the review but in terms of identifying the underlying cause/solving the "medical mystery" GWAS aims to do that --- e.g. the (too) small Norwegian study turned up TPPP gene (thread on this website). So yea forget the medical mystery bit and look at the available tools --- like GWAS
A very brief glance at the Results and Conclusions and the thought occurs that they perhaps they're trying to leave this "study" behind/forget about it ---
Precisely sums up , thank you - "---we have no treatments---". We need research (such as GWAS) to identify the cause/underlying disease mechanism --- then we can move to treatments.
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