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The article is the blurb. I don't see any insight into biological processes. It just seems to be an exercise in putting ducks in a row without knowing what you are going to do with them when they are in a row. I find it hard to see the point of studying fatigue in condition slike rheumatoid...

I cannot think of any reason why they should.

The blurb suggests a total lack of insight into the problem - unsurprisingly.

I am thinking of the example of lupus, which is probably as 'complex' as any disease. Identifying rare genes was very useful - particularly complement gene deficiencies. By about 1980 we knew that a tiny proportion of lupus cases could be entirely accounted for by individual complement gene...

I am not sure. I don't want to appear to be telling anyone what to do. I am just trying to point out that there may be unexpected consequences of our actions and that we should all take responsibility for those actions.

Also: Is wrong. Most Long Covid gets better before it qualifies as ME/CFS. 'POTS' is so vaguely defined, beyond orthosttic tachycardia, which may be normal, that it is absurd even to make this statement. This is make believe quack medicine pure and simple.

Yup. None of these have been identified convincingly to my knowledge. Certainly nothing has been shown to be an 'important mechanistic factor' even if there are a few data showing differences from normals. The mechanisms are completely unknown.

I continue to be glad that I never signed on for social media meme-rolling in this field!! There was an old saying about empty vessels.... I seem to remember.

Yes, but the chances that tickling the vagus nerve would be the right thing to do seem remote and a duff trial in RA is probably not the place to start anyway.

Merged post Eric Topol seems to be a science magpie. I think we looked at the studies on this and were underwhelmed.

I disagree. This is an issue that affects young women because ME/CFS is common in young women. Young women are normally more hypermobile than men or older women. The labelling as 'hEDS' was done by physicians who took these people seriously. It then became a problem for other physicians who...

As they are written, I hope. Which is not: It is bound to be a sensitive issue but when I re-read what I wrote think my position was made clear. Perhaps I should put it from a slightly different angle. I do not hold the vast majority of patients and carers responsible for causing problems...

I assume that you would look at their functions and make intelligent guesses much in the way that that has been done for the Zhang study and Liz Worthy's study. The advantage of multicase family studies is just that it seems likely that rare but heavily risk-bearing gene variants would show up...

Just plain wrong again, unsurprisingly.

My understanding is that GWAS data on families will not tell us more because that is a statistical game with common variants that are not likely to be causing disease in any direct way. Although members of a family will share 50% of each others DNA my guess is that if rare variants turn up in...

Yes, at the last meeting there seemed to be a change of approach.

As do I. But I have not seen that narrative here.

Not that I am aware of, as I pointed out at the relevant meeting.

Chris is clearly aware of the option. There may be major practical or statistical difficulties in setting up a good quality study of multi-case families. I would be interested to know what everyone's thoughts on that might be.

My information when first re-joining the process recently was that there was no point in asking for severe services because they were not going to happen. I am hoping that position has changed.