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I am afraid that I agree. Using Maes and Twisk as a comparator is unwise. Maes produces as much nonsense as BPS people. The suggestion that what is needed is more training of psychologists is wrong. If we do not know what is wrong with people and we have no evidence that psychological...

I think it may be quite useful for this sort of disinformation to come out in a national newspaper just now. The people at NICE involved with the new guideline are likely to redouble their commitment to sticking to their guns. Having spent four years working with Adam, Sally, Saran, and...

A story wearing rather thin.

EDS is defined as a cluster of monogenic disorders where connective tissues are abnormal because of a defect in a single collagen or related gene. In that respect it is akin to haemophilia or Marfan's or sickle cell disease or a wide range of other gene defects. EDS III was posited as a...

NO I think they are just looking at joint hypermobility per se. The problem is that some fringe physicians are now conflating that with what used to be called EDS III and is now called hEDS, which as far as I can see isn't really a form of EDS anyway. There is very little evidence for monogenic...

It is more subtle in that you want to make sure that the ascertainment of a diagnosis of ME/CFS and of JH is not coloured by beliefs about JH and ME. There are some population studies in children that tend to suggest that JH isn't associated with anything much to do with ME. There is the ME...

Not sure what your question is. A lot of ME/CFS services are run by immunology/infectious disease departments in the first place - or at least they act as a primary route of referral for suspected ME/CFS. Amolak Bansal is an immunologist. My cousin who saw a lot of ME/CFS was an infectious...

I get the impression that in the UK this study would be considered unethical. One group were advised how to get rehab and the others were not. For those in the rehab group to bother they would have to be told rehab was good. The other group would have to be told something different. Maybe I have...

To me it belongs to this conversation: "Did you go out into the garden yesterday evening?" "MNYES (wait for it)" "Did you lock the kitchen door when you came back in?" "MNYES, erm, I think so, er maybe not." "How many times have I told you... And so on. So it's: "Do you know what's wrong with...

A very heartening read.

Wonderful that they base their case on a Canadian trainee psychiatrist's hot air.

I am afraid to me it reads as a scattershot blast of old and rather tired ideas.

The only long term acquired imbalance I can think of would be due to an autoantibody to an inhibitor or complement clearance process. I would expect the effects of that to be both unstable and evident in some obvious change in levels - markedly low levels of some factor like CD55. Maybe not but...

Indeed. I may have been a bit corrosive in my responses, which might have got me off the list as usual.

I was thinking that a complement imbalance might make some sense for ME. It ought to be too much complement to make it different from complement depletion as in lupus. High C1q would be too much. Low MBP would allow C1q to build up. It would point to a problem with too much classical pathway...

You must have given good answers.

This is just an essay done by a trainee sent off as a review publication. The first author probably knows little or nothing about CFS.

JH evolves during childhood but is probably largely genetically programmed. It can probably be modified by stretching activities during childhood - maybe in ballet dancers - although I am not sure there is evidence on this. By the age of 18 nearly all ligament insertions have ceased growing and...

I think the limited evidence comes from inadequately controlled studies from Rowe and from Knoop.

I blame the Nasi goreng.