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There is a lot wrong with the medical profession but not this. The reason there is nothing to treat ME/CFS with is that there are no clues as to what to do. It is an illness with a mechanism that so far we have no understanding of. It is a bit like saying why didn't Peter Higgs find his Higgs...

The implication is that there is useful care that the NHS is not providing. There isn't. But I think it is an important point that the NHS is not even attempting to provide competent advising and supporting staff. If ME/CFS is real like diabetes is real then it should be handled by the public...

I am afraid that I totally disagree with this @butter. The reason progress has been made in Parkinson's disease is simply that for over a century people have known where the structural pathology is. So there is a lead. In ME there is no lead. Money is no use if you do not know what to do with...

It is an important milestone that was well aired in the pre-S4ME days. I think it was presented in Bristol in 2014. TGF beta should probably be taken seriously. The conclusion is fair but only in the sense that serum levels are clearly not the whole story. That would not be at all surprising...

That appears to be non sequitur to my quoted comment, Peter, which was that most of these studies turn out to be artefact. They are not for generating hypotheses, they are for testing them. The idea that post-infective disease is due to autoantibody is sixty years old and has failed to show any...

It looks as if by psychosomatic they simply mean mind and body - as in sound in mind and body. In which case we all want to have a good psychosomatic status. There is a saying that old soldiers never die - they just fade away. Someone also said that old immunologists never die - they just lyse...

The basic point is that EDS is defined as a monogenic dominant or sex linked recessive disorder. There has always been a group called type III, or hypermobile only. The problem with the term hEDS is that it has become a standard term simply for hypermobility, which in 99% of cases will be...

As far as I can see this is just a report of a gene variant in two families with EDS. I would forget the hEDS. In these families it is presumably the basis of their EDS, which I guess has limited visceral involvement and so comes under type III (hyper mobile type) although the knock in mice had...

I thought it was that the foods stimulated release of histamine. Do any foods actually contain a lot of histamine? Histamine wouldn't produce an allergic reaction as such. Allergy releases histamine through binding of IgE antibodies but for foods I think the histamine release is based on a...

I am not clear that either of these are meaningful? A number of foods stimulate histamine release in the GI tract - strawberries and seafood I think most often. Histamine is otherwise a normal mediator in most tissues. MCAS seems to be a category so ill-defined that it has no clinical value.

I am afraid it is just a word salad, @Hutan. Anyone familiar with the clinical pathology of inflammation can see that they do not actually think through what they are saying. If there is inflammation with increased flow the bit goes pink and warm - you can see it and feel it. I haven't even...

It's actually completely meaningless, I think, @Hutan. As are the data on interferons I think. One of the authors here is a serious red flag in autoimmune research.

It is reasonable to question why there should be scepticism, but from my perspective the scepticism is founded on years of experience with this sort of study. The problem with that is that it is only too easy to get a result like that which is pure artefact, combined with some wishful thinking...

Almost nothing is known about turnover of these wall signals. But observations on rheumatoid nodules suggest that the signals are dependent on things like ongoing physical forces - probably a bit like what controls the thickness of skin on the palms of our hands (which may be mediated by exactly...

It would require some careful systematic work to establish normal patterns. Maybe Rob Wust's group might have an interest in looking at muscle.

The increasing emphasis on amino acid metabolism in ME/CFS seems interesting. A shift in metabolism that might in a crude sense be 'anti-inflammatory rather than inflammatory might make some sense. I doubt, however, that simply increasing availability of substrates for down regulated pathways...

That would be my thought. As far as I can see 'POT' is not dysautonomia (almost the opposite) because it is a sign of a competent autonomic response to a haemodynamic stress. I have not yet seen any evidence of dysautonomia in ME/CFS or LC. Unusual autonomic activity maybe, but that may have...

That sentence to me is unimpressive. The way to screen for these is already established. What exactly is being said here? I fear it is 'Why don't we measure everything we can charge a fee for measuring? Send them along'.

I wouldn't be so sure. The big problem with ME/CFS is that even the most mainstream biomedical inclined physicians specialising in it have a tendency to pick up fringe ideas like this. So, currently, people are being treated with triple anticoagulant therapy on the basis of 'micro clots' and by...

I would like to see how well controlled this study is. I am a bit leery of antibodies that react both to meninges and sciatica nerves being related to headache. It would also be more convincing if they mentioned a bit about what they didn't find too.