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Nice succinct letter. I see they chose a nice slightly mauve ribbed cardigan with casual neckscarf. It adds a nice little irony.

Whew, I was getting thirsty. Over the £20,000 now. Just needs another push.

Com on guys, make it £20,000 by drinks time. And then some more tomorrow.

Keep the donations coming. Keith's work has been crucial - he deserves all the support members can muster.

Interesting to see a prominent patient activist taking part in a GIGO study like this. Th first author is of Cours a health psychologist. I cannot see what psychology has to do with refractory inflammatory disease - other than of course as a term for use in healthcare marketing.

I don't think they did that in any meaningful sense. They stated the reported improvements in all groups. Both absolute and relative change were explicit - and both are relevant in interpreting a study. This is about the one thing that they did not get wrong - except perhaps maybe in press...

Blue pills can be quite pricy!

The irony is that Pariente is really repeating Knoop and White when they said that CBT is really working as a placebo. The problem with that for White was that he claimed that placebos had no effect on ME, but that cannot right if PACE showed CBT effective and it is a placebo. But the key thing...

Well, if BPS people like Pariente feel the need to respond to Monbiot by reiterating muddled arguments about placebos being good because you have to have placebo controls in trials then hopefully Monbiot will be encouraged to believe that the story sold him by the patient activists was spot on...

I cannot see any good reason why plasma and total blood volume should behave differently in this study. They may use the words semi-interchangeably, assuming that measured plasma volume reflects blood volume?

Are you sure? That is not the physiology I was taught. As I understand it almost nobody is short of salt in developed countries at least. Historically people were entirely healthy on much lower salt intakes.

Interestingly, blood volume was lower in POTS patients then that of healthy control subjects, even with a high-sodium diet. (From the review) But that does not seem to be what the abstract says? It says there was no difference, despite the other variables still being different?

I have not tried to access the full paper but two things strike me as odd about the abstract. Firstly, although they say that high salt altered values in POTS patients they give no results for this (and no statement about statistical significance), while they do give results showing that the...

I agree, I don't see that we can extrapolate from studies on afferent signals in fatiguing in normal people to speculation about what is the cause of abnormal fatiguing. There are a hundred and one unanswered questions about what is causing what down the line!

If patients have long lived plasma cells contributing to pathology then they pretty much have to be non-neoplastic, since Ig levels are normal. So they are part of an immune response. Everything we know from theory and practice in autoimmunity suggests that trying to deal with the problem just...

The key thing to remember I that the weight of evidence is that none of these people are responders to anything here. They got better during studies but looking at all the evidence together much the most likely explanation is that these were coincidental or placebo responses. When I originally...

Yes, what I said: it does not kill a high percentage of non-malignant plasma cells. And so I also said: Which was simply to agree that it is a plasma cell targeting agent and therefore likely to fall under F & M's patent. I have been hoping for years for a combination protocol that kills...

Bortezomib has had a reputation for having side effects but does reduce plasma cells, at least in some situations. I don't know if the patent is still central to the ideas of F & M. I suspect the right thing to do would be to find a more intensive B/plasma cell protocol that works better than...

This of course makes no sense. An RCT is needed to see if the treatment has any useful effect. What on earth do they mean by solving issues around randomisation? The wording strongly suggests that they haven't a clue. What is the point of investigating timing without whether it works?

I am afraid that this reads like a computer-generated word salad based on popular memes about 'hEDS'. Real scientists are not 'excited to share'. They let their data speak for itself.