Search results

Why is any study that acknowledges ME/CFS as a physiological illness using the Chalder Fatigue Questionare at all, let alone as a primary outcome?

Oh to be a fly on that wall 'While biological understanding of ME is still limited, planning for the future is essential. This includes preparing for the delivery of potential treatments, as identified by the ME Priority Setting Partnership.' So many questions that can't currently be answered...

If we think that ME/CFS after long covid is the same as ME/CFS after any other illness, then within a couple of years we will have pretty definitive answers on some JAK inhibitors with this, Wes Ely's bari trial and another one which I can't currently remember. I assume that different JAK...

Very well put. As someone who studied a lot about systems of control, capitalism etc etc, it was bizarre to find that I had still managed to be completely hoodwinked by said system, and then sort of be strapped into a front row seat to observe and be a victim of the emptiness and cruelty of the...

Oh this is very interesting, i didn't know about this. Edit: it says in the link that Finngen results are now 'publically available for the whole research community'. So it's entirely possible it's concurrent.

I reckon this is probably the Lipkin study that had funding pulled. Some of the US institutions seem to have won a court case to reinstate funding so maybe that will go ahead eventually.

Am I correct in thinking nature scientific reports is more prestigious than nature communications? Either way it's shocking this got published anywhere.

That occured to me but I didn't know if it was even possible to increase NK cells

A lot of the physical tics assoicated with schizophrenia are actually caused by the drugs commonly prescribed to treat it.

We are living in an age of utter delusion parading around as science. This is as nonsensical as any belief in wellness/antivax circles. And it sounds like it uses the PACE trick of telling the patients how effective it is, which tells us everything we need to know. I sometimes feel like the...

I guess I meant could it be a factor - this process going awry somehow. If ifn-g and cd8 t cells are the medium by which PEM is triggered during/after activity essentially. And in terms of long term deterioration I don't know. I suppose I was thinking of this process as adding fuel to the fire...

Could this possibly explain why pwME get PEM and sometimes deteriorate after exercise? I note IFN-G increase which is of course relevant to the Edwards/Cambridge/Cliff hypothesis.

JE has said a few times that there may be repurposeable mabs that will do the trick. I think it depends entirely on what drug targets come to light. For example yesterday: As for developing a new one, here is JEs best case scenario from a while back. I think the broad point is that if pharma...

'In how many years' is the pressing question about all this no one can answer it seems . Would it also block the monoclonals? Damn I didn't realise that.

Perhaps that is true if Daratumumab works but it may well point the way to other treatments with a different mechanism that are more universally effective.

Every damn treatment that trends - mestinon, ldn, this, whatever - always seems to come with reports of worsening as well as improvement. At least we will have the data from the placebo controlled Rapamycin study and the lift ldn mestinon study in the next year or two.

It's not the first time I've seen him make it either.

I'll get my chequebook! Do you think that Jackie is likely to get that kind of funding once all of our DecodeME etc ducks have lined up over the course of the next little while?

Forgive me if I missed this in your paper, but how would we establish whether this is the case?

Younger says that a 72% response rate is unlikely because we know the ME/CFS label contains 3 different pathologies. Unless I have missed something major, or he has seen advance results I haven't, we don't know anything of the sort.