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This story has been going for at least thirty years for things like Prevotella. As a general story of course it goes back a century. People had their teeth taken out to cure everything including RA in the nineteenth century if I remember rightly. I doubt these are blinded studies and if not the...

Yes, I did suspect it might be motivated by the idea that ME/CFS was due to lingering viruses. Chia's work has consisted of a series of disconnected observations, none of which convincngly show involvement of viruses in ME/CFS. I suspect it harks back to the original concept of 'ME' that was...

A little premature maybe.

The suggestion of synapses in the Zhang paper will probably hold up I think. The anterior midbrain makes sense as somewhere that might be relevant in ME/CFS and my hunch is that all this sifting through is getting us a bit warmer. I am less sure about the lymphocyte clues but they recur. It...

So do we have any information about the possible link to NEGR1 in ME/CFS in terms of where the relevant (different) SNPs would have altered expression. I am doubtful one could draw any sensible conclusion but it might be interesting. I am sorry that I cannot keep up with the detail of the...

That makes sense. I am surprised that such data exist for brains. If they can collect 1000 brains and study expression profiles for every part for thousands or hundreds of thousands of SNP variants that is impressive an suggests that all the needed brain studies on ME/CFS could be done by next...

I am ready to believe that LDN might turn out to show some benefit in ME/CFS (but not holding my breath) but I am prepared to bet 97 pints of good beer it has nothing to do with an infinitesimal 'anti-inflammatory' or 'immuno-modulatory' effect.

All the ones we are discussing. ;)

But how did they possibly get enough bits of brain tissue from people with positive and negative SNP variants to home in on one region like hypothalamus? That seems to me like the sort of thing machine learning spits out but without any rea justification.

This is more or less exactly what my genetics friends at UCL did when they gave me a presentation of why they thought it was worth picking CA10 for a basic biology project.

Having long standing lumbar disc problems I am very aware that viral infections, presumably through cytokine and prostanoid signals, love to tickle up lumbar discs, which presumably swell and therefore hurt. The resulting pain is partly in the back area but diffuse and often as much in the legs...

So how do they link the NEGR1 genetic linkage specifically to hypothalamic expression? That is what I am confused about.

I am not sure how they established that NEGR1 expression in hypothalamus and DRD2 in nucleus accumbens was relevant.

As indicated in the paper this is less a proposal for a preferred theory than an exercise in theory-building. And if this theory is roughly right there ought to be T-cell inhibiting strategies to find. Nor does it discount a success for daratumumab by any means.

S Blitshteyn MD, FAAN, Dysautonomia Clinic ® @dysclinic.3h FYI: I will be blocking you if you come attacking me. I practice evidence- based medicine with the goal of improving function and encourage movement via an individualized approach that we outline in our paper. We don't do GET, we do...

I agree. It seems that these people cannot get rid of their competing interest in "Sports Medicine". The more I see of poorly constructed analysis the less confidence I have in data.

I was going to write exactly that !

Isn't Henningsen the guy who was planning to do 'body psychotherapy' or something on people in association with Moss-Morris at some rehab centre in East London?

I cannot think of a reason for someone with ME/CFS wanting more IFN gamma. It is a mediator of feeling bad. The last time I heard of people being treated with T cell cytokines in a pilot drug trial they all got very ill and I think one died!

When narcolepsy was fund to be associated with HLA-DQ (as ME/CFS probably is, but in an obscure and much more limited way) we settled in to the idea that it was an autoimmune disease like a lot of others - tick box, job done. But two age peaks throws up major questions about how that would fit...