NIH: Accelerating Research on ME/CFS meeting, 4th and 5th April 2019

I'm finding the low definition stream more reliable than the HD stream. If you're having frequent dropouts in the video, try turning off HD.

 

Younger now. Taking the time to define what he means by neuroinflammation, so someone must have gotten a word in Uses it in the crudest sense, whenever he means any form of micro glial activation.

 

https://twitter.com/user/status/1114228204905086976

 

Don't know how well his science stands up (which is a comment on my ability to judge, not necessarily on his science) but I do think Younger presents well.

 

Elzakker: “Neuroinflammation” is imprecise, “microglial activation” is a proxy

ETA: Apparently both Younger and Van Elzakker are aware of the issues with the vague language around neuroinflammation, a good sign that they are addressing it.

 

OK but what is microglial activation a proxy for? And why is it just a proxy rather than important in its own right? If microglial activation is just a bystander then we seem to be chasing even less inflammation.

If microglial activation occurs in the absence of other aspects of inflammation ( vascular changes or cell migration) it may be a response to something non-inflammatory like neuron death or degeneration.

I would like to get away from proxies for invisible snarks amd stick to data and mechanisms.

I may be a grumpy old crust but I don't think these guys are doing themselves justice. Real science answers are REAL; they don't need gilding with excuses. What's more they are there to be found if you look. And they aren't what you are expecting - at least not until you finally seehow it works (unexpectedly).

 

I'm sure you're right! He said A LOT more but he's talking very fast and to be honest I'm starting to fog over too much to follow. I picked a couple of lines from one of his slides as an example. Just wanted to comment that they are addressing it in some way. Hopefully this will all be posted online so people can take it in in more detail. He was very clear that we can't tell if any of this is particular to ME either, this stuff (whatever it is) is going on in a lot of diseases.

ETA: I think it's great that you are so critical, it can be hard to know what to believe sometimes, especially when processing power ~ 0.

ETA2: I think (just my understanding and vague recollection) that he used 'proxy' because in reality the field is not advanced enough to really be completely sure what they are measuring.

 

(I haven't been able to follow all of the presentations because of caregiving responsibilities.)
What sort of discussion has taken place during this conference about cognitive problems in ME?

 

Is this serum switching (healthy cells in sick serum vs sick cells in healthy serum) independent of Davis' research? Would be pretty strong boost to have honed in on the same observation.

 

This is great. Is this the first announcement of the paper being accepted or my failing memory?

 

Aren't there multiple observations of increased... can't remember the right word... cell death (apoptosis?)? Which seems to fit well with observations of decreased telomeres if the cell replacement cycle has to replace cells more than usual.

Do we know what else happens to the cells put in ME plasma (or serum, I think Davis is with plasma and there's another presentation today finding changes with serum?) besides the weird impedance signal? Do they also die quicker or just mostly crap out on energy production but otherwise continue otherwise merrily functioning badly with the same lifespan?

 

https://twitter.com/user/status/1114249259594014721

 

If there "something in the blood," I wonder if that might be related to why patients feel better following an infusion - i.e. the blood becomes more dilute, possibly reducing the concentration of "x" to below some kind of symptomatic threshold.

Similarly, if patients have low blood volume, then the concentration of "x" may go up if it is entering the bloodstream at a constant rate unrelated to blood volume.

 

The "something in the blood" news is very encouraging. Mostly because it has the potential to be a biomarker. No more BPS crap, but instead accurate animal models.

 

We like grumpy old crusts......

 

Oh dear. The end roundup is depressing. The concentration so far on Sickness Behaviour

 

Always low expectations for Komaroff, who is editor for UpToDate's improved but still-awful CFS section. UpToDate still hasn't completely rejected PACE, and states GET and CBT are beneficial for some ME/CFS patients.

2 decades ago, Komaroff did a presentation for the Medical Board of California where he recommended GET and CBT . He's never corrected this, to the best of my knowledge. It's still on the Medical Board of California website.

Edit: supportive links if anyone is interested
https://www.s4me.info/threads/uptodate-me-cfs-information.5755/
https://www.s4me.info/threads/my-le...still-recommending-get.2085/page-4#post-49180

 

Professor Maureen Hanson gave an amazing speech.

 

First I'd heard.

 

And in PNAS, no less!