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

It is, however, exhausting.

 

While listening to this afternoon's presentations, one cannot help but realize how out of touch, incorrect, shallow, and harmful the CBT/GET brigade is regarding this disease. Thank you to the knowledgeable scientists/clinicians presenting at this conference. I do so hope this message gets through to those promoting the harmful CBT/GET ideology and that they stop it! But most importantly I hope this information gets through to those rewriting the NICE guidelines. Patients deserve a lot better than what they have received in the past.

 

Funny that i was thinking the exact same thing during Dr Systrom's presentation, this is what the PACErs have spent decades suppressing.

It will not. They refuse to abandon their religious fanaticism

+1

 

It was very interesting, am looking forward to tomorrow!

I really liked the guy who was responding to David Systrom, who was not familiar with me/cfs, but was an expert on exercise intolerance. He said: this is a circulatory control problem, until proven otherwise. I thought it was pretty funny how he said it, like it was really obvious and he was really wondering how people could have missed that until now. He sounded a bit intrigued though, I think that is what we need: experts in fields that are now giving clues to being involved. How interesting must this disease be, if you're an expert on exercise intolerance?

 

I'm not entirely sure I can get behind his solution tho.

I mean how much exercise can you do on one leg?

 

Hopping should be good cardio?

 

Biking with one leg, I think? If the problem is in the vascular system in the muscles, I can imagine it’s interesting to compare the active muscle with the inactive muscle during exertion.

I think there are a lot of people working on the disease from very different angles and it would be interesting if there were more people following the same angle as well, because they can critize each others work better and pitch new ideas to each other.

 

By chance did folks keep track of/remember other questions that were asked and whether the person asking was new to the field?

 

The word "Neuroinflammation" has been used in about half the talks so far and will be used again extensively tomorrow. I know @Jonathan Edwards has said there is no evidence of NI in CFS, only microglial activation. Should speakers be asked to define NI? Advice @JaimeS ? If there is no NI, then it is bad that the speakers are claiming NI because it could be a waste of research effort.....

Thanks

 

I only had the opportunity to see a few of the presentations, but I was really impressed by Dr. Systrom's talk. It struck me as a real tour de force of how to effectively convey a lot of complex information in a short time.

 

One of the people discussing neuroinflammation in ME is Mike VanElzakker, whose speciality is neuroscience. While it's possible he's using the term incorrectly, it's unlikely. And if he is using the term in its correct sense, it's unlikely he'd change it because 'neuroinflammation' isn't really an inflammatory process the way we understand it. It's a bit of a tangle and I'm far from an expert in neurology myself! I'll ask Mike if he can clarify tomorrow if I have time.

I probably can't engage much here, but JayBee reached out to me via email and so summoned me from the Conference aether.

 

I only watched his as well. It was a very good presentation. One question I had, because it was hard to follow and now I'm going off my (poor) memory was his diagnosis process - it seemed like for someone to qualify for me/cfs they had to have the preload failure and then these patients were measured against the other fatigued patients?

44% of the preload patients had small fiber neuropathy, but the sfn wasn't linked to cardio-pulmonary performance. And, strangely, did he say saline infusions during cardio-pulmonary testing normalized the results? If so, I'm not sure that sfn or the patients without preload failure are irrelevant. I'll have to review it later.

About the video: it worked fine for me after I de-selected the auto-HD button in the top right.

 

From what i've seen so far it is interesting to note that MAIT Cells have been mentioned by Derya Unutmaz and also found increased to the latest paper by CureME team. I ran a text analysis through all papers discussing MAIT cells and i got the following text cloud :







Without getting very technical, the larger the text size, the more important the term. Of course, "liver" is there because MAIT cells are mostly found on the liver. What is also interesting is the term "exercise" so i looked for relevant papers in PUBMED and here is one i found :

I am compiling a list with material from the latest presentations with information relevant to the "Liver Injury Hypothesis" and will post shortly.

 

Don't forget, different URL to use for streaming day two, https://videocast.nih.gov/live.asp?live=31640&bhcp=1 - due to start in 5hr 24mins from time of this post, so 1.30pm UK time.

 

The problem is that there is no definition of NI. It is a slogan rather than a scientific term.

A sad fact about biomedical science now is that it is mostly shouting slogans. I am afraid that being a neuroscientist does not mean someone is not bullshitting.

I am not alone in this view someone found a review a year or two back where an eminent neurobiologist was bemoaning the meaninglessness of NI just like me.

Things seemed to change around 1985. Before that we talked about our data and about theories of mechanism in biomedocal science. By 1990 we had slogans like 'cytokine imbalance' or th1/2 imbalance, which mean nothing much.

There is an interesting difference with the story of rheumatoid ( ra) and multiple sclerosis ( ms). We could see inflammation in joints and brain with th naked eye. When we found cytokines we said maybe these are causing the inflammation we can see.

But in ME people find a whiff of cytokine and suggest it is causing inflammation that nobody had found so was not needing to explain. Its a bit like finding a loose tile and saying that will explain the water getting in when nobody had noticed any water getting in. It is back to front science.

It makes perfect sense to suggest the cytokines may be causing symptoms in ME but why say they are causing them via smething we do not see? Maybe they are causing the symptoms another way?

I fear that when you hear slogans in science you can be pretty sure people are clutching at straws of evidence. It is a bit like the slogan 'evidence-based therapy' - we know what that amounts to now.

A lot of the tine NI is used to mean microglial activation, but why not call that microglial activation. The reason is that it has not been found yet. Moreover the various measures Younger snd Bergquist talk about do not seem to indicate microglial activation particularly.

 

I didn't have trouble live-streaming this, but that may be because I was watching it at a relatively low bit-rate. In my experience, it's fairly unusual to have multiple bit-rate streams available during a "livestream." This suggests that they have multiple processors/computers generating each selectable bit-rate stream in realtime. This is usually done after the fact on, say, youtube.

Long story short, if people are having trouble with the video failing, it may be that too many people are watching the HD bit stream. Try selecting a lower bit-rate on the right hand side of the video.

I don't know if it will work, but... "couldn't hurt."

 

Cort has a lot of tweets on the presentations.

https://twitter.com/CortJohnson

 

The hashtag for the conference has many more tweets now.

https://twitter.com/hashtag/MECFSatNIH19?src=hash