News From Jarred Younger / Neuroinflammation, Pain, and Fatigue Laboratory at UAB, From Aug 2020

SNT Gatchaman said:
"This is called the anterior mid-cingulate cortex, or the aMCC. Now this region drives motivation, will power and perseverance and sustained effort. And it does this by monitoring available energy in the brain and assessing whether there's sufficient energy to do the thing that you're thinking of doing."
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Hard to see any relevance, I have almost never heard of those things being any lower in pwME. In fact they might even be above normal. It's not the traditional definition of effort, but when simply existing requires massive effort on a second-by-second basis, that's still a high degree of sustained effort.

Plus all those "drive motivation, will power and perseverance and sustained effort" as far and as best as current neuroscience defines them, which is obviously crude and superficial.
 
SWA said:
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In the video Younger shows 3 ME patients where 'active' microglia are colored red through a tracer, one shows them present in amygdala, one in the thalamus and brainstem and one in broad areas of the brain, the latter being the persons scans you showed in a picture earlier in this thread.

Younger speculates that maybe there are these 3 groups of 'inflammatory' patterns in patients with ME but acknowledges at the same time that he hasn't enough data/scans to confidently claim that, so it's unclear if he has seen and compared 10, 20 or 100 of those scans.

What seems clear though is
a) that there isn't one pattern of inflammation that can be connected to the symptoms of ME and
b) none of the patterns he shows has 'activated' microglia primarily present in the anterior mid-cingular cortex, 2 even show no presence of them in this area, so if we equate this with neuroinflammation like he does it seems unlikely for neuroinflammation to explain abnormalities in this area.

Like I said above the red areas are marked by a tracer that is said to bind to 'activated' microglia, what that exactly means remains unclear. Younger then equates this hightened density of 'activated' microglia with neuroinflammation, as a layman it's also not clear to me if this equation is something that can be done so easily.
 
Silip said:
Like I said above the red areas are marked by a tracer that is said to bind to 'activated' microglia, what that exactly means remains unclear. Younger then equates this hightened density of 'activated' microglia with neuroinflammation, as a layman it's also not clear to me if this equation is something that can be done
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As someone with a doctorate in inflammation science I can assure you that it can't.
The real problem with all these imaging methods is that it is too easy to turn knobs so that certain areas look really different when the difference probably has no biological significance. Pictures on their own are not enough. Using pictures to suggest that they show something on their own is misleading people.
 
He cites this paper at 2:38 that he suggest convergence. I think it he’s been teasing his own results for over a year now, what happened to that?? He keeps saying chronic inflammation in this area. This video posted is possibly the least informative yet, lots of conjecture

forestglip

Thread 'Microstructural alterations in brain tissue of ME/CFS and long COVID using diffusion tensor imaging and diffusion kurtosis imaging, 2026, Singh et al'

Microstructural alterations in brain tissue of ME/CFS and long COVID using diffusion tensor imaging and diffusion kurtosis imaging

Singh, Tanoj Bahadur; Marshall-Gradisnik, Sonya; Barnden, Leighton; Eaton-Fitch, Natalie; Huynh, Tuong Hieu; Inderyas, Maira; Thapaliya, Kiran

Introduction
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and long COVID have overlapping symptoms, such as profound fatigue, cognitive impairment, post-exertional malaise, pain and sleep disturbances that are debilitating and reduce quality of life. While Magnetic Resonance Imaging...
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Jared says this is the site of ME/CFS “inflammation” he also states in this video this area is not reachable by photobiomodilation. Odd that he is supporting the renagade research photobiomodulation trial if he is so sure this is truly the area where things have gone awry.

Edit: I don’t want to be such a huge downer. I do think you can chase two things at once, just neither here seems to have sound or reproducible data to chase just yet. Show the data then find the target and then apply the therapeutic. We’re not even seeing the data, and for the photobiomodulation I don’t think there is any either yet it’s being promoted and will inadvertently cost desperate ill people money.
 
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The founder of the Neuroimmune, Pain and Fatigue Lab at UAB talks on measuring energy levels in the brain, what may be the brain hub for ME/CFS, FM and long COVID, why the fatigue and pain in these diseases has a brain origin, the biggest disappointment in his academic career, and more.
 
I've been trying to make my way through this thread (and others) to understand what the objections or evidence against the neuroinflammation theory in ME/CFS are. But mental energy and screen tolerance are limited at the moment.

Would anyone be able to do a quick TL;DR on the problems with Younger's claims? He says he has shown brain inflammation in his research, but was the research not done well?

I was not aware that his stance was disputed before joining S4ME and was under the impression that brain inflammation was a least a major player here. I did read two other threads on the topic, but I'm still unclear on the discrepancy. If anyone's able to do a quick summary, many thanks.
 
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In short:
The idea that there is neuroinflammation in ME/CFS stems from the word 'encephalomyelitis' which was never relevant to ME/CFS as we now use the term (it applied to an acute illness).

Researchers appear to have assumed that they should be looking for neuroinflammation but as far as I am aware there are no studies that show anything that deserves the name. There was a study of microglial activation by Nakatomi that seemed to show something but it was not confirmed and did not look like pathological change anyway.

I am not aware that Younger has produced any convincing published data.
 
Hutan said:
Oh, he is promoting the Renegade Research trial of photobiomodulation device, funded by Solve ME. The one with the head harness and an infra-red light. (and also the vagus nerve stimulator)

Jarred Younger is in full-on hype mode:



I think we probably need to look at the evidence base for all of those claims, because so many people with great influence in the ME/CFS community are lining up to throw their authority behind the idea.

Younger talks about the 'great design choices' of the study. Specifically the testing of two treatments at one time:

There is no mention there of the possibility that a treatment doesn't work, or that neither treatment works.... Or that the trial design is so hopeless that actually there is no chance of null results. There is no criticism of this study at all.

Solve ME is doing a talk on the study on November 6, when they will share the protocol. Perhaps there will be some sham treatments, although SolveME didn't seem to be saying that there will be yesterday. Perhaps there is still time to lobby Renegade Research, SolveME.
Younger is involved, from memory Todd Davenport is too, we've talked about this elsewhere. So, that is more people to lobby.
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Is this stronger than the infra red skin masks the influencers have all been sporting the past few years? Looking like demented cyber men.

ETA really though, how much different is the wavelength of the red light in the photo-bio-mod thing he is using coz I can get one of these for £20 and try it and let you know.
 

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Joni said:
I've been trying to make my way through this thread (and others) to understand what the objections or evidence against the neuroinflammation theory in ME/CFS are. But mental energy and screen tolerance are limited at the moment.

Would anyone be able to do a quick TL;DR on the problems with Younger's claims? He says he has shown brain inflammation in his research, but was the research not done well?

I was not aware that his stance was disputed before joining S4ME and was under the impression that brain inflammation was a least a major player here. I did read two other threads on the topic, but I'm still unclear on the discrepancy. If anyone's able to do a quick summary, many thanks.
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This is one of those science things which is a lot of hype and headlines but there isn’t any good factual evidence for it.
We found this! We found that! So it means the other must be true! (Reads paper….oh but they didn’t really find much of “this” or “that” hmm, so really it’s a bit of a stretch to use those as a basis for saying the other thing must be true)



Like all things ME, the more you look at something, the less clear it becomes.

Also this place is kind of like a university on steroids, it’s extremely robust science with experts. Just being a professor is like basic. It’s good though, the smartness is catching!
 
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I didn't know brain inflammation was a widely spread misinformation. My brain MRI was clear and I've heard the same from other patients who were sent for one. The caveat is that we had an indication to be referred for a brain MRI.

I thought encephalomyelitis in ME/CFS was yet another nonsense I had faced with the healthcare system.
 
Agree with Utsikt it's all over the internet. I suspect the interest in neuroinflammation is arising as a compromise between the fact that many aspects of ME/CFS look neurological, and the fact that the concept of a problem occurring in the brain has been monopolized and used for harm by the psychologizers/BPS/brain-trainers.

If I tell someone I have a problem with my brain they might think I can therapy my way out of it. Whereas if I tell someone I have *neuroinflammation* that automatically sounds like I need medical treatment.
 
Jonathan had made good comments on this before in other threads. Using the search function you can search for the term “Neuroinflammation” and filter by his username. Here is one good comment addressing it:
Jonathan Edwards

Post in thread 'ME/CFS Atlas site'

Robius said:
What do you think the real underlying mechanism is more specifically?
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I wish I knew but I have a rough idea of what sort of thing it might be. The link to viral infection suggests to me that immune signals such as cytokines are being generated as part of an immune response and that for some reason these persist. My work in the past was on autoimmune diseases and we have a reasonably good idea how persistent signalling can be set up for those, but involving specific autoantibody. We also know that persistent signalling can occur in autoinflammatory disease like psoriasis without...
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Inflammation is really popular at the moment as well, it’s a perfect storm with neuro- prefixed stuff being popular.
I’m sure we are soon to be victimised by the term “biohacking” it’s also gaining popularity.

Has anyone invented “bio maxxing” oh no - I looked and they have. Urgh.
 
Jonathan Edwards said:
Researchers appear to have assumed that they should be looking for neuroinflammation but as far as I am aware there are no studies that show anything that deserves the name.
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Thank you; I appreciate that.

Yes, I assumed that the word encephalomyelitis was based on definitive evidence of neuroinflammation. And the theory is repeated in ME/CFS spaces online, with the microglia activation being presented as fact.

Hearing Dr Younger say that brain inflammation has been confirmed by higher levels of lactate and higher temperatures probably cemented the idea for me.


I would normally fact check and read studies to verify claims. But as I've grown sicker that has become less feasible to do. Unfortunately, to cut corners, I've had to trust that seemingly grounded people know what they are talking about. But of course that is often problematic!

Jonathan Edwards said:
It would be interesting to know where you got the impression from
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