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

Yann04 said:
Didn’t one of the only studies on recovered people find that people who described themselves are “recovered” were still quite limited ability wise compared to people who never had ME. (I don’t have the energy to dig and confirm so relying on my dysfunctional brain memory for this…)
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I’ve heard that said as well, but I don’t know where it’s from or if it’s right. For all we know, it’s a result of just partial recovery to a better than mild-state.

I guess we won’t know for sure until we get some long term follow up from effective treatments.
 


So, there is a way to simulate immune/microglial activation and ME/CFS fatigue. I wonder if there is a way to simulate PEM. Chronic activation means chronic fatigue, but PEM may require acute activation on top of the chronic one. I suppose you could simulate it by giving more dose of endotoxin on top of what is already given.
 
Jonathan Edwards said:
If there is actual inflammation in the brain (increased vascular permeability) then you are drowsy, comatose or, if it is local, may appear to have had a stroke. People with ME/CFS do not have those features, however dreadful and unable to do things they may feel.
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"Inflammation" in ME/CFS context only means neuroimmune activation, and the subsequent flooding of pro-inflammatory cytokines, rather than the actual swelling of the brain. You can fault people conflating the terms, but you well know swelling is not what they meant.
 
So what is "neutoimmune activation" or even activation, pray? Why bother with bullshit when you can do science where words actually mean something? All this stuff is dross that goes below the line on a Bridge score sheet. It may pass for science but that is just because biomedical science has largely been drowned out by bullshit in this century.

I know what these people mean - something they don't actually understand that isn't actually there.
 
poetinsf said:


So, there is a way to simulate immune/microglial activation and ME/CFS fatigue. I wonder if there is a way to simulate PEM. Chronic activation means chronic fatigue, but PEM may require acute activation on top of the chronic one. I suppose you could simulate it by giving more dose of endotoxin on top of what is already given.
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I’m really confused by this video. LPS are structures on the outside of bacteria that immune cells recognize during bacterial infections through TLRs. This is just a model of immune response to actual bacterial infection.

And as far as I knew, all the PET tracers for “activated microglia” had serious interpretational problems. None of them were actually for cytokines so it’s just using a certain protein as a proxy for a “activated” phenotype that is itself a big oversimplified category. Has he provided any details for how “activation” was determined?
 
Another video stating activated microglia as fact without data, though this time he lets slip only 35% of people with ME/CFS have (according to him) activated microglia. If this is his new results I’m unimpressed. Also in what world is injecting endotoxin the same as ME/CFS.

How many more videos is he going to make on his imaging that he isn’t making public, while stating this as fact. I’m convinced he’s posting weekly for the YouTube algorithm.
 
ChronicallyOverIt said:
Another video stating activated microglia as fact without data, though this time he lets slip only 35% of people with ME/CFS have (according to him) activated microglia. If this is his new results I’m unimpressed. Also in what world is injecting endotoxin the same as ME/CFS.
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I’m glad you mentioned this because I ducked out of the video before the end and didn’t catch this sentence. Even if the findings were real and there weren’t huge methodological issues with detecting “activated microglia” by PET, 35% means that you can’t even claim it’s a decent biomarker. And certainly not that it’s CAUSAL for ME/CFS symptoms. I’m actually shocked
 
jnmaciuch said:
Has he provided any details for how “activation” was determined?
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He can’t because then he wouldn’t be able to make weekly YouTube videos on it. He apparently is still writing the paper, but decides to present on it weekly.

I have to say having science “influencers” have got to be some of the worst outcomes for this disease. People personally investing in who they like the most/fits their theory the best. Then people who can spend the most time on social media getting funding. It’s abysmal, I definitely fell for this thinking when I first started my research.
jnmaciuch said:
I’m glad you mentioned this because I ducked out of the video before the end and didn’t catch this sentence.
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Got to watch him on 3x speed. No point in wasting more time
 
OrganicChilli said:
Does this really impact his funding? Does anyone who reads a grant application care about his influencer status? Is this why Prusty announces his papers on Twitter?
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Prusty for sure gets face time with Ron Davis due to his social media presence I’d say, which is akin to getting funding. Which bothers me a bit since I spent a lot of time raising money and having family and friends donate to OMF.
 
ChronicallyOverIt said:
How many more videos is he going to make on his imaging that he isn’t making public, while stating this as fact.
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Is there a limit?

A lot of these types of folks who are in over their skis end up trying to be patient allies, etc., but in reality, in the long run they end up doing harm by diverting resources from researchers who are not in over their skis. The researcher from Florida also comes to mind.
 
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ChronicallyOverIt said:
I have to say having science “influencers” have got to be some of the worst outcomes for this disease. People personally investing in who they like the most/fits their theory the best. Then people who can spend the most time on social media getting funding.
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This phenomenon is even worse for “Long Covid”. There is whole suite of researchers, largely based in the USA, promoting various theories about viral persistence, spike proteins, etc., for patients who almost certainly have ME/CFS. Umm speaking of the devil….

 
ChronicallyOverIt said:
Prusty for sure gets face time with Ron Davis due to his social media presence I’d say, which is akin to getting funding. Which bothers me a bit since I spent a lot of time raising money and having family and friends donate to OMF.
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And not just OMF. He's also funded by WE&ME. That's a shame because I think they're able to collect a decent amount of donations.


They have Ron Davis and Putrino on their scientific advisory board.
 
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