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This paper is interesting also in the sense that it is a recommendation/invitation to pharma scouts to at very least sponsor some daratumumab. It's much easier for pharma to do this with a paper like this one out.

Would your model still hold if a significant number of patients had low IFN-γ levels in blood, @Jonathan Edwards? Or asked differently, would it hold in patients with low IFN-γ?

Very interesting! I’m a long-term very severe patient. NSAIDs change things a bit for a while—not just the pain. I have no elevated inflammatory markers on standard labs; quite the opposite—mine have been described as 'suspiciously low.' Interestingly, there was a Gulf War illness paper showing...

What do you make of the fact that some people — and I’d say it might not even be a small subgroup — can lessen the impact or occurrence of PEM with NSAIDs? And it seems to help specifically with PEM. How, if at all might this fit with your ideas? I remember a renowned specialist in diabetes and...

If gamma interferon is really the issue, isn't treatment likely to only or mostly work in acute and subacute scenarios? Secondary pathologies (like 'mitochondrial dysfunction' or persistent glial activation,...) may persist independently of the original trigger?

I don't know who you are and what you are working on exactly, but I think if you do something rather than nothing that's a good thing for all of us. Also, having read only a few of your posts, I agree with a lot of what you say, and I am sure many others do as well. Absorb and learn from what is...

This is certainly an interesting finding, I think time course of the disease will be relevant, though. We need to find better ways to stratify ME/CFS patients in the future. Quoting the study re IL-3: Among the cytokines measured, the differences between controls and Long-COVID patients were...

I am not sure any of the findings (low VitE, low Q10, low Selenium, increased 8ISO-pgf2alpha, low GSH, etc.) pointing towards increased oxidative stress/ROS/redox imbalance have been replicated, but I think these might be significant findings that could be easily replicated.

Would it still be a 'non inflammatory condition' then? It would maybe not be surprising if the same patients (patients were recruited in 2021 and 2022) would show an 'exhausted phenotype' or at least some significant changes by now? Fascinating how many seem to assume these conditions are static.

There exists no such thing as the one and only way/modality/model for research funding allocation. That's because people simply don't/can't know what will pan out in the end. At best you can make sure that obvious nonsense doesn't get funding, but even that is fraught with issues. There are...

I don't think any of this is really known, in part because we don't collect data during the acute phase from people with symptoms suggestive of these conditions. Doing this could turn out to be useful to delineate patients. The 1 year cut off, where does that come from? I heard 2 and 3 years...

Missing the different stories? Then you’re surely missing the whole story. :)

Very interesting, thank you! PS: I am not certain, but I think IL6 and TNFa were also elevated in Montoya's paper?

What you are describing is only one of many effects of IFNg? So, while what you are describing as silent, might not be the whole story? I am certainly very interested to see how this will pan out in your paper!

Wait, excessive IFN-γ means inflammation, right? (Isn't that quite a new direction for you?) Is the idea then that excessive IFN-γ activates macrophages as part of the innate immune response? If so, the difference between PVFS and ME/CFS might then be: The level and duration of this...

This might be so, what you are describing is still sepsis. Please explain how exacty I changed my story! (Edit: Please don't; waste of energy) You could study inflammation for another 100 years, and still have zero clue about what happens in ME/CFS acutely and subacutely without testing it...

What you are describing is sepsis, and I am aware most (definitely not all) use the term hyperinflammatory exclusively for that. Please think of it as increased iflammation, that's what I meant. The fact remains, we know next to nothing about the initial (acute and subacute) inflammatory (!)...

There is no infection (=trigger of ME/CFS in most cases) without a hyperinflammatory state, unless you want to use that term exclusively for sepsis etc. You will naturally miss this 'signal' if you diagnose patients only 6 months later. It's like saying there is no inflammation in post sepsis...

'There is no inflammation in ME/CFS' is as problematic as 'there is strong inflammation in ME/CFS'. Chances are high inflammation is involved in the diseases process, it's just a question of timing. There is somewhat of an emerging pattern in LC that patients might have an inadequate initial...

There are some quite serious people like Wolfram who think it's essentially impossible to explain and understand AIs' 'reasoning.'