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It's a good question, I've seen plenty of the images in powerpoint meetings but not sure if any of this is published or public facing. I think that is a bit odd. So the work they do relies upon the upright MRI because they are looking at the ligaments. I believe they do flexion X rays too. If...

Yes there are some attempts to test it but it's quite difficult to prove or disprove these hypotheses. That's the main limitation of working on this hypothesis IMO. Obviously you want to be able to test it in a way that gives a definitive answer, that's not possible yet.

No I wouldn't, this hypotheses suggests there might be hundreds of genetic variations in an ME cohort that lead to a similar phenotype. So what Ponting and co landed on is plausible, a very heterogeneous disease that is compounded by the fact that healthy controls may have the same genetic...

Yeah I'd say most of the research has been around mitochondrial diseases because they have quite a strong field presence for research and funding. There may be many more beyond these that may be infection-onset. Check out POLG1 infection onset.

Kaufman has been involved in a number of trials for ME/CFS medications. I think he's at least responsible in that he continues to work on trialling the treatments offered in his practice. I agree that the surgery itself is dangerous and I wouldn't personally recommend it. I've known some...

It's a board of varied opinion. OMF doesn't dictate to the board members how they should comport themselves and what advice they give their patients and scientists. These clinicians/researchers add their perspective to discussion but have a common respect. I think it would be more dangerous if...

That would be the expectation. The increased use of amino acids is meant to happen in a stressed state, it's more Carbon efficient than glucose/fat (which is why we use it during stress, females go to this well faster) but it produce more negative byproducts and removes amino acids from the...

The basis of this hypothesis is that the increased reliance on amino acids for ATP production has consequences that could explain many of the symptoms and that the increased reliance on amino acids could be driven by many factors that may be different between people.

This work has had delays on my side trying to work out some red tape. It is expected to be completed in 2026. The pilot work was done.

I haven't heard of this group in ME/CFS circles before. Has anyone else?

You probably know this but my understanding is that POT is postural orthostatic tachycardia, it occurs in healthy people too. You stand and your HR jumps up and stay up by 20bpm from resting for over 10 minutes. POTS is that you have a suite of symptoms along with POT. Clinicians are confident...

It's annoying that they took the "it's a diagnostic test" approach to the data when simply comparing ME/CFS to healthy people. You don't need a test to know they are not a healthy population, you need to know why they aren't a healthy population, what is it that is causing this and what markers...

Have never met Maes, has anyone here?

Yes I think adding IFN-a as a stimulant is worth trying. We were already thinking about it.because of the itaconate shunt theory.

So CD24 was elevated on ME/CFS B cells compared to healthy when we take them straight out of the blood. CD38 only popped up as significantly different between ME and controls when we stimulated the B cells in vitro. CD38 elevating suggests the B cells may be more rapidly transitioning to...

Still meaningful. But if they come to this idea from different data unpublished suggesting it then we'd have 2 studies rather than 1. That's all I meant.

Part of me wonders if Norwegians thought to trial this drug based on our study as I think we showed them this data before 2020. Took a long time to publish the paper as it kept getting rejected and Fane had finished his PhD (he was driving the cell work). I say that because this may not be two...

We cultured the ME/CFS patient and healthy control B cells after both t cell dependent and t cell independent stimulation. We measured CD markers at day 0, day 3 and day 6. What we noticed was that the % of B cells with CD38 grew significantly faster in ME/CFS compared to healthy. We also found...

I agree with you regarding burden of proof. Not saying your take on controversial at all, I'm being controversial because I have these questions on what can be done for what I fear is a wild West of treatments in the absence of approved ones. If we were in a situation where there were some...

I haven't seen anything promising from Long COVID. The treatments I think have strongest weight of evidence amongst majority of clinicians with least risk (though without trials) are pacing for ME, LDN for Fibro, salt/water for POTS.