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Is the suggestion then simply that EBV is more likely to cause some problems in neurons/synapses because the febrile response takes longer, or will there be 2 separate arguments for why EBV is good at causing PVF and good at causing ME/CFS?

So in short, the argument might really only work in one way due to the complexity of the brain and the inability to somehow view it as isolated?

Yes, but if I'm not wrong the 2 theories for that are: Increasing the likelihood of "bad B-cells doing bad things" or "something to do with viral persistence" and of course these effects take place years, sometimes decades after infection so how could a common pathway look (especially if we...

What is not quite clear to me about a neurological hypothesis: Why are these problems apparently more common after glandular fever? How does EBV seemingly have more influence on synapses or neurons than other viral infections? If we accept a comparison to something like a "ongoing sickness...

Whilst I can understand that people might be reluctant to such a model, because it might currently not be explain muscular problems in a straightforward way, there’s been an abundance of metabolic, muscular and so forth theories on ME/CFS but none of those have even tried to explain the...

I know plenty of athletes measure their core temperature (for example for heat adaptation training) using devices that look no different to the usual heart rate monitors they wear. Sounds like something that might be up the lane of someone like Wüst.

I think it can be consistent with the sort of neurological models that are being proposed here, something along the lines of "A typically noisy network is calmed down by a specific firing constellation of neurons" (for example acting like a sink that removes too much excitation) but of course...

Underarmpit temperature should have a good enough accuracy to tell you whether it's a thing, without having any extra hassle. Is that not what most people do?

Computational neuroscientists love to model things with no practical relevance, so they might have a field day here.

There have already been quite a few decentralized trials for Long-Covid with a similar setup to the one above. The Paxlovid study by Iwasaki had a similar setup. I agree that Long-Covid diagnosis will make things very tricky, if not meaningless, if these things aren't taken care of very...

I've only now come across this post by Hilda Bastian. I think she puts it beatifully and it's a strong piece. Patients deserve better than this regurgitated nonsense!

In my head I'm thinking of 2 different stories. For a GWAS to pick out genes that are linked to confounders in controls (say illnesses) the confounders have to be systemic. I think it may be rather hard to get systemic confounders from controls having a host of varying conditions that were...

I think there is no evidence of this and that such evidence should be easy to establish. I think there is the fact that people feel hot or feel like there is temperature dysregulation, but that might be something rather different to actual fever.

So if I'm understanding you correctly doing a specific very task that is largely cognitive in nature often let's you get normal sleep and you wake in a way akin to healthy people, whilst pretty much all other tasks give you "ME/CFS unrefreshed sleep, foggy brain and ME/CFS symptoms the next...

Maybe results of the larger phase 3 study didn't show anything tangible.

Yes, however in the DecodeME delivery plan it's mentioned that it won't be possible to use the same exclusion criteria for controls as for ME/CFS patients (https://www.decodeme.org.uk/app/uploads/2024/03/2024-03-15_DecodeME_Data_Analysis_Plan_v2_final.pdf).

I do wander whether this combinatorial approach won't carry some risks related to my previous question...

This still seems quite black boxy to me and I think in some sense one could maybe expect things to be easier to interpret for DecodeME, right? Here they use that fact that there was a massive GWAS meta-analysis for endometriosis (60 000 cases 701 000 controls) that identified 42 risk loci. They...

Thanks for bearing with me, hopefully after my necessary repair period things will sit more naturally with me tomorrow.

Thanks, I think that makes things clearer to me. So if I'm understanding correctly: In ME/CFS synapses become broken more easily or stop functioning as they should. This doesn't change network firing rates due to synaptic scaling (for example if Neuron B looses connection to Neuron A it now...