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Congratulations @Tom Kindlon and thank you for what you have done for others!

Well, studies have already shown Pax not to work, so you purposefully don't have a only Pax group because otherwise you'd run into the problem of showing something works as well as something that doesn't work at all. But of course Putrino has already published a largely identical study for only...

To some extent yes, but to some extent no. This discussion might be very vague, handwavy and a full of belief but of course an actual model would not be that (and nobody has ever even tried developing a neurological model of ME/CFS). I'm thinking of something that should be examinable if you...

Yes, but I don't think there's a need to invoke a very localized theory nor global detactable changes, if I'd guess one would probably anyways want to do the opposite precisely because things would have otherwise been seen. Firing patterns are anyways pretty noisy and complex, if one say was to...

Soon w.r.t. research timelines, not w.r.t to the immense suffering that ME/CFS causes.

I think it is quite clear that any model would have to avoid such scenarios, but I wouldn't see why there's not enough wiggle room for them to exist but that's probably something where serious neuroscientists have to get involved. To avoid an epilepsy-like phenomena one might invoke something...

The situation is quite different though. F&M observations on Rituximab came at a point where they were not setting out making observations about ME/CFS. That tends to give such observations far more meaning due to the role of the observer. If someone sets out to see what they want to see, they...

But the whole point is that this has nothing do with ME/CFS. One thinks to see "responders" in any intervention for any condition because of things like regression to the mean, natural recovery, Hawthorne effect, placebo-like effects, subjective outcomes etc, there's countless papers and books...

Because you have to establish efficacy on a population level basis first. For the most part, all the drugs that work have been shown to work in phase 3 studies, even when they don't work for everybody (or there is a reasoning why they should work a sensible dose-response curve or something...

Yes but increased activitation in one region in one study (but not other regions) then increased activation in a different region (but not the previously mentioned one) is pretty much an opposing finding already in that it doesn't support the previous results. There is nothing consistent in the...

I think the problem is that the possibility of chance findings there is extremely high as there's lots of noise. If the sort of problems that exist in ME/CFS are not tied to a specific region, not global and not very stark either but more like "occasionally a bit of extra neurological noise here...

Yes, I think the models that are being discussed here are all more or less a version of such thoughts (maybe not specifically regional hyperexcititation which should possibly be seen in EEGs so things have to be more subtle). The problem of course is anybody is in their right to say: This is...

The risk are unlikely to be the same and maybe not even the benefits for the individual even if the treatment eventually turns out to be effective. For a given individual the risk of an off-label attempt is likely much higher than the risk of participation in the trial for the reasons already...

Above you mentioned the mtDNA study that looked at calcium-dependent mtDNA release and synaptic signaling and used that as a possible metabolic mechanism to explain cognitive PEM. I assumed that the explanation was metabolic in the brain but that the symptoms produced come from neurological...

Yes, people that think of donating to a phase 2/3 study as being "you get treatment vs I get treatment" probably won't be donating, but I have hope that there are enough ME/CFS patients that are sensible enough to understand that this is not what is occuring and that understand that the point of...

I understand that vague references to "something to do with synapses/neurons" are not be more insightful than "something to do with brain-metabolism" but is this not essentially all the same? If the suggestion is simply that there is diminished synaptic signalling that could explain symptoms of...

I'm not sure what you'd want to be pointed at. Cytokines are standard enough to have been measured in blood in numerous studies of ME/CFS (certainly more than 50 studies possibly more than 100), for instance in the intramural study and there's meta-analyses on these topics as well. Someone might...

@nataliezzz this would be evidence against your idea that OSA plays a role in ME/CFS if one was to believe the authors, right? Because the authors claim TNFalpha and IL-6 to be elevated in OSA and we know that they are not elevated in ME/CFS.

According to Google there are also responses with Rituximab in Lupus for 12 months, but google also says that it's suggested that "memory isn't removed in general". The study you cited above only had a 12 month follow-up so I'm not sure whether it is relevant to the discussion on whether "memory...

But if you don't know this then the comparison fails. If one was to believe the remissions in ME/CFS were drug related (for which there is of course no evidence) then they were permanent and there was no need for maintenance dosages, if this in not the case in Lupus then things have to be...