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I can see that, and maybe it’s what’s needed to get a result. But like you, I think it’s high risk, as well as not the right way to go. The numbers are already pretty big, and I wonder if making them even bigger make the case that much stronger. Especially as a lot of politicians are even...

Yes. We have no data on whether or not these people have the same illness – no evidence at all. What we do know is that long Covid is “defined place great by a couple of hundred symptoms – it’s not based on a limited number of course symptoms. Some definitions of long Covid, which have been used...

We do. The 50% figure comes from biased samples, either specialist clinics or social media groups, who are likely to be more severe. And the massive numbers come when you apply the 50% figure to the ONS data. It is the ONS data itself that undermines the 50% claim. Because the ONS studied also...

Yes, that frustrates me too, especially when it comes to LC-ME estimates, which don't square with the data. But this higher estimate of 0.6% (previous best estimate was probably Jason, 1999, 0.42%), largely using pre-LC data, looks good.

I think there is a question mark about UK biobank diagnostic reliability. People were asked either if they had ever had a diagnosis of chronic fatigue syndrome, or Myalgia and celery -itis/ Chronic fatigue syndrome. It’s too easy for people with a diagnosis for chronic fatigue – which is pretty...

Agreed, it’s not a Mendelian disorder. But each individual hit could point to a biological process that plays a part in the illness. It could be one of several parts. Or it could reflect some of the likely-several different sub groups. Ideally, you would find several genes that played a...

I’m guessing it wouldn’t make a great deal of sense of people to start pursuing 115 different candidates on the basis of a small study and a potentially over fitted model. But comparing these results with other studies might be very useful eg the DecodeME GWAS and the precision life work on...

Thank you, that’s still encouraging.

You said this on the 25th of March. Are you still thinking of making your ideas public on that kind of timescale? And I seem to remember you said you theory would also indicate a potential existing treatment. Does that still look like a possibility? thanks

Thanks, and to @forestglip for the explanations. You could say that a GWAS is essentially scanning all of human biology to find clues about what processes have gone wrong. But with a relatively small study, such as DecodeME at 20k, it's likely you will miss a lot of clues.

What an extraordinary database string is, and brilliantly explained. Also, what a cool red chair in the background

What is A3, Mario? Still means a paper size to me, I’m afraid. Because I thought that was an amazing list, , Including some quite sophisticated points. Basically over my head. I’ve messaged Chris! A few points based on a limited amount I know: I had previously heard that the minimum useful...

Thanks, I hadn’t seen that. I had a feeling I had seen a survey results of a similar question before, but I couldn’t say where. But just to recap the results For those who have PEM after both physical and cognitive exertion: Fundamentally different: 9 (13%) Fundamentally the same: 17 (25%) Some...

I don't remember doing so, but as this was yesterday morning there is no chance I would recall :) Possibly - but a small difference vs none isn't much of an effect. Someone on PR, who I think is here too, did a brilliant analysis of 6MWT results of clinical trials of modest exercise...

That’s very possible. And Negative findings are hard to publish in any field. But I would like to see a better version of this study done that gives us clear answers. I suspect that answer would be a clear-cut negative, which would be useful, as you say – but either way I’d still like to see a...

Do you have any indication of how this group’s severity compares with people who took part in the Pace trial? The six minute walking test worked perfectly well there to expose the problems. But yes, a Fitbit test would be more useful. The Pace trial also did a fitness test, which showed that...

Thanks for pointing that out. As I said, I only skimmed. So, they calculated the right measure, and highlighted wrong ones that looked better? I had credited them with simple incompetence.

I’ve only had the energy to skim the thread and the paper, so this might be a little off track, or repeating what’s already been said. But I think this study is a step forward, for a couple of reasons: – it uses several sensible objective physical measures Which we’ve been calling for for such...

It is, thank you. I think I understand the key metabolic ideas more clearly. Though presumably the central question for any theory to answer is, “how does this cause ME?“ And as you say, this is where you rely on speculation to bridge the gap. I will bow out at this point, but thanks for taking...

Thanks. I was hoping for something more succinct because of my brain fog. From a quick scan of your other post, malate seems to play a central role, but I wasn’t sure if the underlying issue was presumed reduced Mitochondrial reduction of NAD(P). Can you sum it up in a couple of sentences?