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To test the non-existent biomarkers related to SGB or ME/CFS or both. It ties into the reason for doing the trial in the first place.

@rvallee the problem isn’t the level of reasoning, but being able to understand why an AI-model gives any given output. This is important to avoid e.g. discrimination.

You’d need to properly justify running it in the first place.

10.5 In conclusion, on the validity of the study The basic assumption about what causes PEM/PESE thus influences the choice of study population and outcome measures, which in turn systematically affects study results and perceptions of the generalizability of the results, i.e. the validity of...

SGB can be risky as well: Out of a total of 1909 articles, 67 articles met our inclusion criteria, yielding 260 cases with adverse events. In 134 of the 260 (51.5%) cases, SGNB was performed with image guidance. Sixty-four (24.6%) and 70 (26.9%) of the complication cases reported the use of...

Rituximab showed large placebo effects with blinding. This was unblinded and without controls. SGB is already hyped in some communities. I worry this will make it worse.

«No measureable abnormalities are found». That’s a blatant lie. There are plenty of things that are wrong, we just don’t know how the pieces fits together.

We don’t know if it’s impossible or not. So I tend to not take extreme opinions very seriously. Also, there are proxies for «reasoning» that could be meaningful even if we’re unable to get at the pure reasoning, if that’s even a thing.

I don’t have the capacity to explain fully now, but the field of Explainable AI (XAI) would probably be the best bet when it comes to insight. In short, XAI tries to find out what the model has learned or how it made its choice. In the iMCD example, you would use different techniques to try...

The journal didn’t admit it though, only former employees. The journal would probably prefer to keep it an open secret.

Sooo.. Open-label and subjective outcomes?

Idk what it is, but that’s a fair guess. No model is valid before we know the mechanism(s) of ME.

Ron Davis claims to have ME/CFS models in bacteria, zebrafish and mice/rats. A team in Utah, apparently. They are using them to screen all FDA-drugs++.

I don’t know anything about GWAS, but I do know that a lot is happening in AI. And AI is really, really good at spotting patterns in data. So it has never been more likely that we would be able to find something if it actually existed. I hope that DecodeME makes the data publicly available. If...

That’s bleak…

That’s a savage line! Luckily the conclusion describes gender as demographic. But it wouldn’t put it past certain people to conclude that the gender influences the psyche.

I understand what the lobby wanted and why. But I don’t understand what kind of leverage they had on Cochrane to get them to agree to doing it that way. Cochrane must have understood that pwME would not let this pass, so something must have made them think that it was worth it to please the...

When did sleep disturbances become psychological?!

Given the lack of testing, the control group is bound to be contaminated with undetected infections. 5-6 % lower bound prevalence of LC within 180 days is equivialent to ~17-20 million Americans.

I wonder what kind of leverage the BPS lobby has on them. Surely they must have known that S4ME and pwME wouldn’t give up on this.