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JB Handley is also a vaccines-cause-autism guy.

That is a modelling study with far too many questionable assumptions. As such, it is important not to confuse pre-symptomatic and individuals who are deliberately not reporting symptoms (there is a strong incentive to do so if you wish to disembark!) with being asymptomatic. Likewise, PCR...

Yes, participation biases, a desire to please the investigators, and the fact that this is not an unheard of explanation can lead to an exaggeration of questionnaire reports.

There isn't reasonable evidence that there are any "asymptomatic" cases at all. I suggest such assumptions based on poor test specificity. There can be pre-symptomatic cases if tested right before the patient realises they are developing symptoms. Similarly, survey questions can be limited (eg...

Brain scanning, 19th century style! https://www.npr.org/2014/08/17/340906546/the-machine-that-tried-to-scan-the-brain-in-1882 Also notably, Angelo Mosso wrote a textbook on fatigue (La fatica) in 1891, the ideas of which have been repeatedly (re)"discovered" over the decades since.

Exactly. If cognitive and/or behavioural therapies actually led to remission, we'd all be in remission by now! It boggles the mind that anyone could think that LP could be any more effective than generalised CBT. Stoic, is that a nice way of saying laid-back and lazy? :p

Nothing new here. Lloyd claiming that CFS/ME can be a positive dianosis and extensive testing should be ruled out. He states the fatigue is not genuine weakness. He says that besides the fever, the symptoms of CFS are like that of an infection that never resolves and that occurring after an...

I must admit I first thought theDurdle Door cliff thing was a joke about people being lemmings...

Indeed. Seems strange that we can't find any more info about what they are actually doing.

Wow, how did all the crap about "moderate" make it through to the final publication, given all that discussion?

None of those conclusions are justified given the tiny sample size and no control group. The claims of CRHR2 upregulation do not seem to be associated with any (hitherto) published data. The higher dosage may have resulted in slightly lower symptom scores in 2(!) participants, but one of those...

Which begs the question how?

I've long been suggesting that ACE2 dysregulation is the key problem, but I doubt very much that it is genetics that will explain the variance.