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I already stated the problem: participation and reporting biases. Such biases certainly apply to whether financial or relationship problems were significant enough to mention. The controls in Sailit 1997 are not recruited in an unbiased way either. All of the studies you mentioned are...

Retrospective studies which used questionnaires, and recruited people who were willing to answer those questionnaires having some idea of what the hypothesis is. (Such evidence is only ever suggestive, not conclusive).

No, there has been insufficient study. But they can trigger autoimmune conditions (rarely), some of which (Guillain–Barré syndrome) cause ME and CFS like symptoms long term in many patients.

Sharpe just says stuff he thinks suits the message he wants to provide, regardless of the facts. He's been caught out making misleading/wrong statements to the media before too. Both the depression and genetics stuff are equivocal, there is some familial association but that could be due to...

Seems like a confusion of cause and effect. Those who are capable do more and become more flexible as a result...

I've experienced this occasionally, sometimes I feel a bit more energetic when I get an infection, but it is still far from being well. It's kinda irrational but everytime I have an infection, I hope I'll get well again - but it was years ago since I met someone who coincidentally became well...

The only proven "placebo effect" is the short term reduction of pain through conditioned activation of the endorphin system, everything else is speculative aka pure bullshit.

What are they measuring exactly? It is important not to confuse the various reporting biases with a true placebo effect. I daresay, across ME patients as a whole, these reporting biases are likely to be similar to any other patient group.

87% is very poor for a cherry picked/post-hoc threshold.

For any marker to be used as a diagnostic test it needs to have very high sensitivity and specificity, demonstrated by replication studies comparing to other illnesses as well as healthy controls. As far as I know, no numbers of sensitivity/specificity have been published for the buspirone...

I've suggested something similar to DT, namely that the goal is to encourage scientists to join the field, so we need positive stories of scientists becoming involved.

All the minus SD stuff is bullshit because the general population distribution is highly skewed with a prominent ceiling effect. The should be comparing to a population percentile. For the general population with demographics similar to the people in the PACE trial, a SF36 PF score of 60 is...

It is true that "stress" is not a disease, it is a mostly meaningless buzzword used to mean all sorts of things. See: http://journals.sagepub.com/doi/10.1177/1745691616635593 Leaving work due to "stress" is a bad idea. Instead there are more meaningful underlying reasons. But ME or CFS are not...

Whether or not ME/CFS is considered a psychosomatic disorder or not is irrelevant (by the researchers at Columbia). The problem with Fink is his comittment to poor quality science and use of authority to harm certain patients (KH).

I don't think people should get their hopes up at all. I'm predicting minimal changes at most.

Most of us don't discuss that though - it is deliberate mischaracterisation of our arguments by people who haven't bothered to listen to us.

The review is not going to disappear permanently. The best we can hope for is a downgrade of the evidence, with note that unblinded study combined with subjective outcomes is an unreliable form of evidence.

The article is still on the Cochrane site as of right now.

The bias is they trust authority over what I have to say.

Anyone else afraid to watch this? I'm about to visit relatives who might have watched it (and they are not the most supportive...)