Have you looked at the spin in his previous papers?How can anyone look at these details and think of Simon Wessely? This is going to be the deepest biological investigation of ME ever conducted.
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Have you looked at the spin in his previous papers?How can anyone look at these details and think of Simon Wessely? This is going to be the deepest biological investigation of ME ever conducted.
I haven't read the papers yet, but how can he be our SW when he plans to look at extensive physiological data?Have you read the prior papers from the lead clinical investigator? Because I'm up to three for three looking pretty bad. The 3rd one is musing on the evolution of the symptoms of fibromyalgia, and it's similarities to neurasthenia, with the attraction of being a "real illness" ...
I think we've found the American version of Simon Wessely.
Because he specializes in burying physiological data, or explaining how that data proves the problems aren't really that real. Wessely has certainly done the same thing, such as with low-dose hydrocortisone trials.I haven't read the papers yet, but how can he be our SW when he plans to look at extensive physiological data?
Even if mouse 'models' were any use at all (doubtful), how on earth can they create a model of an illness with unknown aetiology and unknown biology? Not to mention such complexity that it requires sufferers to be able to describe how it affects them.- NIH will make stem cells + neurons + humanized mice with ME patient cells - they are making a mouse model of the illness
Your welcome! I was able to record the audio on my computer. @mango has put up a recording here:Did you record it? How? Thank you for the transcript!
I don't think the main criticism was ever that the NIH is not serious. The main criticisms are to do with patient selection and exclusion criteria and choice of control groups.If anyone looks at that plan and decides NIH is not serious about this, they need to take a few steps back from the screen.
and another seems to be going the central sensitization route (your brain just thinks you're fatigued) for GWS/CFS.
The central sensitisation route is what is supposed to explain FMD, so that is a worry, because the use of FMD as a control is very odd.also a deep weirdness with the FMD control group. I hope Dr Nath will respond more fully about that control group in days to come,
Worrying, but hope you can share some titles/abstractsHave you read the prior papers from the lead clinical investigator? Because I'm up to three for three looking pretty bad. The 3rd one is musing on the evolution of the symptoms of fibromyalgia, and it's similarities to neurasthenia, with the attraction of being a "real illness" ...
Probably can tomorrow, but it's getting late here.Worrying, but hope you can share some titles/abstracts
Here is Fred Gill.I don't think the main criticism was ever that the NIH is not serious. The main criticisms are to do with patient selection and exclusion criteria and choice of control groups.
Again, we're getting bombarded with information from various sources and none have been consistent. The unintentionally posted protocol says Reeves, advocates speaking to NIH say all criteria including IOM, these slides say Fukuda+CCC. Again, I will continue to reserve further judgement until the full protocol is posted in its entirety on the NIH website.
Here are the screen shots
Perhaps that's where the Reeves idea came from.
Gill’s a big fan of the Centers for Disease Control’s Empirical case definition, AKA the Reeves definition. He loves the—gasp—"excellent" questionnaires that the Reeves definition used, as well as the CDC's 2006 gene study.
To be sure, we're going to turn these people inside out. I don't think it will change anything though. The study will go on and these are the people that will be involved whether we like it or not.I think we systematically have to go through all the names to see whether these people will be helpful or not.
Kati, may I post these on Simmaron Research, if I give you credit, and how do I identify you for that credit?
I think I heard that the plan is to transplant some patients' cells to the animal, to see if the animal then has an illness response. But I might be wrong and I didn't catch any further details.Even if mouse 'models' were any use at all (doubtful), how on earth can they create a model of an illness with unknown aetiology and unknown biology? Not to mention such complexity that it requires sufferers to be able to describe how it affects them.
Principal investigator: Avindra Nath.
Lead clinical investigator: Brian Walitt.
So there are some concerns about Walitt, while Nath is looking good with his comments on welcoming patient involvement and AIDS activism.
Does anyone know what their roles are exactly? I suspect ultimately Nath is in control here.
Nath doesn't seem to have any prior experience of ME/CFS, so might be relying on Walitt for his "expertise" in FM and GWS.Does anyone know what their roles are exactly? I suspect ultimately Nath is in control here.
This is not a study of those two illnesses.Nath doesn't seem to have any prior experience of ME/CFS, so might be relying on Walitt for his "expertise" in FM and GWS.
Because he specializes in burying physiological data, or explaining how that data proves the problems aren't really that real. Wessely has certainly done the same thing, such as with low-dose hydrocortisone trials.