Video, Emerge Symposium 2019: Dr Neil McGregor, An Omic Analysis of ME/CFS – an Assessment of Potential Mechanisms

There is a lot of biomedical research underway lately, showing clear physiological changes in pwME compared to healthy controls. Is it possible to also show that these physiological changes differ significantly from people who are solely deconditioned? Because it seems this could be a key diagnostic - Yes, pwME can be shown to have clear physiological discrepancies, and No, they are not (solely) deconditioned. I say 'solely' because people with any illness that severely inhibits their ability to exercise, must also be deconditioned; the key distinction being also not solely.
 
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Aroa said:
I thought ME was a hypometabolic disease :cry:. I am confused.....
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Same here ! I thought that ME/CFS is hypometabolic.

@Andy Thank you for the shout out. I just want to take the opportunity to say that Professor Fiehn at UC Davis may also be onto something because he mentioned Bile acids at his presentation at time mark 1:37:39. I am very excited about his work, this is what we need to put things together and ultimately to find how everything is connected.

Also at one point i also heard one person from the audience asking Jose Montoya at 7:38:52 mark on day 2 whether it is possible to join by Network Analysis all of the findings we have so far. This is how we must start thinking.

IMHO We are getting very close, we just have to see the big picture.
 
Aroa said:
I thought ME was a hypometabolic disease :cry:. I am confused.....
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strategist said:
Confusing indeed, but maybe it just depends on the point of view. In the cell versus what is going on outside.
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My current take: the cells are working flat out (hyper) but due to some glitch in the system still cannot produce enough energy (hypo).
strategist said:
I'm glad researchers are finally looking into abnormal glucose tolerance.
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Same here. There's some very odd things going on with my glucose levels and I'd love to know what, if any, connection there is to ME (for the record: I think there is a connection but what and which way I've no idea). Though in my case the link seems to go through hyper- rather than hypoglycaemia, for example during PEM my glucose levels are significantly higher.
 
All looks very interesting. I like the way he is trying to start linking things together.

The conclusion slide is quite good apart from the taurine one which looks a bit shoehorned in ...a lot of the word “may” for my liking...this looks like it’s too early to tell or that there isn’t enough/any mainstream science to key into for what appears a very loose hypothesis. I worry when I see things like this in the conclusion section (regardless of venue/context).
 
Is anyone here able to explain McGregor's hypothesis in simple terms?

I've watched the talk twice, with lots of pauses to read the slides and try to process everything but I remain confused.

He covered lot of interesting ground and I felt I understood each individual point but somehow I can't get them all to hang together to form a coherent whole.

So what exactly is his hypothesis? Hypermetabolism, I guess, but what precisely does he mean by that? And how does he propose testing his hypothesis?
 
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