Blog by Cort on Simmaron's site (haven't read it all yet):
http://simmaronresearch.com/2015/09...une-exhaustion-and-new-gut-findings-in-mecfs/
http://simmaronresearch.com/2015/09...une-exhaustion-and-new-gut-findings-in-mecfs/
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They’re finding evidence of significant changes in the gut flora of ME/CFS patients vs healthy controls. For one, altered levels of butyrate producing bacteria have been found in the ME/CFS patients. Noting that similar differences have been found in autoimmune diseases, Dr. Hornig proposed that an autoimmune process may be fueling the symptoms in a subset of patients.
That nice concurrence between immune findings in the spinal fluid and in the blood was encouraging, and the group is digging deeper into those CSF samples. Thus far a factor called cortisol binding globulin (CBG) has popped up in protein analyses.
oThe first cerebrospinal fluid study using Dr. Peterson’s carefully collated samples found a similar pattern of immune system down regulation. That study (supported by CFI and Evans Foundation) included only longer duration patients. These two studies – the first to find similar issues in these two different compartments of the body – suggested that the immune system had taken a system wide punch to the gut.
What could cause this kind of immune exhaustion? Dr. Hornig stated it’s usually associated with chronic infections.
[my bolding]Noting that similar differences have been found in autoimmune diseases, Dr. Hornig proposed that an autoimmune process may be fueling the symptoms in a subset of patients.
I don't quite follow this sentence. Is @Cort saying that classical patients have more immune down-regulation while complex atypical patients have higher (more normal?) levels of the measured immune factors? Or that complex atypical patients have immune up-regulation? Or something else entirely?Virtually all the immune factors tested were higher in the complex atypical vs the classical patients.
How so? Does this mean the the immune dysregulation in atypical patients is less clear, or nonexistent, or in the opposite direction to the immune dysregulation in classical patients?Similarly, without excluding Peterson’s subset of atypical patients, the cerebral spinal fluid study findings would have been insignificant.
Wow, hadn't heard that before...very much looking forward to what the next few years will bring. She said she was cautiously optimistic that the IOM and P2P reports, the positive immune study, plus the signs that the National Institute of Neurological Disorders and Stroke (NINDS) may be interested in taking ME/CFS on, indicate that a turnaround for ME/CFS funding is in store. - See more at: http://simmaronresearch.com/2015/09...w-gut-findings-in-mecfs/#sthash.b4pbN8xI.dpuf
I've looked at that gene (SERPINA6) before, with the 31 patients I have full data and roughly matched controls for. We're totally normal - more so than the controls even."@Valentijn, can you possibly see anything odd in your n=50 material from 23andme?
the signs that the National Institute of Neurological Disorders and Stroke (NINDS) may be interested in taking ME/CFS on, indicate that a turnaround for ME/CFS funding is in store.
I thought she was sympathetic and constructive and relatively well-informed. I thought we'd do well to have ME moved to her department. (Can't remember her name.)This sounds like happy-talk based on hand waving at the recent CFSAC meeting. Some people watching the meeting thought the NIH rep was sympathetic, while she was mindlessly repeating the party line about lazy researchers won't repeatedly resubmit grant applications and the ones that do are too stupid to fill out the forms properly.
Perhaps it fits the recent autoantibody research too? i.e. adrenergic receptors. (But I don't know how adrenergic receptors would interact with CBG.)"That nice concurrence between immune findings in the spinal fluid and in the blood was encouraging, and the group is digging deeper into those CSF samples. Thus far a factor called cortisol binding globulin (CBG) has popped up in protein analyses. "
Like @Bob I found this interesting. Did it "pop up" as a high or low value? As the CBG has to do with the distribution of cortisol in blood and so many of us seem to have cortisol disturbances with great impact on health it would be interesting to know if it might be of genetic reasons the CBG value isn´t normal in PWME.
Well, there is this:Like @Bob I found this interesting. Did it "pop up" as a high or low value? As the CBG has to do with the distribution of cortisol in blood and so many of us seem to have cortisol disturbances with great impact on health it would be interesting to know if it might be of genetic reasons the CBG value isn´t normal in PWME.
I thought she was sympathetic and constructive and relatively well-informed. I thought we'd do well to have ME moved to her department. (Can't remember her name.)
Yes, we liked Dr. Vicky Whittemore from the National Institute of Neurological Diseases and Stroke.I think there were two NIH reps - one who favourably impressed me and one who didn't.