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so the question might just as likely be why do so few people get ME/cfs?
Infection dose and enough rest?
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so the question might just as likely be why do so few people get ME/cfs?
Infection dose and enough rest?
Also about the fact that they have been looking at some autoantibodies I think regarding the hypothalamus? I cant remember now if I am using the correct word.
Very interesting, do you have a link to this work?
A bit too much emphasis on stress, in my opinion, especially the troubling slide at the very end that he skipped over which had a diagram featuring "worry and stress that something may be wrong" leading to "mild hyperventilation".
Please note that while CBG is considered by most as a transporter molecule, to a biochemist this view sets up red flags. CBG has the physical structure of a hormone, including the ability to partially bind to a cell membrane and interact like a hormone. I forget the details, I was looking into this around 2000.
This researcher could be valuable to us if we can get him looking at glucocorticoid resistance.
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I agree, but this depends both on how CBG is affected and the kind of assays used. I have not looked into this in enough detail.Thanks for this post. Another thing. I think it might be worth keeping in mind that the CBG is important concerning serum cortisol testing. If the CBG is affected, the serum cortisol isn´t valid, but a saliva cortisol is, as the saliva cortisol is independent of the CBG level. There are probably lots of "normal" serum cortisol results among PWME due to this. I learnt this from an endocrinologist.
auto-immunity to cell nuclei in the hypothalamus;
Ah, thanks Jonathan. I did wonder why he used the specific term 'nuclei'. On reflection, to my recollection, he didn't say "cell nuclei" in the presentation - that was my interpretation.I had a double take both this time and when Amolak said nuclei to me on Friday. I actually think he is talking of nuclei in the sense of clusters of neurons, not nuclei inside cells. The hypothalamus is divided into several such cluster 'nuclei' which are just groups of closely packed cells with white matter in between. Elsewhere in the brain there are caudate nuclei, nucleus caeruleus, nucleus gracilis, olivary nucleus etc. But I am still not totally sure what he is referring to. I think we need to wait and see because it is clearly very early days yet.
That was my understanding too.I actually think he is talking of nuclei in the sense of clusters of neurons, not nuclei inside cells.
This description of glucocorticoid resistance syndrome doesn't match CFS: http://www.ncbi.nlm.nih.gov/pubmed/17161335 (Note: I have only read the abstract, but HPA axis hyperactivity is not a typical finding in CFS).
What am I missing here?
Glucocorticoid resistance does not explain most of the evidence gathered so far. In fact major reviews and models have been written trying to explain findings of enhanced GCr sensitivity, which makes the most sense given all of the neuroendocrine studies so far in CFS.
The best (in my opinion) review of the neuroendocrine findings, despite being out of date and written by a protege of an unpopular psychiatrist is still this one:
http://www.ncbi.nlm.nih.gov/pubmed/1270018 (Cleare 2003)
There was a more recent attempt, but I was not as impressed:
http://www.hindawi.com/journals/isrn/2013/784520/ (Tomas, Julia Newton, Watson 2013)
(Anyone who is seriously interested in this stuff needs to read the above two articles).
The SNPs found by the CDC group, in the papers mentioned by @Helen have been suggest as a possible cause for this increased sensitivity (note again: opposite of resistance). And indeed this assumption is specifically mentioned in these papers (which does have some author continuity)
http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1000273
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0084839
Glucocorticoid resistance might be a problem in a few people, but it does not fit with the rest of the evidence gathered in CFS so far.
If there is a central problem here, then I am willing to bet that it will be something other than GCr SNPs, or alpha/beta ratios.
@alex3619
Polymorphisms in the glucocorticoid receptor NR3C1 has been shown to be connected to CFS.
http://www.ncbi.nlm.nih.gov/pubmed/16610957
http://www.ncbi.nlm.nih.gov/pubmed/16740143
The best (in my opinion) review of the neuroendocrine findings, despite being out of date and written by a protege of an unpopular psychiatrist is still this one:
http://www.ncbi.nlm.nih.gov/pubmed/1270018 (Cleare 2003)