Purinergic Signalling and Thyroid

debored13

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Given that Naviaux has been talking about CFS as hypometabolism, and has been doing some of the most robust research on CFS, I wonder if anybody has tried to find the links between his model of purinergic signalling being disrupted, and thyroid issues. Also curious about how these two connect to mast cells. I haven't had the energy to look into this stuff for awhile but I think it's possibly a promising area. Dumping some links in case anybody is curious/wants to follow up.

the leading theory on cfs/me now is by robert naviaux. IT's an idea that CFS is an illness state caused by an initial response to a pathogen causing purinergic signalling to be switched on, and never get switched off.http://www.pnas.org/content/113/37/E5472

I've started to find a little evidence for purinergic signalling crossing over with thyroid issues, which is not surprising, as purinergic signalling is very important for intracellular signalling across a number of physiological systems

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3944044/

search and you may find more... i'm very tired

https://www.hindawi.com/journals/jtr/2013/434727/
 
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Also curious about how these two connect to mast cells.
I thought this Aug 3 paper was a good read. It ties a lot of the research together in one place and hypothesizes that Mast Cells are activated in the brain by CRH.
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome-Metabolic Disease or Disturbed Homeostasis due to Focal Inflammation in the Hypothalamus?
http://jpet.aspetjournals.org/content/jpet/early/2018/08/03/jpet.118.250845.full.pdf
Mast cells are also found in the pineal, the pituitary and the thyroid glands (Theoharides, 2017) further extending their contribution to the symptoms of ME/CFS such as sleep disturbances dysfunctional HPA axis and fatigue due to thyroid dysfunction.
And this is the third paper I've read lately talking about CRH activating mast cells. CRH is at the heart of the Cortene hypothesis.
 

Wishful

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Whenever I read papers such as this, about ME/CFS metabolics, I wonder whether their patient samples were only from the sub-group of those with physical limitations. If so, then the findings are about a common symptom, not necessarily the core cause.