new Alan Light paper... alpa-2a, glutocorticoid implication

[lansbergen]

Some people with CFS/ME and POTS have ganglionic acetylcholine receptor antibody.
http://www.ncbi.nlm.nih.gov/pubmed/17352367

I understand that it is a muscarine receptor. My immunemodulator acts on the a7 nicotine receptor.

As B1 cells pump out large amounts of none specific anitbodies there could be some that can bind to acetylcholine receptors.

Then there is less acetylcholine release and receptors blocked by antibodies.

 

[Snow Leopard]

http://pharmacologycorner.com/alpha-receptors-1-2/

Snow Leopard and lansbergen,

Give me some help on my speculation here, please. Speaking specifically about the Alpha receptors, would one want to damp down the receptor response by using a antagonist? If so, then that would increase acetylcholine and norepinephrine, correct? Any spec speculation on what else an antagonist might do?

That and a million other things (as is usual in biological systems). It's all speculation from here on out.

The first question that comes to mind is whether the increased Alpha-2A receptor expression is serving a positive response or not. But the only way you'd really find out is by using an antagonist and associating a reduced Alpha-2A receptor function with reduced post-exertion severity.

 

[voner]

Thanks. I'm sure this is much much more complex and we should use caution in individual interpretation of these receptor studies. I wrote a blog about a presentation given by Dr. Bateman in Denver this summer where she discussed the various results of earlier studies by Dr. Light. She showed slides for individual patients and it became pretty apparent that patient to patient the responses of these receptors after exercise varied immensely. While most of the patients (with ME/cfs and fibromyalgia and NO orthostatic intolerance) had a similar response of increased alpha-2a receptor expression, there was a subset of patients with ME/cfs and fibromyalgia AND orthostatic intolerance who had a decrease in alpha-2a receptor expression.

http://www.cortjohnson.org/blog/201...yndrome-subset-if-doctors-will-just-look-for/

The impression given was that this decrease in the alpha-2a receptor receptor expression was correlated with orthostatic intolerance. I remember she said that the patients averaged a increase in heart rate upon standing of 28 beats per minute, thus she was forced to not call it POTS, rather "orthostatic intolerance", although she indicated clinically and symptomatically it was all the same.

I suspect the doctor Light group is also trying to ferret out what is evidence of pain pathways being activated and what is the evidence of fatigue pathways being involved, if any.

 

[MeSci]

voner
Valentijn is the guinea pig. So far so good,

Nicotine can replace acetylcholine on the nicotine acetylcholine receptors.

I use an a7nAchR modulator and smoke like a chimey. It helped me a lot. Improvement is slow but steady. I am not cured yet but compared to what it was when I started it I went from hell to heaven.

Safer to use electronic cigarettes, I would think, and you can control the nicotine hit better with them.

 

[MeSci]

Some people with CFS/ME and POTS have ganglionic acetylcholine receptor antibody.
http://www.ncbi.nlm.nih.gov/pubmed/17352367

From a quick look I didn't see anything about control groups in this paper. Also, it says

ganglionic acetylcholine receptor antibody was detected in 14.6%

so a minority, and would it be different from control groups?

 

[Valentijn]

The first question that comes to mind is whether the increased Alpha-2A receptor expression is serving a positive response or not. But the only way you'd really find out is by using an antagonist and associating a reduced Alpha-2A receptor function with reduced post-exertion severity.

I've been using the most potent antagonist, Yohimbe, and thus far it seems like it's reducing PEM. But I haven't really tried to provoke an episode, aside from a 10 hour flight + airport time (with wheelchairs).

 

[voner]

I've been using the most potent antagonist, Yohimbe, and thus far it seems like it's reducing PEM. But I haven't really tried to provoke an episode, aside from a 10 hour flight + airport time (with wheelchairs).

@Valentijn ..... How has your Yohimbe trial turn out? I would love an update...

 

[Valentijn]

@Valentijn ..... How has your Yohimbe trial turn out? I would love an update...

Still generally helpful, but doesn't prevent my episodes where I end up bedbound for a week or three due to intense OI. I had a couple of those happen a while ago, and had hoped that the Yohimbe was keeping them away! Still, I definitely do a lot better with the Yohimbe.

 

[ukxmrv]

Just resurrecting this thread and hoping that the fine minds here will comment on the next stage of the same research on this other thread

They are moving on now to measuring brain function before and after exercise

http://forums.phoenixrising.me/inde...-study-women-in-madison-wi.32633/#post-506209

 

[alex3619]

Is it possible that the up-regulation after exertion is resulting in the receptors getting worn out and under-performing at other times?

I doubt it. However over-expression might set in motion feedback effects leading to other problems.