The Gut: Fixing the Root of all my Problems

[JPV]

I use a vaporizer but that's because I'm addicted to nicotine. Maybe there's a reason for that though.

 

[aquariusgirl]

https://m.youtube.com/watch?ebc=ANy...HVnihNFrbW1_T7A&time_continue=8&v=J6z7tkwrfso

This woman says she has found something to help w/gastroparesis

 

[kangaSue]

@douglasmich

You might like to do a search on the work of Diane Driscol (sorry can't provide a link at the moment) who cured her gastric motility problems with a nicotine patch after she worked out that the problem was being caused by a sluggish vagus nerve. I think others chew nicotine gum when they wish to move their bowels.

Dr Driscoll said the effect of nicotine patches on stimulating bowel movement was only short lived, continuous use induced an inflammatory reaction that prevented enhanced acetylcholine signalling of nicotine patches from working to move the bowels (the vagus nerve is a nicotonic acetylcholine receptor) so she ended up developing her own supplement, Parasym Plus.

 

[JPV]

Dr Driscoll said the effect of nicotine patches on stimulating bowel movement was only short lived, continuous use induced an inflammatory reaction that prevented enhanced acetylcholine signalling of nicotine patches from working to move the bowels (the vagus nerve is a nicotonic acetylcholine receptor) so she ended up developing her own supplement, Parasym Plus.

Anybody interested in trying Parasym Plus might want to read this thread before going forward...

Acetylcholine caused crash

It's seeming that messing around with one's acetylcholine mechanism is potentially dangerous. In fact, I have now come to believe that the onset of my CFS started because of over-stressing my body's acetylcholine/acetylcholinesterase mechanism.

 

[douglasmich]

@douglasmich

You might like to do a search on the work of Diane Driscol (sorry can't provide a link at the moment) who cured her gastric motility problems with a nicotine patch after she worked out that the problem was being caused by a sluggish vagus nerve. I think others chew nicotine gum when they wish to move their bowels.

Interesting that you mention that because i have actaully watched her video. I have already been doing gargling for a year but its not working anymore. I have not tried nicotine. I have some ALPHA-GPC to try but i have not yet due to supplement intolerance.

 

[kangaSue]

Anybody interested in trying Parasym Plus might want to read this thread before going forward...

Acetylcholine caused crash

It's seeming that messing around with one's acetylcholine mechanism is potentially dangerous. In fact, I have now come to believe that the onset of my CFS started because of over-stressing my body's acetylcholine/acetylcholinesterase mechanism.

Conversely, having antibodies to voltage-gated calcium channels (N-type and P/Q-type) and or ganglionic nicotonic acetylcholine receptors can seriously screw up acetylcholine signalling resulting in chronic autonomic dysfunction.

I'm waiting on blood test results from Mayo to see if my chronic g.i. dysfunction (I don't have ME/CFS) is attributable to this because of Autoimmune Gastrointestinal Dysmotility (AGID, a restricted form of Autoimmune Autonomic Ganglionopathy) which coincidentally has been found as a standalone cause of chronic slow transit constipation.
http://www.mayoclinic.org/medical-p...ces/autoimmune-gi-dysmotility-a-new-direction
http://www.mayomedicallaboratories.com/test-catalog/Clinical and Interpretive/89886 AGID test panel.

Antibodies to N and P/Q type calcium channels also feature in Lambert-Eaton Myasthenic Syndrome which has a lot of overlap with ME/CFS symptoms. I see it mentioned a bit that N-type CGCC antibodies are being detected in some cases of CFS too.

 

[JPV]

Conversely, having antibodies to voltage-gated calcium channels (N-type and P/Q-type) and or ganglionic nicotonic acetylcholine receptors can seriously screw up acetylcholine signalling resulting in chronic autonomic dysfunction.

Interesting. Do you have any more information on this subject that you can point us to?

 

[kangaSue]

Interesting. Do you have any more information on this subject that you can point us to?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739271/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360501/
http://www.ncbi.nlm.nih.gov/pubmed/18474849

I haven't found any paper specific to ME/CFS in connection with calcium channel and acetycholine receptor antibodies but looking into Autoimmune Autonomic Ganglionopathy (AAG) and LEMS, some of the papers have mentioned finding these antibodies in some cases with a co-morbidity of ME/CFS

There's a lot of PR articles pondering the same question re ion channel dysfunction but without specifics, for instance; http://phoenixrising.me/research-2/...annelopathy-in-chronic-fatigue-syndrome-mecfs

sushi says Dr Kenny De Meirleir finds calcium channel dysregulation to be the case for some with ME/CFS, KDM's of the view not to take calcium supplement because of some irregularity in the calcium ion channel and holds the position that the fragmentation of RNase L indicative of viral reactivation in CFS/ME patients is what leads to ion channel disruptions. Not sure whether that means the problem is with voltage-gated calcium channel (VGCC) or potassium channel (VGKC) antibodies affecting calcium dysregulation.

http://phoenixrising.me/research-2/...elopathy-an-overview-from-patrick-englebienne
It's slightly off the subject but KDM's article above has an interesting perspective for nitrates though. This article says;
[The SUR I channel controlling intracellular potassium levels seemed a likely candidate for malfunction in CFS patients. (The SUR I (sulfonylurea receptor) ATPase dependent K+ ion channel is of special interest because its activity is a function of ATP activity.
Low levels of ATP cause the SUR I channel to open and release K+. Dysregulation of the SUR I channel typically causes severe muscle weakness because of severe K+ losses.) The body attempts to rebalance ion distribution caused by SUR I channel dysfunction through increased aldosterone production (by the adrenal glands) which leads to increased tubular secretion. None of the CFS patients exhibited, however, the severe K+ losses typically associated with SUR I dysregulation.]

The mitochondrial K+ATP channel is opened with nitrates. With chronic g.i. dysfunction, I tested negative for VGKC but have a low titre (normal range) for N-type VGCC Ab but taking nitrates (nicorandil and GTN patches) helped a lot with symptoms even in the absence of any muscle pain or K+ deficiency and my low bp increased which I've just realised is probably due to reduced aldosterone as per above. A lot of that symptom relief with nitrates has reduced for me, I'm hoping nicotonic acetylcholine Ab explains it, either AGID or AAG.

gingergrrl here on PR has positive N-type VGCC antibodies causing chronic lung issues but no problems with g.i. stuff. POTS or some form of OH is prevalent too in most cases, if not all.

I haven't had a chance to look at any of her work but Jonathon Edwards says a Dr Angela Vincent at Oxford University in the U.K. is a world authority on ion channel autoimmunity.