i read through posts mentioning acetylcholine on the forum, for anyone interested here are some pieces (please read the threads for complete understanding, some context is lost here):
Nightingale - June 2012Acetylcholine seems to be a major player in this boy's symptoms, and maybe ours. Lecithin supplementation sounds like a good thing to try, in conjunction with fatty acid supplementation. The vitimin B6 deficiency seems to cause major increases in neurotransmitter receptors, and might lead to a burnout of transmitters that Acetylcholine seems to help make. I am going to look into it more, and pick up Lecithin tomorrow.
haidcat - September 2012?I discovered that it might have to do with lack of acetylcholine going to the Iris sphincter, Ciliary muscle, and extraorbital muscles. Norepinephrine leads to dilation of all these, and for me its really the trouble contracting these muscles that negatively impacts my life. So, I am trying to increase my acetylcholine levels to try to activate the acetylcholine receptors in those areas. The only ways I know are: 1. Huperzine A, 2. Alpha GPC, and 3. Nicotine.
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One more very very important point: ON many many receptors throughout the body norepinephrine competes with Acetylcholine; with NE being primarily a sympathetic nerve effector(triggers fight or flight responses) and acetylcholine being a parasympathetic nerve effector( calms you down, slows heart rate, allows better use of eye muscles, increases tear production, helps with digestion, etc.) This norepinephrine/acetylcholine competition of sorts, could be why huperzine A and acetyl-L carnitine work so well for Kurtosis. Indeed, it would seem that nicotine and alpha GPC would also help alot with POIS too if this is correct.
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I find that with my eyes, its not just a sense of tension + dry eyes. I find that the actual ability to focus using my ciliary eye muscles is severely weakened.The best way to describe it is taht my eyes constantly want to go out of focus, its like their natural state is to want to relax the ciliary muscles and hence effectively blur out my vision, making it nearly impossible to focus for sustained periods of time on any book or computer.
Now, in regards to this problem, I know acetylcholine/norepinephrine play a huge role because the actual contraction of the ciliary muscles requires acetylcholine impulses, and is negated by norepinephrine due to NE's dilation effect.
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So glutamate and acetylcholine are essential to contraction of muscles, and are culprits in conditions where muscles are too rigid/spastic/painful(Fibromyalgia, parkinsons, etc).
So it seems release of too much glutamate/acetylcholine cause rigid/painful muscles, while not enough release of these things would cause muscle weakness, and inability to contract muscles for extended periods.
kurtosis - September 2012There are some theories of ADHD which suggest the symptoms of poor concentration and hyperactivity result from impairment in the acetylcholine (calm thinking), dopamine (focus/concentration) functioning caused by too much noradrenaline (fast reaction & bodily defence).
poiseidon - November 2013The histamine H3 receptor has also been shown to presynaptically inhibit the release of a number of other neurotransmitters (i.e. it acts as an inhibitory heteroreceptor) including, but probably not limited to dopamine, GABA, acetylcholine, noradrenaline, histamine and serotonin.
which is annoying I add because such anti histamines are not yet available and I strongly feel they would do a major improvement on symptoms.
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lets say semen or "orgasm" or whatever is a flock of unharmful birds. the immune system is a radar that sends the signal producing histamines thinking the birds are actually 'zee germans'. the h3antihistamine blocks the reception of the alarming histamines. a friendly fire that would mess with our bodys headquarters the brain. making a chain effect that lasts a few days.
Jimmy - August 2014The difference is that the orgasmic stress occurs instantaneously upon orgasm and during sexual tension (extreme arousal), but both orgasmic and work stresses can last very long. To solve the orgasmic headache and nausea Orgasmic Stress), you have to
1. reduce the dopamine-norepinephrine-epinephrine conversion in the brain and adrenal medulla, and the epinephrine level in the bloodstream (who can do those? 5-HTP and Kava Kava!);
2. partially block the sympathetic alpha receptors;
3. increase the DHEA/androstenedione (for balancing testosterone and estrogen!) levels;
4. increase the acetylcholine and serotonin levels to modulate the sympathetic function for orgasm - de-stress the body for orgasm;
5. partially inhibit the acetylcholine re-uptaking in the synapses and power the parasympathetic nervous functions to balance the sympathetic functions that induce stress against the cardiovascular, digestive, liver, kidney and adrenal functions;
6. increase the prostaglandin E-1 (PGE-1) production in the local tissues by increasing the DHEA, acetylcholine (and its neurochemicals), and androstenedione levels;
VagSmasher - April 2015I think NE's and P0iS in general is caused by high levels of acetylcholine. I think when they finish there research, the answer will be in acetylcholine. Good luck...
b_jim - October 2015About acetyl-choline(AC), this is something we didn't look enough for and it's probably more complicated. It's linked to dopamine as a booster neurotransmitter (I remember dopamine is the accelerator and acethylcholine is the gas).
Some guys had improvment only by eating eggs (1 egg = about half of choline needed a day).
Some guys had improvment with acetylcholinergic meds.
Taurine seems to regulate AC.
I have the same problem with caffeine.
Nightingale - October 2015Look at the posts by Outsider and FloppyBanana about Myetelase. This drug increases acetylcholine levels. Low acetylcholine can cause muscle weakness. Consider lecethin as a supplement, and Huperzine A
Mr Raba - November 2015Trying pure encapsulations alpha-GPC an advanced delivery form for phosphatidylcholine to increase acethylcholine. It is a big help in 3 non POIS days so far. I am in my fourth day. And day 1 after O.
Quantum - March 2016Memantine is a NMDA receptor blocker. I have benefit from less potent NMDA receptors blockers, like magnesium, flaxseed oil ( lignam), L-Theanine, zinc, and the like. I have recently found that rosmarinic acid, that I have been using for years for POIS relief through rosemary extract, has acetylcholinesterase properties ( in addition to its gabaergic properties and its IDO inhibitor properties).
Mr Raba - July 2016Note that this is NOT a suugestion you for try this drugs Just good info related to vagus and what doctors may use to affect it.
"A bevy of drugs, many of which have not been tried ME/CFS or FM, can improve parasympathetic nervous system functioning. They do so either by blocking aceytlcholine from being degraded (e.g. Mestinon), or by increasing acetylcholine release, or by inhibiting sympathetic nervous system activity.
Reversible parasympathomimetic drugs include Donepezil, Edrophonium, Neostigmine, Physostigmine, Pyridostigmine, Rivastigmine, Tacrine, Caffeine (non-competitive) and Huperzine A."
http://www.healthrising.org/blog/2016/06/17/mestinon-chronic-fatigue-vagus-nerve-stimulation-exercise/Bookmark site. Lots of gems here. ??joelawrence - January 2016?A very useful article that could explain the Vagus theory of POIS that is currently being researched at Rutgers.
http://drsircus.com/medicine/vagus-nerve-inflammation-heart-rate-variability/The article touches upon how if the vagus nerve is not stimulated enough it leads to inflammation and that Acetylcholine helps control the inflammation. This explains Outsider and Floppybanana s treatment success with increasing Acetylcholine, as it helps control the inflammation.
Ejaculation is inflammatory (There are a few articles propsosing this, I have posted one of those articles below) but vagus nerve manages the inflammation by secreting the required Acetylcholine.
https://www.researchgate.net/publication/24421089_Frequent_ejaculation_associated_free_radical_and_lactic_acid_accumulation_cause_noninfectious_inflammation_and_muscle_dysfunction_A_potential_mechanism_for_symptoms_in_Chronic_ProstatitisChronic_PelviWhen the vagus nerve is not able to stimulate properly the inflammation is not reduced for a long time which is the POIS period for us. As you may all know systemic inflammation to the joints and bones is what causes pain throughout the body. Then the inflammation to brain and parts of eyes is what causes blurred vision, headaches, cognition issues, etc? An inflamed prostate also causes all types of issues including premature ejaculation.
Vagus nerve is also required for increasing testosterone in the body. The body?s free testosterone level naturally drops following ejaculation and again a normal functioning vagus nerve should get it back to normal levels soon, but happens slowly in our case.
So low testosterone and systemic inflammation of the body are the main reasons why we get the POIS symptoms IMO. This explains why Testosterone replacement therapy has worked for a few and anti-inflammatory stuff like Nicain, anti-histamines, fenugreek, acetylcholine stimulators work for some. IMO there will be 100% permanent cure only if the vagus nerve heals and starts functioning as it would in a non-POIS person.
These are all strictly my theories, please let me know your thoughts and challenge me if you disagree with something so that I can research a bit more.
Bluesbrother - January 2016(too long to paste here)?http://poiscenter.com/forums/index.php?topic=2194.msg17905#msg17905
b_jim - February 2016It seems garlic has a real effect on brain and memory functions vua acetylcholine :
http://poiscenter.com/forums/index.php?action=dlattach;topic=27.0;attach=447POISse - October 2016I made some research and found out about CFS / fibromyalgia which are accroding to me really close to pois. Why do I believe that ?
- A lot of symptoms are similar with POIS
- They are also convinced that the vagus nerve is involved
- What cure CFS also cure me : specific diet, no sport, acetylcholinesterase inhibitor, protein intake
Now from my experience with sports-related symptoms, the best way to prevent the apparition of symptoms for me is to take a protein shaker 20 min before doing sport. In fact high dose of protein help me not only with sport but in general. For the ones who are eating eggs every day, I guess it is the same effect, but shakers are more concentrated in protein and easier to take when needed. However I tried different brands and not all kinds seems to work.
Acetylcholinesterase inhibitor (mytelase) also work for me after sport (with brain fog and insomnia) but I prefer protein shaker since it works very good and it?s more natural.
Quantum - December 2016the use of cholinesterase inhibitors in order to boost acetylcholine activity is totally in line with the current Rutgers study n POIS involving vagus nerve stimulation ( for those wondering,, the vagus nerve is one of the most important cholinergic nerve in the whole body). The use of cholinesterase inhibitors like galantamine is just another way to achieve this, and to stimulate the Cholinergic Anti-inflammatory Pathway ( CAP) . For more information about all this, those interested can see this post I have written about CAP and the ways to stimulate it : http://poiscenter.com/forums/index.php?topic=2200.msg17995#msg17995 .
nanna1 - September 2017Unlike NORE, SAM-e can cross the blood brain barrier. SAM-e has a proven track record of elevating mood, reducing inflammation (downregulating a1-adrenergic receptor/ see reference #7) and elevating neurotransmitters (dopamine, serotonin, acetylcholine and epinephrine) in the brain. But please consult your healthcare professional about drug interactions with your medications.
trusttheprocess - April 2017Although Kynurenine seems to have many upsides, it has equally as many downsides, making it only useful as an emergency measure. The first downside is that it blocks ?7-nicotinic acetylcholine receptors (non-competitive antagonistic effect). What this does is block an incredibly important process from performing it's anti-inflammatory effects. This response to excess inflammation is known as the Cholinergic Anti-Inflammatory Pathway (CAP), and it is how the Vagus Nerve is able to reduce inflammation. It does this specifically by activating the efferent (from the CNS) portion of the Vagus Nerve, causing the release and the binding of acetycholine to the ?7-nACh receptors. This blocking of the CAP by Kynurenine explains the prolonged inflammatory response in POIS, as the bond between Kynurenine and the ?7-nAChr is non-competitive, meaning it completely blocks many receptor sites that acetycholine should be activating. The body produces more acetycholine to compensate for this, explaining lowered heart rate in POIS. Even VNS devices will probably have some but limited effect (reported by Colm_2), as VNS stimulation releases serotonin and acetylcholine by firing the same nerve as the CAP (Although there is the possiblity that this just means we need a stronger or higher frequency VNS device).
