From
https://www.me-pedia.org/wiki/Acetylcholine#Acetylcholinesterate_inhibitors"Acetylcholine is a neurotransmitter that is thought to play a role in many human diseases including Myalgic Encephalomyelitis and postural orthostatic tachycardia syndrome.
Function
Acetylcholine is used in the autonomic nervous system, both as an internal transmitter for the sympathetic nervous system and as the final product released by the parasympathetic nervous system. It plays an important role in regulating the inflammatory response and is used at the neuromuscular junction by motor neurons in order to activate muscles.
In the central nervous system, acetylcholine modulates arousal and temperature regulation, is important for attention, memory and motivation, and may play a role in central fatigue.
Immune system
The vagus nerve speaks directly to the immune system via acetylcholine.[1][2][3]
Acetylcholine plays a role in innate immunity through nicotinic acetylcholine receptors and in the adaptive immune response via M3 muscarinic acetylcholine receptors (M3R).[4]
Muscarinic receptors
Knockout mice, that is mice lacking the gene that encodes for M3R, had impaired response to bacterial infection, while normal mice given a muscarinic agonist (to increase the activity of M3R) had enhanced production of IL-13 and IFN-γ.[5] Another study used a muscarinic agonist and an antagonist (reduce activity) and found antagonist suppressed the immune response while the agonist exaggerated it.[6]
Mast cells
Several studies suggest a relationship between autonomic nervous system dysfunction and mast cell activation via acetylcholine.
One study found that acetylcholine via muscarinic receptors strongly inhibited the release of histamine in mucosal mast cells.[7]acetylcholinesterase activity was found to be significantly increased in 64% of patients experiencing flares of ulcerative colitis.[8]
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Chronic fatigue syndrome
In 2015, a large German study found 29% of ME/CFS patients had elevated autoantibodies to M3 and M4 muscarinic acetylcholine receptors, as well as ß2 adrenergic receptors.[15][16] A 2016 Australian study found that ME/CFS patients had significantly greater numbers of single nucleotide polymorphisms associated with the gene encoding for M3 muscarinic acetylcholine receptors.[17]
Anecdotally, some ME/CFS patients have tried Mestinon, an aceytlcholinesterase inhibitor that increases circulating acetylcholine and is used to treat myasthenia gravis, with some success.[18] A work in progress study of exercise intolerance in preload failure found that Mestinon improved exercise tolerance, but the study has not yet been published.[19]
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Many classes of drugs including benzodiazepines, opiods, anesthetics, and some antihistimanes such as Benadryl are anticholinergic. During exercise, levels of acetylcholine drop."
Doesn't this explain so much?
I always thought that ME/CFS was separate from the benzo withdrawal or that you might have been put on benzos because of ME/CFS but the mechanisms of ME/CFS and benzo withdrawal were different. But apparently benzos can actually worsen or even trigger that actual ME/CFS mechanisms.
To be honest reading Jennifer Brea's blog opened my eyes as to why I suffer so much and why the common advice of "pushing yourself" is actually making me worse.
If you are in protracted you might want to research ME/CFS a little more to see if any of the ME/CFS treatments and/or coping strategies can be useful for you.