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Benzos are are anticholinergic. What does it mean:


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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]

 

...

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]

 

...

 

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.

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Interesting.

 

Glutamate is also implicated in ME/CFS and Dr Cheney prescribes Clonazepam to ME patients because it seems to help them.

 

I think ME is a big rag bag of different things.

 

This man is very severe with ME and Ativan seemed to help him:

 

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Oh yes, I actually think that I had normal levels of acetylcholine prior to benzo wd because Ativan made me feel just wonderful the first time I took it, I never had a problem with benadryl and felt great after exercise. Then I believe benzos messed up my glutamate first because my atypical severe migraines are triggered by even the tiniest amount of glutamate in the food and these migraines only started while on benzos. Never had them before. However, I could still take Benadryl and exercise. Only after stopping Klonopin I started having ME/CFS symptoms and wasn't able to take Benadryl or exercise anymore.

 

I think it's your specific body chemistry and risk/benefit analysis that determines whether benzos would be an appropriate treatment.

 

Have you read up on CCI? Craniocervical instability. When Jennifer Brea had her surgery and went into ME/CFS remission I thought of you and all of your neck symptoms.

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My story:

 

I was also diagnosed with ME/CFS. They didn't know, what the problem was.

 

I met a tough, and very good neurologist. He said "you're here on a visit. A very good sign!". And he asked, if I was completely bedridden, and forced to avoid TV and the Internet. My answer, of course, was"no".

 

He said, my symptoms were probably side effects painkillers. And then Benzo during many years.

 

It's written, in Swedish healthcare pages, that Benzo is not the right treatment for neurological diseases. The brain is too sensitive. And then tolerance.

 

Aside from WD, all old symptoms have disappeared! FOR MY PART my problems were probably side effects painkillers. And then Benzo during many years.

 

So Benzo- and painkillers-free, has saved my future, and there is hope. So I'm so happy!

 

 

:smitten:

 

 

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Yes, aware of CCI and is definitely a possibility for me but they don’t do the surgery in the U.K.

ppl have to raise £100k to go to Spain for it.

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I found this. I hope it's another article, and not the same. :)

 

https://www.healthrising.org/blog/2016/06/24/benzodiazepine-fibromyalgia-chronic-fatigue-withdrawal/

 

 

 

Additionally, although technically not in the anticholingeric class of drugs (such as antihistamines) benzodiazepines do appear to have anticholinergic properties.  This means they can inhibit (or lower) the action of the parasympathetic nervous system by blocking the binding of the neurotransmitter, acetylcholine, to its receptor in the nerve cells.  Many people with ME/CFS and/or fibromyalgia may have  autonomic nervous system problems.

 

The effects these anticholingeric drugs have on the nervous system dysfunction depends on many factors including their pharmacological action andhow people metabolize the drug

 

 

I believe the possibility that anticholingeric drugs may be counterproductive in persons with ME/CFS/FM should be investigated further.  That idea suggests, however, that a drug taken for symptomatic relief could actually be worsening the illness in some ways.

 

The literature provided by the drug experts at the Point of Return organization states that benzodiazepines reduce the brain’s output of excitatory neurotransmitters, including norepinephrine, serotonin, dopamine, and acetylcholine – all necessary neurotransmitters for normal functioning and emotional well being.

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  • 3 weeks later...

On the other hand:

 

I had ME priorto Benzos and think they may have been covering g some of the sensory symptoms I had from ME.

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The weird thing is that the only benzo that ever worked for me was Ativan. I also developed tolerance and started having interdose withdrawal within 2 weeks. With Klonopin it was 2 years.
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  • 2 years later...

Benzo withdrawal increases acetylcholine especially in the amygdala(the fear center of the brain)

 

I was thinking the same and that could reduce dopamine. Do you have a source for it?

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  • 3 weeks later...

Benzo withdrawal increases acetylcholine especially in the amygdala(the fear center of the brain)

 

I was thinking the same and that could reduce dopamine. Do you have a source for it?

 

Acetylcholine in the accumbens is decreased by diazepam and increased by benzodiazepine withdrawal: a possible mechanism for dependency

 

Pedro Rada 1, Bartley G Hoebel

 

Affiliations expand

 

PMID: 15680263 DOI: 10.1016/j.ejphar.2004.12.016

 

Full text linksCite

 

Abstract

 

Diazepam is a benzodiazepine used in the treatment of anxiety, insomnia and seizures, but with the potential for abuse. Like the other benzodiazepine anxiolytics, diazepam does not increase dopamine in the nucleus accumbens. This raises the question as to which other neurotransmitter systems are involved in diazepam dependence. The goal was to monitor dopamine and acetylcholine simultaneously following acute and chronic diazepam treatment and after flumazenil-induced withdrawal. Rats were prepared with microdialysis probes in the nucleus accumbens and given diazepam (2, 5 and 7.5 mg/kg) acutely and again after chronic treatment. Accumbens dopamine and acetylcholine decreased, with signs of tolerance to the dopamine effect. When these animals were put into the withdrawal state with flumazenil, there was a significant rise in acetylcholine (145%, P<0.001) with a smaller significant rise in dopamine (124%, P<0.01). It is suggested that the increase in acetylcholine release, relative to dopamine, is a neural component of the withdrawal state that is aversive.

 

https://pubmed.ncbi.nlm.nih.gov/15680263/

 

 

 

 

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ME ts an awfull condition,  but i dont understand the use of this drug as help.. , and when his brain get affected by this injury from benzodiazepines like t did for us ? .. how its going to be?...
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