My 2 cents. Acetylcholine is increased through xenoestrogens (in women, higher estrogen more focus, earlier puberty n such ) but is decreased in men. Maybe the ratio of testosterone to estrogen becomes imbalanced and makes men not as focused and mood becomes lower. If testosterone is lower when acetyl choline is higher then why is testosterone really important, for men, for motivation and a lot of good stuff that targets acetylcholine too.
@@DocSnipes See, for an example, clarifying the distinctions between activating and inhibiting the nicotinic and muscarinic receptors with symptoms and medications without putting jargons into it, is a really nice thing to do. We all can find the information in books but in order to absorb all that we first have to get the simple ideas and then later on dive into the intricacies gradually. So, to start with Neurotransmitters, this video is certainly helpful.
All your presentations are interesting to me.. as a 61 yo female, many useful tidbits, I'm someone that needs more acetylcholine..I feel like all my neurotransmitters are flatlining, but near the end 2 things caught my attention, one, I'm on hrt w additional progesterone..supposed to be good for my sleep which I struggle with and two, I've been taking ZQuil to help me get a good night's rest.. maybe these 2 things are actually sabotaging my acetylcholine which might explain my absolute loss of energy or motivation lately.. I'll speak w my doc to see what she suggests regarding this.
Thank you! I am grateful to be of service and I appreciate you watching the video. Please don’t hesitate to share the videos you find useful to help those in need.
Receptors: At min 31:12 Dawn says that dopamine and acetylcholine are low in people with RLS and parkinsons. I think she means that the receptors are low and not the dopamine and acetylcholine themselves.
Not necessarily. The dysfunction in neurotransmitter levels can come from insufficient axons, insufficient dendrites, insufficient production or even imbalance in other neurotransmitters or hormones causing low levels of dopamine or dysfunction.
I’m confused. At 38.05 you start talking about acetylcholinesterase (which breaks down acetylcholine) and then you switch to talking about increasing/decreasing acetylcholine.
Acetylcholinesterase is enzyme that breaks the Acetylcholine into Choline and Acetate now if the action of Acetylcholinesterase is inhibited, no more Acetylcholine will convert into Choline and Acetate which will eventually cause accumulation and increase level of Acetylcholine at Synaptic cleft
14:36 but it seems we make acetylcholinesterase endogenosly, as an enzyme. So if it gets bogged down it won't produce its effect of breaking down acetylcholine making it accumulate and GO UP
I know this is an older video but was wondering how after i started using Alpha GPH my idiopathic neuropathy in my feet improved a lot and some days never bothered me.
You're absolutely right! Acetylcholine, often overshadowed by its more popular counterpart dopamine, plays a crucial role in cognitive functions and muscle control. It's like the unsung hero of neurotransmitters, quietly doing its job to keep our brains and bodies in sync.
I’m kind of confused. I have panic disorder and heard that the body will stop the autonomic nervous system panic response by activating the parasympathetic nervous system, and I heard that it does this with acetylcholine. So I was thinking that raising my acetylcholine levels would help preventing the body from going into a panic response. But on here you say that acetylcholine increases memory associated fear - which is kind of a big factor of panic disorder. Didn’t watch the rest of the video yet, but curious if acetylcholine would be something positive or negative regarding panic attacks, or if it’s basically a non factor. Hopefully there’s more clarity as I go through the rest of the video
Anytime you modify the level of one neurotransmitter, it impacts the levels of other neurotransmitters. Here is a good article. www.ncbi.nlm.nih.gov/pmc/articles/PMC3466476/
Greetings, I'm exposed to a specific organophosphate at work that can cause "irreversible inhibition of acetylcholinesterase" and I believe it's at least contributing to some issues I'm having. While this video has been more helpful than any other single resource I've found so far, I still have questions. Basically, all these studies about tricresyl phosphate mention "irreversible inhibition of acetycholinesterase" but none of them describe what is meant by "irreversible". Does your body make a finite supply of this enzyme? For example, if this enzyme becomes a new AChe-Organophosphate molecule, are you out of luck in producing new enzyme that is not affected? I'm also wondering if the body can clear this compromised molecule. While it's a big topic in my industry right now, it's not well known outside the industry and it's tough to get help. I'm also trying to help some of my coworkers who have been affected more than me and are extremely unwell and having trouble getting help. It's not about going after anyone and placing blame, but about figuring out how to get better and providing helpful information to our healthcare providers. Any information is helpful
Hello! Irreversible inhibition occurs when a substance (like an organophosphate) binds permanently or for an extended period to an enzyme (like acetylcholinesterase). This binding alters the enzyme’s structure or function so that it can no longer perform its normal role. Your body continuously produces new acetylcholinesterase enzymes. However, if an organophosphate irreversibly inhibits AChE, the enzyme becomes inactive and cannot break down acetylcholine effectively. Because the inhibition is irreversible, the body needs to produce new acetylcholinesterase to replace the inactive ones. This process can be slow and depends on how quickly the body can generate new enzymes. The production of new AChE enzymes happens in the body’s cells, such as in the liver or other tissues. If exposure to organophosphates continues, it may outpace the body’s ability to produce and replace the enzyme. Now, the body cannot directly clear the organophosphate-AChE complex. Instead, the solution involves generating new, unbound AChE enzymes. The rate of enzyme production and the extent of inhibition influence recovery. The irreversible inhibition of AChE leads to an accumulation of acetylcholine in the nervous system, causing overstimulation of nerves and resulting in symptoms like muscle twitching, respiratory issues, and neurological effects. Treatment for exposure typically involves using antidotes that can reactivate some of the inhibited AChE or mitigate the symptoms, such as atropine and pralidoxime, but they come with their own sets of potential side effects and interactions, so please provide this information to your healthcare providers to help them understand the nature of the exposure and the specific challenges related to enzyme inhibition. They may need to monitor enzyme levels and provide targeted treatments to manage the symptoms and support recovery. All the best!
that makes complete sense as when i would quit nicotine and experience the withdrawal effects my mood would be extremely terrible, i would be in a very irritable state of mind, so much so that i would have to advise people around me before i even have any interaction with them. i do wonder if this has to do with the fact that nAChR agonists (such as nicotine) regulates mood, and the withdrawal of that constant agonism results in mood dysregulation.
I was diagnosed with an autoimmune disease 1 year ago. My legs are currently paralyzed from it. Do you think acetylcholine would be good for my motor nerves?
Bless you as well. I also have another UA-cam Channel: Good Orderly Direction | Practical Bible Study ua-cam.com/channels/YYJCD94NU3_qdbkSEyHLrg.html Please consider liking and subscribing.
Bless you. I also have another UA-cam Channel, I just started: Good Orderly Direction | Practical Bible Study ua-cam.com/channels/YYJCD94NU3_qdbkSEyHLrg.html Please consider liking and subscribing.
Mechanisms of Myofascial Pain M. Saleet Jafri "This nonquantal spontaneous acetylcholine release at the motor end plate as a result of CGRP is termed as acetylcholine leakage" The psychological stress after a physical injury can interfere with mitochondrial biogenesis and the leakage of acetylcholine at the neuromuscular junction. How can this be mediated or modulated with breathing or nutrition? HOW CAN ACETYLCHOLINESTERASE BE DISINHIBITTED ?
Sorry to bother you so much recently. Am very interested in the subjects of your talks. Slide twelve, which is titled Acetlycholinesterase, has a subtitle called "Reduces" and then diphenydramine as one that reduces it. And I emphasize "it" because I got kinda confused. If I am not wrong, diphenhydramine reduces acetylcholine, not acetylcholinesterase. I kept looking back at the title.
What is the connection between plavix and onset of cussing and mania thought maybe it was the adenosine break on the dopamine inhibited also have aggressiveness that lose by any type or any amount of hydrocodone as a painkiller for major surgery what's the neural modulator neurotransmitter connection between the outburst the hypervigilance the aggressiveness almost tourette's like cussing from plavix and the damn near going postal connection with hydrocodone in a person who doesn't drink doesn't use doesn't smoke and eats healthy to where you can't take those medications
Yes, marijuana can impact acetylcholine levels in the brain. It's believed to have both inhibitory and stimulatory effects on acetylcholine release, which could contribute to various physiological and cognitive effects experienced when using marijuana. However, the exact mechanisms are complex and not fully understood.
Hello doc. I deleted acetylcholine from brain and I'm delaying with rhythmic muscle movement. I depleted it from years of daily masterbation. I quit my addiction 2 years ago. Can the brain heal of burned out acetylcholine receptors and low acetylcholine? Please tell me can the brain recover on its own?
This was excellent information. Thank you.
Very welcome. Thanks for watching
My 2 cents. Acetylcholine is increased through xenoestrogens (in women, higher estrogen more focus, earlier puberty n such ) but is decreased in men. Maybe the ratio of testosterone to estrogen becomes imbalanced and makes men not as focused and mood becomes lower. If testosterone is lower when acetyl choline is higher then why is testosterone really important, for men, for motivation and a lot of good stuff that targets acetylcholine too.
Excellent milestone for understanding the relationship between acetylcholine and diabetes insipidus. Thank you :)
Thanks for watching.
Another great video that is underrated.
Thanks for watching the video. What did you find most useful from it?
@@DocSnipes See, for an example, clarifying the distinctions between activating and inhibiting the nicotinic and muscarinic receptors with symptoms and medications without putting jargons into it, is a really nice thing to do. We all can find the information in books but in order to absorb all that we first have to get the simple ideas and then later on dive into the intricacies gradually. So, to start with Neurotransmitters, this video is certainly helpful.
All your presentations are interesting to me.. as a 61 yo female, many useful tidbits, I'm someone that needs more acetylcholine..I feel like all my neurotransmitters are flatlining, but near the end 2 things caught my attention, one, I'm on hrt w additional progesterone..supposed to be good for my sleep which I struggle with and two, I've been taking ZQuil to help me get a good night's rest.. maybe these 2 things are actually sabotaging my acetylcholine which might explain my absolute loss of energy or motivation lately.. I'll speak w my doc to see what she suggests regarding this.
Holy Basil
Very Glad You Talk about it
loved it! great class
Thank you! I am grateful to be of service and I appreciate you watching the video. Please don’t hesitate to share the videos you find useful to help those in need.
Interesting. The sub cortisol in some PTSD people I saw yesterday made sense, probably a dissociation that helps stay calm maybe (or so seems)
Receptors: At min 31:12 Dawn says that dopamine and acetylcholine are low in people with RLS and parkinsons. I think she means that the receptors are low and not the dopamine and acetylcholine themselves.
Not necessarily. The dysfunction in neurotransmitter levels can come from insufficient axons, insufficient dendrites, insufficient production or even imbalance in other neurotransmitters or hormones causing low levels of dopamine or dysfunction.
I’m confused. At 38.05 you start talking about acetylcholinesterase (which breaks down acetylcholine) and then you switch to talking about increasing/decreasing acetylcholine.
Acetylcholinesterase is enzyme that breaks the Acetylcholine into Choline and Acetate now if the action of Acetylcholinesterase is inhibited, no more Acetylcholine will convert into Choline and Acetate which will eventually cause accumulation and increase level of Acetylcholine at Synaptic cleft
14:36 but it seems we make acetylcholinesterase endogenosly, as an enzyme. So if it gets bogged down it won't produce its effect of breaking down acetylcholine making it accumulate and GO UP
I know this is an older video but was wondering how after i started using Alpha GPH my idiopathic neuropathy in my feet improved a lot and some days never bothered me.
Unfortunately, I am not finding any peer reviewed studies. It would be interesting to ask your neurologist.
Acetylcholine is underrated! And unfortunately less well known than Dopamine as a neurotransmitter and neuromodulator.
You're absolutely right! Acetylcholine, often overshadowed by its more popular counterpart dopamine, plays a crucial role in cognitive functions and muscle control. It's like the unsung hero of neurotransmitters, quietly doing its job to keep our brains and bodies in sync.
@@DocSnipes Hence why they used this in Trauma Based Mind Control! Thank you so much for this presentation! Blessings!
@@DocSnipes FYI Hawthorn Berry has Acetylcholine! Check out Dr. Christopher!
I’m kind of confused. I have panic disorder and heard that the body will stop the autonomic nervous system panic response by activating the parasympathetic nervous system, and I heard that it does this with acetylcholine.
So I was thinking that raising my acetylcholine levels would help preventing the body from going into a panic response.
But on here you say that acetylcholine increases memory associated fear - which is kind of a big factor of panic disorder.
Didn’t watch the rest of the video yet, but curious if acetylcholine would be something positive or negative regarding panic attacks, or if it’s basically a non factor. Hopefully there’s more clarity as I go through the rest of the video
Anytime you modify the level of one neurotransmitter, it impacts the levels of other neurotransmitters. Here is a good article. www.ncbi.nlm.nih.gov/pmc/articles/PMC3466476/
magic mushrooms will help
Check out Hawthorn Berry, Dr. Christopher!
What kind do you suggest is good. Thank you!
I appreciate you watching. Sadly, I can’t recommend medication.
Great lecture. Thanks, Doc.
Thanks for watching!
Greetings, I'm exposed to a specific organophosphate at work that can cause "irreversible inhibition of acetylcholinesterase" and I believe it's at least contributing to some issues I'm having. While this video has been more helpful than any other single resource I've found so far, I still have questions. Basically, all these studies about tricresyl phosphate mention "irreversible inhibition of acetycholinesterase" but none of them describe what is meant by "irreversible". Does your body make a finite supply of this enzyme? For example, if this enzyme becomes a new AChe-Organophosphate molecule, are you out of luck in producing new enzyme that is not affected? I'm also wondering if the body can clear this compromised molecule. While it's a big topic in my industry right now, it's not well known outside the industry and it's tough to get help. I'm also trying to help some of my coworkers who have been affected more than me and are extremely unwell and having trouble getting help. It's not about going after anyone and placing blame, but about figuring out how to get better and providing helpful information to our healthcare providers. Any information is helpful
Hello! Irreversible inhibition occurs when a substance (like an organophosphate) binds permanently or for an extended period to an enzyme (like acetylcholinesterase). This binding alters the enzyme’s structure or function so that it can no longer perform its normal role. Your body continuously produces new acetylcholinesterase enzymes. However, if an organophosphate irreversibly inhibits AChE, the enzyme becomes inactive and cannot break down acetylcholine effectively. Because the inhibition is irreversible, the body needs to produce new acetylcholinesterase to replace the inactive ones. This process can be slow and depends on how quickly the body can generate new enzymes. The production of new AChE enzymes happens in the body’s cells, such as in the liver or other tissues. If exposure to organophosphates continues, it may outpace the body’s ability to produce and replace the enzyme. Now, the body cannot directly clear the organophosphate-AChE complex. Instead, the solution involves generating new, unbound AChE enzymes. The rate of enzyme production and the extent of inhibition influence recovery. The irreversible inhibition of AChE leads to an accumulation of acetylcholine in the nervous system, causing overstimulation of nerves and resulting in symptoms like muscle twitching, respiratory issues, and neurological effects. Treatment for exposure typically involves using antidotes that can reactivate some of the inhibited AChE or mitigate the symptoms, such as atropine and pralidoxime, but they come with their own sets of potential side effects and interactions, so please provide this information to your healthcare providers to help them understand the nature of the exposure and the specific challenges related to enzyme inhibition. They may need to monitor enzyme levels and provide targeted treatments to manage the symptoms and support recovery. All the best!
that makes complete sense as when i would quit nicotine and experience the withdrawal effects my mood would be extremely terrible, i would be in a very irritable state of mind, so much so that i would have to advise people around me before i even have any interaction with them.
i do wonder if this has to do with the fact that nAChR agonists (such as nicotine) regulates mood, and the withdrawal of that constant agonism results in mood dysregulation.
Yes, same thing has happened to me after quitting smoking 7 yrs ago.
Brain not normalising,without nicotine.
Starting soon on choline supplements.
I was diagnosed with an autoimmune disease 1 year ago. My legs are currently paralyzed from it. Do you think acetylcholine would be good for my motor nerves?
Thank you so much . Please talk about dopamine. God bless
Bless you as well.
I also have another UA-cam Channel:
Good Orderly Direction | Practical Bible Study
ua-cam.com/channels/YYJCD94NU3_qdbkSEyHLrg.html
Please consider liking and subscribing.
Bless you.
I also have another UA-cam Channel, I just started:
Good Orderly Direction | Practical Bible Study
ua-cam.com/channels/YYJCD94NU3_qdbkSEyHLrg.html
Please consider liking and subscribing.
Mechanisms of Myofascial Pain
M. Saleet Jafri
"This nonquantal spontaneous acetylcholine release at the motor end plate as a result of CGRP is termed as acetylcholine leakage"
The psychological stress after a physical injury can interfere with mitochondrial biogenesis and the leakage of acetylcholine at the neuromuscular junction.
How can this be mediated or modulated with breathing or nutrition?
HOW CAN ACETYLCHOLINESTERASE BE DISINHIBITTED ?
Can CHRNA3 and CHRNA5 mutations affect you is you are not a smoker and you never smoked?
Sorry to bother you so much recently. Am very interested in the subjects of your talks. Slide twelve, which is titled Acetlycholinesterase, has a subtitle called "Reduces" and then diphenydramine as one that reduces it. And I emphasize "it" because I got kinda confused. If I am not wrong, diphenhydramine reduces acetylcholine, not acetylcholinesterase. I kept looking back at the title.
Production ideas have a goodnight 😀
Thanks for watching
What is the connection between plavix and onset of cussing and mania thought maybe it was the adenosine break on the dopamine inhibited also have aggressiveness that lose by any type or any amount of hydrocodone as a painkiller for major surgery what's the neural modulator neurotransmitter connection between the outburst the hypervigilance the aggressiveness almost tourette's like cussing from plavix and the damn near going postal connection with hydrocodone in a person who doesn't drink doesn't use doesn't smoke and eats healthy to where you can't take those medications
Check out Hawthorn Berry by Dr. Christopher
Does marijuana block acetylcholine?
Yes, marijuana can impact acetylcholine levels in the brain. It's believed to have both inhibitory and stimulatory effects on acetylcholine release, which could contribute to various physiological and cognitive effects experienced when using marijuana. However, the exact mechanisms are complex and not fully understood.
@@DocSnipes That totally makes since! Thank you!
Sugar and salt.... CBD VS THC Ratio Mix 😅 I think abt it all da time 😂
Thanks for watching
God bless you and your family and friends forever in Jesus name
Jesus Christ is the Lord 🙏
Acts 2:38
Thanks for watching.
Hello doc. I deleted acetylcholine from brain and I'm delaying with rhythmic muscle movement. I depleted it from years of daily masterbation. I quit my addiction 2 years ago. Can the brain heal of burned out acetylcholine receptors and low acetylcholine? Please tell me can the brain recover on its own?