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I'm confused about Potassium
Posted by Richard
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Richard
I'm confused about Potassium November 05, 2003 03:02AM |
I was hoping I'd get a bite on this link from my previous post, because this confused me:
"Sympathetic activation, which releases norepinephrine (NE), increases pacemaker rate by decreasing gK+ and increasing slow inward gCa++ and gNa+, all of which increase the slope of Phase 4. Parasympathetic (vagal) activation, which releases acetylcholine (ACh), decreases pacemaker rate by increasing gK+ which decreases the slope of Phase 4 thereby increasing the time to reach threshold. Vagal activity also hyperpolarizes the pacemaker cell during Phase 4 which results in a longer time to research threshold voltage."
[www.oucom.ohiou.edu]
So let me see if I understand this. There is a push-pull drive between the SNS and the PNS, a kind of yin and yang. So as the SNS pushes, it releases Ca, Na and norephinephrine, and reduces K, to drive the force, and to counter this action, the PNS increases acetylcholine and K (and probably Mg, that wasn't mentioned), to oppose the push and balance the SNS, hence a normal heartbeat. So forgive me if I sound dense in this matter, especially after all that has been posted on this topic, but it would seem that if one is vagally dominant there is either too much acetylcholine and/or potassium at the synaptic cleft. I know when I took beta blockers, this blocked my adrenalin or noradrenalin, actually not sure which one, and caused devastating effects for me. My heartbeat would plummet, only at night, upon sitting or lying down, which leads me to believe I was stopping the balance of the SNS, and the release of norepinephrine. And being that I was not too energetic during the day with much more irregular heartbeats, and really bad at night, I needed adrenalin. On the other hand flecainide works well, and blocks Na, yet I had normal Na in serum and normal K and Mg in the cells. So I'm left to believe that norepinephrine is my problem, especially in lieu of the fact that my pathway to NE had problems on my metabolic profile, and also that s-adenosyl methionine, which I was low in (methionine), is necessary for this pathway. I've re-read Hans's explanation on pgs. 18/19 and still feel dense. One other thing that I would like to point out, is that in the case of an overdose of flecainide, dopamine, which is the precursor to epinephrine and norepinephrine, is the protocol for alleviating the overdosage. If one was low in epinephrine or norepinephrine, could this cause PAC's, PVC's and ectopics during the day, as the SNS struggles to maintain balance, but when night falls and the PNS becomes more dominant, then the SNS just can't keep up with its struggles, therefore causing AF. It would also seem to me that the adrenergic would be the one who needs Mg, K, and/or acetylcholine. Maybe some here are more mixed than they know, and Mg helps, but they still haven't gotten a balance of either choline, necessary for acetylcholine or dopamine, necessary for norepinephrine.
Another point I'd like to make, is that Parkinson's disease is a problem with dopamine synthesis, hence why L-dopa is used. The symptons are shakiness and loss of control of muscles. Could we have Parkinson's of the heart, so to speak?
Why I can't understand all this is beyond me. What is confusing me is the drive to get more K into the body for vagals and Hans was taking sea salt in his water. It should be the opposite, as I see it. It seems to be a fairly simple concept, even though I know how complicated the body is, but I just don't get it. I've read and re-read, so could someone pls. explain to me what I might not be seeing. Maybe we all need more choline, B vitamins, Mg. and tyrosine with less emphasis on K and Na.
Thank you in advance for any clarifications anyone can give me.
Richard
"Sympathetic activation, which releases norepinephrine (NE), increases pacemaker rate by decreasing gK+ and increasing slow inward gCa++ and gNa+, all of which increase the slope of Phase 4. Parasympathetic (vagal) activation, which releases acetylcholine (ACh), decreases pacemaker rate by increasing gK+ which decreases the slope of Phase 4 thereby increasing the time to reach threshold. Vagal activity also hyperpolarizes the pacemaker cell during Phase 4 which results in a longer time to research threshold voltage."
[www.oucom.ohiou.edu]
So let me see if I understand this. There is a push-pull drive between the SNS and the PNS, a kind of yin and yang. So as the SNS pushes, it releases Ca, Na and norephinephrine, and reduces K, to drive the force, and to counter this action, the PNS increases acetylcholine and K (and probably Mg, that wasn't mentioned), to oppose the push and balance the SNS, hence a normal heartbeat. So forgive me if I sound dense in this matter, especially after all that has been posted on this topic, but it would seem that if one is vagally dominant there is either too much acetylcholine and/or potassium at the synaptic cleft. I know when I took beta blockers, this blocked my adrenalin or noradrenalin, actually not sure which one, and caused devastating effects for me. My heartbeat would plummet, only at night, upon sitting or lying down, which leads me to believe I was stopping the balance of the SNS, and the release of norepinephrine. And being that I was not too energetic during the day with much more irregular heartbeats, and really bad at night, I needed adrenalin. On the other hand flecainide works well, and blocks Na, yet I had normal Na in serum and normal K and Mg in the cells. So I'm left to believe that norepinephrine is my problem, especially in lieu of the fact that my pathway to NE had problems on my metabolic profile, and also that s-adenosyl methionine, which I was low in (methionine), is necessary for this pathway. I've re-read Hans's explanation on pgs. 18/19 and still feel dense. One other thing that I would like to point out, is that in the case of an overdose of flecainide, dopamine, which is the precursor to epinephrine and norepinephrine, is the protocol for alleviating the overdosage. If one was low in epinephrine or norepinephrine, could this cause PAC's, PVC's and ectopics during the day, as the SNS struggles to maintain balance, but when night falls and the PNS becomes more dominant, then the SNS just can't keep up with its struggles, therefore causing AF. It would also seem to me that the adrenergic would be the one who needs Mg, K, and/or acetylcholine. Maybe some here are more mixed than they know, and Mg helps, but they still haven't gotten a balance of either choline, necessary for acetylcholine or dopamine, necessary for norepinephrine.
Another point I'd like to make, is that Parkinson's disease is a problem with dopamine synthesis, hence why L-dopa is used. The symptons are shakiness and loss of control of muscles. Could we have Parkinson's of the heart, so to speak?
Why I can't understand all this is beyond me. What is confusing me is the drive to get more K into the body for vagals and Hans was taking sea salt in his water. It should be the opposite, as I see it. It seems to be a fairly simple concept, even though I know how complicated the body is, but I just don't get it. I've read and re-read, so could someone pls. explain to me what I might not be seeing. Maybe we all need more choline, B vitamins, Mg. and tyrosine with less emphasis on K and Na.
Thank you in advance for any clarifications anyone can give me.
Richard
|
PC
Re: I'm confused about Potassium November 05, 2003 04:14PM |
|
Richard
Re: I'm confused about Potassium November 05, 2003 05:09PM |
PC,
Thank you for taking any time you can to just explain this one point, PC. Why do you feel it's so important to get K and Mg into your cells, when, from this article, it would seem that, that is what stimulates the parasympathetic side, and it is my understanding that you want to block this dominance. I know once you go into AF that your heart beats irregular and faster, but from what I've read in Hans's book, it appears that the PNS takes over in vagals before the heart kicks into AF. It would seem to me that you would want more Na and Ca to stimulate the SNS, to keep this vagal dominance at bay, and from happening in the first place. I understand that vagals don't do well on beta blockers, because this suppresses the SNS, which is something we wouldn't want. I'm soooo confused.
The effect of Magnesium Di-Potassium EDTA suppositories on the nervous system
The autonomic nervous system (ANS) is divided into two parts, the sympathetic (SNS) and the parasympathetic systems (PNS). The SNS creates what is commonly known as the fight or flight response. In the event of a perceived emergency, the body will suppress all non-critical physiological systems and push the blood into the muscles for quick action. Non-critical systems include digestion, reproduction, gestation, milk production, immune function, higher brain functions, growth and repair processes, and sleep. Thats not to say that any SNS response is bad. For instance, its the SNS that keeps a person from passing out due to the effects of gravity upon their blood when they stand up quickly. The point is that continual activation of the SNS is very detrimental to our health.
The PNS is the counterpoint to the SNS. It generates what might be termed the relaxation response, and when activated, helps suppress the SNS. When the PNS is activated, the body digests well, reproduction, gestation, and milk production are supported, the immune system is active, our brains are happy and functional, injured tissue is repaired, new tissue is formed, and we get a good nights sleep.
Thus it makes sense to keep the body in a slightly PNS dominant state whenever possible. This can be accomplished very easily with Magnesium Di-Potassium EDTA.
To understand the effect that Magnesium Di-Potassium EDTA can have on the nervous system, we need to review the effect of minerals on the autonomic nervous system (ANS). There are four minerals that play key roles in the balance of the autonomic nervous system namely, magnesium, potassium, sodium and calcium. They work as follows:
Sympathetic system Parasympathetic system
Magnesium Blocking action Potassium Stimulating action
Sodium Stimulating action Calcium Blocking action
Thus, Magnesium Di-Potassium EDTA can have a very powerful calming effect on the nervous system by both blocking the stress response as well as stimulating the relaxation response. Many clients report feelings of profound relaxation within 5 to 20 minutes of taking Magnesium Di-Potassium EDTA precisely because of how it affects the (ANS).
On the other hand Di-Sodium EDTA and Calcium Di Sodium EDTA can do the exact opposite. They turn off the relaxation response and stimulate the fight or flight response. This is most easily observed by the increase in pulse rate these forms of EDTA can cause.
Heart Rate Variability tests results
Heart Rate Variability (HRV) testing is a recognized and well researched method for determining the stress level of a client.
The Red range represents the sympathetic system, and is associated with the "fight or flight" stress response.
The Green range represents a mixture of both the sympathetic (2/3rds) and parasympathetic (1/3rd) systems.
The Blue range represents the parasympathetic system and so is responsible for relaxation.
In this first test, you can see that the client is all sympathetic and virtually no parasympathetic (all in the red range). In this state, all the blood is sent to the muscles for survival. Digestion, growth and repair, immune function, higher brain functions, and the ability to sleep are all suppressed. Cortisol, adrenaline and noradrenaline are the predominant hormones in this state.
This second test was taken after one Magnesium Di-Potassium EDTA suppository. You can see the shift from the sympathetic to parasympathetic systems (blue range). With this reading, a client will be relaxed, and the growth and repair, immune function, higher brain functions, and the ability to sleep are enhanced.
[www.medicardium.com]
Richard
Thank you for taking any time you can to just explain this one point, PC. Why do you feel it's so important to get K and Mg into your cells, when, from this article, it would seem that, that is what stimulates the parasympathetic side, and it is my understanding that you want to block this dominance. I know once you go into AF that your heart beats irregular and faster, but from what I've read in Hans's book, it appears that the PNS takes over in vagals before the heart kicks into AF. It would seem to me that you would want more Na and Ca to stimulate the SNS, to keep this vagal dominance at bay, and from happening in the first place. I understand that vagals don't do well on beta blockers, because this suppresses the SNS, which is something we wouldn't want. I'm soooo confused.
The effect of Magnesium Di-Potassium EDTA suppositories on the nervous system
The autonomic nervous system (ANS) is divided into two parts, the sympathetic (SNS) and the parasympathetic systems (PNS). The SNS creates what is commonly known as the fight or flight response. In the event of a perceived emergency, the body will suppress all non-critical physiological systems and push the blood into the muscles for quick action. Non-critical systems include digestion, reproduction, gestation, milk production, immune function, higher brain functions, growth and repair processes, and sleep. Thats not to say that any SNS response is bad. For instance, its the SNS that keeps a person from passing out due to the effects of gravity upon their blood when they stand up quickly. The point is that continual activation of the SNS is very detrimental to our health.
The PNS is the counterpoint to the SNS. It generates what might be termed the relaxation response, and when activated, helps suppress the SNS. When the PNS is activated, the body digests well, reproduction, gestation, and milk production are supported, the immune system is active, our brains are happy and functional, injured tissue is repaired, new tissue is formed, and we get a good nights sleep.
Thus it makes sense to keep the body in a slightly PNS dominant state whenever possible. This can be accomplished very easily with Magnesium Di-Potassium EDTA.
To understand the effect that Magnesium Di-Potassium EDTA can have on the nervous system, we need to review the effect of minerals on the autonomic nervous system (ANS). There are four minerals that play key roles in the balance of the autonomic nervous system namely, magnesium, potassium, sodium and calcium. They work as follows:
Sympathetic system Parasympathetic system
Magnesium Blocking action Potassium Stimulating action
Sodium Stimulating action Calcium Blocking action
Thus, Magnesium Di-Potassium EDTA can have a very powerful calming effect on the nervous system by both blocking the stress response as well as stimulating the relaxation response. Many clients report feelings of profound relaxation within 5 to 20 minutes of taking Magnesium Di-Potassium EDTA precisely because of how it affects the (ANS).
On the other hand Di-Sodium EDTA and Calcium Di Sodium EDTA can do the exact opposite. They turn off the relaxation response and stimulate the fight or flight response. This is most easily observed by the increase in pulse rate these forms of EDTA can cause.
Heart Rate Variability tests results
Heart Rate Variability (HRV) testing is a recognized and well researched method for determining the stress level of a client.
The Red range represents the sympathetic system, and is associated with the "fight or flight" stress response.
The Green range represents a mixture of both the sympathetic (2/3rds) and parasympathetic (1/3rd) systems.
The Blue range represents the parasympathetic system and so is responsible for relaxation.
In this first test, you can see that the client is all sympathetic and virtually no parasympathetic (all in the red range). In this state, all the blood is sent to the muscles for survival. Digestion, growth and repair, immune function, higher brain functions, and the ability to sleep are all suppressed. Cortisol, adrenaline and noradrenaline are the predominant hormones in this state.
This second test was taken after one Magnesium Di-Potassium EDTA suppository. You can see the shift from the sympathetic to parasympathetic systems (blue range). With this reading, a client will be relaxed, and the growth and repair, immune function, higher brain functions, and the ability to sleep are enhanced.
[www.medicardium.com]
Richard
|
PC
Re: I'm confused about Potassium November 06, 2003 08:19AM |
Richard,
The situation wrt cations and the ANS is much more complicated than that. It's not like some math problem where there is a natural symmetry. The PNS is not K/Mg and the SNS is not Na/Ca. The ion pairs function in opposite ways, but their relationship to the ANS is bipartisan. Ca and Na are predominantly extracellular and K and Mg are predominantly intracellular. There is a Na/K pump and a Mg/Ca pump (as well as many others) to maintain this separation. But these ions are involved in the function of all cells not just the ANS. The interactions are exceedingly complex with many feedback mechanisms, making an attempt at explanation of the ANS wrt LAF via such a simplistic approach untenable.
If it was possible, it would already have been worked out. There are numerous researchers and investigators far more intelligent than you and I. We have a bit of an advantage because we are highly motivated and that makes up for a lot. We can grasp the larger picture, whereas many of them can't see the application of their research.
I think the best approach is to read as much as possible from as many sources as possible (the facts), incorporate your own LAF experience and those of others (the experimental) and try to connect the dots to produce some kind of unifying theory.
Having said that, your perseverance and perspicacity are an example to all.
PC v54
The situation wrt cations and the ANS is much more complicated than that. It's not like some math problem where there is a natural symmetry. The PNS is not K/Mg and the SNS is not Na/Ca. The ion pairs function in opposite ways, but their relationship to the ANS is bipartisan. Ca and Na are predominantly extracellular and K and Mg are predominantly intracellular. There is a Na/K pump and a Mg/Ca pump (as well as many others) to maintain this separation. But these ions are involved in the function of all cells not just the ANS. The interactions are exceedingly complex with many feedback mechanisms, making an attempt at explanation of the ANS wrt LAF via such a simplistic approach untenable.
If it was possible, it would already have been worked out. There are numerous researchers and investigators far more intelligent than you and I. We have a bit of an advantage because we are highly motivated and that makes up for a lot. We can grasp the larger picture, whereas many of them can't see the application of their research.
I think the best approach is to read as much as possible from as many sources as possible (the facts), incorporate your own LAF experience and those of others (the experimental) and try to connect the dots to produce some kind of unifying theory.
Having said that, your perseverance and perspicacity are an example to all.
PC v54
|
PC
Re: I'm confused about Potassium November 06, 2003 08:35AM |
Richard,
I forgot to mention as an example that acetylcholine is not only the neurotransmitter for the entire PNS, but is also the neurotransmitter for the first part of the SNS. Preganglionic neurons (from the CNS) use acetylcholine as a neurotransmitter, whereas most postganglionic neurons (from around the spinal cord) utilize norepinephrine (noradrenaline) as a neurotransmitter.
This is just an example. Human physiology is for the most part not straightforward. As one goes from math to physics to biology, complexity increases. Evolution was not an exercise in mathematics.
PC
I forgot to mention as an example that acetylcholine is not only the neurotransmitter for the entire PNS, but is also the neurotransmitter for the first part of the SNS. Preganglionic neurons (from the CNS) use acetylcholine as a neurotransmitter, whereas most postganglionic neurons (from around the spinal cord) utilize norepinephrine (noradrenaline) as a neurotransmitter.
This is just an example. Human physiology is for the most part not straightforward. As one goes from math to physics to biology, complexity increases. Evolution was not an exercise in mathematics.
PC
|
Richard
Re: I'm confused about Potassium November 06, 2003 10:27AM |
PC,
Thank you for taking the time to explain this. I did not know that acetylcholine was involved in both systems. That just adds more complications to this AF puzzle, however I feel like there's a piece to the puzzle that's just within reach, but I can't see it, to grasp it. I try to visualize the process of the ANS telling the heart what to do, and then follow it from the brain stem down to the heart, imagining the pumps and transmitters, in my primitive, mental way. The distance is not that great, yet it's like trying to discover another universe. There are a few things that I have discovered about myself, but who knows where it will lead.
Normal in Ca, Mg, K, Na, Cl
Mercury problem
Low in Molybdenum, tryptophan, tyrosine, norepinephrine, lithium, B12, folate, and possibly phosphorous.
A bit high in fibrinogen and a bit low in reduced glutathione, with some indicators of oxidative stress.
My metabolic analysis of the Kreb's cycle was pretty normal.
My neurotransmitter metabolism was low in vanilmandelic acid and homovanillic acid, and I need to read more on this, but it has to do with dopamine and the norepinephrine pathway.
In the mean time, I'm happy to be alive, love my family, and am happy that flecainide is working for me. Thank you, PC.
Richard
Thank you for taking the time to explain this. I did not know that acetylcholine was involved in both systems. That just adds more complications to this AF puzzle, however I feel like there's a piece to the puzzle that's just within reach, but I can't see it, to grasp it. I try to visualize the process of the ANS telling the heart what to do, and then follow it from the brain stem down to the heart, imagining the pumps and transmitters, in my primitive, mental way. The distance is not that great, yet it's like trying to discover another universe. There are a few things that I have discovered about myself, but who knows where it will lead.
Normal in Ca, Mg, K, Na, Cl
Mercury problem
Low in Molybdenum, tryptophan, tyrosine, norepinephrine, lithium, B12, folate, and possibly phosphorous.
A bit high in fibrinogen and a bit low in reduced glutathione, with some indicators of oxidative stress.
My metabolic analysis of the Kreb's cycle was pretty normal.
My neurotransmitter metabolism was low in vanilmandelic acid and homovanillic acid, and I need to read more on this, but it has to do with dopamine and the norepinephrine pathway.
In the mean time, I'm happy to be alive, love my family, and am happy that flecainide is working for me. Thank you, PC.
Richard
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