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Prolonged Standing and Aldosterone
Posted by PC
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PC
Prolonged Standing and Aldosterone October 16, 2003 05:57AM |
Over many months Ive noticed the coincidental appearance of AF episodes upon hitting the sack on evenings after Ive been out and about all day, i.e., golfing, running or just prolonged standing. At first I thought this was due to dehydration, given my previously poor habits in this area. I have previously posted my view of the importance of hydration wrt aldosterone and LAF (see post on 8/5/03). However, although definitely an improvement, as usual, this doesnt appear to be the whole story (now isn't that a surprise). Despite improved hydration my episodes continue on such days. In fact I can almost predict their evening appearance with remarkable accuracy depending on the days activities. Instead of a post workout vagal rebound, there appears to be a post prolonged standing vagal rebound. And, of course, this is always in the evening during a period of increasing vagal tone. This used to just happen on weekends, but being semiretired with more free time seems to have an adverse impact in this area.
A sampling of the medical literature
Aldosterone secretion increases in certain conditions such as poor salt intake, oral estrogen therapy, pregnancy, prolonged standing, and excess levels of stress.
[www.antibodyassay.com]
During prolonged standing is there stimulation of aldosterone secretion over and above that stimulated by dehydration? My ankles are never swollen, so I dont think theres lower limb venous pooling during such times (decreasing effective blood volume).
I think there is additional stimulation, because renal perfusion in the upright position is compromised by gravity, even in the absence of dehydration. Not only is blood flow to the JGA (juxtaglomerular apparatus) in the kidney compromised but there is also less hydrostatic pressure perceived by the carotid body in the neck. The latter is vagolytic. I tend to think theres reflexive vagotonia after prolonged standing. Im sure many of you vagal fibbers try to restrict vigorous activity just before bedtime for this very reason. I believe this is the defective substrate (atrial wiring) for both adrenergic and vagal LAFers. Whatever else is going on, our atrial wiring not only potentiates AF, but also is required for AF.
What other contributing factors could there be? When you're active and on your feet, you do require more glucose.
Ive recently posted on postprandial reactive hypoglycemia (PRH) and many appear to have the problem. Hans recent survey underscored the association between hypoglycemia and LAF. However, exactly how does this work?
According to the medical literature
Insulin-induced hypoglycemia caused an increase in plasma aldosterone as well as in renin activity and cortisol. ACTH is largely responsible for this.
Journal of Clinical Endocrinology & Metabolism, Vol 43, 173-177, Copyright © 1976 by Endocrine Society
[jcem.endojournals.org]
Administration of captopril resulted in a blunted plasma aldosterone response to hypoglycemia, but no concomitant blunting of the plasma cortisol response. We conclude that angiotensin II may be required for ACTH to stimulate aldosterone secretion. Alternatively, the possibility that captopril may selectively inhibit aldosterone secretion at the adrenal cellular level cannot be excluded.
Acute Effect Of Captopril On Aldosterone Secretory Responses To Endogenous Or Exogenous Adrenocorticotropin
Journal of Clinical Endocrinology & Metabolism, Vol 66, 46-50, Copyright © 1988 by Endocrine Society
[jcem.endojournals.org]
from previous post
Susceptibility Of The Right And Left Canine Atria To Fibrillation In Hyperglycemia And Hypoglycemia
[www.ncbi.nlm.nih.gov]
which states that The refractory period was shortest under hypoglycemia in the left atrium and longest under normo or hyperglycemia in the right atrium. We all know that approximately 90% of LAF starts in the left atrium, especially the pulmonary veins.
Mechanisms of Abnormal Cardiac Repolarization During Insulin-Induced Hypoglycemia
[diabetes.diabetesjournals.org]
Sympathoadrenal stimulation is the main cause, through mechanisms that involve but are not limited to catecholamine-mediated hypokalemia.
So it seems that not only can hypoglycemia trigger LAF via aldosterone mediated intracellular K imbalance but also via catecholamine mediated K imbalance. In short both the adrenal medulla (catecholamines) and the adrenal cortex (aldosterone and cortisol) can get into the act (of triggering LAF) during hypoglycemia.
However, while I can feel somewhat fatigued on such occasions, Im never sweating, anxious or agitated, as would be expected in hypoglycemia induced catecholamine mediated K imbalance. Perhaps for me its just the mineralicorticoids (aldosterone and cortisol). And then again, perhaps there is a component of GERD (along with PRH) that in concert with the rising vagal tone of the night is enough to trigger an episode.
At this point, Im going to study my diary some more and try to sit down whenever possible. These conditions (PRH, K imbalance, increase in aldosterone, etc.) are transient and very difficult to document. So observing and experimenting are about the only recourse left to us.
An angiotensin II antagonist trial might prove interesting. Perhaps we could interest some pharmaceutical company in sponsoring a trial in an appropriate subgroup of LAFers.
PC v54
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Fran
Re: Prolonged Standing and Aldosterone October 16, 2003 06:53AM |
How very timely PC
For the last few days I have non stop been doing up our new house. This has involved lots of up and down ladders and steps to paint ceilings and walls and lots of bending and straightening to lay wooden floor coverings etc. Last night I went to bed and had - is it bigiminy (no I didn't get married again) - one normal beat another normal beat then an extra for about two hours. (I used to get trigiminy? when I had AF). I went to sleep with it and it had gone by morning. This is the nearest I have come to AF in long long time.
Now I am used to being active - but maybe not to the aerobic step ups of sharing a paint container and having to stepp up and down each time I wanted to load the roller or brush - a lot.
I have also been famished. Can't seem to get enough food and am really craving simple carbs!! Managed so far to stay off and just made an extra snack of 2 scrambled eggs, three rashers of bacon and a pile of leaves with olive oil. Followed by 6 sundried dates. 8.30 in the evening. After an evening meal at 5 of roast lamb, parsnips, cauliflower and carrots - made by my mother in law.
Been eating wee local grown plums and almonds all day to keep up energy with slices of cold roast beef - on the hoof. No hypoglycemic episodes so I assume this may have been caused by catecholamine mediated K imbalance?
IF this is the cause then I am wondering how is best to eat. More or less fruit? Perhaps more salt - I was craving it - I put a lot in my eggs and of course there was some in the bacon (home cured).
We have to lay another floor tomorrow and paint the skirting boards and doors in another room. I DO NOT WANT TO INITIATE AN EPISODE OF AF nor ?bigiminy.
For the last few days I have non stop been doing up our new house. This has involved lots of up and down ladders and steps to paint ceilings and walls and lots of bending and straightening to lay wooden floor coverings etc. Last night I went to bed and had - is it bigiminy (no I didn't get married again) - one normal beat another normal beat then an extra for about two hours. (I used to get trigiminy? when I had AF). I went to sleep with it and it had gone by morning. This is the nearest I have come to AF in long long time.
Now I am used to being active - but maybe not to the aerobic step ups of sharing a paint container and having to stepp up and down each time I wanted to load the roller or brush - a lot.
I have also been famished. Can't seem to get enough food and am really craving simple carbs!! Managed so far to stay off and just made an extra snack of 2 scrambled eggs, three rashers of bacon and a pile of leaves with olive oil. Followed by 6 sundried dates. 8.30 in the evening. After an evening meal at 5 of roast lamb, parsnips, cauliflower and carrots - made by my mother in law.
Been eating wee local grown plums and almonds all day to keep up energy with slices of cold roast beef - on the hoof. No hypoglycemic episodes so I assume this may have been caused by catecholamine mediated K imbalance?
IF this is the cause then I am wondering how is best to eat. More or less fruit? Perhaps more salt - I was craving it - I put a lot in my eggs and of course there was some in the bacon (home cured).
We have to lay another floor tomorrow and paint the skirting boards and doors in another room. I DO NOT WANT TO INITIATE AN EPISODE OF AF nor ?bigiminy.
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peggy merrill
Re: Prolonged Standing and Aldosterone October 16, 2003 07:19AM |
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Sig
Re: Prolonged Standing and Aldosterone October 16, 2003 11:57PM |
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Richard
Re: Prolonged Standing and Aldosterone October 17, 2003 06:56AM |
PC and Fran and All,
I thought these links to be thought provoking.
Serotonin - The metabolic biosynthetic pathway from tryptophan to serotonin is shown here. Serotonin plays multiple roles in the nervous system, including neurotransmission. It is a precursor to melatonin, which is involved in the regulation of sleepiness and wakefulness. In the intestine, serotonin regulates intestinal peristalsis. Serotonin is also a potent vasoconstrictor, which helps regulate blood pressure.
[oregonstate.edu]
Plasma tryptophan and total neutral amino acid levels in men: influence of hyperinsulinemia and age.
- Fukagawa NK, Minaker KL, Rowe JW, Young VR
Metabolism 1987 Jul;36(7):683-6.
Because of the well-recognized age-related changes in peripheral tissue sensitivity to insulin and the demonstrated impact of insulin on blood amino acid profiles in young individuals, we evaluated the influence of insulin level and age on the concentrations of tryptophan and its ratio to the sum of the large neutral amino acids (LNAA). The ratio of the plasma concentrations of tryptophan and the LNAA (leucine, isoleucine, valine, tyrosine, and phenylalanine), may be an important determinant of the rate at which tissues synthesize neurotransmitters, such as catecholamines and serotonin. Each of five healthy young (21 to 34 yr) and five healthy old subjects (67 to 85 yr) received, on separate occasions, euglycemic insulin infusions at rates of 6, 10, 30, and 400 mU X m-2 X min-1. Basal plasma tryptophan concentrations and LNAA levels were similar in young and old. Both tryptophan and LNAA levels decreased in an insulin dose-dependent manner (P less than .02). The dose-response effect of insulin on tryptophan levels in the elderly was less than in the young (P less than .03), while the response of the LNAA was similar in both age groups. The ratio of tryptophan to LNAA was less in the old when compared to the young (P less than .03) but increased in the two age groups in an insulin-dose-dependent fashion (P less than .02). Maximal plasma tryptophan decrements were 39% and 32%, and maximal LNAA declines were 58% and 61% in young and old, respectively, during the 400 mU X m-2 X min-1 studies.
[www.arclab.org]
Depression and Amino Acids
The building blocks of protein, amino acids can affect various central nervous system-controlled mechanisms such as pain threshold, mood, and sleep patterns. Low tyrosine or phenylalanine, for example, can result in abnormal levels of mood regulating chemicals in the brain, such as dopamine and catecholamines. Low tyrosine can also create subnormal levels of thyroid hormone--a well-known cause of depression. This may be why pre-treatment with supplemental tyrosine appears to prevent the behavioral depression observed following an acute stress.1
Because catecholamines rely on S-adenosyl methionine (SAMe) for proper function, low levels of SAMe have been observed in some cases of depression.2 For this reason, it is recommended that the status of the amino acid methionine, the precursor of SAMe, and its various metabolic pathways, be studied in patients with depression.3
Another amino acid, tryptophan, is the body's source material for producing the powerful hormone serotonin, which also influences sleep patterns and mood. Depletion of tryptophan can spur an increase in depressed mood states, particularly in individuals sensitive to affective disorders.4-6 In fact, one study found that a lower tryptophan level corresponded with a higher depression score even for patients who were already under treatment with anti-depressant drugs.7
The Amino Acids Analysis (blood, or 24-hour urine) can reveal deficiencies of tryptophan, tyrosine, methionine and other amino acids which may be significant contributing factors in depression. Should test results uncover important deficiencies, a helpful amino acid supplement schedule is included.
[www.gsdl.com]
PC, It would seem that low catecholamines could be a possible cause of hypoglycemia, rather than catecholamine induced hypo., due to excess, if I understand you right, which I would propose doesn't cause anxiousness or sweating, but instead, simply, lack of glucagon that should inhibit insulin, as my wife was pondering, and we've been discussing.
This is a very interesting article on the different pathways of neurotransmitters, and I found this highlight, of particular importance in regards to orthostatic problems.
The catecholamines that act as neurotransmitters include dopamine and norepinephrine. Epinephrine is not produced in the central nervous system. The catecholamines share a common synthetic pathway. The rate limiting step is tyrosine hydroxylase. The activity of tyrosine hydroxylase can be modified by phosphorylation. This provides a point of regulation for the neuron. Clinically there are no agents capable of modulating tyrosine hydroxylase. However, treatment with agents such as methyldopa can compete with dopa for further processing. The result is a formation of false neurotransmitters. The false neurotransmitters are packaged in the synapse as though they were the catecholamine but when released into the synapse they are ineffective at the receptor. False neurotransmitters such as octopamine are also thought to be increased in hepatic encephalopathy. The packaging of false transmitters in the periphery is thought to be increased by inhibiting MAO. This is thought to explain the orthostatic blood pressure effects caused by therapeutic doses of MAO inhibitors.
[www.dendrites.com]
So if the MAO's are being inhibited by lack of, or formation of false neurotransmitters, then could this be the same effect as a MAO inhibitor, which causes the orthostatic problem? More food for thought. Is your plate full yet? I know mine is.
Fran,
This is why you were so hungry.
According to the glucostatic hypothesis, appetite control is determined by the use of glucose by brain cells. If glucose is low, neurons are activated and hunger increases. Conversely, when the rate of glucose is high, the activity of the brain cells sensitive to glucose is diminished, and the sensation of satiation is attained. Unlike peripheral tissues, such as muscles, the brain does not need insulin to metabolize glucose, suggesting further that the metabolism of glucose may have a unique place in the controlling ones appetite.
[www.matol.com]
Richard
I thought these links to be thought provoking.
Serotonin - The metabolic biosynthetic pathway from tryptophan to serotonin is shown here. Serotonin plays multiple roles in the nervous system, including neurotransmission. It is a precursor to melatonin, which is involved in the regulation of sleepiness and wakefulness. In the intestine, serotonin regulates intestinal peristalsis. Serotonin is also a potent vasoconstrictor, which helps regulate blood pressure.
[oregonstate.edu]
Plasma tryptophan and total neutral amino acid levels in men: influence of hyperinsulinemia and age.
- Fukagawa NK, Minaker KL, Rowe JW, Young VR
Metabolism 1987 Jul;36(7):683-6.
Because of the well-recognized age-related changes in peripheral tissue sensitivity to insulin and the demonstrated impact of insulin on blood amino acid profiles in young individuals, we evaluated the influence of insulin level and age on the concentrations of tryptophan and its ratio to the sum of the large neutral amino acids (LNAA). The ratio of the plasma concentrations of tryptophan and the LNAA (leucine, isoleucine, valine, tyrosine, and phenylalanine), may be an important determinant of the rate at which tissues synthesize neurotransmitters, such as catecholamines and serotonin. Each of five healthy young (21 to 34 yr) and five healthy old subjects (67 to 85 yr) received, on separate occasions, euglycemic insulin infusions at rates of 6, 10, 30, and 400 mU X m-2 X min-1. Basal plasma tryptophan concentrations and LNAA levels were similar in young and old. Both tryptophan and LNAA levels decreased in an insulin dose-dependent manner (P less than .02). The dose-response effect of insulin on tryptophan levels in the elderly was less than in the young (P less than .03), while the response of the LNAA was similar in both age groups. The ratio of tryptophan to LNAA was less in the old when compared to the young (P less than .03) but increased in the two age groups in an insulin-dose-dependent fashion (P less than .02). Maximal plasma tryptophan decrements were 39% and 32%, and maximal LNAA declines were 58% and 61% in young and old, respectively, during the 400 mU X m-2 X min-1 studies.
[www.arclab.org]
Depression and Amino Acids
The building blocks of protein, amino acids can affect various central nervous system-controlled mechanisms such as pain threshold, mood, and sleep patterns. Low tyrosine or phenylalanine, for example, can result in abnormal levels of mood regulating chemicals in the brain, such as dopamine and catecholamines. Low tyrosine can also create subnormal levels of thyroid hormone--a well-known cause of depression. This may be why pre-treatment with supplemental tyrosine appears to prevent the behavioral depression observed following an acute stress.1
Because catecholamines rely on S-adenosyl methionine (SAMe) for proper function, low levels of SAMe have been observed in some cases of depression.2 For this reason, it is recommended that the status of the amino acid methionine, the precursor of SAMe, and its various metabolic pathways, be studied in patients with depression.3
Another amino acid, tryptophan, is the body's source material for producing the powerful hormone serotonin, which also influences sleep patterns and mood. Depletion of tryptophan can spur an increase in depressed mood states, particularly in individuals sensitive to affective disorders.4-6 In fact, one study found that a lower tryptophan level corresponded with a higher depression score even for patients who were already under treatment with anti-depressant drugs.7
The Amino Acids Analysis (blood, or 24-hour urine) can reveal deficiencies of tryptophan, tyrosine, methionine and other amino acids which may be significant contributing factors in depression. Should test results uncover important deficiencies, a helpful amino acid supplement schedule is included.
[www.gsdl.com]
PC, It would seem that low catecholamines could be a possible cause of hypoglycemia, rather than catecholamine induced hypo., due to excess, if I understand you right, which I would propose doesn't cause anxiousness or sweating, but instead, simply, lack of glucagon that should inhibit insulin, as my wife was pondering, and we've been discussing.
This is a very interesting article on the different pathways of neurotransmitters, and I found this highlight, of particular importance in regards to orthostatic problems.
The catecholamines that act as neurotransmitters include dopamine and norepinephrine. Epinephrine is not produced in the central nervous system. The catecholamines share a common synthetic pathway. The rate limiting step is tyrosine hydroxylase. The activity of tyrosine hydroxylase can be modified by phosphorylation. This provides a point of regulation for the neuron. Clinically there are no agents capable of modulating tyrosine hydroxylase. However, treatment with agents such as methyldopa can compete with dopa for further processing. The result is a formation of false neurotransmitters. The false neurotransmitters are packaged in the synapse as though they were the catecholamine but when released into the synapse they are ineffective at the receptor. False neurotransmitters such as octopamine are also thought to be increased in hepatic encephalopathy. The packaging of false transmitters in the periphery is thought to be increased by inhibiting MAO. This is thought to explain the orthostatic blood pressure effects caused by therapeutic doses of MAO inhibitors.
[www.dendrites.com]
So if the MAO's are being inhibited by lack of, or formation of false neurotransmitters, then could this be the same effect as a MAO inhibitor, which causes the orthostatic problem? More food for thought. Is your plate full yet? I know mine is.
Fran,
This is why you were so hungry.
According to the glucostatic hypothesis, appetite control is determined by the use of glucose by brain cells. If glucose is low, neurons are activated and hunger increases. Conversely, when the rate of glucose is high, the activity of the brain cells sensitive to glucose is diminished, and the sensation of satiation is attained. Unlike peripheral tissues, such as muscles, the brain does not need insulin to metabolize glucose, suggesting further that the metabolism of glucose may have a unique place in the controlling ones appetite.
[www.matol.com]
Richard
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PC
Re: Prolonged Standing and Aldosterone October 17, 2003 08:01AM |
Richard,
Catecholamines, as you indicated, should not cause hypoglycemia. I was reiterating that they could cause hypokalemia. The agitation, sweating, etc., that they precipitate during hypoglycemic episodes are a reaction to the hypoglycemia (increased release of catecholamines attempting to increase blood glucose). Sorry that I wasn't more clear on that.
Hypoglycemia, as you stated, could be caused by either a problem with glucagon (too little) or insulin (too much or a hypersensitivity to it).
Insufficient catecholamines are rarely responsible for hypoglycemia, since glucagon is the main counterregulator to insulin.
PC
Catecholamines, as you indicated, should not cause hypoglycemia. I was reiterating that they could cause hypokalemia. The agitation, sweating, etc., that they precipitate during hypoglycemic episodes are a reaction to the hypoglycemia (increased release of catecholamines attempting to increase blood glucose). Sorry that I wasn't more clear on that.
Hypoglycemia, as you stated, could be caused by either a problem with glucagon (too little) or insulin (too much or a hypersensitivity to it).
Insufficient catecholamines are rarely responsible for hypoglycemia, since glucagon is the main counterregulator to insulin.
PC
|
Richard
Re: Prolonged Standing and Aldosterone October 17, 2003 11:32AM |
PC,
You said, "Insufficient catecholamines are rarely responsible for hypoglycemia, since glucagon is the main counterregulator to insulin."
I apologize for our neurotransmitter deficient brains, but we're just not understanding. If epinephrine facilitates the release of glucagon, and one is deficient in the former, then why wouldn't catecholamines have anything to do with hypoglycemia?
Thank you for taking the time to clarify.
Richard
You said, "Insufficient catecholamines are rarely responsible for hypoglycemia, since glucagon is the main counterregulator to insulin."
I apologize for our neurotransmitter deficient brains, but we're just not understanding. If epinephrine facilitates the release of glucagon, and one is deficient in the former, then why wouldn't catecholamines have anything to do with hypoglycemia?
Thank you for taking the time to clarify.
Richard
|
PC
Re: Prolonged Standing and Aldosterone October 17, 2003 04:33PM |
Richard,
I've never heard (or read) that catecholamines were required for (or even involved in) the release of glucagon.
Glucagon is produced by the alpha cells in the pancreatic islets and its secretion is caused directly by hypoglycemia, just like insulin's secretion from the beta cells in the islets is stimulated by hyperglycemia.
Glucagon can also be secreted in response to elevated blood amino acids and exercise. This should be right up your alley.
As far as I know (and that's not a whole helluva lot, because I always have to look things up), catecholamines are secreted in direct response to hypoglycemia (amongst other things) and do not need glucagon to function in this regard.
However, its role is secondary to that of glucagon wrt hypoglycemia. Similarly for GH and cortisol wrt hypoglycemia.
Please don't apologize for questioning (especially something that I posted).
PC v54
I've never heard (or read) that catecholamines were required for (or even involved in) the release of glucagon.
Glucagon is produced by the alpha cells in the pancreatic islets and its secretion is caused directly by hypoglycemia, just like insulin's secretion from the beta cells in the islets is stimulated by hyperglycemia.
Glucagon can also be secreted in response to elevated blood amino acids and exercise. This should be right up your alley.
As far as I know (and that's not a whole helluva lot, because I always have to look things up), catecholamines are secreted in direct response to hypoglycemia (amongst other things) and do not need glucagon to function in this regard.
However, its role is secondary to that of glucagon wrt hypoglycemia. Similarly for GH and cortisol wrt hypoglycemia.
Please don't apologize for questioning (especially something that I posted).
PC v54
|
Richard
Re: Prolonged Standing and Aldosterone October 17, 2003 07:51PM |
PC,
I guess I was a bit confused by reading this link, and this is what it said:
9. What stimulates glucagon release?
A: low blood glucose, amino acids (prevents hypoglycemia after a "protein meal"), epinephrine (adrenal), norepinephrine (sympathetic innervation of pancreas);
[www.med.uiuc.edu]
Stimulates and fascilitates are two entirely different words. I read it wrong.
By the way, I am amazed at how much you know, and how very well you understand it. You definitely keep me on my toes. The body, and it's processes, are extremely difficult to understand. It is an amazing and complex machine. Thank you for clarifying.
Richard
I guess I was a bit confused by reading this link, and this is what it said:
9. What stimulates glucagon release?
A: low blood glucose, amino acids (prevents hypoglycemia after a "protein meal"), epinephrine (adrenal), norepinephrine (sympathetic innervation of pancreas);
[www.med.uiuc.edu]
Stimulates and fascilitates are two entirely different words. I read it wrong.
By the way, I am amazed at how much you know, and how very well you understand it. You definitely keep me on my toes. The body, and it's processes, are extremely difficult to understand. It is an amazing and complex machine. Thank you for clarifying.
Richard
|
peggy merrill
Re: Prolonged Standing and Aldosterone October 18, 2003 12:56AM |
|
PC
Re: Prolonged Standing and Aldosterone October 18, 2003 02:07AM |
Richard,
The complex and exceedingly intricate nature of human physiology makes the biochemical approach to understanding AF daunting indeed. Your persistence on the amino acid front is admirable. I'm sure you're far more knowledgeable there than I.
Regarding sympathetic innervation of the alpha cells of the pancreatic islet cells, the situation is not clearcut. Although NE is involved as a neurotransmitter, secretion of glucagon is not blocked by alpha or beta blockers at doses that completely block insulin release (alpha adrenoreceptors) and sympathetically mediated HR increase (beta adrenoreceptors).
It's also important to differentiate between NE the neurotransmitter (a "localized" hormone that doesn't reach the blood) and the systemic hormonal version of catecholamines (NE and E) that are secreted by the adrenal into the blood. Perhaps during certain conditions, e.g., exercise, they can in some way contribute to glucagon release.
Just another small example of this complexity.
Medical School and 29 years of pathology do help in creating some understanding of human disease. However, the details are constantly changing and I'm constantly visiting google (like you and Fran and many others) in an attempt to keep abreast. My central brain is small (and shrinking) but my peripheral brain (google) is constantly growing.
PC v54
The complex and exceedingly intricate nature of human physiology makes the biochemical approach to understanding AF daunting indeed. Your persistence on the amino acid front is admirable. I'm sure you're far more knowledgeable there than I.
Regarding sympathetic innervation of the alpha cells of the pancreatic islet cells, the situation is not clearcut. Although NE is involved as a neurotransmitter, secretion of glucagon is not blocked by alpha or beta blockers at doses that completely block insulin release (alpha adrenoreceptors) and sympathetically mediated HR increase (beta adrenoreceptors).
It's also important to differentiate between NE the neurotransmitter (a "localized" hormone that doesn't reach the blood) and the systemic hormonal version of catecholamines (NE and E) that are secreted by the adrenal into the blood. Perhaps during certain conditions, e.g., exercise, they can in some way contribute to glucagon release.
Just another small example of this complexity.
Medical School and 29 years of pathology do help in creating some understanding of human disease. However, the details are constantly changing and I'm constantly visiting google (like you and Fran and many others) in an attempt to keep abreast. My central brain is small (and shrinking) but my peripheral brain (google) is constantly growing.
PC v54
|
Richard
Re: Prolonged Standing and Aldosterone October 18, 2003 04:04AM |
PC,
That goes to show that I didn't know about the differences in NE's versions. I keep getting distracted on the homefront, but I'm trying to focus on my Metabolic Analysis Profile test, and get a more in depth understanding.
I'll present one finding that I've not heard of.
Formiminoglutamic Acid (FIGlu) Ref range <=9.0 My result 22.6
This is what it said:
It is an intermediate in the histidine-to-glutamatic acid pathway, and it is elevated if tetrahydrofolate is deficient. Tetrahydrofolate (from folic acid) is the coenzyme that helps covert FIGlu into glutamic acid. Elevated FIGlu can be consistent with: megaloblastic anemia, birth defects (facial clefts, neural tube defects), and homocystinuria/emia with increased susceptibility for cardiovascular disease. Additionally, if folic acid dysfunction affects the metabolism of methionine, causing homocystinuria, many diverse disease conditions could be related to this dysfunction. Such conditions include mood disorders, neurological problems and diseases associated with vitamin B12 disorder, because B12 activity depends upon folate function in many instances.
Dr. Gersten's schedule of supplements includes a multi vitamin by Montiff, 1 @ 3x's day with meals, TriPhos B - 2 @ 2x's day before and aft. breakfast (Montiff), Intrinsi B12/Folate 1 @ 3x's days w/meals (Metagenics), and B-Complete 1 @ 2x's day at bkft/dinner (Montiff). This is just 4 items of 25. He's hitting me big time with B-s.
I was low in methionine, again, but not as much as on the urine amino analysis.
Serum amino Methionine - Ref range. 2.5-4.9 Result 2.7
Urine amino Methionine - Ref range 7-35 Result 2.1
Homocysteine(HS) - I was at the lowest risk w/0.6
So this tells me that I'm just not getting enough methionine in my diet, and it has nothing to do with pathway disruption, otherwise I'd have a higher level of HS, or I'm simply passing it through, but then you'd think my urine levels would be higher. I was reading a rather interesting site last night about autism, www.newtreatments.org/fromweb/sulfur.html (it's worth a read, but lengthy), of the importance of sulphur and molybdenum. As you may have read in the CR, my very low level of molydbenum was possibly the most important finding in my tests.
I may not do it now, but Dr. Braley (I think that's his name) and Metagenics are located right here in Gig Harbor, and I may approach his clinic about doing a clinical trial on arrhythmias. They use nutritional approaches. The last time I spoke with them, they were doing a clinical trial on rheumatoid arthritis. My daughter's best friend's dad just went to work for Metagenics. I believe there is a connection between the two companies.
PC, I can't completely substantiate my stand on methionine, but based on my own findings, common sense of lacking foods and diseased animals using up their own stores, and what I've read, I feel that this is an important component of our needs. Maybe by simply adding more B-6 (coenzymated) B-12 and folate to our diets, this could help, but by way of methylcobalamin or a coenzymated form, as cyanocobalamin may be too large of a molecule. You get your highest content of methionine from meat, and I've been eating that 2-3x's per day, since Feb., and I'm still low, even with organic meat. So why is that?
Richard
That goes to show that I didn't know about the differences in NE's versions. I keep getting distracted on the homefront, but I'm trying to focus on my Metabolic Analysis Profile test, and get a more in depth understanding.
I'll present one finding that I've not heard of.
Formiminoglutamic Acid (FIGlu) Ref range <=9.0 My result 22.6
This is what it said:
It is an intermediate in the histidine-to-glutamatic acid pathway, and it is elevated if tetrahydrofolate is deficient. Tetrahydrofolate (from folic acid) is the coenzyme that helps covert FIGlu into glutamic acid. Elevated FIGlu can be consistent with: megaloblastic anemia, birth defects (facial clefts, neural tube defects), and homocystinuria/emia with increased susceptibility for cardiovascular disease. Additionally, if folic acid dysfunction affects the metabolism of methionine, causing homocystinuria, many diverse disease conditions could be related to this dysfunction. Such conditions include mood disorders, neurological problems and diseases associated with vitamin B12 disorder, because B12 activity depends upon folate function in many instances.
Dr. Gersten's schedule of supplements includes a multi vitamin by Montiff, 1 @ 3x's day with meals, TriPhos B - 2 @ 2x's day before and aft. breakfast (Montiff), Intrinsi B12/Folate 1 @ 3x's days w/meals (Metagenics), and B-Complete 1 @ 2x's day at bkft/dinner (Montiff). This is just 4 items of 25. He's hitting me big time with B-s.
I was low in methionine, again, but not as much as on the urine amino analysis.
Serum amino Methionine - Ref range. 2.5-4.9 Result 2.7
Urine amino Methionine - Ref range 7-35 Result 2.1
Homocysteine(HS) - I was at the lowest risk w/0.6
So this tells me that I'm just not getting enough methionine in my diet, and it has nothing to do with pathway disruption, otherwise I'd have a higher level of HS, or I'm simply passing it through, but then you'd think my urine levels would be higher. I was reading a rather interesting site last night about autism, www.newtreatments.org/fromweb/sulfur.html (it's worth a read, but lengthy), of the importance of sulphur and molybdenum. As you may have read in the CR, my very low level of molydbenum was possibly the most important finding in my tests.
I may not do it now, but Dr. Braley (I think that's his name) and Metagenics are located right here in Gig Harbor, and I may approach his clinic about doing a clinical trial on arrhythmias. They use nutritional approaches. The last time I spoke with them, they were doing a clinical trial on rheumatoid arthritis. My daughter's best friend's dad just went to work for Metagenics. I believe there is a connection between the two companies.
PC, I can't completely substantiate my stand on methionine, but based on my own findings, common sense of lacking foods and diseased animals using up their own stores, and what I've read, I feel that this is an important component of our needs. Maybe by simply adding more B-6 (coenzymated) B-12 and folate to our diets, this could help, but by way of methylcobalamin or a coenzymated form, as cyanocobalamin may be too large of a molecule. You get your highest content of methionine from meat, and I've been eating that 2-3x's per day, since Feb., and I'm still low, even with organic meat. So why is that?
Richard
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