GERD, H2O, glucose, K, Stress and LAF

Sit back, put on your thinking cap and prepare for a brain cramp.

Many, including Jackie most recently, have speculated on the mechanism connecting GERD and LAF. It could be related to stimulation of vagal afferent or sensory nerve fibers (via gastric distention, irritation, etc.) that send signals to the brainstem resulting in motor signals back to the stomach (vagal efferents) instructing it to contract. This results in better mixing of gastric contents and its digestion and then its passage into the small bowel. However, these same initial signals to the brainstem could simultaneously result in crossover stimulation of vagal fibers to the heart (located immediately adjacent in the nucleus ambiguus). This would be akin to what happens with swallowing. This is a well known trigger for AF and plagued me for many months.

However, there is another perhaps additional mechanism connecting GERD and LAF. GERD is characterized by an increase in gastric acid secretion. H+ and Cl- are secreted into the gastric lumen and HCO3- and K+ are simultaneously secreted (maintaining intracellular electrical neutrality) into the blood draining the stomach. In anticipation of a meal this process results in what is called the alkaline tide, an increase in blood pH that triggers an increase in excreted urinary HCO3- to maintain the tightly controlled blood pH (7.35-7.45). You’ve hopefully read my posts on alkalosis and its impact on blood K+.

Hypokalemic alkalosis is a condition in which loss of K+ (profuse diarrhea, thiazide diuretics, etc.) causes alkalosis. However, I think there is an argument in the other direction, i.e., for alkalosis causing the hypokalemia. For a good explanation of how this might happen please visit
[www.compendium.com.ar]
Read the last paragraph just before “The Aldosterone Paradox” section. Given high potential for a brain cramp, let me try to distill the main point wrt us lone afibbers.

The aldosterone paradox basically relates to the dual sometimes conflicting actions of aldosterone. On the one hand, it springs into action when stretch receptors in the small vessels of the kidney (called the juxtaglomerular apparatus) perceive too little stretch, i.e., a drop in BP. It takes this to mean that blood volume is down (blood loss, dehydration, etc.) and triggers the release of aldosterone from the adrenal gland (via renin, angiotensin, etc.). This results in the rreabsorption of Na+, the main determinant of blood volume, at the expense of K+ loss in the urine. On the other hand, its release is also triggered when there is elevated blood K+. However, sometimes these two “secretagogues” (fancy word for the stimulus to an organ to secrete a hormone) are in opposition, e.g., dehydration and hypokalemia. This is the paradox.

This article seems to imply that increased urinary HCO3- will result in greater K loss when aldosterone levels are increased. For example, dehydration might be especially detrimental to K balance in the face of alkalosis. Perhaps this is why some participants in the waller water (pH 8.3) trial may have encountered worsening of their LAF. Perhaps this is just another mechanism associating GERD with LAF. This implication is not based on any hard data, but on an integrative approach to the topic, and if any disease needs an integrative approach, it’s lone atrial fibrillation.

For many months I would routinely go into AF every Sunday morning around 10 or 11 AM. These mornings were characterized by a small breakfast (if any) of cereal and OJ at 5:30 AM, minimal if any water during the subsequent round of golf with a glazed donut and OJ at the turn (sorry Fran, I know you’re cringing). I’d finish around 10 AM and would go into AF after walking up the hill to the parking lot and sitting down in my car. I probably couldn’t construct a better scenario to trigger AF.

First of all, there’s the vagal tone caused by being on my feet (I never take a cart) all this time, walking up a hill and then sitting down.
Secondly, there’s the dehydration and possibly GERD related impact on intracellular K+. Although I have occasional dyspepsia, I don’t know that I have GERD. However, it could be subclinical. It has been documented that GERD is more frequently encountered in the physically fit. I once ran the Boston Maraton in 2h45m and in my younger years routinely ran more than 100 miles per week. All the while my hydration habits were atrocious.
Thirdly, there is the question of hypoglycemia. Please see p. 65 of Hans book for a discussion of the yo-yo effect on blood glucose of the above Sunday morning diet. I will shortly explain why this just adds fuel to the fire.

Hypoglycemia (v. hyperglycemia) is problematic for many lone afibbers. Hans survey showed that diabetes was nearly completely absent amongst LAFers, a rather surprising finding in this age of syndrome X (AKA metabolic syndrome) and rampant obesity (67% of Americans are overweight or obese according to a recent JAMA article) and diabetes. Quite to the contrary, many perhaps most LAFers complain of symptoms referable to hypoglycemia, a condition much less frequently encountered in the general population.

So why should hypoglycemia be a problem for LAFers?

One of the two most important factors triggering AF is shortening of the atrial effective refractory period (AERP). The other is dispersion of this refractoriness, causing creation of the wavelets necessary to sustain AF. Vagal tone, hypokalemia and hypoglycemia all cause shortening of the AERP. Catecholamines can also do this. Vagal tone and cardiac fibrosis also cause increased dispersion of refractoriness and slowing of cardiac conduction velocity. Please see

[www.westhertshospitals.nhs.uk]
Please read the last paragraph under Arrhythmia Mechanisms.

“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.

“Proarrhythmic effects of reactive hypoglycemia”, Rokas S, Mavrikakis M, Iliopoulou A, Moulopoulos S.
Pacing Clin Electrophysiol 1992 Apr;15(4 Pt 1):373-6
which states “that reactive hypoglycemia was the trigger for aggravation of arrhythmia.”

“Mechanisms of Abnormal Cardiac Repolarization During Insulin-Induced Hypoglycemia”
[diabetes.diabetesjournals.org]
which states that “Our data indicate that hypoglycemia causes an acquired long QT syndrome. Sympathoadrenal stimulation is the main cause, through mechanisms that involve but are not limited to catecholamine-mediated hypokalemia.”

The bottom line is that hypoglycemia appears to cause shortening of the AERP over and above any caused concomitantly by hypokalemia. This latter also causes shortening of the refractory period and increases the dispersion of this refractoriness. Vagal tone does both of the latter as well as slowing cardiac conduction velocity.

What’s surprising is that LAF isn’t more common amongst those with GERD, those that don’t hydrate sufficiently, and those that constantly snack on sweets. But I believe that LAFers have a predilectiion over and above these factors. Our atria are wired differently. Vagal nerve fibers (only present in the atria) are located in a pattern that enhances the required dispersion. As we grow older, there is the inexorable increase in cardiac fibrosis caused by aldosterone and cortisol, amongst others, that further aggravates this dispersion. Stress is capable of enhancing automaticity and shortening AERP through its associated increase in catecholamines (?K mediated) and increasing dispersion of refractoriness through the above two steroids, both with affinity for the aldosterone receptors in the kidney and the heart.

This BB is full of highly recommended strategies for longevity. However, I believe that hydration, stress avoidance, GERD management, K and Mg balance, lower carbohydrate diet all deserve special mention in particular for LAF.

Nonetheless, at some point ablation may be unavoidable. However, improvement and avoidance strategies may allow us to delay our date with the EP. Hopefully the technique will be sufficiently advanced by then to make it less risky and more successful.

PC, brain crampist

Excellent post. I know there is a connection. I have faired much better on a lower carb diet.

blessings,
MLM

PC,

Very little I can add to your excellent summary........... except to say what a great brain cramp and that I'm personally grateful for, and most appreciative of, your continuing endeavours as regards unravelling the intricacies of LAF. Your sentence:
"However, I believe that hydration, stress avoidance, GERD management, K and Mg balance, lower carbohydrate diet all deserve special mention in particular for LAF."
kinda sums up my own future approach as regards dealing with frequent ectopy and occasional VMLAF.

Mike F.

P. C.
I wonder how certain symptoms that I experience tie in with what you have outlined above with regard to hypoglycemia?

During the last eight years, I have occasionally experienced a deep and unshakable near "comatose" state that comes on in the evening after supper when sitting still, watching t.v. It is NOT a matter of being "sleepy" or tired or a sign that I need to go to bed. It is usually accompanied by PACs or PAVs. It almost always precedes a night of VAFIB. It hit again last night and at the same time I had numerous premature beats. I forced myself to get up and experimented with drinking a lot of water, which seemed to help. In this instance, I did not go into afib last night. I attribute this to drinking water and the safety net of magnesium supplementation. It seems to hold afib in check.

During my life I have had numerous episodes during the daytime of what I thought was hypoglycemia, but it didn't showed up on a single lab test. My doctors dismissed my symptoms. Symptoms were sleepiness, lightheadedness, a feeling of passing out, nausea, desperate need for or craving for food , always protein, red meat - a hamburger. After eating meat, symptoms would subside.

Incidentally, my blood work is absolutely normal.

Does this sound like a symptom of hypoglycemia? If so, it might be a graphic example of the connection between hypoglycemia and arrhythmia.

Thank you for your hard work in trying to solve this afib puzzle. You appear to be on track for a Nobel Prize!

Carol

Your comments are always much appreciated.

Carol,

As a pathologist, I can comment specifically on your hypoglycemia question. Hans and I have communicated several times in the past on just this point - how to diagnose hypoglycemia?

For many years an oral glucose tolerance test was the only lab test for diagnosing hypoglycemia. At present the only way to diagnose reactive hypoglycemia is to demonstrate a low blood sugar (less than 3.3 mmol = 60 gm/dl) concomitant with symptoms, i.e., diaphoresis (sweating), agitation or anxiety, etc. However, although the oral glucose tolerance test (OGTT) is far from diagnostic, a characteristic pattern is often seen in PRH. The release of insulin is sluggish and the insulin peak delayed with respect to the peak value for blood glucose.

See pp 63-64 of Hans’ book in section on hypoglycemia where he states, “It is also possible, but purely speculative on my part, that a blunted glucose response could be associated with LAF”.

In mid February of this year I posted something on postprandial reactive hypoglycemia. I remember that Fran took special interest in it. Hopefully Hans won't mind my repeating portions of it for some who may not have seen it. Please visit the below website for details.

Diabetes & Metabolism (Paris), 2000, 26, 337-351
POSTPRANDIAL REACTIVE HYPOGLYCEMIA
J.F. BRUN, C. FEDOU, J. MERCIER
[www.alfediam.org]

Accordingly, I would like to second Hans' suggestion via the following evidence lifted from that article and the medical literature:

1)Insulin hypersensitivity is present in more than 50% of those with PRH.
2) High carbohydrate-low fat diet increases insulin sensitivity, and this pattern is frequently found in PRH patients.
3) Glucagon like peptide (GLP-1) is also significantly increased in most. GLP-1 (also known as incretin) controls blood glucose after a meal via stimulation of insulin secretion.
4) Insulin enhances epinephrine, norepinephrine and cortisol secretion in response to hypoglycemia.
5)Insulin sensitivity alone can induce hypoglycemia, since high values like those found in PRH are found in young, lean people who never report suffering PRH.
6) An increase in insulin sensitivity associated with a deficiency in glucagon secretion is the widely accepted explanation for hypoglycemia in the late postprandial phase.
7) Glucose production secondary to glucagon requires Mg (see above post).
8) Glucagon receptor activity is mediated by adenylate cyclase, which is Mg dependent.
9) This failure of glucagon induced glucose production in response to insulin induced hypoglycemia stimulates epinephrine secretion.
10) Insulin and catechlamines both stimulate cellular uptake of K.
11) Hypokalemia is highly arrhymogenic.
12) LAF is a well known symptom of hypoglycemia.

Other pertinent particulars:
1) Very lean people or in women with moderate lower body overweight are prone to hypoglycemia.
2) Insulin sensitivity is twofold higher in follicular than in luteal phase. These women frequently describe hypoglycemic symptoms late in the morning.
3) Slimming increases insulin sensitivity.
4) PRH individuals have high HDL cholesterol.
5) Symptomatic hypoglycemia typically occurs after a sugar drink or alcohol while in the fasting state.

Conclusion: Many LAFers whose episodes are triggered by hypoglycemia have PRH, because they have insulin hypersensitivity due to increased GLP-1. They also have the required defective glucagon secretion and sensitivity due to Mg deficiency. This results in LAF because the insulin and reflexive catecholamine secretion result in lower blood K levels. Hypoglycemia (see my first post) causes AF over and above any catecholamine mediated hypokalemia.

PC

PC--

Your initial post in this thread has been anything but a brain cramp. What it does, even if we cannot follow fully the discussion of the physiology, is to tie our successful experiences dealing with afib to underlying principles. This in turn can only help convince those who need encouragement to follow the successful pattern for nutrition and lifestyle changes.

I would emphasize stress management as an important lifestyle change that is most likely to be overlooked. In this vein, I think it is so very interesting that during Hans' Hawaiian vacation, his afib did not occur. So, if anyone needs a primer on slowing down and avoiding stress, a Hawaiian vacation is possibly the easiest introduction.

From my own experience, I think that nutient depletion from drinking coffee and alcohol need to be emphasized as important problems regarding afib.
The common emergency-room afib syndrome "holiday heart" testifies to the afib consequences of alcohol.

Finally, PRH is an element in my afib scheme that I had not noticed until this thread. My afib episodes all followed high-carbohydrate, late evening meals which included desserts and some (moderate, eg two glasses of wine) alcohol intake. I also have relatively high HDL in my cholesterol profile.

PC, [or anybody else who might want to answer me], i am trying to fit this with my own experience. My first 2 episodes took place in mid to late 1999, in the context of a very stressful and taxing convenience store job involving lots of overtime and no benefits whatever. I was working long hours and long weeks, at one point 11 days without a break. I was drinking a really lot of coffee, which is the only way you can work like that. This was only the last in a long series of such jobs, what i call 'b shift' jobs, the ones where you be there when it opens and be there when it closes, that's the be shift. My diet tended to be whatever i could find in the store, a sorry selection. Most of my waking hours were in the store, i would go home, eat whatever leftovers i found in the refrigerator, and collapse into bed, getting up to go back and do it some more. I was taking a lot of supplements but magnesium was not among them.
These first 2 episodes happened at night after i had gone to sleep, both times around midnite. You know the sensation of something being very, very wrong, heart doing jigs without rhythm, breathless, sweaty, have to pee, etc. The first one only lasted a few hours, terminating when i tried to get more comfortable by taking a cool shower. This was in late August or early September, still pretty hot. I went to a doctor a few days later. Of course he could not find anything wrong at that time as there was no afib at that time, but he asked me please to go to an emergency room if that ever happened again. He insisted on that point, asked me to promise that i would, and i did promise.
In mid October i gave 2 weeks notice on the job, having gotten enough cash together to get me to Staten Island where i had a promise of a job and a place to stay. I should mention that i had been staying with my brother and his wife in Maine while working the convenience store job. I had recently broken up a 17 year bad marriage, too. While working the second week of that notice, again i was awakened around midnite by the same feeling of impending doom, madly thumping heart, etc. I didn't want to awaken my brother and sister in law, sleeping the sleep of exhaustion just as i had been and going to work tomorrow too, so i tried the cool shower trick and it didn't work. At last i did apologetically awaken them, and my sisterinlaw took me to the nearest emergency room, about 15 miles away.
That hospitalization lasted 3 days and got me a debt of nearly $3000. They told me i would have to give up coffee and i said yes,yes, i'll cut down. Second or third morning out of the hospital i poured myself my usual cup of good strong coffee, drank about half of it right down, and went into afib. Only lasted 15-20 minutes, but i poured the rest of the coffee out and became a teadrinker on the spot.
The hospital doctor had put me on digoxin, the smallest dose possible, i don't recall what. I moved to Staten Island and the job and place to stay worked out ok, a much easier job than the convenience store. This job was in a thrift store with 3 floors to it. Staten Island is very hilly, and the residences all had 3 floors too. Everything was uphill and upstairs, and that digoxin was keeping me feeling worn out all the time. I had no endurance and stairs were a real problem. If i lay down at all during the day i would fall right to sleep. Eventually i ran short of digoxin at a time when i didn't have the money to refill it, and i began taking it every other day to conserve it til payday. The days i didn't take it i felt a whole lot better, so i stopped taking it.
August 2000 i didn't sleep a couple of nights due to a neighbor's dog barking all night. Summer is pretty hot in Staten Island, and i had no air conditioning, neither at work nor at home. I am way too heavy and the heat bothers me. The second day i was pretty groggy at work and i drank probably 4-5 cups of green tea in an effort to stay awake. My workplace was stifling hot, a small room on the second floor. I decided some exercise would wake me up, so i took a break and walked down to the foot of the hill and back up again. It's a real steep hill, you have to lean forward to keep from falling back down it. At the top i realized everything was not all right at all. I called my doctor [had health insurance by then] and she said meet her at the hospital.
Stayed there a day and a half before reverting to NSR, cardizem drip while there. Quit caffeine altogether after that and have had only a few short episodes of afib since, not connected to anything i can identify. Got airconditioning the next summer, had no problems. Have since added magnesium to my supplements, recently changed to the glycinate form due to information gotten here.
I don't have diabetes and i don't think i have hypoglycemia. I am considerably overweight and i fit the profile for syndrome x, insulin resistance and all. Since discovering this board i have changed my diet to a more paleo kind, cutting out grains, potatoes, etc. Years ago i cut out processed food and white flour, never drink sodas. Have been paying much more attention to proper hydration, also due to information found here. Had a little afib episode a couple months ago but they are rare these days and go away by themselves. Hopefully the Mg glycinate will abolish even those. I don't have health insurance right now so i really must take good care of myself.
So how do i relate to PC's post? Any comments greatly appreciated.
Peggy

P. C.

I am so grateful for your contributions to this BB. While there has been a large amount of pooling of invaluable information on this board, I honestly think that you and Hans are getting close to sorting it all out and solving the riddle of LAF. I also think that it is interesting that anecdotal evidence presented on this board , that science tends to shun, may play a large part in finding the answer.

I was astonished to discover that I fit ALL FIVE of the "other pertinent particulars" in your recent post. I am tall and lean, have had episodes of PRH in late morning in addition to after supper, have very high HDL cholesterol, episodes used to occur while fasting following drinking alcohol, ( I no longer drink) ,etc.

Now, am I correct in thinking that the way to prevent PRH is to stick to a strict Paleo diet? That is, no starches, sugar, potatoes, rice, sugar drinks, etc. and eat protein, veggies, fruit? What about fruit juices?

Am I also correct in thinking that Mg. depletion contributes to PRH?

The previous post was from me, Carol - I clicked the post button prematurely!

Peggy,

Best of luck to you. You seem to be on the right track. I also know what it's like to be without health insurance, but the best insurance is plenty of exercise and a good diet. I too struggle mightily on the latter. I have a real sweet tooth.

Carol,

Thanks to Hans, I think we are making progress in understanding LAF. However, there seems to be so much variability from one LAFer to another. Our bodies are so complex and its physiology so intricate that I'm not sure we'll ever see the total picture wrt LAF.

There are many diseases much worse. LAF is a constant reminder to me that life is precious and to be thankful for the good health I do have. If I didn't have the affliction, I don't think my appreciation of such would be as keen.

Easy for me to say, since my episodes are shortlived, relatively gentle and occurring predominantly during sleep.

PC

P.S. Stay away from fruit juices unless you're also eating protein or low glycemic food. Until reading Lam and Mercola I always thought that fruit juices were good for you. Shows you what a sugar junkie I am.

P. C.

Thanks for the reply.

What do you suggest with respect to my last two questions regarding magnesium and type of diet to prevent PHR? (please scroll up to my last post)

I agree that afib is probably a symptom with a number of separate causes or combinations of causes, but I still think that patterns will emerge and that afibbers will fall into one or perhaps several categories.

Stress management, hydration, nutrition, magnesium may be the constants underlying all the variations.

Carol

Carol,

Don't you know that MDs don't know anything about proper diet and nutrition. Fran is the expert here. I'm out of my league.

Having said that, about all I can do is quote the recommendations in the main article I cited above

DIETARY TREATMENT
Harris, in his first paper [4], advocated treating PRH with a low carbohydrate diet and frequent small split meals. This dietary approach remains the first treatment of this disorder [1, 10, 28-30, 73]. The first important point is to add small meals at the middle of the morning and of the afternoon, when glycemia would start to decrease. If adequate composition of the meal is found, the fall in blood glucose is
thus prevented.
The second cornerstone of this diet is that patients should avoid rapidly absorbable sugars and thus avoid popular soft drinks rich in glucose or sucrose. They should also be cautious with drinks associating sugar and alcohol, mainly in the fasting state. If the breakfast is hyperglucidic, adding proteins to it frequently reduces its insulin response and thus its
power to induce further excessive falls in blood glucose [45].
Addition of soluble dietary fibers that lower the glycemic and the insulinemic index has a similar effect and has thus been recommended. Soluble fibers as pectin and guar delay gastric emptying and prolong the intestinal transit time. Mirouze [89] reported in a series of nineteen patients that treatment with pectin protected against falls in blood glucose after OGTT by increasing the glucagon response in the late period of the test [89]. The addition to the meal of 5 to 10 g hemicellulose, guar or pectin often improves postprandial hypoglycemia. Dietary fibers are mainly interesting when PRH is associated with decreased glucose
tolerance or occurs after gastric surgery [29]. As shown above, the risk of reactive hypoglycemia is markedly enhanced by the simultaneous ingestion
of ethanol and sucrose or glucose, mainly in the fasting state. Decreasing the amount of sucrose (glucose) ingested or replacing it with either saccharin or the noninsulinotropic carbohydrate fructose has been
shown to prevent this kind of hypoglycemia [108].
In most patients with idiopathic-reactive hypoglycemia, diet alone is sufficient; but one should be alerted for the aggravation of symptoms on a low carbohydrate diet. If this occurs, one should suspect fructose 1-6 diphosphatase enzyme deficiency, and the diet should be increased in carbohydrates [10].

PC (please don't ask me where to find guar or hemicellulose)

PC,

I haven't posted in a long time, but wanted to thank you for all the information you have shared, over the time that Richard and I have been reading this BB. He's in CA. for his meeting with Dr. Gersten, and I get the use of the laptop for a change. I wouldn't let him take it. You peaked my curiosity, in regards to hypoglycemia, as I believe that I may suffer bouts of it myself. I completely agree, that we are a society that loves our sugar, but as you know, we also deal with enormous stress. As you may remember, we have looked at the diets of the chimpanzees. They are considered frugivorous, but eat leaves, insects, and other monkeys, but only for about 2-3 mths. So, because they are frugivorous, I'm assuming they get a lot of glucose from the sugars, but also from the sap of the trees. So, to my point, and pls. bear with me, as I'm trying to learn, as I go.

How does the body "supposedly" know just how much insulin to secrete? Let's just assume that it doesn't, and it secretes the normal amount everytime. There always seems to be a yin and yang, action and reaction, to everything, such as calcium/magnesium or serotonin/dopamine, etc. Could it be possible, that due to adrenal exhaustion over time, from stress, that epinephrine is the problem, as it stimulates the release of glucagon, and it's not being secreted to offset insulin's effects? As I was reading last night, and today, I found s-adenosyl-methionine, the activated form of methionine, to be the rate limiting step in converting norepinephrine to epinephrine. Richard was the lowest in methionine and cysteine, based on his urine amino test results. Because our society is so bombarded with external sources of pollution, by way of foods and air, I have to believe that methionine is playing a key role here, and your stores are depleted, just as your Mg. stores are. Glucagon is also important for amino acid uptake, and Richard wasn't absorbing his proteins, or other nutrients for that matter. We used to think, and still do, that serotonin and dopamine were playing a key role, but lack of Mg. and vitamins were probably more the problem, and upon some people upping their intake, it helped the necessary pathways for the vital neurotransmitters, yet you all still have the haunting problem.
Here's one of my sources: [www.med.uiuc.edu]

Has anyone studied the anabolic/catabolic cycle of building up and tearing down, within the body. I find it interesting that the catabolic cycle begins at approx. 4pm until around 10pm, especially in regards to Han's cycle of AF. The aminos acids most important for the catabolic process are methionine, taurine, cysteine, (all sulphur containing) and aspartic and glutamic acid, of which the latter two, are probably not a problem. What if the body doesn't have enough sulphur containing aminos for use in tearing down, so the cells cannot be renewed?

It's a bit late, so I must go to bed, but if I seemed confused on the insulin issue, it's because I am, so pls. excuse me, and if you have any comments or clarifications, I would greatly appreciate your input.

Rhonda

Thanks,

I meant to check out the web site you cited. I was so busy trying to "digest" your information packed response that I neglected to check it out.

My printer gets a work out with your posts!

Carol

Rhonda,

It may bear repeating from the above cited article that they believe that PRH is due to a defect in the functioning of glucagon.

Although the article didn't mention it, Mg is critical in the proper function of glucagon both at the receptor site and in at least four of the ten steps by which pyruvate (from intracelluler protein) is converted to glucose.

On the other hand, it could be a problem with catecholamines, as you suggested.

And then again it could be something from left field. For example, Hans has been doing some extensive research on copper. It may turn out to be latest overlooked mineral, now that Mg has ascended to its proper position in the pantheon of vitamins and minerals.

Specifically, as relates to your suggestions wrt catecholamine synthesis

Copper is required for the synthesis of the neurotransmitter norepinephrine from dopamine. Copper imbalances can contribute to imbalances of the norepinephrine/dopamine ratio.

Copper is a cofactor for the enzyme monoamine oxidase (MAO), which plays a role in the degradation of norepinephrine, epinephrine, dopamine and serotonin.

PC v54

Hi PC,

I take it, that I understood about how insulin and glucagon works. I was doubting myself. Richard's neurotransmitter pathways were not working, yet his zinc and copper levels turned out to be normal, per Dr. Gersten. (Please see my post in the conf. room about molybdenum.) His pathway from dopamine to norepinephrine, which is carried out by homovanillic acid, was blocked. I can't expand on that much more, but you can bet I'll be reading more about it. His tryptophan levels were also low, with interruptions in those pathways, as well. When Richard returns, he'll be filling you all in. This is all so fascinating, but very difficult to fully understand. It's nice to have a doctor on board, with such an open mind. Thank you.

Rhonda

Rhonds,

Open but mostly empty.

PC v54

I wouldn't say that PC. Your mind is full of interesting and intellegent facts and inquiry. And for anyone of us to understand the complexities of the human body they would be able to build a human baby from scratch (no egg no sperm) with no disease or illness. Phew, It doesn't bare thinking about.

Fran

Talk about brain cramps! I saw this thread a while ago and needed some time to digest it and re-read it. I am not female, but I am tall and relatively lean. My HDL is off the charts-in the 60's, very unusually high, according to the doctor. As for the hypoglycemic type trance, my wife and kids even have a name for it--they say that Dad is "watching tv with his eyes closed". I am relatively fit--ran a number of marathons in my youth and still, at age 54, play full court basketball a lot and workout frequently. I also get dehydrated frequently, no matter how much I drink. Running up and down a basketball court in South Florida, even in AC, drains one because the humidity is usually in the 90+ range. My most recent discovery has been to be very careful about rehydrating and drinking sports drinks with potassium in them; it seems to help. And, my afib, which is again relatively infrequent, is ALWAYS associated with gastronomical rumblings, heartburn, etc.

There are some very common grounds here, folks, and I think we are learning most valuable information. Mg has been a big help for me, and lately, making sure I get some extra potassium when I sweat a lot has helped. Now, I get to read up on hypoglycemia, which I gather is kind of the opposite of diabetes.

Thanks to all! John.

Hans,
It would really be interesting to do a survey to determine how many lafers experience PRH - postprandial reactive hypoglycemia - or just plain hypoglycemia . There seems to be a lot of correlation popping up here.
Carol