Sympathetic vs Vagal Question

To All,

Alright, I'm going to ask this question one more time, and hopefully someone will help me to understand. Here are the facts about myself, which is the reason I am confused.

Feb. 03 is when I found this site. At the time, I was on dysopyramide and toprol and my condition had changed from flutter to AF, probably due to a flutter ablation, but it could have been the meds. I was convinced I was vagal, because all my episodes came on in the evening. Virtually everytime I finished dinner, my heart would start missing beats. As soon as I would retire to the couch, my heart rate would plummet, and I would go into AF. I became a human yo-yo. If I didn't go to bed with AF, I would wake up frequently in AF. It was continuous and horrible. I had all the symptons of a typical vagally mediated AFer.

Upon learning all I did on this BB, I reflected on my situation prior to diagnosis. All my episodes were during the day, and exertion or exercise induced, especially when walking up slopes. I had either 3 or 4 episodes pre-diagnosis, which all converted, except for the last one, of which I was cardio-converted. I didn't know at the time, what was happening, and even went to a well recommended doctor, but she could find nothing wrong.

When quitting dysopyramide and toprol on 4/1/03, I then went back to flutter and remained persistent for 1.5 mths. Flecainide had worked for 1 yr., but quit working, so I decided to try it again. That was around May 20, and it has worked ever since, with the exception of 3xs. I connected those 3 episodes to glutamate and dining out.

I must add in the above scenario, if memory serves me, that I thought there was a possible correlation to pesticides (organophosphates) on the golf course because I lived on a course, pre-dianosis, and golfed 1-2xs per week, during good weather. At the time I stopped dysopyramide and toprol, I had golfed, and that's when I went into persistent flutter.

I now have every reason to believe that I am mixed, but with different causes. Here's the way it happened:

1) Pre-diagnosis, pre-meds - flutter always during the day and always upon exertion. Lived on the golf course at the time, so it could have been pesticides, therefore adrenergic.

2) Upon taking dysopyramide and toprol - always vagally mediated, with the exception of when I stopped, then I went our during the day.

3) Upon taking flecainide - flutter 2x's during the day and 1x when I awoke in flutter, therefore mixed.

Now because I have a broader understanding of the basics of how the body works, this is what I see.

1) Being that I was probably adrenergic in the very beginning, if flutter can have that terminology, it had to have something to do with acetylcholine, and organophosphates block cholinesterase.

2) I became vagal, along with changing to AF, I believe, due to the blocking of adrenalin. So not only had my heart changed from flutter to AF, but I became worse than before. If I was originally adrenergic, with overstimulation of sympathetic tone, shouldn't the blocking of adrenalin helped me? They use noradrenalin to bathe the hearts of hamsters to gain sympathetic tone.

3) I then found that glutamate could be a problem for me.

So, I have three different neurotransmitters coming into play here. What my tests revealed are the following:

1) Very low in molybdenum (Mo). That could have been my problem with the pesticides, as well as the glutamate. Fran posted that molybdenum helps with glutamate toxicity. Mo could have possibly helped with processing the toxins of the pesticides, as well, had my levels been optimal, and because I was low, the pesticides made their way through my system causing the cholinesterase problem.

2) I was low in methionine, cysteine, taurine, and reduced glutathione. S-adenosyl-methionine is the rate limiting enzyme to produce noradrenalin. So in actuality, I was low in noradrenalin, and the beta blockers were causing further insults to my system by blocking adrenalin, which in turn blocked noradrenalin. This caused me to become extremely vagal. Another point, is that glutathione is 140xs more prevalent in the lungs than elsewhere in the body. Could that have been a further insult by breathing in pesticides, as I had no defense by either glutathione or Mo?

3) I was also very low in tryptophan, which is the orchestrator of all the neurotransmitters.

4) My Mg, K, Na, Ca, Zinc, Copper, and Manganese were all normal in serum and red blood cell, but I was extremely low in folate and low in B12, but all other vitamins were normal.

So, since taking all the supplements and aminos that Dr. Gersten has prescribed, I must say that I feel great. I was on a trip for 5 days, and my eating left a lot to be desired, I had a few drinks, and I stayed in rhythm.

Could it be the 1000mg of tryptophan at night, or the 300mcg. of molybdenum, coupled with taking a multi, extra B's, extra co-enzymated B's, time released C, super antioxidant formula, folate, and gamma linolenic acid, of which was the only fatty acid I had a problem with. I'm also taking an amino acid blend, along with extra N-acetyl-cysteine, taurine, glutamine, tyrosine and N-acetyl-tyrosine.

So to my question. Isn't there a possiblity that being vagally mediated isn't because of a dominant parasympathetic system, but rather a deficient sympathetic system? I still don't understand why we're focusing on trying to fix the parasympathetic system, instead of trying to rectify the sympathetic system. If I was adrenergic in the beginning, and was considered sympathetic dominant, then why did the beta blockers cause me to become so vagally dominant? It would seem to me that I further degraded my faltering sympathetic system.

Please help a neurotransmitter deficient old fool. I will work for answers.

Richard

Richard,

WHat a determined individual you are! I do admire you a lot. As regards your post's main question, I think it's a VERY good one indeed. It struck a chord with me given the likelyhood that my traumatic childhood and anxious adulthood have in all likelyhood left my sympathetic NS a little overstressed to say the least. I've never thought of THAT as being the problem as you put it - i.e. a deficent SNS being at the nub of the problem as opposed to an OTT PNS. Makes sense (except perhaps in the case of athletes) that a component of the ANS would more likely become damaged rather than over-developed.

However, I'm currently intrigued with PC's latest thoughts and speculations as regards AFrs' principal problem being ion channelpathies which are REVEALED by inbalances in the ANS (for whatever reason) as opposed to AFrs getting AF BECAUSE of ANS inbalances per se.

SO do here sitteth I, quite likely with a genetic polymorphism of my IKACh ion channel which predisposes me to AF, with the AF episodes occurring in line with the whims of my slightly out-of-sync ANS??

What to do? Do a Fran and an Erling as regards diet and limited supplements. Those cell membranes are surely ALL important in all of this.

And then if I keep on getting AF (and more than likely with increased frequency) hope firstly that the new RSD1235 and tarantula venom drugs come on stream (problem free and effective) asap, and secondly that abaltion techniques are perfected in the next 2 or 3 years as a fall back should I require it.

BTW Richard, I'm weaning off the SSRI citalopram to go on 5HTP (100mg/day). I can't get tryptophan here in the UK, and neither can I get 5 HTP on prescription (my GP said cos no money in it for the drug companies cos they can't patent it! NOw I knew this already but was impressed that my GP also proffered such a viewpoint). So I've acquired some 5 HTP from a reputable UK outfit who as it happens supply many reputable private clinics and concerns here in the UK. Also, I am, I'm a little sorry to say (to you at any rate!) that I'm still imbibinb a little red wine, but 'only' half a bottle a few times per week.

Best wishes,

Mike F.

I think that Richard's idea of nocturnal vagal afib originating in a burned out/highly sensitive daytime sympathetic nervous system - and not a highly sensitive parasympathetic ns, is SIGNIFICANT.

For example, I am just beginning to learn to monitor my day time activities with respect to stress load as I feel it registering as tension in my body and shallow breathing. A kind of body feed back, if you will. When I begin to overload myself with a whole lot of compulsive "must dos" and push myself into doing "just one more thing" all without resting or pausing in between or find myself racing to make an appointment, I sense the nervous tension building up in mybody and a light goes on in my little head. I draw back and say "no," I'm not going to push myself any more today. Time to cool it. I may leave errands or projects undone for the time being, allow myself to be late, without the slightest guilt or remorse!! It's a nice feeling of being in control.

I believe, this strategy protects my highly sensitive, daytime nervous system and that is probably why I am having more and more nights in NSR.(Magnesium also helps)

This theory of Richard's may not apply to all afibbers, but it seems to ring true here.

Carol

Mike,

Thank you for your kind comments. I admire your fortitude and appreciate your help very much.

I am intrigued by what PC is discussing in the conf. room, and also by the study, but I'm still not convinced. I say this, only because I keep meeting more and more people with AF. It's as if it is an epidemic, and I just can't fathom that all these people have polymorphisms. Genetic predisposition, but not polys. That doesn't make me right, however. The insulin factor that PC has represented could very well have something to do with all this, because insulin is a very big player in our bodies. Maybe it depends on what cells become resistant to insulin, determines what a person's disease will be. Even though I have a crude understanding of insulin and how it works, that makes much more sense to me, due to the population's love for carbs. Fran's theory, and my recent findings, in regards to myself and glutamate, also makes a lot of sense, too, but since enacting my supplement regimen, I had fears of the free glutamate in the pills causing problems for me, but thusfar that hasn't been an issue. I have a strong feeling that the molybdenum has helped. And last, but not least, is my opinion on sub-optimal levels of sulfur, which is an important antioxidant, and precursor to disulfide bonds in the formation of insulin, not to mention that it forms glutathione that is highly prevalent and protective in the lungs, which is where the blood goes, before dispersing into the pulmonary vein to the left atrium. Oh yeah, and enzymes for the poor misunderstood pancreas, who is an underappreciated workhorse in our systems. It produces the enzymes and insulin, and is under constant pressure to perform, due to eating lifeless food.

I wish I had the deeper understanding that so many others here have. I'm still working on it, but feel I have a long way to go, so I'll keep plugging along.

I'm glad to hear that you are trying 5-HTP, Mike, but remember how important the cofactors are, in particular B6 and magnesium. Dr. Gersten has me taking tryptophan before bed. Keep me posted on your results. Glad to hear you are trying to moderate your alcohol consumption. I know it's hard to give up all our vices, especially with you being so young. You might consider taking molybdenum, as well, since it is necessar to break the acetaldehydes down to acetate, when drinking alcohol. In regards to tryptophan, I was just thinking last night, that because chimpanzees are our close relative and considered frugivorous, do they have more serotonin than humans, and if that's so, are we really lacking more than we think. I'll have to check out fruit's contents and see what I find. Chimps love bananas, and I was reading that they actually prefer organic bananas over ones with pesticides. There is a stronger and better taste in the organic bananas.

Well, I'll be off to study more on insulin. Arginine is the most prevalent carrier of insulin, and that has intrigued me.

Thanks, Mike,
Richard

Carol,

That's an interesting observation about yourself. It would seem that stress throughout the day insults the sympathetic system, and by nightfall it's worn down, and then the parasympathetic system kicks in, in its normal way, but the sympathetic system just doesn't have enough steam left to fight against the current of the PNS. Stress, which is what put me over the edge, happened during the day.

Thank you, Carol.

Richard

Richard

I dont think it has to be a polymorphism. I have worked from the premise that it is a mutation - caused by - yes free glutamate.... I know I asked PC what the difference between a polymorphism and a mutation was and he said the p/morphism were long standing. I wanted to ask (and have done now) how can they tell if it is longstanding or a more recent mutation? I have a friend who is head of genetics in a good hospital - maybe I should ask her.

Anyway. Your theory about a burned out adrenal system is good to me. The stress I was under all my life must have burned something out. Even as a child I remember feeling like my heart would explode or burst or wrench in two, especially when hiding and being scared to breathe incase I was heard. Then there is the saying about a broken heart. I lived with one for many years and it did indeed feel broken. Its only relatively recently I have managed to get over stress by changing my outlook and how I get involved in things.

Fran