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