Report on 1 year's progress.

Introduction:

I have been exhibiting chronic a-fib for two years. I have no other known health problems, other than being 66 years old, and having a lifelong history of migraine. I work 60 or more hours per week, and my sports are wind-surfing, mountain biking, and mountain climbing, all of which are now pursued with suitable restraint. My height is 5’11" and weight 145 lbs.

My a-fib does not affect my normal life, nor am I much aware of it. My heart rate is; 70 waking, 80 resting, 100 working, 115-125 exercising (albeit not too vigorously), and 150-160 peak. My blood pressure averages 120/70 when I am far away from medical doctors. All the standard tests failed to show any heart or chemical anomalies

My two children are both MDs, and my daughter-in-law is a physical therapist for the Olympic teams. Our collective judgement is that, as aging continues, in ten or twenty years my health will be better if aging proceeds with my heart in sinus rhythm, rather than in a-fib.

Background:

For years prior to November, 2001 I had what, at the time, seemed like skipped heart beats, but I experienced no a-fib. On a trip to Phoenix that November I stayed up most of a night analyzing a particularly frustrating German patent. This predictably triggered a migraine the following day, which peaked the following night. When I awoke the next morning I was experiencing an irregular heartbeat, but no other symptoms other than what seemed like somewhat stronger than usual post migraine recovery symptoms.

When I returned home my daughter analyzed my problem over the phone as a-fib and had me come in for an ECG to verify her guess.

I did a cardioversion in the spring of 2002 which successfully converted my heart to sinus rhythm. The resultant, if unanticipated, migraine restored my heart to a-fib when the migraine peaked about 36 hours after the cardioversion. This was little different from what had happened months earlier when my a-fib started as a migraine peaked. A month or so later we did another cardioversion, with the same result as obtained with the first cardioversion.

Additional information:

Soon after my heart began a-fib I acquired a used H-P ECG and began regular monitoring of my heart waveforms. Over a relatively short period of time I came to the conclusion that only the random ectopics provided any useful information about the condition of my heart. There were five different ectopics, which could all be seen in the aVF trace: (1) a standard left ventricular ectopic; (2) a half amplitude standard left ventricular ectopic; (3) a standard right ventricular ectopic; (4) a half amplitude standard right ventricular ectopic; and (5) a very low amplitude transient (when seen on the aVF trace) which had a shape somewhat like a right ventricular ectopic. During 2002, the rate of ectopics averaged about 20 per hour, with a range of 0 to 75 ectopics per hour, and predominantly consisting of the (5)th ectopic listed above.

During 2002 I explored the various supplement and nutritional ideas promoted on this a-fib web site as being beneficial without noting any changes in my heart’s ectopic pattern, nor did I notice any other physical
or mental changes.

In November, 2002 I decided to do the following: (1) eliminate all foods known to be high in Tyromine and all foods to which I reacted on a standard allergic skin prick test (to reduce problems with migraine; (2) eliminate all foods known to contain added glutamate; and (3) to consume 1 ounce of ethanol daily in multiple servings of a sulfite free wine (as an anti-stroke measure).

Naturally, this regimen forced other changes: no eating out; no processed foods; etc. My grocery store shopping now takes place entirely in the vegetable/fruit section with a few purchases in the organic dairy section (butter and eggs). I occasionally eat salmon from vitalchoice.com. I use organic oat groats for making cereal.

The ectopic rate started decreasing immediately. Over the next two months the ectopic rate dropped from its one year average of 20 per hour to a sustained average of less than 1 ectopic per hour, and has probably continued to decrease during 2003. But, there are so few ectopics now (30 minutes of monitoring per day) that it is hard to determine specifically
how much the ectopic rate has continued to decline.

The ectopics went away in the following order: (1) the (5)th ectopic listed above disappeared first; (2) the (1)st and (2)nd ectopics listed above (left ventricular ectopics) disappeared next. Generally, only the (3)rd and (4)th ectopics listed above (standard right ventricular ectopics) are seen any more.

I interpreted this change to be a hopeful sign. But, after about 8 months of minimal ectopics, and no return to normal sinus rhythm, I did a third cardioversion in August, 2003, which failed to convert my heart to sinus rhythm.

While the ectoptic rate was decreasing, unexpectedly, my neck’s rotational range increased noticeably and minor pain associated with large quick neck rotations largely disappeared. This improvement is continuing, albeit more slowly now. The literature suggests such neck stiffness and pain may be associated with added dietary glutamate.

The migraines have substantially gone away, and generally energy and thinking clarity seem to have improved.

So, it seems clear that: (1) I seem to have found a way to influence my heart tissue to be generally less irritable; and (2) with the passage of time the root cause of my a-fib is exerting progressively greater power to maintain my heart in a-fib.

It seems like it is time to give serious consideration to a pulmonary vein isolation.

Wil Schuemann

Wil,

Thanks for the fascinating story. As I've said before, your persistence and dedication in tracking down the root cause of your AF, albeit unsuccessful, is admirable.

I would have to agree with your thoughts on PVI ablation. Who have you decided might be best in this regard?

Do you think that you would have been able to arrest the progression to chronic AF, if your dietary regimen had been instituted earlier? I presume Mg is high on your supplement list, especially given your history of migraines.

PC

Hello PC,

I regard the program as successful, even without a return to NSR thus far. I have essentially eliminated ectopics in the ventricles. This should reduce the probability of ever encountering a number of non-afib related heart problems in the future. In addition, assuming the lowered heart irritability will extend to the atriums, if a PVI is successful, should improve the probability of maintaining NSR thereafter.

In my case there was no progression to afib. My heart just switched from lifelong NSR to chronic afib. In a way I can regard this positively, as the possibility exists that some event caused a single aberrant site in a pulmonary vein to switch on, which caused the switch from NSR to afib. If true, this might mean that the PVI has a higher probability of being successful because there may only be one source to isolate.

The Mg, at very high levels, had no effect on the migraines or ectopics during 2002. The ectopic reduction and migraine reduction seems to have resulted from dietary eliminations. Based on how much more productive I am now, and how much better I feel, I would have to agree that had the dietary change been instituted earlier the heart deterioration probably would have been slowed.

I have submitted an application for a PVI to the Cleveland Clinic Heart Center. They haven't responded yet.

The important thought which caused me to convert from being willing to live with the afib to being favorably inclined toward a PVI is that my thinking had to switch from what is best now to what decision now will have been best when evaluated twenty years from now. The few precent PVI complication rate extrapolated to twenty years hence only corresponds to a life expectancy loss of four months. But, the 50% probability of being in NSR for the twenty years is likely to worth far more than four months of high quality life.

Wil:
Sure sounds like you're right on top of things. You didn't mention, have you had a Thallium Stress test and an echo and know that you have no underlying heart disease? I suppose you could consider yourself safe, with being 66 y.o. and wind surfing, mountain biking, and mountain climbing. Surely all that would have brought on anginal pain if you had significant CAD.
It also sounds like you have made vast improvements in ectopy with diet changes. Your chronic afib is at least at a comfortable rate. Do you feel it most of the time? or some of the time? Have you ever tried any of the antiarrhythmics? In consideration of ablation, if you have been reading on this BB for any time, I am the one who had a disasterous ablation result, sustaining a catheter induced mitral valve injury. However, the longer I participate in this site, the more wonderful success stories I read. We just had two this week. I think the doctors are more aware of this threat since what happened to me was well published in EP journals.
I feel much more positive about the possibility that ablation is the first line treatment for persistant PAF. I don't know that it treats chronic afib quite as successfully. I would defer to others opinions on that. I do believe that the endeavor needs to well planned, with a very experienced and successful EP. One needs to measure success by word of mouth, such as this forum, rather than trusting in stories from the doctors web sites, as I have found them to be misleading and possibly inaccurate. I would also rather rely on my own research, rather than being referred by any cardiologist.
Good luck, Wil, with your decision; and I know that you have come to the right place to find good advice and suggestions. You will find a wealth of knowledge and support on this board.

God Bless,
Pam

Wil,

I, too, find your story and scientific approach quite fascinating. I always enjoy reading your posts, and wish you would post more often.

I would like to pose a few questions. From your post, you have found tryamines (and MSG also high in tyramines) to be your culprit, because due to elimination, you have progressed to better health and noticed a remarkable reduction in ectopics. But the question is, why is someone sensitive to tyramine? There must be an underlying cause. What I have read and posted to you before, is higher levels of phenylalanine cause migraines, and to reduce this, one would take l-tryptophan. That still doesn't answer the question of why, however, and my book (THe Healing Nutrients Within) doesn't explain why, but I found the following info, that could be of interest to you, or at least stir you into another avenue of thinking.

From the book, "Laboratory Evaluations in Molecular Medicine" it states:

Intestinal bacteria that contain L-amino acid decarboxylase enzymes degrade tyrosine to tyramine. The tryamine is than deaminated and oxidized to p-hydroxyphenylacetate. High levels of this in urine are of bacterial origin, such as Giardiasis.

Elevated urinary phenylacetate comes from similar degradation reactions starting with phenylalanine. An increase in dietary protein leads to altered products of colonic metabolism.

The neurotoxicity of phenylacetate is probably due to very strong inhibition of synaptic choline acetyltransferase.

Read on:

ANIMAL MODEL
Symula et al. (1997) mapped hyperphenylalaninemia 2 (hph2), a recessive mutation in the mouse that causes deficient amino acid transport similar to Hartnup disease. The hph2 mouse locus was mapped in 3 separate crosses to identify candidate genes and a region of homology in the human genome where they proposed that the human disorder may map. The gene maps to mouse chromosome 7 close to a marker in the fibroblast growth factor-3 gene (164950) which in the human is located on 11q13. The mouse mutant was isolated after N-ethyl-N-nitrosourea (ENU) mutagenesis on the basis of delayed plasma clearance of an injected load of phenylalanine. Symula et al. (1997) found that animals homozygous for the mutation excrete elevated concentrations of many of the neutral amino acids in urine, while plasma concentrations of these amino acids are normal. In contrast, mutant homozygotes excrete normal levels of glucose and phosphorase. Symula et al. (1997) presented experiments indicating that the mouse disorder is a model for heart disease: the urine amino acid profiles were similar; in both species, there was a deficiency in brush-border amino acid transport; and both displayed a niacin-reversible syndrome influenced by diet and genetic background.
[www3.ncbi.nlm.nih.gov]

Hartnup disorder is an autosomal recessive impairment of neutral amino acid transport affecting the kidney tubules and small intestine. It is believed that the defect lies in a specific system responsible for neutral amino acid transport across the brush-border membrane of renal and intestinal epithelium. The exact defect has not yet been characterized. The characteristic diagnostic feature of Hartnup disorder is a dramatic neutral hyperaminoaciduria. Additionally, individuals excrete indolic compounds that originate from the bacterial degradation of unabsorbed tryptophan. The reduced intestinal absorption and increased renal loss of tryptophan lead to a reduced availability of tryptophan for niacin and nicotinamide nucleotide biosynthesis. As a consequence affected individuals frequently exhibit pellegra-like rashes.
Many other nitrogenous compounds are found in the intestine. Most are bacterial products of protein degradation. Some have powerful pharmacological (vasopressor) effects.
[web.indstate.edu]
(under digestive tract nitrogen)

So you could very well be low in tryptophan, not only because it takes 60mg of tryp. to produce 1mg of niacin, but because it's not being transported in the first place.

Richard

Will

Its wonderful to read more of your story. You certainly know how to listen to your body.

I understand from your post you are just over 8 months into your new dietry regime. When I started my dietry regime it was just over a year before I slipped back into sinus. This went hand in hand with me stopping my meds (which I wonder sometimes if they kept me in AF). I am a bit different from you in that sinus came first and my ectopics were last to go (I still get the odd few - but not a patch on the runs I used to experience. I find that grains and dairy are what make ectopics happen now. Like you I no longer get headaches....

You don't mention much in your meat sources of food. But as per Richards post above you will need them for the amino acids. I have a high protein intake but also a lot of veggie carbs.

I couldn't take Mg supplements as they induced AF and ectopics. But what I do do is take lots of high Mg food - pumpkin seeds are the best source I have come across - as well as almonds etc, they are wholly bioavailable and do not induce ectopics in me.

Maybe some of what I found worked for me is worth a try whilst you are waiting for CC to get back to you.

Best of luck

Fran

Wil,
Just wondering how you submitted your application. If you did this online the respond time is not good. I had my cardiologist call them directly, after a week, and I had an appointment within 2 months and a confirmation of the appointment immediately . I know this seems long, but when you are picking your EP personally, and choosing one of so high caliber, I believe it is well worth the wait, if you can actually wait.....

Best wishes!
Joe

begin soapbox mode:

The subtitle of this bulletin board should be, "correlation is not causation".

I made the specific changes listed above, which caused nearly everything else in my life to change, along with, of course, the continuing passage of time. I subsequently experienced a change in ectopic rate. That could have been purely accidental. I hope that it was not, and there are other bits of information that encourage me to believe that the ectopic rate change was related to the changes made (and all the other changes which resulted). But, it was a single experiment with a single data point. To try to isolate any part of what I did and credit it with the ectopic rate change is to ignore, "correlation is not causation".

For instance, the fact that the autonomic nervous system affects afib (correlation), should not be taken to mean that the ANS is implicated, in any way, in the condition of afib (causation).

end soapbox mode:

Pam: (1) stress test - no; (2) angina pain - never; (3) anti-arrhythmics - no; (4) awareness of afib - only the slightest sensation in the chest when not moving around; (5) most people in chronic afib probably got there via a long period of multiple forms of heart cell deterioration - mine appeared suddenly, therefore the chronic afib statistics for PVI may not apply to me.

Richard: You said, "[Wil has] found tyramines (and MSG...) to be [his] culprit". Not true. Correlation is not causation. There are certainly: some people who subscribe to that theory; some data which supports such a theory, said data playing a part in how I defined my experiment of one, and the results of my experiment support the theory. But, it is a long way from there to a conclusion.

Fran: (1) Actually I am 12 months into the experiment: 2 months of declining ectopics; 8 months of low ectopics; a cardioversion to see if I could get back into NSR before the 12 months period you experienced had elapsed; and two more months of low ectopics. I anticipate another 6 to 8 months before a PVI, during which time I hope to revert to NSR spontaneously (ala Fran). But the most recent cardioversion result dampened my hopes a little. (2) The protein forms I tolerate well without headache symptoms are eggs and butter, and some salmon. I haven't tried to do as much in this area as I should have and plan to correct that. You are perhaps lucky, because my impression is that the area you live in has a greater variety of available local (unprocessed) foods.

Joe: Thanks for the heads up on the system at CC. I will tickle them a little. I am not in a hurry for the PVI. I do expect that in 6 or 8 months I will either have spontaneously reverted to NSR or will have given up hope of ever doing so, and would therefore be ready to let the gleeful doctors have some fun with their knives, hammers, and pliers.

Wil,

Your "Correlation vs. Causation" reminded me of funny aside we were told to teach us about that concept in grad school statistic classes.

Here it is:

Fact: Every time Ice Cream Sales Go up, More People Die of Shark Attacks.

Fact: Every time Ice Cream Sales Go down, Less People Die of Shark Attacks.

Conclusion: The Sale of Ice Cream seems to dictate the amount of people being attached by sharks.

*Perhaps you heard of this.....

Answer, the UNKNOWN or HIDDEN 3rd Variable was not looked at or considered.... SUNSHINE and Heat.

The REAL Fact is that sales of Ice Cream go up in the summer when it's warmer. Because it's summer more people are swimming. Because their are more people swimming there is a higher probability of shark attack....

Thus showing that Correlation does not necessarily mean Causation.


Thanks for reminding all of us Wil!

Joe

Gosh, That double "SS" in my name makes a bad sounding surname. I'll have to double check my spelling before I post Next time! Sorry!

Joe

Wil,

I guess I was wrong in jumping to the conclusion that tyramine was the cause of your problem, however I must say that your migraines and tyramine are a good correlation and place to start. It also seems strange that you have correlated the consumption of proteins to headaches. It's as if there is the possibility that your problem could be phenylalanine and/or tyrosine. I find it strange however that you can eat eggs and some salmon with no problem. Have you ever wondered why that is, or figured that out? Could it be a higher content of the sulfur containing amino methionine, or the higher content of calcium, or fatty acids, by way of Omega 3s or lecithin that helps in some way? Common sense tells me it would be the latter. Are you able to eat legumes, nuts or english peas? I find your case very interesting. If you have any further insight about your past and any other symptons you have experienced, I would be very interested to hear about it. Thank you, Wil.

Richard

Richard: I only have the data from the allergic scratch test for guidance on what foods cause my migraines. I find that generally those foods that I reacted to in the skin test are also foods that seem to predictably cause migraines, and the larger the serving the more intense the migraine.

In my case the migraine occurs about 24 hours after ingesting the food and lasts for about 20 additional hours. But, the timing isn't precise and the intensity of the migraine symptoms can range from mental lethargy to serious pain. That makes it difficult to determine precisely what caused a migraine.

One obvious puzzle is beef. I didn't react to beef on the skin test. But, beef seems to consistently cause migraine. Another puzzle is Salmon, which I also didn't react to on the skin test. One shipment of salmon from vitalchoice caused no migraine, even with very large servings. The second shipment caused a migraine with each serving, even when I reduced the size of the servings. As usual, there are too many unknowns and too little data.

I reacted to peas, some legumes, etc. on the skin test, and have mostly excluded nuts during the experiment because I was unable to determine what might have been done to them.

Wil,

If you don't mind me asking, could you tell me what foods you had the severest reactions to? I did a blood allergy test two different times, and found reactions to red snapper on one, but not the other, pistachios, sole (the highest reaction), and clams. I had a slight reaction to milk, yogurt, oysters, alfalfa, olives, zucchini, almonds, corn and corn gluten, lentils, oats, rice, rye, sesame, and chocolate. I was tested for beef and salmon, as well, but showed no reactions.

It would be interesting to compare, and see if there were any commonalities. I had severe migraines for quite some time, and was plagued with headaches prior to getting migraines. I lived on aspirin for my head and Tums for my indigestion. I quit having headaches once I started taking beta blockers for my arrhythmia, but have since discontinued (May 03) . Betas block adrenalin, and Phe. is the precursor to adrenalin (epinephrine). Maybe your pathway to noradrenaline (norepinephrine) is disrupted, as was mine, leaving more adrenalin in the system. Noradrenalin requires s-adenosyl-methione as a precursor. There was a study done on, I believe, salmon that showed when they were exposed to mercury, that the mercury attached to cysteine (breakdown product of methionine) to form methylmercurycysteine, which then, when ingested by humans, would carry out of their system, therefore preventing toxicity. But what if the salmon didn't have any cysteine or methionine left, for utilization in humans, due to their own deficit. Maybe the salmon you ate, that caused no problems, still had methionine and/or cysteine still in its system.

Just thinking out loud. Thank you for responding.

Richard