Lone Atrial Fibrillation: Towards a Cure


Nutritional Treatment for Atrial Fibrillation (Revised July 4, 2001)   2000 by Victor Thuronyi 

This short article talks about nutrition as a possible treatment for atrial fibrillation. It is not "new" 
information, but confirms what can be found in books about nutritional therapy. Nevertheless, it 
seems important to document such cases, since the mainstream medical profession seems not 
yet to have caught on to the importance of nutrition in treating this condition, perhaps because of 
the absence of clinical trials (see below for a suggestion). An important caveat: Nothing in this 
article should be considered as offering medical advice. I have no medical training; therefore 
please do not act on anything written here without consulting your physician.   In addition, what is 
stated here may be more relevant to so-called "lone" AF, and particularly vagally mediated AF, as 
opposed to AF that is related to underlying heart disease or other factors.

I first came down with Atrial Fibrillation (AF) at the end of December 1999. For several months 
thereafter I  had frequent and lengthy AF episodes (about 2 per week, lasting usually around 8 
hours and up to 39 hours). Fortunately my primary care physician was knowledgeable about 
effects of nutritional deficiencies and ordered a test for intracellular minerals. When the results 
came back they were remarkable: very low levels of magnesium and potassium and very high 
levels of mercury. Even before the test I started taking magnesium supplements, but when the 
results came back these were increased and I also started on a regime to detoxify the mercury. 
This consisted of alphalipoic acid (3 capsules of 6o mg. daily), Vitamin C (3 grams daily, in 3 or 
more divided doses), and spirulina. I was also taking multivitamins, fish oil, mineral supplements 
(multiminerals, including magnesium, calcium, potassium and others), and coenzyme Q10. When 
I took another blood test 2-1/2 months later, the magnesium level had gone up only slightly, but 
the mercury had been cut in half. Apparently if the body has very low levels of magnesium it is 
difficult to build it up with oral supplements alone; therefore, in mid-May 2000 I started on a 
course of magnesium through an IV (once a week, four times). The nutritionist managing the IV 
therapy suggested that I take for mercury detoxification for a one-month period floressence tea 
(2-4 ounces daily) and, separately, a fistful of cilantro blended up with water a few times a week (I 
found that adding a dash of lemon juice to this made it more drinkable). I don't whether these 
worked, but drinking a cilantro and lemon juice cocktail can hardly do one any harm. Meantime I 
was also pursuing more "traditional" cardiological approaches. I had a stress test done which, as 
had the echocardiograms which I got when I was first hospitalized, showed nothing significantly 
wrong with my heart from a structural point of view. On March 20, I checked into the hospital as 
an outpatient when I went into one of my AF episodes to test my reaction to Flecainide. I was 
given a high dose -- 300 mg. -- and no adverse effects (e.g. no lengthening of the QT interval) 
were noted. I converted to NSR (normal sinus rhythm) in a half hour with this dosage. 
Subsequently I used a dose of 200 mg. flecainide to convert when I had an episode; most of the 
time it worked within a few. In late April I got fed up with having all these episodes and started 
taking a flecainide pill nearly every evening (I figured I needed it only in the evening since all my 
AF episodes were in the evening or at night). This greatly reduced the frequency and length of 
episodes. I only had four in May, all under 8 hours, whereas I had had 7 episodes in February 
and March and 6 in April. My last magnesium IV was June 14, 2000. I stopped taking flecainide at 
that point.  I had no further episodes for nearly 8 months, and during this period took no medicine, 
but did keep up with supplements.

In February of this year I again had a few episodes, but not as frequently as the previous year 
(only 7 between February and the end of June).  I had been slacking off on the supplements, and 
so I started on them again at full strength.  I also went in for several more IVs of magnesium.  A 
blood test revealed that my mercury level was up somewhat.  I decided to have all the amalgams 
removed from my teeth: the resulting dental work has not been simple, but it will result in better 
oral health and will reduce my overall exposure to mercury, which over the long run can cause 
even more serious problems than AF.  I have invariably taken flecainide to help convert quickly to 
NSR.  My episodes have averaged only a little over 2 hours with this regime  much shorter than 
last year.  This may also have contributed to having fewer episodes, by preventing "remodeling" 
from taking place.  I also presume that stroke risk is minimised by keeping the episodes short.

I have also found it helpful in the past few months to take some homeopathic remedies, Cactus 
Grandiflorus extract (manufactured by Herb Pharm) and Cytisus Scop. (manufactured by Boiron).  
I take about 5-6 drops of the former and 2 drops of the latter sublingually before bed (and 
sometimes also in the afternoon).  These remedies have stopped ectopic beats, and therefore 
seem to have prevented  episodes that otherwise would have occurred.  I would strongly caution 
anyone not to try this on their own without consulting a doctor, particularly if they are taking any 
other medicines.  The fact that these are over-the-counter remedies does not mean that they 
cannot interact with prescription drugs, potentially quite dangerously.

Because I have been taking so many supplements (magnesium, other minerals, CoQ10, L-
carnitine, taurine, fish oil, multivitamin) plus other measures identified above, it is impossible to 
determine which of these has been beneficial and which might be superfluous.  (The supplements 
seem important, even over the short term: my most recent episode seems to have resulted from 
skipping my supplements for about 3 days.)  Overall,  it seems that my strategy is working.  Thus, 
I had 35 episodes in the first 6 months, went 8 months without any episodes and any medicine, 
and have had only 7 short episodes in the past 5 months.  It may, however, be another 6 months 
or a year before I will be able to report more definitively, including on the effects of removing my 
amalgams.  In the meantime this may be considered a progress report.

I believe that my experience demonstrates not only the benefits of supplementation but the need 
to have tests done and to do the supplementation under medical supervision. The fact that I had 
high levels of mercury, for example, probably meant that I would not have benefited from taking 
magnesium supplements alone, since the mercury apparently interferes with the magnesium. 
Moreover, given the important effects for the body that all these minerals have (beyond their 
effect on the AF alone), I feel better knowing what my levels are rather than just guessing. 
Obviously, because these tests involve an expense it is not something to be done too often. 

The need for clinical trials 

The apparent success of nutritional therapy in my case and the reports of success by others 
suggests that this is a fruitful area for clinical trials. Moreover, it would be simple and inexpensive 
to conduct such trials. As far as I am aware, some clinical trials have been done for the use of 
magnesium for acute treatment of recent onset AF. What should be confirmed is the benefits of 
this therapy for chronic conditions. I am not sure what the population should be. It might make 
sense to restrict it to those with idiopathic paroxysmal AF, but there would also be an argument 
for extending the test population so as to be able to ascertain the group of patients for which 
nutritional therapy might be beneficial. The first step would be take a blood sample from the 
patients and analyze it for intracellular minerals, noting which patients have high levels of mercury 
and/or low levels of magnesium. It would be interesting in and of itself to see what proportion of 
the patient population has abnormal levels of one or both. The hypothesis would be that, at least 
for the idiopathic group one would see a substantial difference from the average population. (It is 
striking how many long distance runners seem to have AF. These are persons who lose large 
amounts of magnesium and potassium by sweating and therefore may well suffer from 
deficiencies unless they have been taking supplements.) Those patients with abnormal levels 
would then undergo nutritional therapy to correct the levels (for best results, those with low levels 
of magnesium could be administered magnesium intravenously once a week for 4 weeks). After a 
suitable interval, the intracellular blood test should be repeated to verify that the magnesium 
levels had been corrected. Then the results in terms of decrease in episodes would be compared 
to the control group. Because AF is not a life-threatening condition, there would be little risk in 
such a trial, which to exclude other factors probably should be done keeping patients off 
antiarrythmic drugs. (As considered appropriate, patients could as a precautionary matter be 
anticoagulated with warfarin for the duration of the trial). 
While it seems likely that magnesium is a key factor, other supplements could also be evaluated 
in other trials.

The bottom line

I feel that in many cases AF is a symptom of some other problem, in many cases a nutritional 
deficiency or a poisoning (mercury).  It seems plain to me that every effort should be made to 
ascertain whether there is an underlying problem and to deal with that directly, rather than just 
dealing with the symptom.  Otherwise, the underlying nutritional problem can lead to even more 
serious conditions.   


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ISSN 1203-1933.....Copyright © 2001 by Hans R. Larsen

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