Summary as at September 2018:
The following are the measures taken to eliminate my atrial fibrillation and all ectopic beats:
Maintain serum vitamin D at approximately 160 nmol/L (approx 65 ng/mL). This is a level which is absolutely normal for anyone who experiences extensive sun exposure, such as outdoor workers, and is a level which was therefore normal for the vast majority of people throughout history until very recent times. It is achieved in my case by taking five 5000iu capsules of vitamin D3 per week, but see details on this site.
Maintain calcium consumption just below 500 mg/day. Some familiarity with the calcium contents of various foods is required to achieve this, but that information is easily obtained from sources like the USDA “Food Composition Database”.
Maintain total serum cholesterol around 5.2 mmol/L or 200mg/dL (in other words: around the top of the recommended range rather than simply as low as possible) and maximise the HDL component. To achieve this, I maintain high fitness and consume several eggs per day.
Increased protein intake, increased magnesium intake, and consumption of certain fruits, are also beneficial as detailed below.
The focus of this site is the treatment of Lone Atrial Fibrillation (“LAF”) by means other than medication or surgery. It has arisen because of my own success in totally eliminating a full-blown and completely typical case of this arrhythmia, without medication or surgery. A senior medical practitioner, extremely surprised by this, then urged me to put the information online, strongly backed by my three children who are also medical doctors (or about to qualify). While the focus is on LAF, it is not excluded that my dietary approach may be of benefit in some cases of Atrial Fibrillation (“afib” or “AF”) of types other than LAF, but this site is not suggesting that to be the case. If other LAF sufferers experience and report relief through the approach described here, it should be feasible to stimulate formal medical research into the underlying mechanisms, and to produce improvements in effectiveness and convenience of treatment.
If you have found your way to this site, I will assume you are a sufferer of LAF, or are someone very familiar with it, and not waste your time with definitions or descriptions of the condition. That is all well covered in many places on the internet. (However, for any other visitors, a brief outline is here). I will just note the following four things which are frequently not well emphasised elsewhere, and then push on to the details of my own case and my successful elimination method.
1) By definition, in having diagnosed LAF, a cardiologist can find no cause for the sufferer’s atrial fibrillation. There are many millions with the diagnosis, which strongly suggests that there is at least one unknown but relatively common cause of the condition which is yet to be discovered or recognised by science. UpToDate.com, the medical profession’s leading “bible” for overall summary of absolutely current medical knowledge, acknowledges this real possibility by politely summarising, with understatement: “The factors that precipitate paroxysmal atrial fibrillation (PAF), particularly in patients without apparent structural heart disease, are incompletely understood”. So it is not the least bit implausible that this cause, or these causes, may be found amongst dietary or lifestyle inadequacies which have simply not yet been recognised to be contributing factors.
2) For reasons well documented, available medical and surgical treatments are far from ideal, and this is recognised and lamented by most medical experts in the field.
3) In addition to the long-term dangers, sufferers often find the episodes extremely unpleasant, despite the relative lack of external symptoms. Certainly, many victims seem to think that their condition is not fully able to be “empathised” by others.
4) The graph below highlights the typical course of Paroxysmal (ie: intermittent, or episodic) AF as the episodes relentlessly become longer and more frequent after the initial diagnosis. For 171 patients initially suffering from Paroxysmal AF, it shows the progressive decline in the fraction of patients who remain Paroxysmal after several years, ie the fraction who have not transitioned to Permanent (Chronic) AF. Of these 171 subjects, 88 were Paroxysmal Lone AF (“PLAF”) sufferers and 83 had structural heart disease (ie, were initially Paroxysmal but not “Lone” AF sufferers). After 10 years, 43% had not yet reached Permanent AF; after 20 years only 10.6% were free of it, and the difference between the LAF group and the “structural heart disease” (non-Lone) group was very small. It should be noted that all patients were treated with optimum antiarrhythmic drugs as determined by the treating physicians and as varied whenever necessary according to their judgement  (all published scientific references are numbered in square brackets and listed in full at the end). Clearly, the conventional outlook for paroxysmal afib sufferers is certainly not a good one.
Figure 1. Evolution over time of the proportion of patients remaining substantially in normal sinus rhythm, ie without developing permanent atrial fibrillation, over the follow-up periods indicated. The year zero represents the initial diagnosis, and therefore the presumed onset of paroxysmal AF, in all patients studied. Adapted from reference 1: Kato, T., Yamashita, T., Sagara, K., Iinuma, H., & Fu, L. T. (2004). Progressive nature of paroxysmal atrial fibrillation. Circulation journal: official journal of the Japanese Circulation Society,68(6), 568-572.
My history; treatment approach; and the rationale behind it
I was a classic Paroxysmal or Intermittent LAF sufferer. Here are the details:
- First attack: May 2004, aged 50.
- Maximum length of individual attack: 13 hours.
- Typical length of individual attacks: several hours.
- Direction of the change in intervals between attacks (when untreated): ever-decreasing, ie increasing in frequency.
- Maximum frequency of attacks: every eight days.
In addition, ectopic beats, sensed as “missed” or “crowded” beats, could frequently be detected between the actual atrial fibrillation attacks, and these showed an ever-increasing prevalence overall, reaching a maximum of over 1,000 per day. Possibly due to a slim build, all ectopic beats and all AF attacks were always highly symptomatic to me. That is, they were very noticeably apparent. Twentyfour-hour Holter monitoring verified this fact -- the cardiologist noted that his request for me to manually diarise all irregularities which I detected, had confirmed my recognition of all ectopic beats during waking hours (it was a period of much lower abundance than the maximum referred to above). Although unpleasant, being highly-symptomatic was probably a great assistance in eventually being able to clearly determine which factors opposed or promoted the irregularities!
There were also several features which defined me as a classic “vagal” afibber:
- Time of occurrence of attacks: frequently in the early hours of the morning, or, to some extent, whenever my heart rate and/or blood pressure dropped to a minimum.
- Postural position during occurrences: by far most often while lying on my left-hand side. Frequently, in the initial years, an emerging attack could be “aborted” by quickly flipping to my right side.
- Vagal “triggers”: cooling down after strenuous exercise was always a risk time, especially the consumption of chilled liquids or subjection to air-conditioning at such times.
- Increased aerobic fitness only worsened the frequency of attacks.
What was attempted to deal with the problem?
As ectopic beats became more frequent, I began to seek any and every dietary and lifestyle change which could conceivably have a bearing on the problem. This hunt began after just my second atrial fibrillation attack.
Over almost nine years, there were 96 individual factors which I systematically varied. Many of these were varied in both a positive (increased) and, separately, a negative (decreased) manner. Operating from a home environment, and having a light workload, I was free to approach the variation of dietary and other factors in an extremely rigorous and consistent manner. In addition, my science qualifications and generally scientific inclination ("About the author") made it very clear to me what had to be done and how to go about it.
My approach was to vary only one factor at a time, and to allow that variation typically two weeks to see if any reduction (or increase) of ectopic beats occurred. I had noticed early on that this time period was adequate to identify changes in the frequency of ectopics which resulted from the first two effective factors that I identified, which are described below, and I considered that the long-term time constraints involved in sequentially testing many factors therefore made this a suitable duration over which to run each individual test. I typically adhered to an absolutely fixed diet and daily regime, in relation to all other factors, while the one “target” factor was under variation. Of course, due to the potentially huge number of interactions between factors, a considerable amount of “backtracking” occurred, where I would retest some factor, let us call it “X”, but, on the second occasion, specifically in conjunction with factor “Y” which had not previously been employed when “X” was first tested.
It is worth repeating that my adherence to the numerous regimes was extremely rigorous and consistent: I was absolutely determined to find a solution and to avoid at all costs the often undesirable and frequently inadequate outcomes of either an ablation operation or currently existing medications (more here). As a result, I have not had any surgical intervention or taken arrhythmia-related medications.
A couple of underlying aspects were usually in my mind:
1) The relatively “cyclical” nature of the condition, in which an AF attack would lead to an apparent period of “immunity”, followed by a re-emergence of and then gradual increase in frequency of the ectopic beats, until another AF attack became imminent.
2) The overall, apparently relentless, march of the problem towards increasing frequency with increasing age: amply borne out by population statistics for the prevalence and incidence of AF (more here); by the condition’s typical age-progressive course outlined in the graph and point (4) above; and by my own pattern.
Both these aspects suggested that, at least to some extent, there may be an underlying, age-progressive “metabolic” or “biochemical” problem or imbalance as yet unrecognised by medical science -- something which the body was constantly striving to rectify, but with decreasing efficiency at older ages. Whenever the hypothesised imbalance could not be adequately brought back into line, and it therefore reached a critical threshold, some sort of “safety valve” seemed to be released via an atrial fibrillation attack, and the cycle would then begin again. Permanent AF would then represent the state where the body's "rectifying" procedures could no longer achieve even temporary correction of the imbalance.
Explanations which were more-or-less purely anatomical in nature, such as those related to essentially anatomical electrical abnormalities of the myocardial substrate, seemed to be unsatisfying in regard to the cyclicity, and possibly to the relentless age progression.
In addition, it seemed to me that if any modifiable dietary or lifestyle factor existed which was giving rise to an underlying “metabolic” or “biochemical” imperfection or misalignment (in so many million people), it was by far most likely to be found in some previously unrecognised deviation of modern diets or lifestyles from those to which humans had evolved ideal genetic adaptations over several million years. This idea, that what we do now may not be what we have ideally evolved for, over the vast majority of the 6 million years since we diverged from chimpanzees, may loosely be described as a “Palaeo” or “Paleo” approach to diet and lifestyle adjustments, but there are many ideas upon exactly what constituted our Palaeo diet and/or lifestyle, and the devil is certainly in the detail.
Nevertheless, it always seemed doubly encouraging if my experiments showed that something which appeared to be beneficial also made good sense from a “Palaeo” perspective, and I frequently looked for ways to pursue this angle.
My successful method
Within months of the first attack, when I took a small dose of a calcium-based antacid for indigestion, I noticed that although the calcium diminished ectopic beats in the short term (the period from 40 minutes to a couple of hours), any sustained increase in daily calcium intake worsened ectopic frequency overall (and atrial fibrillation attacks). With further experimentation, it was relatively easy to isolate the effect to the calcium component and not the other components of an antacid (or of any other calcium source) by varying the antacid employed and by trying various calcium and other supplements -- thereby varying both the cation (eg calcium, magnesium, aluminium, potassium, sodium, iron, zinc) and the anion (carbonate, bicarbonate, hydroxyapatite, lactate, orotate, citrate, etc). The effect was clearly and strongly due to the calcium alone.
After considering what could possibly be disturbing the body's calcium homeostasis in such a way that acute calcium ingestion acutely reduced ectopic beats, but that any sustained increase in calcium ingestion worsened ectopic beats overall, and suspecting something which could have a “Palaeo” type of explanation, vitamin D status seemed a likely candidate.
After all, humans did not ingest modern-day “Western” quantities of calcium prior to approximately 5,000 years ago, when dairying began (and mostly much more recently than that). In contrast, for several million years, right up until the Industrial Revolution, all humans were consistently exposed to extensive solar radiation and must have been “saturated” with vitamin D by modern standards (more info on this aspect here). Even in the last few decades, solar exposure has fallen further. Vitamin D has very powerful effects on calcium metabolism at every level, from absorption via the gut to final excretion from the kidneys, and multiple stages in between. Vitamin D also interacts powerfully with other powerful calcium-stabilising hormones manufactured within the body, such as parathyroid hormone.
A little research indicated that while the US threshold for serum (blood) vitamin D deficiency is now 12 ng/mL (30 nmol/L), true sufficiency is variously suggested to range from 20 ng/mL (50 nmol/L) to 100 ng/mL (250 nmol/L). In addition, any individual who is heavily exposed to the sun, such as surfers or outdoor labourers in sunny climates, etc, will have a serum vitamin D of around 160 to 170 nmol/L (~65ng/mL). Levels naturally plateau around this mark regardless of further solar exposure. In earlier times, the vast majority of all humans would have exhibited such levels, existing, as they did for millions of years, as hunter-gatherers, and then later almost entirely as agricultural workers. There is a large, thoroughly reputable, school of thought that optimum vitamin D levels should be around this mark . It is then often thought that calcium intakes do not need to be so high at these vitamin D levels (since vitamin D increases calcium absorption and decreases calcium excretion, among many other effects) and that too much calcium may then be deleterious.
So I rapidly increased my serum vitamin D levels to the 160 to 170 nmol/L (~65ng/mL) range by use of supplements (I found that 5 doses of 5,000 IU of vitamin D3 per week was the required maintenance amount in my case).
Quite rapidly, ectopic beats were much reduced and afib attacks seemed eliminated, but only if calcium intake was also maintained at a reduced level. More calcium meant more ectopics and the return of atrial fibrillation. To be certain about this, before finalising the desirable daily calcium and vitamin D intakes, I increased calcium and/or reduced vitamin D over several experimental periods, but each time ectopics increased and afib returned.
Once I stabilised serum vitamin D around the 160 nmol/L level (~65 ng/mL), and reduced calcium intake, atrial fibrillation attacks ceased. But not all ectopic beats did, and when I increased my fitness levels, by transitioning from regular walking to jogging, the ectopics increased and atrial fibrillation returned after a six month absence.
A frustrating period of seven years then ensued, during which I methodically, but seemingly endlessly, tested many further potential factors consecutively. Throughout this period, any significant reduction in vitamin D levels or sustained increase of calcium intake resulted in increased ectopics and afib, but holding serum vitamin D at ~165 nmol/L (~65 ng/mL) and calcium intake not far below 500 mg/day did not successfully eliminate ectopics or atrial fibrillation. I did not experiment with holding vitamin D at higher levels, or calcium intake at lower levels, so cannot comment on the obvious possibility that those steps alone or in combination would have been completely successful.
Continual experimentation, however, eventually revealed that increased animal protein consumption caused a reduction in ectopic beats, but still did not entirely eliminate them or the afib, even at very high intakes. In any event, extreme protein intake seemed somewhat artificial and not in accord with typical hunter-gatherer diets, which I had good familiarity with, and seemed to almost certainly risk adverse long-term health outcomes other than atrial fibrillation.
What else could be missing? What other deviations from a “Palaeo” type situation could be operating, particularly ones which might influence calcium metabolism or calcium homeostasis? It seemed that one should be able to, indeed obviously needed to, consume a significant proportion of fruit and vegetables in a healthy diet, yet what was it that seemed to be deleterious about fruit and vegetables compared to a diet containing large amounts of animal protein?
There is an enormous amount of “pop health” material on the web about the supposed health benefits of an overall “alkaline” metabolism derived from an “alkalising” diet. This mainly means eating lots of fruit and vegetables. I had always consumed large amounts of both, yet I had afib. (It is important to note that the alkalising effect of fruits and vegetables in a metabolic sense has little to do directly with the "high school chemistry" meanings of "acid" and "alkali" -- for example acidic lemon juice is alkalising in its metabolic effect). I looked at numerous blood test results I had (all of which were always within the normal reference ranges). I noted that my serum bicarbonate was always near the top of the normal range. Elevated serum bicarbonate, even beyond the normal range, is not an absolutely conclusive test for alkalosis or alkalemia (roughly, “being too alkaline”) -- that would require drawing arterial blood gases, which was not appealing and would have been difficult to persuade my doctor to order. But, all things being equal, the serum bicarbonate did seem to suggest an existing tendency toward alkalosis/alkalemia rather than to the opposite. Eating lots of animal protein (which I had noted to reduce ectopics) is certainly something which would push the body’s metabolism away from alkalosis/alkalemia, ie in an “acidic” direction . Alkalosis/alkalemia can certainly disturb calcium metabolism and homeostasis, and can also directly disturb cardiac myofilaments’ responsiveness to calcium . Was this a factor which could be at work despite no obvious, full-blown (“clinical”) alkalosis/alkalemia technically being apparent?
Further research also revealed that alkalemia (there are two kinds) is the most common acid-base disorder in hospitals, being present in 80% of patients who have an abnormal acid-base status , and that alkalosis and alkalemia become ever more common with increasing age. Could an increasing tendency to alkalosis/alkalemia with age, perhaps even merely at a subclinical level, be one factor related to the increased prevalence of AF with age? Perhaps the tidal wave of “alkalising” propaganda on the web was misguided or excessive and this was not necessarily, or even probably, a wise course as one aged?
Nevertheless, apart from a massive meat intake, what could one practically, and hopefully healthily, do to pursue this line of reasoning? Were there any fruits and/or vegetables (with all their other beneficial effects) that were not alkalising, even perhaps acidifying?
In short, the answer is: "Yes, but not many". The explanation is given here. In summary, the fruits which have been documented to have the strongest “acidifying” metabolic effect are cranberries [6,7].
Experimenting with an intake of 500 grams of cranberries per day, blended into a smoothie with other foods, the effect was rapid. Within a week, all trace of ectopic beats was gone! (This was a perfectly typical consumption of fruits like cranberries throughout the millions of years of mankind's Palaeo existence.)
I am not necessarily claiming that the mechanism of action of the cranberries is as intimated above, merely indicating the reasoning which led to my testing them, and that it is one possible mechanism. Cranberries have been associated with a range of other beneficial health effects (discussed here), and there are good reasons why this would be so, linked to the fact that they contain a wide variety of known active components in much larger amounts than modern table fruits (explained here), so there are other possible explanations for an effect on atrial fibrillation, some of which are discussed here. From the perspective of most sufferers, the exact mechanism will be pretty unimportant: what will be important is whether it works!
There are obvious experiments which could be undertaken to narrow down the mechanism, some of which are discussed here; in some cases very simple dietary ones. But it could be argued that the hard part has been done and that it should be relatively straightforward to track down the active component of the cranberries, and from there perhaps the interacting mechanisms of the active ingredient and the calcium. One such known interaction is discussed in a link, below, regarding connections between atrial fibrillation and the epidemiology of other diseases. At the cellular level, a mechanism is already known for calcium-overload-induced ventricular arrhythmia [8,9]. After nearly nine years of strictly-regimented dietary experimentation, 11 years since the first episode, and being extremely happy with my current treatment method and all its health outcomes, further experiments are not my own priority, but reports by other sufferers of positive responses to the factors highlighted here would ensure that at some point professional researchers would take interest, with likely subsequent gains in medical treatment of LAF.
Two episodes of reduced cranberry intake caused ectopic beats to temporarily return, albeit that at 250 grams per day relatively few recurred (and see improved results in "Updates" below). Apart from that, and a short return of ectopics due to a temporary, hidden, but substantial calcium intake, which I describe in the section discussing details of my diet, I have been totally free of afib and ectopic beats for two years, while consuming nothing other than a very realistically Palaeo or hunter-gatherer balanced diet (with many other likely health benefits) and while increasing my fitness to three vigorous running sessions per week as a 61-year-old, with many further beneficial effects noted! The latter was something that was previously impossible in terms of atrial fibrillation risk! I have no other health problems on this treatment protocol, take zero medications, and all blood tests always register within normal ranges.
It is impossible to over-emphasise how dramatic the improvement has been. It is relevant to add that our three children, all of whom either are, or are about to qualify as, medical doctors, are amazed by the outcome they have witnessed first-hand at home, considering what they are taught in medical school about the inevitably one-way, irreversible path of lone atrial fibrillation.
Apart from my approach's apparent requirements to maintain vitamin D and cranberry intakes, and to keep calcium intake relatively low, complete flexibility in all other dietary components seems to be perfectly acceptable and to have no adverse atrial fibrillation effects. Complete elimination of a very well-advanced and absolutely archetypal case of lone atrial fibrillation has therefore been achieved on nothing more than a very well balanced diet! I have not been able to locate any similar reports anywhere. (However, some comparisons with other non-medical, non-surgical attempts to reduce AF are here.) Since the characteristics of the case were so absolutely typical for lone AF, and since the course of the condition was so well-advanced and the attacks and ectopic beats were so strongly developed, it seems very likely that the information will be of assistance to others. In addition, repeated testing of the sharply and decisively reversible dosage effects of all three of the protocol's specified factors (calcium, vitamin D and cranberries) has provided very strong indications of the underlying cause(s) of LAF, and considerable confidence that the fundamental, underlying mechanism(s), as yet undescribed in medicine, are being directly manipulated by this diet. The dominant connection to the underlying thread of calcium homeostasis is very clear.
Predisposing genetic variations are known to be involved in particular individuals’ susceptibility to LAF. Indeed, numerous candidate genes have already been identified . It seems likely to eventuate that these genetic variations cause some percentage of the population to be more sensitive to the factors raised on this site and thence to exhibit the typical age-progressive changes related to the condition.
UPDATE, AUGUST 2015
A few months ago, I reduced my total calcium intake to 300 mg/day and then commenced testing a reduced cranberry intake of one cup per day (100 grams). Over the following months I have continued to be completely free of afib and ectopic beats, again confirming the crucial role of calcium in the condition. As discussed elsewhere on this site, 300 mg/day of calcium is an intake associated with excellent bone health in much of the world's population. I continue with high protein and vitamin D intakes and with 100 gm/day of cranberries, which are absolutely minor and easy dietary adjustments to maintain long-term. I have now been completely free of atrial fibrillation and ectopic beats for two and a half years and have returned to fitness levels last seen in my 20's, by greatly increasing running pace.
UPDATE, DECEMBER 2016
I have now been free of afib for nearly four years and my overall approach remains very similar. However, about a year ago, I discovered a strand of previously published scientific research which appears to hint that atrial fibrillation may be less common (and without other adverse outcomes) in individuals who have higher levels of "good cholesterol", ie high density lipoprotein, "HDL". (That is my greatly abbreviated and simplified distillation from, for example, the following references): [11,12,13,14,15,16]
As mentioned elsewhere on this site, my total cholesterol levels have always been low (ie far within the recommended range). In addition, numerous studies show no overall increase in mortality with raised HDL levels, or from total cholesterol at the top of the medically recommended range, and probably the contrary -- ie reduced mortality compared to that at lower HDL levels. Therefore I decided to experiment with increasing my serum total cholesterol level. This was achieved by consuming several eggs per day as the main source of protein. Other animal protein is consumed intermittently. The remainder of my diet is very low fat and I maintain a lean physique. This approach, of high direct cholesterol consumption; low overall fat intake; and high physical fitness (also well documented to elevate HDL at the expense of LDL), maintains my total cholesterol around 5.2 mmol/L or 200 mg/dL (ie at the top of the recommended range) but with an HDL component of 2.2 mmol/L or 85 mg/dL and therefore a Total/HDL ratio ("Coronary Risk Ratio") of just 2.4 (and with very low triglycerides).
It appears likely that this maintenance of a higher HDL and total cholesterol (but the latter still within or at the top of the recommended range) is indeed beneficial to afib control, because eggs contain significant calcium and so my intake of the latter is now around 500 mg/day -- a level which previously, unless accompanied by 500 gms rather than 100 gms of cranberries per day, did not provide as good an afib outcome as 300 mg/day of calcium -- yet my elimination of afib, and of ectopic beats, remains at 100%.
So my overall regimen of high vitamin D, high HDL, high-ish protein, 100 gms of cranberries per day, and 500 mg of calcium per day is working superbly. I'm also very pleased by the fact that the diet and lifestyle closely reflect that which would have been experienced by our hunter-gatherer ancestors for tens of millennia, in a coastal, estuarine or riverine environment (now recognised to be the "preferred habitat" of most ancestral hunter-gatherer populations), providing great comfort that this is an approach which genuinely provides a "natural" correction to the problems underlying PLAF.
UPDATE, MARCH 2018
My freedom from afib and medications, and generally excellent health, continues, and my overall approach remains very similar. Further scientific research continues to emerge which suggests a protective anti-afib roll for optimum levels of cholesterol, particularly HDL -- most recently that published in February of this year. [17,18,19] So my high egg intake and other dietary aspects continue as above, along with high fitness from three multi-kilometre runs per week and two strength and sprinting sessions per week (increased fitness is well documented to increase the HDL/LDL ratio). It may also be worth noting that eggs are one of the most acidifying of all foods, and so a high egg intake has a similar effect to cranberries in that regard; but it is not my intention to elevate that connection above the apparent positive effect of adequate cholesterol which is increasingly now being documented (especially for HDL), eg in the scientific research references mentioned above and listed below.
UPDATE, SEPTEMBER 2018
I recently added to my regular diet a small amount (~30g/day) of soluble dietary fibre in the form of "inulin FOS" (inulin fructo-oligosaccharides) derived from chicory root. This form of root-vegetable soluble fibre was a significant part of our ancestral diets but is greatly reduced in modern table vegetables (and fresh chicory root is not available in my vicinity). It is increasingly being associated with health benefits, which are beyond the focus of this website, but a couple of weeks after beginning regular consumption occasional ectopic beats began to occur. Very significantly, a little research revealed that one of the well-documented effects of inulin is to increase the body's absorption of calcium from whatever food is ingested! So the recurrence of ectopic beats is far from a coincidence, and once again highlights the central role of calcium intake in PLAF.
So I reduced my total calcium intake from ~450mg/day to ~350mg/day, and the ectopics ended within three days. Retaining the inulin consumption, I then returned my calcium intake to ~450mg/day but also newly added 60mg of magnesium per day -- an amount which thereby reduced the previous overall Ca/Mg ratio of my diet. The ectopics have since remained completely absent. This is notable because, in all my earlier experimentation, added magnesium failed to previously deliver a beneficial effect, although others have reported such an effect. Magnesium is certainly intimately entwined in the metabolism and homeostasis of calcium, for example interacting directly itself with vitamin D and parathyroid hormone, so these are all closely related tools that are being employed, but space is limited to fully discuss here.
Possibly the newfound positive effect of the magnesium is being facilitated by the presence of the inulin. Alternatively, perhaps beneficial effects of magnesium can only occur when calcium intakes are below a certain threshold: that was something I did not trial in my earlier experiments. At any rate, the added magnesium is best supplied via small amounts of various foods which have high magnesium and low calcium contents. Since these are no-doubt a healthy addition, I have no incentive or desire to experiment further at this stage.
So, within a not very restrictive diet, there are now a number of different "levers" the manipulation of which could be trialled by anyone else seeking to eliminate their LAF. But, overall, the centrality of calcium metabolism is extremely clear (and the interrelated effects of vitamin D, parathyroid hormone, magnesium, acid/base effects, etc).
REFERENCES NUMBERED IN THE TEXT ABOVE
 Kato, T., Yamashita, T., Sagara, K., Iinuma, H., & Fu, L. T. (2004). Progressive nature of paroxysmal atrial fibrillation. Circulation journal: official journal of the Japanese Circulation Society,68(6), 568-572.
 Vieth, R. (2004). Why the optimal requirement for Vitamin D is probably much higher than what is officially recommended for adults. The Journal of steroid biochemistry and molecular biology, 89, 575-579.
 Remer, T., & Manz, F. (1995). Potential renal acid load of foods and its influence on urine pH. Journal of the American Dietetic Association, 95(7), 791-797.
 Morgan, J. P. (1991). Abnormal intracellular modulation of calcium as a major cause of cardiac contractile dysfunction. New England Journal of Medicine,325(9), 625-632.
 Hodgkin, J. E., Soeprono, F. F., & Chan, D. M. (1980). Incidence of metabolic alkalemia in hospitalized patients. Critical care medicine, 8(12), 725-728.
 Blatherwick, N. R., & Long, M. L. (1923). Studies of urinary acidity II. The increased acidity produced by eating prunes and cranberries. Journal of biological chemistry, 57(3), 815-818.
 Fellers, C. R., Redmon, B. C., & Parrott, E. M. (1933). Effect of cranberries on urinary acidity and blood alkali reserve. The Journal of Nutrition, 6(5), 455-463.
 Jiang, D., Xiao, B., Yang, D., Wang, R., Choi, P., Zhang, L., ... & Chen, S. W. (2004). RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR). Proceedings of the National Academy of Sciences of the United States of America, 101(35), 13062-13067.
 Chelu, M. G., & Wehrens, X. H. T. (2007). Sarcoplasmic reticulum calcium leak and cardiac arrhythmias. Biochemical Society Transactions, 35(5), 952-956.
 Tucker, N. R., & Ellinor, P. T. (2014). Emerging Directions in the Genetics of Atrial Fibrillation. Circulation research, 114(9), 1469-1482.
 Psaty, B. M., Manolio, T. A., Kuller, L. H., Kronmal, R. A., Cushman, M., Fried, L. P., ... & Rautaharju, P. M. (1997). Incidence of and risk factors for atrial fibrillation in older adults. Circulation, 96(7), 2455-2461.
 Annoura, M., Ogawa, M., Kumagai, K., Zhang, B., Saku, K., & Arakawa, K. (2000). Cholesterol paradox in patients with paroxysmal atrial fibrillation.Cardiology, 92(1), 21-27.
 Ohira, T., Shahar, E., Chambless, L. E., Rosamond, W. D., Mosley, T. H., & Folsom, A. R. (2006). Risk factors for ischemic stroke subtypes the atherosclerosis risk in communities study. Stroke, 37(10), 2493-2498.
 Imamura, T., Doi, Y., Arima, H., Yonemoto, K., Hata, J., Kubo, M., ... & Kiyohara, Y. (2009). LDL Cholesterol and the Development of Stroke Subtypes and Coronary Heart Disease in a General Japanese Population The Hisayama Study. Stroke, 40(2), 382-388.
 Iguchi, Y., Kimura, K., Shibazaki, K., Aoki, J., Kobayashi, K., Sakai, K., & Sakamoto, Y. (2010). Annual incidence of atrial fibrillation and related factors in adults. The American journal of cardiology, 106(8), 1129-1133.
 Manabe, Y., Morihara, R., Matsuzono, K., Nakano, Y., Takahashi, Y., Narai, H., ... & Abe, K. (2015). Estimation of the presence of small dense lipoprotein cholesterol in acute ischemic stroke. Neurology international, 7(1), 5973
 Watanabe, H., Tanabe, N., Yagihara, N., Watanabe, T., Aizawa, Y., Kodama, M. (2011). Association between lipid profile and risk of atrial fibrillation. Circulation Journal, 75(12), 2767–2774.
 Alonso, A., Yin, X., Roetker, N.S. (2014). Blood lipids and the incidence of atrial fibrillation: the Multi-Ethnic Study of Atherosclerosis and the Framingham Heart Study. Journal of the American Heart Association, 3(5):e001211.
 Boudi, F., Kalayeh, N., Movahed, M. (2018). High-Density Lipoprotein Cholesterol (HDL-C) Levels Independently Correlates With Cardiac Arrhythmias and Atrial Fibrillation. Journal of Intensive Care Medicine, Feb 8.
A dietary approach producing complete elimination of frequent, severe, Paroxysmal Lone Atrial Fibrillation without use of surgery or medication: strong indications of the unknown cause(s) of LAF
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