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

Steven Carr

 

 

Summary as at September 2020:

The following measures eliminated my atrial fibrillation (AF) and all ectopic beats, without surgery or medication:

Maintain serum vitamin D at approximately 160 nmol/L (approx 64 ng/mL). This is a level which is absolutely common amongst those who experience extensive sun exposure, such as outdoor workers or surfers, and is a level which therefore, for nearly everyone throughout the entire seven million years of human existence prior to the last two centuries or so, was a typical serum (blood) level of vitamin D for most of every year -- and is a much healthier level than the typical, current, low levels found throughout all modern societies. It is achieved in my case by taking one 5000iu capsule of vitamin D3 on five days per week. See details on this site.

Maintain calcium consumption at or below 400 mg/day. This is an intake also typical for all humans during the entire seven million years before dairying began, and still is for most of the world's population (who typically have lower rates of osteoporosis than Westerners). We also know with 100% certainty, from the prevalence of lactose-intolerance, that not everyone has genetically evolved to suit even minimal dairy intake (or therefore, with similar probability, unnaturally high calcium intakes) in the very short time since dairying began or the even shorter time since dairy foods became common. At the natural Vit D levels mentioned above (actually much more natural, as explained in detail on this site and elsewhere), less than 400mg/day of calcium provides me with absolutely mid-range blood calcium levels and absolutely normal calcium and bone metabolism tests of every type. See latest update, below, for this month's published scientific proof that such calcium and VitD levels are optimal for many.

Increased protein intake and consumption of certain fruits also appear to be beneficial in my case, as detailed below -- including in the mainly diet-related sequential updates of my latest status, at the bottom of this page.

Maintaining total serum cholesterol in the upper part of the recommended healthy range rather than simply as low as possible, and maximising the HDL component of cholesterol, may also be beneficial. But the two largest factors are definitely calcium and vitamin D (as also witnessed in my 88yo father's similar success against AF).

I cannot locate any other reports of complete elimination by natural methods. My three children, all of whom are medical doctors, strongly endorse this method's use by my father and me, having witnessed the wonderful results. (Repeated "Fasting Metabolic Bone Studies" and X-ray densitometry tests show zero adverse changes resulting from this combination of calcium-intake and serum vitamin D levels.)

[Note re the other pages reachable via the blue clickable links below: many have not been updated and thus may have slightly out of date bits. But this main page is fully up to date: it should be fully considered and understood, before clicking any links, as it contains all the most important information, with only subsidiary info in the links.]

Introduction

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. An internationally renowned medical practitioner, extremely surprised by this, then urged me to put the information online, strongly backed by my three children who are also all 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 necessarily 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 "Lone" AF, 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 probability by politely summarising, with typical 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 mystery 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 very 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 merely Paroxysmal after several years, ie the fraction who have not deteriorated to Permanent (Chronic) AF. Of these 171 subjects, 88 were Paroxysmal Lone AF (“PLAF”) sufferers, whereas 83 had structural heart disease (ie, were initially Paroxysmal but not “Lone” AF sufferers). After 10 years, 43% had not yet deteriorated to Permanent AF; after 20 years only 10.6% had still not deteriorated to Permanent AF, and the difference between the Lone (PLAF) 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 [1] (all published scientific references are numbered in blue 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 in normal sinus heart rhythm, ie the fraction of patients who did not deteriorate to permanent atrial fibrillation over the number of years shown. The year zero represents the initial diagnosis year, 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 well 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, immediately that I detected each of them, had verified my recognition of every one of the ectopic beats which the Holter monitor had shown to occur 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 dietary 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, during the two-week period in which the one “target” factor was being varied. 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 tested 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 notably “cyclical” nature of the condition, in which an AF attack would lead to an apparent period of complete “immunity” in which absolutely zero ectopic beats occurred, followed by a re-emergence of ectopic beats and then a gradual increase in their frequency of occurrence, 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 above and in 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.

 

In contrast, 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 very 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 the diets and lifestyles which we follow, now, may not be what humans have ideally evolved for over the vast majority of the 7 or so million years since we diverged from other species, 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 the frequency of atrial fibrillation attacks). With further experimentation, it was relatively easy to isolate the effect to the calcium component and not any 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 separately testing both the cations (eg calcium, magnesium, aluminium, potassium, sodium, iron, zinc) and the anions (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 (ie short-term) 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 first began (and, in almost all regions, 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 due to their ever-present outdoor activities and therefore had very high vitamin D levels by typical modern standards; indeed they were usually “saturated” with the natural maximum blood levels generated by sunlight (more info on this aspect here). Even in the last few decades, most people's solar exposure has fallen further. Vitamin D has very powerful effects on calcium metabolism at every level, from the latter's 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). Furthermore, 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). Serum levels naturally plateau around this mark regardless of further solar exposure, and I have carefully checked this outcome on myself by heavy sun exposure alone, ie without vitamin D supplements. (This level can, however, be exceeded by consuming excess supplement VitD). 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. So there is a large school of thought, thoroughly medically reputable, that optimum vitamin D levels should be around this mark of 160 nmol/L (~64ng/mL)[2]. It is then often thought that calcium intakes do not need to be anywhere near 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 intake 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. [But note that heavier dosing -- ie a "loading dose" -- is typically required if one wishes to increase serum VitD levels within days or weeks rather than months.]

 

Quite rapidly, ectopic beats were much reduced and afib attacks seemed eliminated, but only if calcium intake was then maintained at a significantly reduced level. More calcium intake caused 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 (64 ng/mL), and reduced my calcium intake, atrial fibrillation attacks ceased. But not all ectopic beats did, so I therefore continued to search for other factors by consecutively testing many possibilities. 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 ~160 nmol/L (64 ng/mL) and calcium intake not far below 500 mg/day did not successfully eliminate all ectopics, although doing so had hugely reduced them.

 

Continual experimentation, however, eventually revealed that increased animal protein consumption caused a reduction in ectopic beats. I also 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 [3]. Alkalosis/alkalemia can certainly disturb calcium metabolism and homeostasis, and can also directly disturb cardiac myofilaments’ responsiveness to calcium [4]. Was this a factor which could be at work despite no obvious (“clinical”) alkalosis/alkalemia technically being apparent?

 

But for the practical purpose of addressing the problem at hand, and to go beyond simply consuming massive amounts of animal protein, the question arises whether there are any fruits and/or vegetables (with all their other beneficial effects) that are not alkalising in a metabolic sense (as nearly all are), even perhaps are “acidifying” like high protein foods?

 

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 a large daily intake of cranberries, blended into a smoothie with other foods, the effect was rapid. Within a week, all remaining trace of ectopic beats was gone.

 

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, and obvious experiments which could be undertaken to track down the effect, some of which are discussed here.

 

Two later episodes of reduced cranberry intake caused ectopic beats to temporarily return. Apart from that, and a short return of ectopics due to a temporary, hidden, but substantial additional 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 already are, or are about to qualify as, medical doctors, are amazed by the outcome they have witnessed first-hand at home (and then later with my 88yo father, who was also an AF sufferer), considering what they are taught in medical school about the inevitably one-way, irreversibly downhill path of lone atrial fibrillation (as graphically highlighted in Fig 1, above!)

 

Apart from my approach's main requirements to maintain a steady vitamin D intake and thus serum levels near the natural sun-exposed level, and to keep calcium intake lower than most Westerners do (but not lower than most of the world's population), great 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 calcium and vitamin D 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. (And at the cellular level, mechanisms are already known for calcium-overload-induced ventricular arrhythmia [eg 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.

 

Predisposing genetic variations are known to be involved in particular individuals’ susceptibility to LAF. Indeed, numerous candidate genes have already been identified [10]. 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 more of the world's population (although most of those people also have high serum VitD levels like I now have, thanks to their heavy solar exposure) than are the higher daily calcium intakes in Western countries. 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 suggest that atrial fibrillation may be less common in individuals who have higher levels of "good cholesterol", ie high density lipoprotein ("HDL"), and that this is true without costs in terms of other adverse outcomes -- in fact quite the contrary! 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 "admirably" low (ie far within the recommended range). In addition, numerous studies show no overall increase in mortality rates with raised HDL levels, or from total cholesterol levels at the top of the medically recommended range, and in fact the contrary -- ie overall reduced mortality rates are shown (increased lifespans), compared to mortality rates at lower HDL levels. Therefore I decided to experiment with increasing my serum total cholesterol level. This was achieved by consuming eggs every day as one source of protein. Other animal protein is also consumed. 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 higher HDL and higher 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 back up 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/ectopics 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 hundreds of millennia, in a coastal, estuarine, or riverine environment (now recognised to be the "preferred habitat" of most ancestral hunter-gatherer populations), providing very 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, new, 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 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 metabolically acidifying of all foods, and so a high egg intake has an effect in the same direction as cranberries in that regard (and as protein); but it is not my intention to elevate that connection above the apparent positive effect of adequate cholesterol which is increasingly now being scientifically documented (especially for HDL), eg in the 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 reduced in modern table vegetables (and fresh chicory root is not available in my vicinity). It is said to be 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 other foods are 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 again ended by three days later.

I have since ceased the use of inulinFOS. But, overall, the centrality of calcium metabolism is again extremely clear (and the interrelated effects of vitamin D, parathyroid hormone, acid/base effects, etc).

                                     UPDATE, DECEMBER 2019

 

My generally excellent health and complete freedom from all afib, ectopics and medications continues, and my overall approach remains very similar. On the basis that my diet, because of its effectiveness, now seems to be well settled for the long haul, the following is a summary of the important details.

Total "routine" daily calcium intake is usually below 400mg. This has been calculated from the USDA FoodData Central website, based on my "routine" foods consumption. Minor increases above this level do not cause problems, but normally I avoid all high-calcium foods. This mostly means dairy foods, but there are other things I moderate intake of also. Eggs are my single largest routine source of calcium (see below). When I do have a high-calcium food, such as cream on a dessert for example, I sometimes reduce the other calcium-containing foods that day. I have deliberately adjusted my normal intakes of my "routine" foods to provide a total calcium content below 400mg/day (down from 500mg) precisely so that I have "leeway" for these digressions into higher-calcium "non-routine" foods, which now occur quite often. This is working very well.

I hold my blood serum vitamin D level around 160 nmol/L all year (~64 ng/mL) by supplementing with six 5,000iu capsules of D3 per week for much of the year and with five 5,000iu capsules per week in summer (because of the high solar exposure at latitude 32 degrees where I live). It is important not to significantly exceed the natural 160 nmol/L "solar saturation" plateau level (~64 ng/mL) because doing so further increases the proportion of calcium which is absorbed into the bloodstream (of whatever calcium amount one ingests in total), which negates one's attempted reduction in calcium intake and may cause the recurrence of ectopics (and thus risk AF)! The optimum serum VitD level really does seem to be near 160 nmol/L (~64 ng/mL) as long as calcium intake is sufficiently reduced, so occasional VitD blood tests are needed for a couple of years until one can personally determine what dose of VitD supplementation delivers that test level! Note that it would take a few months for most people to reach and then plateau at that blood serum level, even with a daily dose of 5000iu, so a larger daily dose (a "loading dose") is needed initially if it is desired to speedily reach that plateau.

I consume the following foods every day, but with additions of other foods for variety and when socialising. When I add these other foods (ie the latter, non-routine foods) I simply form a rough mental idea of their calcium content and adjust accordingly. Brief reasons for the routine foods are written below (but far from all of the non-afib-related reasons have been included -- ie the various lines of evidence for various healthy-aging benefits -- due to space limitations).

I eat eggs every day to maintain my total serum cholesterol around 5.2 mmol/L or 200 mg/dL (in other words: around the top of the recommended healthy range rather than simply as low as possible) and to maintain my HDL cholesterol around 2 mmol/L or 80 mg/dL (fitness assists to raise HDL also). Eggs also provide adequate iodine and other critical nutrients. They are my largest single routine calcium source, because I restrain intake of other calcium-rich foods (see below).

I consume approximately four hundred grams of lean meat or poultry every day. [Source of high grade (readily assimilated) protein, etc. I found that the equivalent amount of plant protein was not adequate with increasing age.]

Beyond the meat and eggs, most of my routine foods consist of unprocessed fruits and vegetables. These currently always include a variety of dark fruits, including cranberries and invariably blueberries, black plums, black grapes, tomato. [The general benefits of dark fruits are now well recognised, and I've also seen research indicating their specific merit if one is consuming significant quantities of eggs and meat. All very Palaeo of course.]

I consume (in the routine foods) little fat beyond that which is naturally in the eggs and meats specified above, but don't exclude any foods entirely.

I take no medications and no supplements beyond the vitamin D described above, other than a daily vitamin K1/K2.

Regarding omega-3 fats, which health-conscious people often go out of their way to consume, the following is worth noting: the optimum daily intake to minimise afib occurrence has been reported to be approximately 0.6 gms/day of long-chain omega-3 fats ("DHA+EPA", or "n-3 PUFA"), with greater occurrence of afib at both higher and lower daily intakes than this amount. [20, 21] Eggs and Australian range-fed meat contain some omega-3 fats, so 40gms of cooked mussel meat is enough to top up to around 0.6 gms/day (no great surprise really, since consuming such amounts of these foods should closely imitate a diet likely to be the most "universal" type of ancestral, "Palaeo" diet that most of us are genetically adapted to), so I take no omega-3 supplements and aim to average the sort of seafood consumption just indicated. The omega-3 contents of eggs and meats will differ in other countries with different animal feeding practices, such as the USA, so there is a need to review one's own total omega-3 intake accordingly. Despite experimenting with omega-3 supplements and their withdrawal, I have no personal evidence that they affect afib or ectopic frequency, but choose caution as outlined.

Avoiding excess calcium consumption requires some knowledge of foods with significant calcium content, beyond dairy foods alone. Unfortunately, many processed foods are now deliberately calcium-enriched, so that is a particular problem. As an example, this particular difficulty extends even as far as the fact that many standard packaged flours are now calcium enriched! In Australia, only the cheapest, "Store Brand" varieties are not! In fact, I would go so far as to say that it would be virtually impossible to restrain one's calcium consumption if one ate much processed food, no matter how much one studied the labels! Even amongst fruit and vegetables there are traps for the unaware. Following are some brief examples of some higher-calcium-content fruits and vegetables. These are not so high in calcium that they cause the difficulties of dairy foods or of several varieties of nuts (or of many processed foods, as mentioned), but this sort of knowledge is useful information because when I eat a definitely high-calcium food (containing cheese, cream or yoghurt etc) I can ensure that I restrain foods like the following that day: all dried fruits; citrus fruits; blackcurrants; most legumes; all brassica vegetable varieties; carrots; sweet potato; and several others. But many, many fruits and veggies have Ca contents around the 10mg/100g level, so even a kilo of these will deliver 100mg of Ca, allowing "room" for a high-Ca food.

So a brief summary of my position is that I eat a cross section of foods which all our ancestors ate for hundreds of thousands of years to millions of years, and which we are therefore fully genetically adapted to. I minimise consumption of foods which have only been available to us for a few thousand years, and which we are therefore not fully genetically adapted to -- as unequivocally proven by such conditions as lactose intolerance, gluten intolerance and, I now believe, lone atrial fibrillation! In the process, I consume the sort of total calcium intake, and all other nutrient intakes, that would have been typical of the great majority of humans throughout human history (indeed, before dairying or supplements, it would have been impossible to much exceed my current calcium intake without deliberately eating limestone, shells or bone), and at the sort of vitamin D levels that were virtually universal until a couple of hundred years ago. I am enjoying enormous health benefits from this, and I have a hopeful attitude about it particularly since so many of the Western diseases of aging also have as a major contributing factor some calcification of the vasculature, which it is hard to believe has any cause other than a calcium-related aspect of diet and/or lifestyle such as the one highlighted here.

                                                UPDATE, SEPTEMBER 2020

 

I will add some further minor update material shortly, but one important thing to provide is the result of the very latest genetic and archaeological research, published this month, which has now proven unequivocally that milk consumption was not common in Europe even 3,000 years ago and was not widespread in Europe until just 1,000 years ago. [22] This is nowhere near long enough for evolution to have ensured that all those who are disadvantaged by high calcium consumption have yet been "weeded from the gene pool", especially when this ailment, Lone Afib, normally only occurs well after the main breeding ages of the victims -- thus ensuring that their "Afib genes" mainly pass perfectly successfully to the next generation. So this latest high-quality research is essentially conclusive evidence that large numbers of people are not genetically suited to consume the sort of quantities of calcium which are normally now recommended by doctors, nutritionists and governments, and that many people, if not most, are still best suited to consume typical pre-dairying calcium intakes (but with much higher vitamin D). Without deliberately eating shells, limestone or actual bone (not just the marrow), a natural calcium intake from non-dairy natural foods can barely exceed 400mg/day, and then only with extreme dietary efforts -- but of course these sub-400mg intakes were always combined with much higher levels of serum vitamin D than most people enjoy today, and that combination was entirely natural and optimal!

                           REFERENCES NUMBERED IN THE TEXT ABOVE

 

[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.

 

[2] 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.

 

[3] 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.

 

[4]  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.

 

[5] Hodgkin, J. E., Soeprono, F. F., & Chan, D. M. (1980). Incidence of metabolic alkalemia in hospitalized patients. Critical care medicine, 8(12), 725-728.

 

[6] 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.

 

[7] 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.

 

[8] 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.

 

[9] Chelu, M. G., & Wehrens, X. H. T. (2007). Sarcoplasmic reticulum calcium leak and cardiac arrhythmias. Biochemical Society Transactions, 35(5), 952-956.

 

[10] Tucker, N. R., & Ellinor, P. T. (2014). Emerging Directions in the Genetics of Atrial Fibrillation. Circulation research, 114(9), 1469-1482.

 

[11] 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.

 

[12] 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.

 

[13] 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.

 

[14] 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.

 

[15] 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.

 

[16] 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

[17] 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.      

 

[18] 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.     

 

[19] 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.

[20] Rix, T.A., Joensen, A.M., Lundbye-Christensen, S., Riahi, S., Schmidt, E.B., Overvad, K. (2013). Moderate consumption of marine n-3 fatty acids is associated with a lower risk of atrial fibrillation—a cohort study (Abstract). Europace 2013; 15 (S2), S84.

[21] Metcalf, R.G., Skuladottir, G.V., Indridason, O.S., Sullivan, T.R., Bjorgvinsdottir, L., Sanders, P., Arnar, D.O., Gibson, R.A., Heidarsdottir, R., Cleland, L.G., et al. U-shaped relationship between tissue docosahexaenoic acid and atrial fibrillation following cardiac surgery. Metaanal. Eur. J. Clin. Nutr. 2014, 68, 114–118.

[22] Burger, J., Link, V., Blocher, J., Thomas, M.G., Veeramah, K.R., Wegmann, D., et al. Low Prevalence of Lactase Persistence in Bronze Age Europe Indicates Ongoing Strong Selection over the Last 3,000 Years. Current Biol. 2020, In Press

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Paroxysmal lone atrial fibrillation diet