Link J

Specific details of my successful approach (as optimised up to Jan 2021)

 

 

 

I have broken these items into the following categories:

Those which I am certain provide benefit: eg optimum serum (blood) vitamin D level and calcium intake.

Those I am essentially certain provide benefit: eg raised protein intake; cranberries and dried plums.

Those for which I detected no effect on afib, but which I continue for other reasons.

Various other dietary and lifestyle aspects, with some brief explanations why they are maintained.

 

Summary: keep blood VitD as below; calcium as below; 5 cups of cranberries and 300gm prunes per day; ample meats.

 

Those factors which I am certain provide benefit:

Blood level of Vitamin D3: I take five “Healthy Origins” brand 5,000 IU capsules per week, on Monday to Friday for an easily maintained routine, except for the three summer months, when I take four per week. These, plus an average of probably half an hour per day of direct sun on arms and head, keep my serum 25-hydroxyvitamin D around 160 nmol/L (64 ng/mL). It is certainly necessary to be tested, to check serum levels, until a person has fixed a routine which is ideal to them. Since most will probably find that they have an initial level much closer to 50 nmol/L (20 ng/mL) than to 150 nmol/L (60 ng/mL), what may seem like a very substantial dose is required to first reach the 160 nmol/L (64 ng/mL) zone, before switching to the long-term maintenance dose. I noticed little effect on atrial fibrillation until I got my levels toward this higher range. Waiting for the maintenance dose alone (in my case 5 x 5,000 IU per week) to level off around 160 nmol/L (64ng/mL) will take months, so a “loading dose” may be preferred.

 

A loading dose is a perfectly common and respectable medical strategy. There are many reputable medical studies and protocols for using single doses of vitamin D up to 500,000 IU to achieve an adequate serum vitamin D level, and there are scientific articles summarising some of these [1]. I found that 20,000 IU per day, spread through the day, would lift serum 25-hydroxyvitamin D roughly 10 nmol/L (4 ng/mL) per day (but this would vary between individuals). So, if an initial blood serum test showed 50 nmol/L (20 ng/mL), this would take roughly 10 days, of 20,000 IU per day, to reach a level suitable to then switch to 5 x 5,000 IU per week. But blood tests are importantIt would be easy to overshoot (or undershoot). So a test before supplementing is needed, then an estimate of how long to take a loading dose, then a test at the end of that loading dose. Once a person is anywhere between, say, 130 nmol/L (~50 ng/mL) and 200 nmol/L (80 ng/mL), it would then be best to try a maintenance dose, for example as above, and test again after say two months. If below say 130 nmol/L (~50ng/mL), best to keep loading for a few more days. If over 200 nmol/L (80 ng/mL), best to stop all supplementation for a week or two, before then commencing the maintenance dose, then retest in a month or two. Solar exposure is a factor also. It always takes some jiggling for each individual to find out what works, and so testing, to find out what one’s serum 25-hydroxyvitamin D is, is important (the process of my other family members adjusting their serum vitamin D levels made this apparent). If the tests are not government or insurance supported, then they are well worth paying for!

 

Calcium intake: My routine current intake is close to 400 mg per day. I have assessed this very closely -- the USDA (and other nations' food bodies) have a comprehensive database with calcium contents of thousands of foods. At this intake, my serum calcium levels are always beautifully midrange when tested, and my parathyroid hormone levels are within the normal range. Levels of the latter hormone would indicate a problem, by becoming too high, if calcium intake was too low. It is possible that a good serum (ie blood) calcium level from this amount of calcium intake is only possible with a good Vitamin D level, but that is precisely the balance I am seeking, so all is fine. Apparently paradoxically, my serum calcium levels were usually in the low part of the normal range when my calcium intake was higher, but the complexity and incompletely-understood nature of human calcium regulation is emphasised later, in the section on “Calcium, vitamin D, “wild-type” fruits, and the epidemiology of other diseases” -- Link L.

 

Maintaining daily calcium intake at this level basically requires me to avoid any regular "white" dairy foods (butter for example would be no problem, but no milk, yoghurt or cheese). Believe me, that is a very small price to pay to avoid afib and the threat of multiple ablations and their risks! I substitute with oat milk in coffees (decaf) etc.

 

Basically, a person will need to monitor their calcium well, and have a good idea of its occurrence in foods. There are plenty of traps. For example:

 

  • Many milk substitutes (Oat, Soy, Rice etc) are fortified with calcium. Some aren’t.

  • Multivitamins often contain, say, 250 mg per dose (although I do not take them).

  • Many flours are fortified with calcium! (Therefore numerous baked foods). Some aren’t.

  • Chocolate, or even carob products and white chocolate if you are avoiding caffeine and theobromide stimulants because of your afib, usually contain milk powder (and therefore substantial calcium). But even pure cocoa, carob and cinnamon powders are high-calcium foods in their own right.

  • Almonds and some other nuts and seeds are high in calcium.

  • Eggs are quite high in calcium.

  • Many dried fruits are high in calcium.

  • Molasses: my subtlest trap! (Just as an example). I began using a generous dessert spoon of molasses per day as a tasty sweetener. I noticed a few ectopic beats reappearing. Substitution of the molasses with an equivalent amount of white sugar eliminated them. The USDA database records 205 mg of calcium per 100g for the particular US molasses which they tested, so a single dessert spoon didn’t seem like it should be too disastrous. But it turns out that the molasses I was using had almost nine times the calcium content of the USDA molasses! For your interest, calcium content decreases in the order molasses>treacle>golden syrup>brown sugar>white sugar.

 

Regardless of the comments above, a single serve of high-calcium food has no adverse effect, so long as the overall ongoing calcium intake is consistently acceptable.

 

 

Those factors which I am essentially certain provide benefit (Nil personal evidence re weight loss, or optimum intakes of iodine or omega-3, but there is good scientific evidence re all three):

Raised protein intakeI now routinely consume around 600gms of lean meat/poultry/seafood per day -- about 500g cooked weight of lean meat or poultry, and 100g of cooked mussel meat. This level of high-grade protein consumption maintains my serum protein and albumin at higher (more desirable) levels than previously, and my serum urea (something which would become elevated by too much protein consumption) remains within the normal range. I have noted that it is much easier to add muscle (at 67yo) on this sort of intake, and, with suitable exercise, I now have the highest body proportion of musculature in my life. Meanwhile, body fat has just gradually drained away, without any conscious effort.

Cranberries: We buy 1kg packs of frozen cranberries and I routinely consume around 5 cups per day (approx 550gms).. Because of their relative bitterness and sourness (which, however, I do not find unpleasant) but also because of their acidity, I blend them every morning with water and much smaller amounts of other fruits and veggies, and consume the delicious smoothie through the day. 

 

The reference to their acidity is one concern: would consistent consumption damage tooth enamel? I have not been able to obtain a definite answer, but teeth certainly feel different after chewing cranberries, so that is the main reason for blending them.

It is likely that cranberries provide many other benefits beyond those for afib. There is not space to go into all possibilities here, but, for example, they are amongst the fruits truly highest in resveratrol, many anthocyanins, melatonin, and ursolic acid -- the latter highly beneficial for muscle-production (especially relevant with age).

Dried Plums: The only fruit documented to have similar metabolic acid/alkaline effects to cranberries. Also, like cranberries, extremely high in antioxidants. Also very high potassium/calcium ratio. A bowlful as the last food of the day suffices as "dessert" to prevent me succumbing to much worse alternatives! I routinely consume up to 300gms/day.

Optimum iodine intake: Scientific studies have linked afib to both hyperthyroidism and hypothyroidism. Iodine status is crucial to thyroid status, and deficiency is common. Because I consume no dairy foods routinely (a source of iodine), and no added salt or other foods having government-mandated iodine fortification, I usually consume 100gms of cooked mussel meat per day. This contains the 150 microgram RDI of iodine and, being a "whole animal" (things we no longer often eat -- but regularly did for our entire seven million year history as a species, and before that), contains many other nutrients. But the simplest and most reliable way for most people to ensure that they maintain the RDI is simply to take a 150 microgram supplement (widely available) every day. Using mussels or other shellfish is simply a "Paleo" refinement.

Weight loss and omega-3: I must also include as "essentially certain" these two things, for which there is good published scientific research, even though I have noted no effect myself, despite testing one very thoroughly. Weight loss (presumably of adipose tissue, ie fat, not of muscle) has been scientifically shown to benefit afib. Omega-3 intakes both above and below an optimum intake of 0.6gms/day have been shown to adversely affect afib (see references listed in the main page of this website). I extensively tested large omega-3 doses on myself (before I was aware of the latter research), and also the absence of pretty-much all omega-3 intake, and detected no influence on afib whatsoever in either case. But maybe the time-lag for detectable effects was just too great. Anyway, the published scientific research seems good enough, so it is wise to be cautious. My usual 100gm mussel intake provides about 0.9gms omega-3/day, so that is a bit over the described optimum; but I have no afib problems, and prefer to choose that the 100gm mussel intake optimises my iodine intake as described above. The major risks appear to lie with higher intakes of omega-3.

Those factors with no effect detected, but which I continue for other reasons:

Reduced sodium intake: I always had a very low intake of added sodium anyway, and found no benefit from extensive testing of further sodium reduction. However, the evidence for other adverse health effects from all excess sodium is solid; the natural sodium content of my usual meat and mussel intake (plus other foods) is adequate; and my serum levels of sodium always come back fine, so I add zero sodium to food.

Raised Vitamin K1 or K2 intakeGiven the interrelated effects of vitamin D and calcium on afib, and given that there is scientific research showing an effect of vitamin K to minimise calcification of blood vessels and to increase deposition of calcium into bones, where it belongs, I repeatedly trialled substantial ongoing doses of both vitamin K1 and K2 -- from not only various supplement forms but also from the richest food sources such as natto. I never detected any effect on my afib or ectopics from either addition or removal of any form of vitamin K from my diet. However, given the documented effects mentioned above, and the general scarcity of K2 in modern diets, I continue with a daily supplement of vitamin K1 and K2 (MK-4 and MK-7 forms). It is the only supplement I take apart from the vitamin D outlined above.

Low consumption of cereal grainsAlthough many now abstain from grain-based foods because of supposed gluten-sensitivities, that is not my reason; I have been tested and have no such issue. Furthermore, complete elimination of grains yielded no beneficial effect on afib. However, there is no doubt that grains are not an ancient and therefore natural food for humans (at least not in quantity). They are not such a recent introduction to our diets as are dairy foods, but almost so. The widespread occurrence of gluten-intolerance, like that of lactose intolerance, is current-day proof that we are not yet genetically well-adapted, and archeaology is also clear. Unlike some other seeds, we cannot eat them without cooking; and they are low-nutrient calories. In contrast, some high-nutrient seeds are deliberately "designed" (actually: optimally evolved) for raw consumption by fruit-eating mammals like us and our relatives the great apes (with the intent of some percentage, of the large number eaten, slipping through undamaged to emerge in a patch of ready fertiliser). The most obvious in this category are the many seeds within the fruits of the cucurbit family -- many of which are African and therefore fully typical, human foods for millions of years. So I consume no grains except when socialising, thereby eliminating large amounts of empty calories and freeing space for much more nutrient-packed fruits etc. A daily handful of pumpkin seeds, a teaspoon of dry yeast, and 10 grams or so of walnuts, top up various nutrient odds and ends.

 

Other dietary details:

Caffeinated drinks and chocolate are avoided. Substituting caffeine with decaf was very easy and gave noticeably better energy levels once adjusted to it. Chocolate abstinence is hard, but any sane afibber has to be off both, and this is well documented. I can consume chocolate or caffeine now without AF, but prefer caution!

 

Alcohol is not routinely consumed; but again, occasional digression is not a problem.

 

The description above represents the "base" diet -- that is, the dietary pattern followed at home and whenever possible. Moderate digressions from any aspect of it, eg when socialising, have no adverse effects, but obviously any worthwhile experimentation should initially follow closely. It is likely that sufferers in whom the atrial fibrillation is less well-advanced or less severe than it was in my case will not have to adhere as closely, but, again, any initial experimentation should be in a "full-blown" way so that effectiveness can be determined, after which requirements can be moderated as desired. It is likely, once tested, that apart from attention to the specified factors, the protocol can be easily incorporated within any personal, existing, dietary habits.

 

It is not asserted that the mechanism of action of the cranberries and dried plums is definitely via their metabolically acidifying effects; but if that is the mechanism, it would be wise to avoid strongly “alkalising” foods which would counter the acidifying effect of the cranberries and dried plums. At times, I have thought that I have detected this problem, although I have not rigorously tested it. But for anyone concerned at this possibility, or wishing (sensibly) to initially test my dietary protocol in a “full-blown” way, it would be easy and highly desirable to avoid, at least initially, strongly alkalising fruits and vegetables. They are listed in many websites.

 

[1] Whiting, S. J., & Calvo, M. S. (2010). Correcting poor vitamin D status: do older adults need higher repletion doses of vitamin D3 than younger adults?.Molecular nutrition & food research, 54(8), 1077-1084.

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Paroxysmal lone atrial fibrillation diet J