Specific details of my dietary approach
The following details are relevant regarding intakes of the various factors which I have identified in my protocol. There are also a few other, minor, dietary points, which do not seem to have any specific effect on atrial fibrillation, but which are noted at the end of this section for completeness.
Summary: 25,000 IU of vitamin D3/week; 100 g of cranberries/day; calcium as below.
Vitamin D3: I take five “Healthy Origins” brand 5,000 IU capsules per week, on Monday to Friday for an easily maintained routine. These, plus an average of probably half an hour per day of direct sun on arms and head, keep my serum 25-hydroxyvitamin D between about 160 and 175 nmol/L (70 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 165 nmol/L (66 ng/mL) zone, before switching to the maintenance dose. I noticed little effect on atrial fibrillation until I got my levels toward this higher range. Waiting for the maintenance dose alone (say 5 x 5,000 IU per week) to level off around 165 nmol/L (66ng/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 . 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 important. It 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: My routine current intake is very close to 450 mg per day. I have assessed this very closely -- the USDA (and other national 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. The latter would indicate a problem, by becoming too high, if calcium intake was too low. It is possible that a good serum 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 low-normal when 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.
Since eggs contain a reasonable amount of calcium, and I eat quite a few eggs each day (my cholesterol has always been extremely good), maintaining daily calcium intake at this level basically requires me to avoid any regular dairy calcium (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 some baked goods). 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.
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 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.
Cranberries: We buy 1kg packs of frozen cranberries. 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 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.
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!
I consume no added salt beyond that naturally in my eggs and large seafood intake (both have quite significant sodium content) and other foods, but I have never noted a connection between varying salt intake and atrial fibrillation.
I consume considerably more animal protein than previously, and I observed reductions in ectopics with that change, but the effect was not as pronounced as with the calcium, vitamin D and cranberries.
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 in my case will have less stringent requirements, 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 is definitely via acidification, but if that is the mechanism, it would be wise to avoid strongly “alkalising” foods which would counter the acidifying effect of the cranberries. I have not specifically noticed any such problem, and if no such problem exists it would suggest that the effective mechanism is not via acidification. However, I have not rigorously tested this with large doses of strongly alkalising foods while still consuming cranberries. But for anyone concerned at this possibility, or wishing (sensibly) to initially test in a “full-blown” way my dietary protocol, it would be easy to avoid, at least initially, strongly alkalising fruits and vegetables. They are listed in many websites.
 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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