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Calcium, vitamin D, “wild-type” fruits, and the epidemiology of other diseases




This section explores the background of calcium metabolism and two other “Western” disease epidemics. Since the aim of most sufferers would be to optimise their overall health and certainly not just to swap atrial fibrillation for some other major disease, these comments are certainly relevant and indeed are necessary to address some likely questions.


The two “Western” diseases which should be discussed in connection with LAF, and specifically in connection with the information on this website, are osteoporosis and cardiovascular disease (which includes heart diseases, stroke and various other diseases of the entire circulatory system).


Most people know that calcium is connected with osteoporosis (more on this below), but not everyone is yet aware that excess calcium in soft tissues and blood vessels (“calcification”) is intimately involved in most, if not all, forms of cardiovascular disease (CVD). Of course, it is becoming increasingly common to have CAT scans to test for this calcification as a very major risk factor for CVD, so more are becoming aware of it.


It is uncertain whether calcification is the largest factor in all cardiovascular diseases, but it may indeed be so.


So universal is this calcification that virtually everyone over 60 in Western countries has a significant degree of it, and the process generally rockets from these ages onwards. Signs of it are present much earlier.


Cardiovascular diseases of all types were, and to some extent still are, mainly diseases of the developed world. They are now becoming much more common in poorer countries, specifically as these countries rapidly adopt as much of Western dietary and lifestyle practices as they can afford.


One of the other most Western of diseases is osteoporosis. Formerly almost unknown in poorer countries, it too is now increasing rapidly there. Osteoporosis is characterised by depleted calcium in bones, and other aspects of decreased bone strength.


So we have a huge and lethal Western epidemic of too much calcium in elderly blood vessels where it does not belong, and a huge and fairly lethal Western epidemic of too little calcium in elderly bones where the calcium does belong! Neither epidemic existed in poor countries (virtually), but now both are rocketing there too, as those countries adopt Western diets and lifestyles as fast as they can.


What is going on?


The apparent paradox has long been commented upon that it is Western countries that have, or have previously had, hugely greater calcium intakes (through abundant dairy food), yet it is they who “have” osteoporosis. Typical calcium intakes in a country like India are abysmal by Western standards, often averaging maybe 300 mg per day, yet osteoporosis was virtually non-existent. In the West, many people consume many times that amount.


The divergence goes further. The vast majority of the population in poor countries are agricultural and other outdoor workers saturated in vitamin D (ie, up towards the 70 ng/mL, 175 nmol/L level -- explained in main article). The vast majority of US or other Western individuals are indoor workers of one kind or another, with vitamin D levels barely above, or even below, what many experts consider an already inappropriately-low, recommended minimum (more here -- Link D).


Of course, dairy consumption and therefore calcium intake is now increasing in the increasingly affluent poor countries, and their populations are moving indoors and off the land. Hey presto, osteoporosis and cardiovascular diseases are booming. These are transitions that happened in earlier decades in Western countries too, succeeded by the osteoporosis and cardiovascular disease epidemics.


Is there a connection between these factors? Is there something about a high calcium, low vitamin D lifestyle that causes calcium to locate inappropriately: at high levels in the blood vessels and low levels in the bones, and which also leads to (lone) atrial fibrillation in any individuals who are genetically predisposed? It seems sensible not to bet against it. The many positive and negative feedback loops and mechanisms between calcium, vitamin D, parathyroid hormone, and other calcium-sensing and calcium-regulating factors, including numerous diurnal (day-night) variations, are exquisitely sensitive and very complex. It would be through these complexities that any adverse mechanism operated, and the full intricacies of the whole machine are certainly not yet fully understood.


Of course, other factors have been proposed. Quite possibly the sheer physical labour of outdoor work is beneficial for both bones and cardiovasculature. But, in relation to the focus of this website, where one issue must be to consider the benefit, or any risk, of a calcium intake of 450 mg per day (with a high serum vitamin D), emphasising physical effort still ignores the typically excellent bone strength shown in poor countries on very low calcium intakes (by Western standards).


Certainly there are plenty of studies showing normal bone strength on so-called “low” calcium intakes. Just as one example: 105 totally vegan subjects (average duration 33 years) with an average calcium intake of 375 mg/day, were compared with 105 subjects matched for age, height, weight and other characteristics and having an average calcium intake of 683 mg/day, and no significant differences were found in several different measures of bone mineral density [1].


In addition, and contrary to the tidal wave of “high calcium” and dairy promotional material, there are plenty of scientific articles and reputable scientific opinions that more calcium intake is not a good thing for osteoporosis or for cardiovascular disease (e.g. a 50% increase in hip fractures resulting from calcium supplements [2]; a 45% increase in hip fractures associated with two or more glasses of milk per day compared to one glass or less [3]; a 27% increase in myocardial infarctions resulting from 500mg of calcium supplementation [4]). These scientific studies appear to be only very recently beginning to turn the tide in standard medical thoughts on appropriate calcium intakes [5].


Another factor that is very actively under research, with regard to both calcium depletion in bones and calcification of blood vessels, is that of vitamin K. There is some research evidence that various forms of this vitamin may aid both problems. (These are very interesting lines of research: so much so that I consumed what would often be considered very high doses of all three of the apparently most active forms of the vitamin [K1; K2 MK-4; K2 MK-7] for over a year, as one of the factors I investigated in relation to afib, but with no detectable effect, either on their own or in conjunction with anything else which I tested concurrently.)


However, there is no evidence that vitamin K intakes are overall higher in poorer or “pre-osteoporosis”, “pre-CVD” countries. So the extremely provocative question mark certainly remains around the “high calcium, low vitamin D” versus “lower calcium, high vitamin D” life patterns.


It may also be noteworthy that one of the very few treatments, and probably the only “natural” treatment, demonstrated to halt osteoporosis, is supplementing the diet with prunes. Studies now show this effect in both animal and human experiments. Possibly uniquely, even compared to the use of powerful synthetic pharmaceuticals, prunes even appear to increase bone mineral density in several small studies, and therefore, to some extent, to reverse osteoporosis, something normally unattainable [6,7,8,9,10]. Although various mechanisms are proposed, clarity is not yet available. It does not appear that any similar studies have ever been undertaken on cranberries. Perhaps it is pure coincidence that the one fruit which has been shown to have this effect is one of the two readily available commercial fruits which most seem to retain the attributes discussed on this site in relation to their unusual (compared to modern fruits) organic acid components (more here -- main article) and very high polyphenol/antioxidant contents (more here -- Link G). Or alternatively, and probably more plausibly, there are in fact strong inter-relations between the consumption of such “wild-type” fruits and various Western diseases.


Interestingly, just in the last two months, new research in a leading journal has shown that very small changes in blood acidity (“extracellular pH”), much smaller than was previously thought, cause dramatic changes in circulating parathyroid hormone (“PTH”) by suppressing or promoting PTH release from the parathyroid [11]. The senior author is quoted: "What is so important about this research is that we have demonstrated that changes in PTH release can be prompted by very small changes in blood pH level. Before, it was assumed that only a larger change … would cause problems for patients." Although this research arose through studies of kidney disease, circulating (extracellular) PTH is certainly one of the main players, if not the main player, in all calcium metabolism, including bone mineralisation and cardiovascular calcification: and I am definitely proposing in LAF also -- based on the dramatic calcium and vitamin D effects which I experienced. As stated above, “the full intricacies of the whole (calcium regulating) machine are certainly not yet fully understood”, but this newly strengthened linking of acidity/alkalinity and calcium metabolism again attracts strong attention to the acid/alkaline metabolic effects of various dietary components.


So, in summary, it is obvious that an age-related decline in the perfection of human calcium-handling capability is intimately associated with numerous age-related Western diseases (see examples [12]), and this site proposes that most cases of at least the “lone” variant of atrial fibrillation represent little more than one particular genetic manifestation of this gradual decline, until permanent AF represents the complete overwhelming of the system. (The scientifically well-established, age-related decline of the body's vitamin D manufacturing capability, for example, was discussed in Link D). There is a well-argued and well-referenced proposal published in the journal Medical Hypotheses that the ideal calcium intake for osteoporosis avoidance is 300 mg to 500 mg [13]. It is extremely easy to accept that the ideal intake for all mature humans (with adequate vitamin D) would be around this range, and that no calcium-rich foods are required or beneficial, given that all human infants, at the stage of life where the need for calcium is by far the greatest on a weight for weight basis, happily calcify all their rapidly growing bones on breast milk alone, containing only 32 mg of calcium per 100 grams. This is around a quarter the content of cow's milk, and less than some fruits, such as oranges! So it is likely that, in due course, it will eventually be conclusively shown and accepted that all calcium intake beyond these levels becomes progressively more difficult for the calcium-handling systems to cope with as age advances. A good likelihood is that a variety of very serious age-related diseases, of which LAF is just one, result at least partially from calcium overload, vitamin D deficiency, and divergences from our ancestral diets which adversely affect calcium metabolism.






[1] Ho-Pham, L. T., et al. "Veganism, bone mineral density, and body composition: a study in Buddhist nuns." Osteoporosis international 20.12 (2009): 2087-2093.


[2] Reid, I. R., Bolland, M. J., & Grey, A. (2008). Effect of calcium supplementation on hip fractures. Osteoporosis international, 19(8), 1119-1123.


[3] Feskanich, D., Willett, W. C., Stampfer, M. J., & Colditz, G. A. (1997). Milk, dietary calcium, and bone fractures in women: a 12-year prospective study.American Journal of Public Health, 87(6), 992-997.


[4] Bolland, M. J., Avenell, A., Baron, J. A., Grey, A., MacLennan, G. S., Gamble, G. D., & Reid, I. R. (2010). Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis. Bmj, 341.


[5] Bauer, D. C. (2014). The Calcium Supplement Controversy: Now What?.Journal of Bone and Mineral Research, 29(3), 531-533.


[6] Deyhim, F., Stoecker, B. J., Brusewitz, G. H., Devareddy, L., & Arjmandi, B. H. (2005). Dried plum reverses bone loss in an osteopenic rat model of osteoporosis. Menopause, 12(6), 755-762.


[7] Franklin, M., Bu, S. Y., Lerner, M. R., Lancaster, E. A., Bellmer, D., Marlow, D., ... & Smith, B. J. (2006). Dried plum prevents bone loss in a male osteoporosis model via IGF-I and the RANK pathway. Bone, 39(6), 1331-1342.


[8] Bu, S. Y., Lucas, E. A., Franklin, M., Marlow, D., Brackett, D. J., Boldrin, E. A., ... & Smith, B. J. (2007). Comparison of dried plum supplementation and intermittent PTH in restoring bone in osteopenic orchidectomized rats.Osteoporosis international, 18(7), 931-942.


[9] Hooshmand, S., Chai, S. C., Saadat, R. L., Payton, M. E., Brummel-Smith, K., & Arjmandi, B. H. (2011). Comparative effects of dried plum and dried apple on bone in postmenopausal women. British Journal of Nutrition, 106(06), 923-930.


[10] Rendina, E., Hembree, K. D., Davis, M. R., Marlow, D., Clarke, S. L., Halloran, B. P., ... & Smith, B. J. (2013). Dried plum’s unique capacity to reverse bone loss and alter bone metabolism in postmenopausal osteoporosis model. PloS one, 8(3), e60569.


[11] Campion, K. L., McCormick, W. D., Warwicker, J., Khayat, M. E. B., Atkinson-Dell, R., Steward, M. C., ... & Ward, D. T. (2015). Pathophysiologic Changes in Extracellular pH Modulate Parathyroid Calcium-Sensing Receptor Activity and Secretion via a Histidine-Independent Mechanism. Journal of the American Society of Nephrology, ASN-2014070653.


[12] Osteoporosis; heart disease; stroke; other cardiovascular diseases; arthritis; kidney stones; gallstones; ...


[13] Klompmaker, T. R. (2005). Lifetime high calcium intake increases osteoporotic fracture risk in old age. Medical hypotheses, 65(3), 552-558.



The dietary, nutritional, medical and vitamin information provided on this site is not individualised in such a way as to provide suitable care or advice to prevent, manage, treat, cure, or rehabilitate any medical condition, illness, or injury, including lone atrial fibrillation or any variant of atrial fibrillation, for any specific person or group. Visitors to this site with medical conditions -- such as any form of atrial fibrillation -- seeking information on how to treat the condition, should immediately seek counselling from a suitable medical professional. By entering this site, visitors acknowledge that:


1) Information provided in this site may be inaccurate and should not be used in place of advice given by a licensed professional.

2) Information provided in this site and by the author of this site is intended for general use only and is not to be taken as medical, dietary, nutritional or vitamin therapy or as any form of individualized counselling.

3) This site contains only general medical information regarding the experience of a single individual.

4) The medical information is not advice and should not be treated as such.

5) The medical information in this site about one individual is provided without any representations or warranties, express or implied.

6) Without limiting the scope of (5), it is not warranted or represented that the medical information in this website is true, accurate, complete, current or non-misleading.

7) Visitors will not rely on the information on this site as an alternative to medical advice from their doctor or other professional healthcare provider.

8) If visitors have any specific questions about any medical matter, they will consult their doctor or other professional healthcare provider.

9) If visitors think they may be suffering from any medical condition, including atrial fibrillation, they will seek immediate medical attention.

10) Visitors will never delay seeking medical advice, disregard medical advice or discontinue medical treatment because of information on this site.


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