Calcium: A Compendium

Calcium is very important for the proper functioning of the human body, notable for its role in cell signaling, muscle contraction (including the heart–a fairly important muscle), neurotransmitter release from neurons, enzyme-mediated processes like blood clotting, and as a structural component of bone and teeth (1, 2).

Serum calcium (Ca 2+) levels are a well regulated biological system; when dietary levels of calcium are low, parathyroid hormone (PTH) secretion promotes intestinal calcium absorption. When dietary intake of calcium is inadequate, PTH stimulates bone resorption, drawing calcium from bone and releasing it into the blood (3). If bone resorption exceeds bone formation, bone mineral density decreases, which can lead to osteoporosis (3). Osteoporosis, a disease of decreased mineral density, affects an estimated 75 million people in the USA, France, and Canada (5). Given that 1 in 3 women and 1 in 5 men over the age of 50 will experience osteoporotic fractures (7,8), dietary intake of calcium would seem highly important, yet epidemiological studies often fail to demonstrate a correlation between higher intakes of dietary calcium and decreased rates of osteoporosis (9,10,11). Ultimately, this observation becomes explainable when one takes into account the biological systems which regulate calcium metabolism.

Factors Which Improve Calcium Status
Calcium metabolism is affected by several other nutrients, most importantly vitamin D. As previously discussed, parathyroid hormone can help maintain calcium homeostasis. This occurs in part via PTH stimulated renal conversion of hydroxylated vitamin D3 to calcitriol, the hormonally active form of vitamin D (12). Caclitrol increases intestinal calcium absorption and decreases calcium loss in the urine (13,14). Vitamin D deficiency thus significantly affects calcium status in a negative way. Furthermore, numerous studies have found vitamin K has beneficial effects on bone health (15,16,17). Osteocalcin, a protein which facilitates bone mineralization, is produced by vitamin D (18). Vitamin K (specifically K2) has been found to amplify the effect of supplemental vitamin D3 on osteocalcin production (19). This is likely due to the necessity of vitamin K-dependent gamma-carboxylation of three glutamic acid residues involved with osteocalcin mineral binding (20). Thus, vitamin K appears to assist in (and may be integral to) processes which allow for the mobilization and transport of serum calcium to bone cells. Magnesium is also important, primarily for its role in the functioning of the parathyroid gland. Magnesium deficiency often results in a low production of vitamin D metabolites (21). Studies have shown the mineral boron has a potentially positive role in calcium metabolism and bone formation (22,23), however more research is likely needed before major conclusions can be made.

Factors Which Decrease Calcium Status:
Calcium metabolism is also negatively affected by a number of compounds. Studies have shown high intakes of sodium increase renal excretion of calcium (24,25,26). This has been suggested to occur due to calcium and sodium using the same transport system in the proximal tubule, resulting in concurrent renal excretion of both minerals (24,27), although other mechanisms have been proposed. Various methods, including analysis of mineral excretion over 24-h periods, typically demonstrate roughly 9-26 mg of calcium are excreted for every 1000mg of sodium ingested (20-60mg Ca for every 2300mg of Na) (24,28,29,30). Oxalate, a compound found mostly in plants (especially leaves) has been studied for its ability to reduce calcium absorption (31). This occurs when oxalate (C2O4 2−) bonds with calcium (Ca 2+) in the body, forming calcium oxalate which is later excreted in the urine. Though still debatable, observational evidence support the idea that oxalate acts as a calcium anti-nutrient. Spinach, a high oxalate vegetable, contains calcium with a very low bioavailability (32), whereas kale, a low oxalate vegetable, contains calcium with fairly high calcium bioavailability (33). Insoluble fiber also appears to cause dietary calcium losses, increasing calcium excreted in feces (34,35,36). This is likely limited to insoluble fiber, as inulin (a soluble fiber) has been shown increase the absorption of calcium (37). Finally, a lot of scientific literature exists which study the effect of phosphorus, phytate, and protein on calcium balance. Ultimately, the effects of these compounds (whether positive or negative) in the large majority of diets appears to be fairly minimal.

I’d also like to note that the metabolic acidosis can negatively effect calcium status by causing it to be excreted. I covered this in my review of the alkaline diet.

Putting It Into Practice:
Calcium is a vastly important mineral in human physiology. But it takes more than just ingesting the amount of calcium you need; you must also support processes which maximize the efficiency of calcium absorption and utilization, while also minimizing excess calcium excretion and calcification of inappropriate bodily tissues. Here are my tips for achieving this:

1. Take in enough calcium. Your body needs calcium for numerous functions and if you don’t get enough from your diet your body just goes and takes calcium from that big reservoir that is your skeleton. So how much calcium do you need? This, like many things, is probably variable. However, studies by the FAO and WHO have found that calcium loss equals calcium intake at about 640 mg a day:

See where the two lines meet at 640? That’s probably the bare minimum needed, assuming other areas are optimized. It may be safe to shoot for a higher dose to be safe, I think 750 mg is a good daily calcium recommendation. (Note: you will need more if you are growing, healing from a broken bone or osteoporosis, or a woman in menopause).

2. Get vitamin D. First and foremost, go soak up some sunshine. If that’s not an option, eat food sources of vitamin D like fatty fish, liver, and eggs. Or take a supplement. Blood tests for vitamin D are pretty easy to get and it’s definitely worth knowing if your levels.

3. Get vitamin K2. Some people can convert vitamin k1 (in leafy vegetables) to k2, but I wouldn’t bet on it. Good sources of vitamin k2 include butter from grass fed cows, liver (especially from pastured animals), natto (a type of fermented soybean), and certain fish eggs. There are also supplements.

4. Get magnesium. Magnesium can be found in seeds, nuts, beans, whole grains, leafy green vegetables, chocolate, and certain fish. Or supplement it. However, when consumed together, magnesium and calcium compete for absorption. One should avoid taking large quantities of them at the same meal.

5. Understand that bioavailability of calcium in foods varies significantly (this is true of magnesium as well). As covered earlier, 100mg of calcium will be better absorbed from kale rather than spinach. Oxalic acid in spinach, chocolate, tea, beets, and various other foods binds to calcium and cause them to be excreted. Insoluble fibers in whole grains, seeds, and most nuts also increase calcium excretion. Good sources of bioavailable calcium include milk and cheese (unless you have an intolerance). Bone broths are also good sources of calcium, and most leafy green vegetables are too (except spinach). Though a pile of raw kale or chard may seem hard to eat, cooking doesn’t get rid of the abundant calcium (or many of the other health benefits) so try that out if you’re looking for a source of calcium. Finally, you can supplement.

6. An acid forming diet will cause calcium to be excreted. Focus on eating fruits and vegetables to prevent this. Salt and (especially refined) grains may also have negative effects on acidity. Excess salt, in addition to potentially being acid forming, also increases calcium excretion. The overall effect is not hugely significant.

References:

(1) Clapham, D.E. (2007) “Calcium Signaling” Cell, Volume 131 (6), p. 1047-1058.
(2) Junqueira, Luiz Carlos; José Carneiro (2003). Foltin, Janet; Lebowitz, Harriet; Boyle, Peter J.. eds. Basic Histology, Text & Atlas (10th ed.). McGraw-Hill Companies. p. 144. ISBN 0071378294
(3) Albright, F. & Reifenstein, E.C. 1948. The Parathyroid Glands and Metabolic Bone Disease. Baltimore: Williams & Wilkins
(4) Teitelbaum, Steven L. “Bone Resorption by Osteoclasts.” Science 1 Sept. 2000: Vol. 289 no. 5484 pp. 1504-1508
(5) Kanis JA (2007) WHO Technical Report, University of Sheffield, UK: 66.
(6) EFFO and NOF (1997) “Who are candidates for prevention and treatment for osteoporosis?” Osteoporos Int 7:1.
(7) Melton LJ, 3rd, Atkinson EJ, O’Connor MK, et al. (1998) “Bone density and fracture risk in men” J Bone Miner Res 13:1915
(8) Melton LJ, 3rd, Chrischilles EA, Cooper C, et al. (1992) “Perspective. How many women have osteoporosis?” J Bone Miner Res 7:1005.
(9) Food and Agriculture Organization of the United Nations. 1991. Production Yearbook Vol. 44, 1990. Rome, FAO
(10) Maggi, S., Kelsey, J.L., Litvak, J. & Heyse, S.P. 1991. Incidence of hip fractures in the elderly. A cross-national analysis. Osteoporos. Int., 1: 232-241.
(11) Hegsted, D.M. 1986. Calcium and osteoporosis. J. Nutr., 116: 2316-2319.
(12) Voet, Donald; Voet, Judith G. (2004). Biochemistry. Volume one. Biomolecules, mechanisms of enzyme action, and metabolism, 3rd edition, pp. 663–664. New York: John Wiley & Sons
(13) Holick MF. Vitamin D: A millenium perspective. J Cell Biochem. 2003;88(2):296-307.
(14) Sutton AL, MacDonald PN. Vitamin D: more than a “bone-a-fide” hormone. Mol Endocrinol. 2003;17(5):777-791
(15) Sato Y., Kanoko T., Satoh K., Iwamoto J. Menatetrenone and vitamin D2 with calcium supplements prevent nonvertebral fracture in elderly women with Alzheimer’s disease (2005) Bone, 36 (1), pp. 61-68.
(16) Purwosunu Y, Muharram, Rachman IA, Reksoprodjo S, Sekizawa A. Vitamin K2 treatment for postmenopausal osteoporosis in Indonesia. J Obstet Gynaecol Res. 2006 Apr;32(2):230-4. PubMed PMID: 16594930.
(17) Shiraki M, Shiraki Y, Aoki C, Miura M. Vitamin K2 (menatetrenone) effectively prevents fractures and sustains lumbar bone mineral density in osteoporosis. J Bone Miner Res. 2000 Mar;15(3):515-21. PubMed PMID: 10750566.
(18) Skjodt H, Gallagher JA, Beresford JN, Couch M, Poset JW, Russell RGG 1985 Vitamin D metabolites regulates osteocalcin synthesis and proliferation of human bone cells in vitro. J Endocrinol 105:391–396
(19) Koshihara Y, Hoshi K. Vitamin K2 enhances osteocalcin accumulation in the extracellular matrix of human osteoblasts in vitro. J Bone Miner Res. 1997 Mar;12(3):431-8. PubMed PMID: 9076586.
(20)Booth SL. Skeletal functions of vitamin K-dependent proteins: not just for clotting anymore. Nutr Rev. 1997;55(7):282-284.
(21) Zofková I, Kancheva RL. The relationship between magnesium and calciotropic hormones. Magnes Res. 1995 Mar;8(1):77-84. Review. PubMed PMID: 7669510.
(22) McCoy H, Kenney MA, Montgomery C, Irwin A, Williams L, Orrell R. Relation of boron to the composition and mechanical properties of bone. Environ Health Perspect. 1994 Nov;102 Suppl 7:49-53. Review. PubMed PMID: 7889880; PubMed Central PMCID: PMC1566639.
(23) Devirian TA, Volpe SL. The physiological effects of dietary boron. Crit Rev Food Sci Nutr. 2003;43(2):219-31. Review. PubMed PMID: 12705642.
(24) Nordin BEC, Need AG, Morris HA, Horowitz M. The nature and significance of the relationship between urinary sodium and urinary calcium in women. J Nutr 1993;123:1615–22.
(25) Shortt C, Madden A, Flynn A, Morrissey PA. Influence of dietary sodium intake on urinary calcium excretion in selected Irish individuals. Eur J Clin Nutr 1988;42:595–603
(26) Lau EM, et al. Nutrition and osteoporosis. Curr Opin Rheumatol. 1998 Jul;10(4):368-72.
(27) Walser M: Calcium clearance as a function of sodium clearance in the dog. Am J Physiol200 :769– 773,1961
(28) Goulding A, Lim PE: Effects of varying dietary salt intake on the fasting excretion of sodium, calcium and hydroxyproline in young women. N Z Med J96 :853– 854,1983 .
(29) Goulding A, Campbell D: Dietary NaCl loads promote calciuria and bone loss in adult oophorectomized rats consuming a low calcium diet. J Nutr113 :1409– 1414,198
(30) Sabto, J., Powell, M.J., Breidahi, M.J. & Gurr, F.W. 1984. Influence of urinary sodium on calcium excretion in normal individuals. Med. J. Aust., 140: 354-356.
(31) Borghi L, Schianchi T, Mecschi T, et al. Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. N Engl J Med 2002;346:77-84
(32) Heaney RP, Weaver CM. Oxalate: effect on calcium absorbability. Am J Clin Nutr. 1989 Oct;50(4):830-2. PubMed PMID: 2801588.
(33) Heaney RP, Weaver CM. Calcium absorption from kale. Am J Clin Nutr. 1990 Apr;51(4):656-7. PubMed PMID: 2321572.
(34) Reinhold JG, Faradji B, Abadi P, Ismail-Beigi F. Decreased absorption of calcium, magnesium, zinc and phosphorus by humans due to increased fiber and phosphorus consumption as wheat bread. J Nutr. 1976 Apr;106(4):493-503. PubMed PMID: 1255269.
(35) Ismail-Beigi F, Reinhold JG, Faraji B, Abadi P. Effects of cellulose added to diets of low and high fiber content upon the metabolism of calcium, magnesium, zinc and phosphorus by man. J Nutr. 1977 Apr;107(4):510-8. PubMed PMID: 845688.
(36) Kelsay JL, Behall KM, Prather ES. Effect of fiber from fruits and vegetables on metabolic responses of human subjects. II. Calcium, magnesium, iron, and silicon balances. Am J Clin Nutr 1979;32:1876–80
(37) Coudray C, Bellanger J, Castiglia-Delavaud C, Rémésy C, Vermorel M, Rayssignuier Y. Effect of soluble or partly soluble dietary fibres supplementation on absorption and balance of calcium, magnesium, iron and zinc in healthy young men. Eur J Clin Nutr. 1997 Jun;51(6):375-80. PubMed PMID: 9192195.

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One thought on “Calcium: A Compendium

  1. Sabrina Schaefer December 29, 2011 / 12:22 pm

    Ich habe im Internet surfen mehr als 3 Stunden heute, aber ich fand nie irgendwelche interessanten Artikel wie Ihres. Es ist ziemlich wertvoll genug für mich. Meiner Meinung nach, wenn alle Website-Betreiber und Blogger aus gutem Inhalt, wie du getan hast, wird das Netz sehr viel nützlicher als jemals zuvor.

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