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Books on the topic 'Calcium, Dietary'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Institute of Medicine (U. S.). Committee to Review Dietary Reference Intakes for Vitamin D and Calcium, ed. Dietary reference intakes for calcium and vitamin D. National Academies Press, 2011.

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2

Pierre, Colleen. Calcium in your life. Chronimed, 1997.

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3

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: NIH Consensus Development Conference, June 6-8, 1994, Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland. The Institutes, 1994.

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4

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: NIH Consensus Development Conference, June 6-8, 1994, Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland. The Institutes, 1994.

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5

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: [program and abstracts]. National Institutes of Health, 1994.

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6

NIH Consensus Development Conference on Optimal Calcium Intake (1994 National Institutes of Health). NIH Consensus Development Conference on Optimal Calcium Intake: NIH Consensus Development Conference, June 6-8, 1994, Masur Auditorium, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland. The Institutes, 1994.

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7

Wallach, Leah. Food values: Calcium. Perennial Library, 1989.

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8

Leo, Lutwak, ed. The strong bones diet: The high calcium, low calorie way to prevent osteoporosis. Triad Pub. Co., 1988.

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9

Barsoum, Gemal Habib. Cell proliferation and its modification by dietary calcium supplementation in intestinal adaptation and carcinogenesis. University of Birmingham, 1990.

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10

J, Subak-Sharpe Genell, ed. The calcium-requirement cookbook: 200 recipes that supply necessary calcium-rich foods to prevent the bone loss that often begins in a woman's thirties. M. Evans, 1985.

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11

Food values. Perennial Library, 1989.

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12

Wallach, Leah. Food values. Perennial Library, 1989.

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13

Wallach, Leah. Food values. Perennial Library, 1989.

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14

1950-, Garland Frank Caldwell, ed. The calcium connection: A revolutionary diet and health program to reduce hypertension, prevent osteoporosis, and lower the risk of cancer. Simon & Schuster, 1989.

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15

1950-, Garland Frank Caldwell, ed. The calcium connection: A revolutionary diet and health program to reduce hypertension, prevent osteoporosis, and lower the risk of cancer. Putnam, 1988.

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16

Holick, M. F., and Jeri W. Nieves. Nutrition and bone health. Humana Press, 2015.

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17

Bushinsky, David A., and Orson Moe. Calcium stones. Edited by Mark E. De Broe. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0201.

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Key predisposing factors in calcium stone formation are idiopathic hypercalciuria, primary hyperparathyroidism, and hyperoxaluria (dietary, enteric, idiopathic, sometimes genetic). These are described in detail. Other predisposing conditions include renal tubular acidosis, and risk factors identified in epidemiological studies such as hypocitraturia, increased urinary urate. is defined as an excess of urine calcium excretion without a discernible metabolic cause.

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18

Dietary Reference Intakes for Calcium and Vitamin D. National Academies Press, 2011. http://dx.doi.org/10.17226/13050.

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19

Intakes, Standing Committee on the Scientific Evaluation of Dietary Reference, Food and Nutrition Board, and Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride (Dietary Reference Series). National Academies Press, 1999.

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20

Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, and Institute of Medicine. Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride (Dietary Reference Intakes). National Academies Press, 1999.

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21

Kynast-Gales, Susan Anne. Dietary calcium from dairy products and ambulatory blood pressure in male hypertensives. 1990.

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22

Fuchs, Nan Kathryn, Jack Challem, and Kathryn Nan Fuchs. User's Guide to Calcium & Magnesium. Basic Health Publications, Incorporated, 2002.

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23

Institute of Medicine (U.S.). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes., ed. Dietary reference intakes: For calcium, phosphorus, magnesium, vitamin D, and fluoride. National Academy Press, 1997.

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24

Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. National Academies Press, 1997. http://dx.doi.org/10.17226/5776.

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25

Anderson, John J. B. 1934- and Garner Sanford C, eds. Calcium and phosphorus in health and disease. CRC Press, 1996.

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26

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Calcium in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0018.

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Most calcium in the body is present in the skeleton, where it serves a structural role and also as a reservoir for use in other tissues. During pregnancy, calcium is accumulated in the fetal skeleton, mostly during the third trimester when bone growth is at its peak. Although this increases the demand on maternal bone stores, the calcium transfer to the fetus is balanced by increased intestinal calcium absorption in the mother, mediated by compensatory changes in vitamin D synthesis and endogenous hormone levels. Bone loss is minimized if calcium intake is maintained at 1,000#amp;#x2013;1,200

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27

Cheong, Wei-Hua Adeline. Calcium, iron and zinc bioavailabilities in rats fed diets containing cereal dietary fibers. 1991.

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28

Colon cancer promotion, insulin resistance and metabolic measures: The role of dietary calcium, vitamin D and fat. National Library of Canada, 2000.

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29

J. Urban, I. Röhe, and J. Zentek. Effect of dietary protein, calcium and phosphorus concentrations on performance, nutrient digestibility and whole body composition of male Lohmann Dual chickens. Verlag Eugen Ulmer, 2018. http://dx.doi.org/10.1399/eps.2018.231.

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30

Fuchs, Nan Kathryn. User's Guide to Calcium and Magnesium: Learn What You Need to Know About How These Nutrients Build Strong Bones (User's Guides (Basic Health)). Basic Health Publications, 2002.

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31

Sinnott, Bridget, Naim M. Maalouf, Khashayar Sakhaee, and Orson W. Moe. Medical management of nephrocalcinosis and nephrolithiasis. Edited by Mark E. De Broe. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0205_update_001.

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Conditions associated with nephrocalcinosis and nephrolithiasis are described. Some (cystinuria, urate) have specific therapies, and there are some general measure, particular for calcium-containing stones (urine volume, dietary salt, urinary citrate, thiazide diuretics). In the absence of a primary aetiology, urinary biochemical predisposing factors can be manipulated. Properly directed medical therapy is highly effective in preventing recurrence.

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32

R. Nourmohammadi, H. Khosravinia, and N. Afzali. Effects of high dietary levels of citric acid on productive performance, serum enzyme activity, calcium and phosphorus retention and immune response in broiler chickens. Verlag Eugen Ulmer, 2015. http://dx.doi.org/10.1399/eps.2015.97.

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33

Taylor, Eric N., and Gary C. Curhan. Epidemiology of nephrolithiasis. Edited by Mark E. De Broe. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0199.

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Nephrolithiasis is common, costly, and painful. The prevalence of nephrolithiasis, defined as a history of stone disease, varies by age, sex, race, and geography while the incidence of nephrolithiasis, defined as the first stone event, varies by age, sex, and race. Epidemiologic studies have quantified the burden of kidney stone disease and expand our understanding of risk factors. A variety of dietary, non-dietary, and urinary risk factors contribute to the risk of stone formation and the importance of these varies by age, sex, and body mass index.Low fluid intake, high urinary oxalate or cal

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34

Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of plasma magnesium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0177.

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Normal serum magnesium levels are in the range of 0.7–1.0 mmol/l and, as for calcium, most of the total body magnesium is found in bone and soft tissues. Magnesium is essential for normal cell metabolism (as a cofactor for numerous enzymes) and for neuronal function, and regulates parathyroid hormone release. Alterations in serum magnesium levels are usually asymptomatic unless severe. As there are large tissue reserves of magnesium, hypomagnesaemia usually only develops with chronic gastrointestinal or renal losses, or prolonged dietary insufficiency. Hypermagnesaemia is almost always iatroge

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35

Chopra, Bhavna, and Stanley Goldfarb. Approach to the patient with kidney stones. Edited by Mark E. De Broe. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0200.

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A detailed history can identify some risk factors and narrows down the potential causes of kidney stone formation. Radiological investigations confirm the diagnosis and give information on likely stone type. Urine and serum biochemistry is invaluable, but a more comprehensive investigation is reserved for recurrent stone formers. In that case at least two 24h collections, remote from any acute event are recommended, measuring volume, pH, calcium, oxalate, citrate, uric acid and phosphate. Urinary crystals can shed light on some stone types.For single or recurrent stones, analysis of stones the

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36

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly

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37

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly

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38

Hider, Samantha, and Edward Roddy. Epidemiology of gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0038.

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Gout is the most prevalent inflammatory arthritis in men. Data from epidemiological studies conducted in several countries suggest that the prevalence and incidence of gout have risen over the last few decades, although incidence may have stabilized recently. Dietary factors (animal purines, alcohol, and fructose), co-morbid medical conditions (obesity, metabolic syndrome, hypertension, and chronic kidney disease), and medications (diuretics, aspirin, beta blockers, angiotensin converting-enzyme inhibitors, and non-losartan angiotensin II receptor blockers) have been confirmed to be risk facto

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39

Aleksandra Drażbo, K. Kozłowski, Iwona Chwastowska-Siwiecka, Alicja Sobczak, P. Kwiatkowski, and A. Lemme. Effect of different dietary levels of DL-methionine and the calcium salt of DL-2-hydroxy-4-[methyl] butanoic acid on the growth performance, carcass yield and meat quality of broiler chickens. Verlag Eugen Ulmer, 2015. http://dx.doi.org/10.1399/eps.2015.114.

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40

1933-, Simopoulos Artemis P., and Galli Claudio, eds. Osteoporosis: Nutritional aspects. Karger, 1993.

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41

(Editor), Artemis P. Simopoulos, and Claudio Galli (Editor), eds. Osteoporosis: Nutritional Aspects (World Review of Nutrition and Dietetics). S Karger Pub, 1993.

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42

Murer, Heini, Jürg Biber, and Carsten A. Wagner. Phosphate homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0025.

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Inorganic phosphate ions (H2PO4−/ HPO42−) (abbreviated as Pi) are involved in formation of bone and generation of high-energy bonds (e.g. ATP), metabolic pathways, and regulation of cellular functions. In addition, Pi is a component of biological membranes and nucleic acids. Only about 1% of total body Pi content is present in extracellular fluids, at a plasma concentration in adults within the range 0.8–1.4 mMol/L (at pH 7.4 mostly as HPO42−), with diurnal variations of approximately 0.2 mM. A small amount of plasma Pi is bound to proteins or forms complexes with calcium. Under normal, balanc

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43

Voinescu, Alexandra, Nadia Wasi Iqbal, and Kevin J. Martin. Management of chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0118_update_001.

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In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P rest

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