The acid-base hypothesis: diet and bone in the Framingham Osteoporosis Study.
Tucker KL, Hannan MT, Kiel DP.
Eur J Nutr. 2001 Oct;40(5):231-7.
PMID: 11842948
A positive dose-response effect of vitamin D supplementation on site-specific bone mineral augmentation in adolescent girls: a double-blinded randomized placebo-controlled 1-year intervention.
Viljakainen HT, Natri AM, Kärkkäinen M, Huttunen MM, Palssa A, Jakobsen J, Cashman KD, Mølgaard C, Lamberg-Allardt C.
J Bone Miner Res. 2006 Jun;21(6):836-44.
PMID: 16753014
doi: 10.1359/jbmr.060302
We conclude that the current vitamin D recommendation for adolescent girls, at least in the northern latitudes, is too low to ensure sufficient vitamin D status during winter. Intake of vitamin D at rates of 10-15 μg/day aids to maintain stable S-25(OH)D concentrations during winter. Vitamin D induced BMC augmentation by decreasing bone resorption, but not affecting bone formation, which was reflected by the biochemical markers of bone turnover. Optimizing bone mineral gain in adolescence is crucial to the prevention of osteoporosis later in life. Increasing vitamin D intake to 10-15 μg/day aids in attaining this goal.
Vitamin D in preventive medicine: are we ignoring the evidence?
Zittermann A.
Br J Nutr. 2003 May;89(5):552-72. Review.
PMID: 12720576
Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.
Vitamin d deficiency and seasonal variation in an adult South Florida population.
Levis S, Gomez A, Jimenez C, Veras L, Ma F, Lai S, Hollis B, Roos BA.
J Clin Endocrinol Metab. 2005 Mar;90(3):1557-62. Epub 2005 Jan 5.
PMID: 15634725
The prevalence of hypovitaminosis D is considerable even in southern latitudes and should be taken into account in the evaluation of postmenopausal and male osteoporosis.
Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology.
Peterlik M, Cross HS.
Eur J Clin Nutr. 2009 Dec;63(12):1377-86. Epub 2009 Sep 2.
PMID: 19724293
doi:10.1038/ejcn.2009.105
A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.
Long-term effects of giving nursing home residents bread fortified with 125 {micro}g (5000 IU) vitamin D3 per daily serving.
Mocanu V, Stitt PA, Costan AR, Voroniuc O, Zbranca E, Luca V, Vieth R.
Am J Clin Nutr. 2009 Feb 25. [Epub ahead of print]
PMID: 19244376
Dose response to vitamin D supplementation among postmenopausal African American women.\nTalwar SA, Aloia JF, Pollack S, Yeh JK.\nAm J Clin Nutr. 2007 Dec;86(6):1657-62.\nPMID: 18065583
Environmental factors that influence the cutaneous production of vitamin D.
Holick MF.
Am J Clin Nutr. 1995 Mar;61(3 Suppl):638S-645S. Review.
PMID: 7879731
Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors.
Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC Jr.
Am J Clin Nutr. 2002 Dec;76(6):1308-16.
PMID: 12450898
Kerstetter JE, O'Brien KO, Insogna KL.
Low protein intake: the impact on calcium and bone homeostasis in humans.
J Nutr. 2003 Mar;133(3):855S-861S. Review.
PMID: 12612169
Sakhaee K, Maalouf NM, Abrams SA, Pak CY.
Effects of potassium alkali and calcium supplementation on bone turnover in postmenopausal women.
J Clin Endocrinol Metab. 2005 Jun;90(6):3528-33. Epub 2005 Mar 8.
PMID: 15755853
Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC Jr.
Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate.
N Engl J Med. 1994 Jun 23;330(25):1776-81.
PMID: 8190153 [PubMed - indexed for MEDL
Frassetto L, Morris RC Jr, Sebastian A.
Long-term persistence of the urine calcium-lowering effect of potassium bicarbonate in postmenopausal women.
J Clin Endocrinol Metab. 2005 Feb;90(2):831-4. Epub 2004 Nov 30.
PMID: 15572425 [PubMed - indexed for M