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Schleithoff SS, Zittermann A, Tenderich G, Berthold HK, Stehle P, Koerfer R. Vitamin D supplementation improves cytokine profiles in patients with congestive heart failure: a double-blind, randomized, placebo-controlled trial.Am J Clin Nutr. 2006 Apr;

Pittas AG, Lau J, Hu FB, Dawson-Hughes B. The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab. 2007 Jun;92(6):2017-29. Epub 2007 Mar 27. Review. PMID: 17389701 [PubMed - indexed for MEDL

Mullin GE, Dobs A. Vitamin d and its role in cancer and immunity: a prescription for sunlight. Nutr Clin Pract. 2007 Jun;22(3):305-22. Review. PMID: 17507731 [PubMed - indexed for MEDLINE]

Wicherts IS, van Schoor NM, Boeke AJ, Visser M, Deeg DJ, Smit J, Knol DL, Lips P. Vitamin D status predicts physical performance and its decline in older persons. J Clin Endocrinol Metab. 2007 Jun;92(6):2058-65. Epub 2007 Mar 6. PMID: 17341569 [PubMed

Harinarayan CV, Ramalakshmi T, Prasad UV, Sudhakar D, Srinivasarao PV, Sarma KV, Kumar EG. High prevalence of low dietary calcium, high phytate consumption, and vitamin D deficiency in healthy south Indians. Am J Clin Nutr. 2007 Apr;85(4):1062-7. PMID

Broe KE, Chen TC, Weinberg J, Bischoff-Ferrari HA, Holick MF, Kiel DP. \nA higher dose of vitamin d reduces the risk of falls in nursing home residents: a randomized, multiple-dose study.\nJ Am Geriatr Soc. 2007 Feb;55(2):234-9.\nPMID: 17302660 [PubMed -

Hathcock JN, Shao A, Vieth R, Heaney R. \nRisk assessment for vitamin D.\nAm J Clin Nutr. 2007 Jan;85(1):6-18. Review.\nPMID: 17209171 [PubMed - indexed for MEDLINE]

Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003 Nov;78(5):912-9. Review. PMID: 14594776 [PubMed - indexed for MEDLINE]

Vieth R, Chan PC, MacFarlane GD. Efficacy and safety of vitamin D3 intake exceeding the lowest observedadverse effect level. Am J Clin Nutr. 2001 Feb;73(2):288-94. PMID: 11157326

Conclusions: Healthy men seem to use 3000-5000 IU cholecalciferol/d, apparently meeting > 80% of their winter cholecalciferol need with cutaneously synthesized accumulations from solar sources during the preceding summer months. Current recommended vitamin D inputs are inadequate to maintain serum 25-hydroxycholecalciferol concentration in the absence of substantial cutaneous production of vitamin D. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Am J Clin Nutr. 2003 Jan;77(1):204-10. Erratum in: Am J Clin Nutr. 2003 Nov;78(5):1047. PMID: 12499343

Valimaki VV, Alfthan H, Lehmuskallio E, Loyttyniemi E, Sahi T, Stenman UH, Suominen H, Valimaki MJ. Vitamin D status as a determinant of peak bone mass in young Finnish men. J Clin Endocrinol Metab. 2004 Jan;89(1):76-80. PMID: 14715830

Vitamin D fortification of milk products does not resolve hypovitaminosis D in young Finnish men. Välimäki VV, Löyttyniemi E, Välimäki MJ. Eur J Clin Nutr. 2007 Apr;61(4):493-7. Epub 2006 Nov 29. PMID: 17136043 doi:10.1038/sj.ejcn.1602550

McCollum Award Lecture, 1994: vitamin D--new horizons for the 21st century. Holick MF. Am J Clin Nutr. 1994 Oct;60(4):619-30. Review. PMID: 8092101

Decreased bioavailability of vitamin D in obesity. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Am J Clin Nutr. 2000 Sep;72(3):690-3. Erratum in: Am J Clin Nutr. 2003 May;77(5):1342. PMID: 10966885 Conclusions: Obesity-associated vitamin D insufficiency is likely due to the decreased bioavailability of vitamin D3 from cutaneous and dietary sources because of its deposition in body fat compartments.

Vitamin D in pregnancy and lactation: maternal, fetal, and neonatal outcomes from human and animal studies. Kovacs CS. Am J Clin Nutr. 2008 Aug;88(2):520S-528S. Review. PMID: 18689394 Dosing recommendations for women during pregnancy and lactation might be best directed toward ensuring that the neonate is vitamin D-sufficient and that this sufficiency is maintained during infancy and beyond. A dose of vitamin D that provides 25(OH)D sufficiency in the mother during pregnancy should provide normal cord blood concentrations of 25(OH)D. Research has shown that during lactation, supplements administered directly to the infant can easily achieve vitamin D sufficiency; the mother needs much higher doses (100 µg or 4000 IU per day) to achieve adult-normal 25(OH)D concentrations in her exclusively breastfed infant. In addition, the relation (if any) of vitamin D insufficiency in the fetus or neonate to long-term nonskeletal outcomes such as type 1 diabetes and other chronic diseases needs to be investigated.

Evidence for alteration of the vitamin D-endocrine system in obese subjects. Bell NH, Epstein S, Greene A, Shary J, Oexmann MJ, Shaw S. J Clin Invest. 1985 Jul;76(1):370-3. PMID: 2991340 The results provide evidence that alteration of the vitamin D-endocrine system in obese subjects is characterized by secondary hyperparathyroidism which is associated with enhanced renal tubular reabsorption of calcium and increased circulating 1,25(OH)2D. The reduction of serum 25-OHD in them is attributed to feedback inhibition of hepatic synthesis of the precursor by the increased serum 1,25(OH)2D.

Low vitamin D status, high bone turnover, and bone fractures in centenarians. Passeri G, Pini G, Troiano L, Vescovini R, Sansoni P, Passeri M, Gueresi P, Delsignore R, Pedrazzoni M, Franceschi C. J Clin Endocrinol Metab. 2003 Nov;88(11):5109-15. PMID: 14602735 We conclude that the extreme decades of life are characterized by a pathophysiological sequence of events linking vitamin D deficiency, low serum calcium, and secondary hyperparathyroidism with an increase in bone resorption and severe osteopenia. These data offer a rationale for the possible prevention of elevated bone turnover, bone loss, and consequently the reduction of osteoporotic fractures and fracture-induced disability in the oldest olds through the supplementation with calcium and vitamin D.

Vitamin D, nutritional deficiency, and the medical paradigm. Heaney RP. J Clin Endocrinol Metab. 2003 Nov;88(11):5107-8. Review. No abstract available. PMID: 14602734

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.