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Estimation and fortification of vitamin D3 in pasteurized process cheese. Upreti P, Mistry VV, Warthesen JJ. J Dairy Sci. 2002 Dec;85(12):3173-81. PMID: 12512590 The objective of this study was to develop methods for the estimation and fortification of vitamin D3 in pasteurized Process cheese. Vitamin D3 was estimated using alkaline saponification at 70°C for 30 min, followed by extraction with petroleum ether:diethyl ether (90:10 vol/vol) and HPLC. The retention time for vitamin D3 was approximately 9 min. A standard curve with a correlation coefficient of 0.972 was prepared for quantification of vitamin D3 in unknown samples. In the second phase of the study, pasteurized Process cheeses fortified with commercial water- or fat-dispersible forms of vitamin D3 at a level of 100 IU per serving (28 g) were manufactured. There was no loss of vitamin D3 during Process cheese manufacture, and the vitamin was uniformly distributed. No losses of the vitamin occurred during storage of the fortified cheeses over a 9-mo period at 21 to 29°C and 4 to 6°C. There was an approximately 25 to 30% loss of the vitamin when cheeses were heated for 5 min in an oven maintained at 232°C. Added vitamin D3 did not impart any off flavors to the Process cheeses as determined by sensory analysis. There were no differences between the water- and fat-dispersible forms of the vitamin in the parameters measured in fortified cheeses

ScienceDaily (Aug. 25, 2009) - Low levels of vitamin D are known to nearly double the risk of cardiovascular disease in patients with diabetes, and researchers at Washington University School of Medicine in St. Louis now think they know why. They have found that diabetics deficient in vitamin D can't process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. The new research has identified a mechanism linking low vitamin D levels to heart disease risk and may lead to ways to fix the problem, simply by increasing levels of vitamin D.

Zittermann A, Schleithoff SS, Koerfer R. Vitamin D insufficiency in congestive heart failure: why and what to do about it? Heart Fail Rev. 2006 Mar;11(1):25-33. PMID: 16819575 [PubMed - in process]

Bikle DD. What is new in vitamin D: 2006-2007. Curr Opin Rheumatol. 2007 Jul;19(4):383-8. PMID: 17551371 [PubMed - in process]

Robien K, Cutler GJ, Lazovich D. Vitamin D intake and breast cancer risk in postmenopausal women: the Iowa Women's Health Study. Cancer Causes Control. 2007 Sep;18(7):775-82. Epub 2007 Jun 5. PMID: 17549593 [PubMed - in process]

Giovannucci E, Liu Y, Willett WC. Cancer incidence and mortality and vitamin d in black and white male health professionals. Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2467-72. Epub 2006 Nov 28. PMID: 17132768 [PubMed - in process]

Grant WB, Garland CF, Gorham ED. An estimate of cancer mortality rate reductions in Europe and the US with 1,000 IU of oral vitamin D per day. Recent Results Cancer Res. 2007;174:225-34. PMID: 17302200 [PubMed - in process]

Faiz S, Panunti B, Andrews S. The epidemic of vitamin D deficiency. J La State Med Soc. 2007 Jan-Feb;159(1):17-20; quiz 20, 55. PMID: 17396471 [PubMed - in process]

Chatfield SM, Brand C, Ebeling PR, Russell DM. Vitamin D deficiency in general medical inpatients in summer and winter. Intern Med J. 2007 Jun;37(6):377-82. PMID: 17535381 [PubMed - in process]

Reinehr T, de Sousa G, Alexy U, Kersting M, Andler W. Vitamin D status and parathyroid hormone in obese children before and after weight loss. Eur J Endocrinol. 2007 Aug;157(2):225-32. PMID: 17656603 [PubMed - in process]

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.

Vitamin D supplement in early childhood and risk for Type I (insulin-dependent) diabetes mellitus. The EURODIAB Substudy 2 Study Group. [No authors listed] Diabetologia. 1999 Jan;42(1):51-4. PMID: 10027578 DOI: 10.1007/s001250051112 In conclusion, this large multicentre trial covering many different European settings consistently showed a protective effect of vitamin D supplementation in infancy. The findings indicate that activated vitamin D might contribute to immune modulation and thereby protect or arrest an ongoing immune process initiated in susceptible people by early environmental exposures.