Group items tagged

25-hydroxyvitamin D levels inversely associate with risk for developing coronary artery calcification. de Boer IH, Kestenbaum B, Shoben AB, Michos ED, Sarnak MJ, Siscovick DS. J Am Soc Nephrol. 2009 Aug;20(8):1805-12. Epub 2009 May 14. PMID: 19443637 doi: 10.1681/ASN.2008111157 "In conclusion, lower 25-hydroxyvitamin D concentrations associate with increased risk for incident CAC. Accelerated development of atherosclerosis may underlie, in part, the increased cardiovascular risk associated with vitamin D deficiency."

Hypocalcemia as a Cause of Reversible Cardiomyopathy with Ventricular Tachycardia Chandrakant B. Chavan, MD, DNB; Kalavakolanu Sharada, MD, DM; Hygriv B. Rao, MD, DM; and Calambur Narsimhan, MD, DM, AB Annals of Internal Medicine, 3 April 2007, Volume

Wintertime vitamin D supplementation inhibits seasonal variation of calcitropic hormones and maintains bone turnover in healthy men. Viljakainen HT, Väisänen M, Kemi V, Rikkonen T, Kröger H, Laitinen EK, Rita H, Lamberg-Allardt C. J Bone Miner Res. 2009 Feb;24(2):346-52. PMID: 18847321

Wintertime vitamin D insufficiency is common in young Canadian women, and their vitamin D intake does not prevent it. Vieth R, Cole DE, Hawker GA, Trang HM, Rubin LA. Eur J Clin Nutr. 2001 Dec;55(12):1091-7. PMID: 11781676 INTERPRETATION: The self-reported vitamin D intake from milk and/or multivitamins does not relate to prevention of low vitamin D nutritional status of young women in winter. Recommended vitamin D intakes are too small to prevent insufficiency. Vitamin D nutrition can only be assessed by measuring serum 25(OH)D concentration.

Teenage girls and elderly women living in northern Europe have low winter vitamin D status. Andersen R, Mølgaard C, Skovgaard LT, Brot C, Cashman KD, Chabros E, Charzewska J, Flynn A, Jakobsen J, Kärkkäinen M, Kiely M, Lamberg-Allardt C, Moreiras O, Natri AM, O'brien M, Rogalska-Niedzwiedz M, Ovesen L. Eur J Clin Nutr. 2005 Apr;59(4):533-41. PMID: 15714215 doi:10.1038/sj.ejcn.1602108 CONCLUSION: Vitamin D status is low in northern Europe during winter. More than one-third of the adolescent girls have vitamin D status below 25 nmol/l and almost all are below 50 nmol/l. Two-thirds of the elderly community-dwelling women have vitamin D status below 50 nmol/l. Use of vitamin D supplements is a significant positive determinant for S-25OHD for both girls and women (P = 0.001). SPONSORSHIP: The European Fifth Framework Programme (Contract No. QLK1-CT-2000-00623)

Association between serum 25(OH)D and death from prostate cancer. Tretli S, Hernes E, Berg JP, Hestvik UE, Robsahm TE. Br J Cancer. 2009 Feb 10;100(3):450-4. Epub 2009 Jan 20. PMID: 19156140 doi:10.1038/sj.bjc.6604865 The serum level of 25(OH)D may be involved in disease progression and is a potential marker of prognosis in patients with prostate cancer.

Prospective study of predictors of vitamin D status and survival in patients with colorectal cancer K Ng, B M Wolpin, J A Meyerhardt, K Wu, A T Chan, B W Hollis, E L Giovannucci, M J Stampfer, W C Willett and C S Fuchs Br J Cancer 101: 916-923; advance online publication, August 18, 2009; doi:10.1038/sj.bjc.6605262

Vitamin D fortification as public health policy: significant improvement in vitamin D status in young Finnish men. Laaksi IT, Ruohola JP, Ylikomi TJ, Auvinen A, Haataja RI, Pihlajamäki HK, Tuohimaa PJ. Eur J Clin Nutr. 2006 Aug;60(8):1035-8. Epub 2006 Feb 15. PMID: 16482069

Association between serum 25-hydroxyvitamin D and depressive symptoms in Japanese: analysis by survey season A Nanri, T Mizoue, Y Matsushita, K Poudel-Tandukar, M Sato, M Ohta, N Mishima European Journal of Clinical Nutrition (19 August 2009) doi:10.1038/ejcn.2009.96 Short Communication

Towards an adequate intake of vitamin D. An advisory report of the Health Council of the Netherlands R M Weggemans, G Schaafsma and D Kromhout Eur J Clin Nutr advance online publication, July 22, 2009; doi:10.1038/ejcn.2009.67

Diagnosis and treatment of vitamin D deficiency. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Expert Opin Pharmacother. 2008 Jan;9(1):107-18. PMID: 18076342 DOI 10.1517/14656566.9.1.107

Genetic and non-genetic correlates of vitamins K and D.\nShea MK, Benjamin EJ, Dupuis J, Massaro JM, Jacques PF, D'Agostino RB Sr, Ordovas JM, O'Donnell CJ, Dawson-Hughes B, Vasan RS, Booth SL.\nEur J Clin Nutr. 2007 Nov 21. [Epub ahead of print]\nPMID: 18030310 \ndoi: 10.1038/sj.ejcn\n\n

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 -

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]

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

Woo TC, Choo R, Jamieson M, Chander S, Vieth R. Pilot study: potential role of vitamin D (Cholecalciferol) in patients with PSA relapse after definitive therapy.Nutr Cancer. 2005;51(1):32-6.PMID: 15749627 [PubMed - indexed for MEDLINE]

Diagnosis and treatment of vitamin D deficiency. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Expert Opin Pharmacother. 2008 Jan;9(1):107-18. PMID: 18076342 The recent discovery - in a randomised, controlled trial - that daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period dramatically reduced the incidence of non-skin cancers makes it difficult to overstate the potential medical, social and economic implications of treating vitamin D deficiency. Not only are such deficiencies common, probably the rule, vitamin D deficiency stands implicated in a host of diseases other than cancer. The metabolic product of vitamin D is a potent, pleiotropic, repair and maintenance, secosteroid hormone that targets > 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. A common misconception is that government agencies designed present intake recommendations to prevent or treat vitamin D deficiency. They did not. Instead, they are guidelines to prevent particular metabolic bone diseases. Official recommendations were never designed and are not effective in preventing or treating vitamin D deficiency and in no way limit the freedom of the physician - or responsibility - to do so. At this time, assessing serum 25-hydroxy-vitamin D is the only way to make the diagnosis and to assure that treatment is adequate and safe. The authors believe that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich environment, that is, > 40 ng/ml, year around. Three treatment modalities exist: sunlight, artificial ultraviolet B radiation or supplementation. All treatment modalities have their potential risks and benefits. Benefits of all treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As a prolonged 'vitamin D winter', centred on the winter solstice, occurs at many temperate latitudes, ≤ 5000 IU (125 μg) of vitamin D/d

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.

High-dose vitamin D3 supplementation in a cohort of breastfeeding mothers and their infants: a 6-month follow-up pilot study. Wagner CL, Hulsey TC, Fanning D, Ebeling M, Hollis BW. Breastfeed Med. 2006 Summer;1(2):59-70. PMID: 17661565 doi:10.1089/bfm.2006.1.59. Objective: To examine the effect of high-dose maternal vitamin D3 (vitD) supplementation on the nutritional vitD status of breastfeeding (BF) women and their infants compared with maternal and infant controls receiving 400 and 300 IU vitD/day, respectively. Design: Fully lactating women (n = 19) were enrolled at 1-month postpartum into a randomized- control pilot trial. Each mother received one of two treatments for a 6-month study period: 0 or 6000 IU vitD3 plus a prenatal vitamin containing 400 IU vitD3. The infants of mothers assigned to the control group received 300 IU vitD3/day; those infants of mothers in the high-dose group received 0 IU (placebo). Maternal serum and milk vitD and 25(OH)D were measured at baseline then monthly; infant serum vitD and 25(OH)D were measured at baseline, and months 4 and 7. Urinary calcium/creatinine ratios were measured monthly in both mothers and infants. Dietary and BF history and outdoor activity questionnaires were completed at each visit. Changes in skin pigmentation were measured by spectrophotometry. Data were analyzed using chi-square, t-test, and analysis of variance (ANOVA) on an intent-to-treat basis. Conclusion: With limited sun exposure, an intake of 400 IU/day vitamin D3 did not sustain circulating maternal 25(OH)D levels, and thus, supplied only extremely limited amounts of vitamin D to the nursing infant via breast milk. Infant levels achieved exclusively through maternal supplementation were equivalent to levels in infants who received oral vitamin D supplementation. Thus, a maternal intake of 6400 IU/day vitamin D elevated circulating 25(OH)D in both mother and nursing infant.