Clinical Responses to a Mega-dose of Vitamin D3 in Infants and Toddlers With Vitamin D Deficiency Rickets. Soliman AT, El-Dabbagh M, Adel A, Ali MA, Aziz Bedair EM, Elalaily RK. J Trop Pediatr. 2009 Jun 8. [Epub ahead of print] PMID: 19506025 doi:10.1093/tropej/fmp040 Conclusion: An IM injection of a mega dose of cholecalciferol is a safe and effective therapy for treatment of VDD rickets in infants and toddlers with normalization of all the biochemical parameters and healing of radiological manifestations. Measurement of serum 25(OH)D level is highly recommended in all short children with a clear need for a general vitamin D supplementation for all infants and young children in Qatar.

Vitamin D: the alternative hypothesis. Albert PJ, Proal AD, Marshall TG. Autoimmun Rev. 2009 Jul;8(8):639-44. Epub 2009 Feb 12. Review. PMID: 19393200 Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D's ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that may influence disease progression, proliferate over the long-term.

In conclusion, genetic variations of DBP are associated with insulin resistance in Japanese with normal glucose tolerance, which might contribute to the development of type 2 diabetes. Variations in vitamin D-binding protein (group-specific component protein) are associated with fasting plasma insulin levels in Japanese with normal glucose tolerance. Hirai M, Suzuki S, Hinokio Y, Hirai A, Chiba M, Akai H, Suzuki C, Toyota T. J Clin Endocrinol Metab. 2000 May;85(5):1951-3. PMID: 10843180

Vitamin D Binding Protein-Macrophage Activating Factor (DBP-maf) Inhibits Angiogenesis and Tumor Growth in Mice Vitamin D binding protein-macrophage activating factor (DBP-maf) inhibits angiogenesis and tumor growth in mice. Kisker O, Onizuka S, Becker CM, Fannon M, Flynn E, D'Amato R, Zetter B, Folkman J, Ray R, Swamy N, Pirie-Shepherd S. Neoplasia. 2003 Jan-Feb;5(1):32-40. PMID: 12659668 Taken together, these data suggest that DBP-maf is an antiangiogenic molecule that can act directly on endothelium as well as stimulate macrophages to attack both the endothelial and tumor cell compartment of a growing malignancy.

Also known as group specific protein (Gc), vitamin D binding protein (VDBP) is a 52Kda protein that binds monomeric actin in addition to vitamin D. The protein is 458 residues in length (Cooke, 1986), and forms three domains, the first of which contains the sterol binding site

BACKGROUND: To determine the effect of vitamin D binding protein (DBP) genotypes on 25-hydroxyvitamin D [25(OH)D] changes with vitamin D supplements, we studied 98 adults receiving 600 or 4000 IU/d vitamin D(3) for one year. METHODS: The DBP functional variant, T436K, was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). RESULTS: Mean 25(OH)D increases were 97% for TT (n=48), 151% for TK (n=31) and 307% (n=6) for KK genotypes (p=.004). CONCLUSIONS: As with baseline 25(OH)D, T436K genotype predicts 25(OH)D changes after long-term vitamin D supplementation. Common genetic variants of the vitamin D binding protein (DBP) predict differences in response of serum 25-hydroxyvitamin D [25(OH)D] to vitamin D supplementation. Fu L, Yun F, Oczak M, Wong BY, Vieth R, Cole DE. Clin Biochem. 2009 Jul;42(10-11):1174-7. Epub 2009 Mar 18. PMID: 19302999

Alhainen veren D-vitamiinitaso liittyy sydän- ja verisuonitaudin aiheuttamiin kuolemiin, kirjoittaa Archives of Internal Medicine-lehti. Uudet tutkimustulokset ovat vakuuttaneet lääkärit siitä, että 50-60 prosenttia pohjoisamerikkalaisista ja koko maapallon vanhuksista kärsii D-vitamiinipuutoksesta. Tutkimuksen taustatieto antaa viitteitä siitä, että myös nuorempien ikäluokkien D-vitamiinin saanti on liian vähäistä. D-vitamiinin "varastomuotoa", 25-hydroksivitamiinia esiintyi tutkittavien veressa 20-30 nanogrammaa vähemmän millilitrassa. D-vitamiinilla on laajat vaikutukset terveyteen. D-vitamiinipuutos voi johtaa muun muassa kaatumisiin, luiden murtumiin, syöpään, munuaisen toimintahäiriöihin, sydän- ja verisuonitauteihin sekä kohonneeseen verenpaineeseen.

Tuoreen tutkimuksen mukaan D-vitamiini voi toimia apuna taistelussa flunssaa vastaan, erityisesti astmapotilaille.

sunnuntai, lokakuu 19, 2008\nSuomessa oli huono kesä - pitäisikö olla huolestunut D-vitamiinin riittävyydestä?\n*\nKirjoitettu 25.9.2008. Tätä kirjoitusta kommentoidaan vilkkaasti ja asiantuntevasti! Jo 61 kommenttia 19.10.2008. Sano sinäkin mielipiteesi D-vitamiinista! Ystäväni Christel Lamberg-Allardt on valittu Valtion ravitsemusneuvottelukunnan asiantuntijajäseneksi (Osteoporoosiliitto). Uskoisin D-vitamiiniasian tarkentumiseen, ehkä jopa D-vitamiinisuositusten nostamiseen. \n\nMatti Narkia tarjoaa hienon vinkin englanninkielen taitoisille: Lukekaa tohtori John Cannellin uutiskirjeitä D-vitamiinista. Viimeisin löytyy tästä. Koko portaali on erittäin mielenkiintoinen! Kiitos vihjeestä.

The calcitriol receptor, also known as the vitamin D receptor (VDR) and also known as NR1I1 (nuclear receptor subfamily 1, group I, member 1), is a member of the nuclear receptor family of transcription factors.[1] Upon activation by vitamin D, the VDR forms a heterodimer with the retinoid-X receptor and binds to hormone response elements on DNA resulting in expression or transrepression of specific geneproducts. In humans, the vitamin D receptor is encoded by the VDR gene.[2]

The vitamin D3 receptor (VDR) is an intracellular hormone receptor that specifically binds the active form of vitamin D (1,25-dihydroxyvitamin D3 or calcitriol) and interacts with target-cell nuclei to produce a variety of biologic effects

Conclusion The data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury. Froicu M, Cantorna MT. BMC Immunol. 2007 Mar 30;8:5. PMID: 17397543 doi:10.1186/1471-2172-8-5

Robert P. Heaney is John A. Creighton University Professor, Creighton University, Omaha, Nebraska, United States. Hominid evolution took place in an environment (equatorial East Africa) that provided a superabundance of both calcium and vitamin D, the first in available foods and the second through conversion of 7-dehydrocholesterol to pre-vitamin D in the skin, a reaction catalysed by the intense solar ultraviolet (UV) radiation. Seemingly as a consequence, the evolving human physiology incorporated provisions to prevent the potential of toxic excesses of both nutrients. For vitamin D the protection was of two sorts: skin pigmentation absorbed the critical UV wavelengths and thereby limited dermal synthesis of cholecalciferol; and slow delivery of vitamin D from the skin into the bloodstream left surplus vitamin in the skin, where continuing sun exposure led to its photolytic degradation to inert compounds. For calcium, the adaptation consisted of very inefficient calcium absorption, together with poor to absent systemic conservation. The latter is reflected in unregulated dermal calcium losses, a high sensitivity of renal obligatory calcium loss to other nutrients in the diet and relatively high quantities of calcium in the digestive secretions. Today, chimpanzees in the original hominid habitat have diets with calcium nutrient densities in the range of 2 to 2.5 mmol per 100 kcal, and hunter-gatherer humans in Africa, South America and New Guinea still have diets very nearly as high in calcium (1.75 to 2 mmol per 100 kcal) (Eaton and Nelson, 1991). With energy expenditure of 3 000 kcal per day (a fairly conservative estimate for a contemporary human doing physical work), such diets would provide substantially in excess of 50 mmol of calcium per day. By contrast, median intake in women in North America and in many European countries today is under 15 mmol per day. Two factors altered the primitive situation: the migration of humans from Africa to higher latitude

Evidence from clinical trials shows, with a wide margin of confidence, that a prolonged intake of 10,000IU/d of vitamin D3 poses no risk of adverse effects for adults, even if this is added to a rather high physiologic background level of vitamin D. Vitamin D and cancer mini-symposium: the risk of additional vitamin D. Vieth R.\nAnn Epidemiol. 2009 Jul;19(7):441-5. Epub 2009 Apr 11. PMID: 19364661 doi:10.1016/j.annepidem.2009.01.009

What is VITAL? The VITamin D and OmegA-3 TriaL (VITAL) is a research study in 20,000 U.S. men and women investigating whether taking daily dietary supplements of vitamin D (about 2000 IU) or fish oil (about 1 gram of omega-3 fatty acids) reduces the risk of developing cancer, heart disease, and stroke in people who do not have a prior history of these illnesses. Recruitment for the study will begin in January 2010.

Upper levels of vitamin D intake were set at 50 microg/d (2000 IU/d) for all ages. Some individuals would require higher levels than these to achieve serum 25-hydroxyvitamin D concentrations for optimal calcium absorption. So much new information on vitamin D and health has been collected since the requirements were set in 1997 that this nutrient is likely the most in need of revised requirements. Vitamin D requirements: current and future. Weaver CM, Fleet JC. Am J Clin Nutr. 2004 Dec;80(6 Suppl):1735S-9S. Review. Erratum in: Am J Clin Nutr. 2005 Mar;81(3):729. PMID: 15585797

M. F. Holick Vitamin D Deficiency: What a Pain It Is Mayo Clin. Proc., December 1, 2003; 78(12): 1457 - 1459.

Vitamin D related articles in "The Heart Scan Blog" by Dr. William Davis

Together, the earlier data and the data of Heaney et al indicate that an oral dose of vitamin D2 or vitamin D3 would lead to a comparable increase in circulating 25(OH)D concentrations in children and adults when the initial 25(OH)D3 concentrations in the groups are similar and when equivalent oral vitamin D doses expressed per kilogram body weight/d are given. Serum 25-hydroxyvitamin D response to oral vitamin D intake in children. Zittermann A. Am J Clin Nutr. 2003 Sep;78(3):496-7. PMID: 12936937