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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

Tufts University Confirms That Vitamin A Protects Against Vitamin D Toxicity by Curbing Excess Production of Vitamin K-Dependent Proteins Tufts University confirmed my hypothesis that vitamin A protects against vitamin D's induction of renal calcification (kidney stones) by normalizing the production of vitamin K-dependent proteins in December, 2008, without citing my hypothesis or telling me they had confirmed it. I am, of course, very grateful that they thought it significant enough to investigate.

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.

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

"Calbindin describes calcium binding proteins first described as the vitamin D-dependent calcium binding proteins in intestine and kidney."

Bioactive vitamin D or calcitriol is a steroid hormone that has long been known for its important role in regulating body levels of calcium and phosphorus, and in mineralization of bone. More recently, it has become clear that receptors for vitamin D are present in a wide variety of cells, and that this hormone has biologic effects which extend far beyond control of mineral metabolism. The active form of vitamin D binds to intracellular receptors that then function as transcription factors to modulate gene expression. Like the receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has hormone-binding and DNA-binding domains. The vitamin D receptor forms a complex with another intracellular receptor, the retinoid-X receptor, and that heterodimer is what binds to DNA. In most cases studied, the effect is to activate transcription, but situations are also known in which vitamin D suppresses transcription. Each of the forms of vitamin D is hydrophobic, and is transported in blood bound to carrier proteins. The major carrier is called, appropriately, vitamin D-binding protein. The halflife of 25-hydroxycholecalciferol is several weeks, while that of 1,25-dihydroxycholecalciferol is only a few hours. The vitamin D receptor binds several forms of cholecalciferol. Its affinity for 1,25-dihydroxycholecalciferol is roughly 1000 times that for 25-hydroxycholecalciferol, which explains their relative biological potencies

Vitamin K2 is produced by animal tissues, including the mammary glands, from vitamin K1, which occurs in rapidly growing green plants. A growing body of published research confirms Dr. Price's discoveries, namely that vitamin K2 is important for the utilization of minerals, protects against tooth decay, supports growth and development, is involved in normal reproduction, protects against calcification of the arteries leading to heart disease, and is a major component of the brain. Vitamin K2 works synergistically with the two other "fat-soluble activators" that Price studied, vitamins A and D. Vitamins A and D signal to the cells to produce certain proteins and vitamin K then activates these proteins. Vitamin K2 plays a crucial role in the development of the facial bones, and its presence in the diets of nonindustrialized peoples explains the wide facial structure and freedom from dental deformities that Weston Price observe

MedWire News: Calcitriol, the active form of vitamin D, has been found to induce the tumor-suppressing protein CCAAT enhancer-binding protein (C/EBP)α, which can inhibit the growth of breast cancer cells, researchers report.

"Vitamin D-dependent calcium binding proteins were discovered in the cytosolic fractions of chicken intestine, and later in mammalian intestine and kidney, by workers including Robert Wasserman of Cornell University. They bound calcium in the micromolar range and were greatly reduced in vitamin D-deficient animals. Expression could be induced by treating these animals with vitamin D metabolites such as calcitriol. They were found to exist in two distant sizes with a molecular weight of approximately 9 kDa and 28 kDa. They were renamed calbindin; calbindin-D9k is found in mammalian intestine and calbindin-D28k in avain intestine and in kidney."

"Defensins are small cysteine-rich cationic proteins found in both vertebrates and invertebrates. They are active against bacteria, fungi and many enveloped and nonenveloped viruses. They consist of 18-45 amino acids including six (in vertebrates) to 8 conserved cysteine residues. Cells of the immune system contain these peptides to assist in killing phagocytized bacteria, for example in neutrophil granulocytes and almost all epithelial cells. Most defensins function by binding to microbial cell membrane, and once embedded, forming pore-like membrane defects that allow efflux of essential ions and nutrients

VITAMIN D LOWERS C-REACTIVE PROTEIN (CRP) Van den Berghe and colleagues at the University of Leuven in Belgium appear to be the first to show that simple, natural and cheap vitamin D (cholecalciferol) lowers CRP in critically ill patients. Even small amounts of cholecalciferol (500 IU) lowered CRP by more than 25% in a small group of critically ill patients. Another marker of inflammation (IL-6) was reduced even more. The researchers also found that critically ill patients were profoundly deficient in vitamin D.

Vitamin D status: measurement, interpretation, and clinical application. Holick MF. Ann Epidemiol. 2009 Feb;19(2):73-8. Epub 2008 Mar 10. Review. PMID: 18329892 Conclusion The only way to determine whether a person is vitamin D deficient or sufficient is to measure their circulating level of 25(OH)D. There are a variety of assays used to measure 25(OH)D. The radioimmunoassays and competitive protein binding assays for 25(OH)D are useful in detecting vitamin D deficiency and sufficiency. However, these assays are fraught with technical difficulties, especially if they are not run routinely (Fig. 4) (33). Several reference laboratories have now switched to LC-MS ,which measures both 25(OH)D2 and 25(OH)D3 quantitatively. The total 25(OH)D, i.e., 25(OH)D2 plus 25(OH)D3, is what physicians need to be aware of for their patients. A level >30 ng/mL is

Why would vitamin D be prescribed when vitamin D3 is available over-the-counter? Let's review the known differences between vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol): --D3 is the human form; D2 is the non-human form found in plants. --Dose for dose, D3 is more effective at raising blood levels of 25-hydroxy vitamin D than D2. It requires roughly twice to 250% of the dose of D2 to match that of D3 (Trang H et al 1998). --D2 blood levels don't yield long-term sustained levels of 25-hydroxy vitamin D as does D3. When examined as a 28-day area under the curve (AUC--a superior measure of biologic exposure), D3 yields better than a 300% increased potency compared to D2. This means that it requires around 50,000 units D2 to match the effects of 15,000 units D3 (Armas LA et al 2004). --D2 has lower binding affinity for vitamin D-binding protein, compared to D3 --Mitochondrial vitamin D 25-hydroxylase converts D3 to the 25-hydroxylated form five times more rapidly than D2. --As we age, the ability to metabolize D2 is dramatically reduced, while D3 is not subject to this phenomenon

A new study has concluded that one key part of the immune system, the ability of vitamin D to regulate anti-bactericidal proteins, is so important that is has been conserved through almost 60 million years of evolution and is shared only by primates, including humans - but no other known animal species.

"Last Wednesday night I gave a lecture to my clients on hunter-gatherer diets. The turnout was great and the information was well-received. I had it professionally video-recorded and will probably offer this as a DVD for sale (with the handout included). Watch for it in the future. Part of what I discussed was vitamin D3 supplementation. Since I have been supplementing with 4,000-10,000 Units of D3 per day I have noted enhanced recovery and size response from my training. Apparently, skeletal muscle has both surface receptors and nuclear receptors for D3 that augment calcium flux during contraction (from surface receptors) and have steroid-like effects at the nuclear level WRT protein synthesis. This D3 supplementation is not really "supplementation" but is instead "augmentation" to levels that would be normal if we got normal sun exposure as we did in our evolutionary past. Check out www.vitamindcouncil.org for more information. Also, check out this abstract below for your consideration. Also, check out this article."

Vitamin D-induced up-regulation of tumour necrosis factor alpha (TNF-alpha) in prostate cancer cells. Golovko O, Nazarova N, Tuohimaa P. Life Sci. 2005 Jun 17;77(5):562-77. Epub 2005 Feb 25. PMID: 15904673 doi:10.1016/j.lfs.2004.10.072 Combined addition of human recombinant TNF-alpha with calcitriol or CB1093 cause enhanced effect in induction of apoptosis. We conclude that under physiological conditions vitamin D activates only the transcription of TNF-alpha gene, for TNF-alpha protein synthesis additional cofactors are required. Therefore a cooperation of vitamin D and TNF-alpha may play an important role in the control of cell growth in prostate cancer.

Dairy and bone health. Heaney RP. J Am Coll Nutr. 2009 Feb;28 Suppl 1:82S-90S. PMID: 19571166

Dietary acid-base balance, bone resorption, and calcium excretion. Jajoo R, Song L, Rasmussen H, Harris SS, Dawson-Hughes B. J Am Coll Nutr. 2006 Jun;25(3):224-30. PMID: 16766781 Conclusions: Diet changes that increase renal NAE are associated with increases in serum PTH, bone resorption, and calcium excretion over a 60-day period.