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Not enough vitamin D: health consequences for Canadians. Schwalfenberg G. Can Fam Physician. 2007 May;53(5):841-54. Review PMID: 17872747 Conclusion Low levels of VTD are considered a major public health problem in Canada, especially during the winter. Those with risk factors should be screened for low 25(OH)D levels and repletion therapy instituted if needed. Researchers have estimated that the oral dose of vitamin D3 to attain and maintain 25(OH)D levels >80 nmol/L is 2200 IU/d if baseline levels are 20 to 40 nmol/L, 1800 IU/d if levels are 40 to 60 nmol/L, and 1160 IU/d if levels are between 60 and 80 nmol/L.64 We need to ensure that patients have healthy blood levels of 25(OH)D to prevent levels of parathyroid hormone from rising and to maximize absorption of calcium, magnesium, and phosphate. Positive effects on bone are marginal at best unless patients consume at least 800 IU/d of VTD. The emerging and exciting role of the VTD receptor and the actions of VTD in maintaining health in other cell types have become more apparent during the last decade.

Vitamin D's days of obscurity seem pretty much over. Once just an afterthought to most people-relegated to the sides of milk cartons and the pages of medical texts-it's now on the cusp of becoming a full-fledged disease prevention star. Although vitamin D has long been known as an important factor in bone health, a quickly growing body of evidence now shows that it may also help lower the risk of cancer, heart disease, and even premature death.[1], [2] Not surprisingly, scientists and the public have started to take note, particularly of vitamin D's potential to protect against cancer

March 11, 2009 -- Low vitamin D levels greatly increase a teenager's risk of diabetes and heart disease, Johns Hopkins researchers find. It is becoming clear that adults who get too little vitamin D are at higher risk for diabetes and heart disease. Now, it appears vitamin D levels also affect these risks earlier in life, say Johns Hopkins researchers Jared P. Reis, PhD, and colleagues.

Evidence continues to pile up that the sunshine vitamin protects against much more than bone-softening rickets. Vitamin D, also found in milk and oily fish, is becoming king, from fighting colds to preventing cancer. \n\nInvestigators at the Medical University of South Carolina shut down part of a National Institutes of Health study that left nursing mothers and infants deficient, even though the mothers received the maximum safe amount of vitamin D allowed by the Institute of Medicine.\n\nBut here's the kicker. New research suggests we're not getting nearly enough, and recommended levels may be woefully inadequate.

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

ScienceDaily (Feb. 10, 2009) - Vitamin D is significantly associated with muscle power and force in adolescent girls, according to a new study. Although vitamin D is naturally produced in the body through exposure to direct sunlight, vitamin D deficiency has become widely common in the United States. Vitamin D deficiency has been shown to have a significant negative impact on muscle and bone health, and can lead to conditions including osteoporosis and rickets.

Vitamin D deficiency is the cause of common obesity. Foss YJ. Med Hypotheses. 2009 Mar;72(3):314-21. Epub 2008 Dec 2. PMID: 19054627 doi:10.1016/j.mehy.2008.10.005 Common obesity and the metabolic syndrome may therefore result from an anomalous adaptive winter response. The stimulus for the winter response is proposed to be a fall in vitamin D. The synthesis of vitamin D is dependent upon the absorption of radiation in the ultraviolet-B range of sunlight. At ground level at mid-latitudes, UV-B radiation falls in the autumn and becomes negligible in winter. It has previously been proposed that vitamin D evolved in primitive organisms as a UV-B sensitive photoreceptor with the function of signaling changes in sunlight intensity. It is here proposed that a fall in vitamin D in the form of circulating calcidiol is the stimulus for the winter response, which consists of an accumulation of fat mass (obesity) and the induction of a winter metabolism (the metabolic syndrome). Vitamin D deficiency can account for the secular trends in the prevalence of obesity and for individual differences in its onset and severity. It may be possible to reverse the increasing prevalence of obesity by improving vitamin D status.

"The major factor which stimulates weight gain in winter months is vitamin D. Human bodies get vitamin D from sunlight; as the hours of sunlight become less with the onset of fall, so our levels of vitamin D decrease. Low levels of vitamin D affect the brain's production of the hormone leptin. Leptin plays a vital role in controlling appetite and metabolism; so as the amount of vitamin D in our bodies decreases so does the leptin, and this causes an increase in our appetite and a change in our metabolism. Researchers at Aberdeen University found that obese people had 10% less vitamin D than people of average weight. The study also found that excess body fat absorbed vitamin D so the body couldn't use it. Scientists now believe that there is a direct correlation between obesity and low levels of vitamin D.

"So why is Dr Vieth so frustrated? You might think he'd have cause for celebration. But for him and other vitamin D researchers around the world, the good news comes with a bitter aftertaste. They believe they can prove vitamin D could help millions live longer and be healthier and yet they have not been able to convince their own governments. In the US and Canada, official vitamin D policy is set by the Institute of Medicine. And in the opinion of Vieth, the current recommendations - 200 International Units per day for people under 50, 400 for people aged 51-70, and 600 for those 71 and older - are outrageously low. Bruce Hollis, professor of paediatrics at the Medical University of South Carolina, calls 400 IU a day "a joke". That's because the best research suggests that to achieve the higher vitamin D blood levels associated with disease prevention, most adults in the US would need to take 1,000-2,000 IU a day: five to 10 times more than the current official recommendation for adult In 1999, Reinhold Vieth (pictured right) published a review of vitamin D research in response to the IOM conclusions. In it, he argued that there was no evidence that amounts lower than 20,000 IU a day could be toxic. "Throughout my preparation of this review, I was amazed at the lack of evidence supporting statements about the toxicity of moderate doses of vitamin D," Vieth wrote. Studies have since shown 10,000 IU a day of vitamin D to be safe. While any substance will become toxic in excess, vitamin D researchers today accept that the current vitamin D recommendations could be more than quadrupled with no fear of toxicity.!

Table of Contents Ch. I Is calcidiol an active hormone? 1 Ch. II Vitamin D as a neurosteroid hormone : from neurobiological effects to behavior 29 Ch. III Inhibitors of vitamin D hydroxylases : mechanistic tools and therapeutic aspects 67 Ch. IV Vitamin D analogues as anti-cancer therapies 145 Ch. V Paricalcitol : a vitamin D2 analog with anticancer effects with low calcemic activity 169 Ch. VI Vitamin D use among older adults in U.S. : results form national surveys 1997 to 2002 181 Ch VII Vitamin D deficiency in migrants 199 Vitamin D is a fat-soluble steroid hormone precursor that contributes to the maintenance of normal levels of calcium and phosphorus in the bloodstream. Strictly speaking, it is not a vitamin since human skin can manufacture it, but it is referred to as one for historical reasons. It is often known as calciferol. The major biologic function of vitamin D is to maintain normal blood levels of calcium and phosphorus. Vitamin D aids in the absorption of calcium, helping to form and maintain strong bones. It promotes bone mineralisation in concert with a number of other vitamins, minerals and hormones. Without vitamin D, bones can become thin, brittle, soft or misshapen. Vitamin D prevents rickets in children and osteomalacia in adults -- skeletal diseases that result in defects that weaken bones. This book gathers international research on the leading-edge of the scientific front.

"A recent article in the New York Times highlighted an ongoing problem with the accuracy of vitamin D testing at the largest commercial clinical laboratory, Quest Diagnostics. It has become clear from shared experience among vitamin D experts, including myself, that Quest Diagnostics has a problem with seemingly random over-estimation of vitamin D levels."

Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase. Jiang F, Bao J, Li P, Nicosia SV, Bai W. J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12. PMID: 15485861 doi: 10.1074/jbc.M410395200 Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression. Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene. It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro

Small but significant breakthrough studies on people who have been able to overcome or control HIV were presented at a major world conference on ways to stem the three-decade-old disease. One study focused on a group of 12 patients in France who began treatment on antiretroviral drugs within 10 weeks of becoming infected with human immunodeficiency virus, but then stopped the therapy after nearly three years.