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Plasma calcidiol, season, and serum parathyroid hormone concentrations in healthy elderly men and women. Dawson-Hughes B, Harris SS, Dallal GE. Am J Clin Nutr. 1997 Jan;65(1):67-71. PMID: 8988915 Plasma calcidiol and serum PTH concentrations were inversely related, with PTH rising slowly as calcidiol concentrations declined below 110 nmol/L (95 CI: 60, 168 nmol/L). More than 90% of the men and women had calcidiol concentrations below this value in the wintertime. The high prevalence of lower wintertime calcidiol values may increase risk of bone loss in elderly men and women.

Defining Adequate Vitamin D Intake : Cross-sectional and Intervention Studies Viljakainen, Heli Tuulikki University of Helsinki 2008-05-23 Doctoral dissertation (article-based) Vitamin D is required for normal bone growth and maintenance of the skeleton throughout life. In Finland, like in many other Western countries, the population suffers from inadequate or deficient vitamin D status, especially during winter, which is thought to increase the risk of osteoporosis. New strategies to prevent osteoporosis are actively being sought. The main objective of this thesis was to determine whether vitamin D is feasible in the primary prevention of osteoporosis; does it affect bone mineral accrual during the growth period? A second goal was to ascertain whether seasonal variation in calcitropic hormones affects bone remodelling, and to elucidate the vitamin D intake needed to overcome this variation in different age groups. In summary, vitamin D intake remains inadequate among the target groups of this thesis, as reflected by seasonal variation in calcitropic hormones and bone metabolism. Dietary intake of vitamin D should be increased to achieve at least an adequate vitamin D status (S-25-OHD>50 nmol/l) and possibly an optimal vitamin D status (S-25-OHD>80 nmol/l) throughout the year. This could be accomplished by introducing new vitamin D-fortified foods to the market."

Vitamin D in preventive medicine: are we ignoring the evidence? Zittermann A. Br J Nutr. 2003 May;89(5):552-72. Review. PMID: 12720576 Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. Calcitriol receptors are present in more than thirty different tissues. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. In institutionalized subjects 25(OH)D levels are often in the deficiency range. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d.

Strong correlations have been noted between cardiovascular diseases and low bone density / osteoporosis-connections so strong that the presence of one type of pathology is considered a likely predictor of the other. This potentially causal relationship has led to the hypothesis that these conditions share core mechanisms. Recent advances in our understanding of the complimentary roles played by vitamin D3 and vitamin K2 in vascular and bone health provide support for this hypothesis, along with insight into key metabolic dysfunctions underlying cardiovascular disease and osteoporosis. Part I of this review summarizes current research linking vitamin D deficiency to cardiovascular disease, the physiological mechanisms underlying vitamin D's cardiovascular effects, and leading vitamin D researchers' recommendations for significantly higher supplemental doses of the pro-hormone. Part II reviews the vitamin K connection to cardiovascular disease; the ways in which vitamin D and vitamin K pair up to prevent inflammation, vascular calcification and osteoporosis; and the necessity of providing vitamin K along with vitamin D to preclude adverse effects associated with hypervitaminosis D, which include vascular and other soft tissue calcification.

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

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]

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.

Conclusion We demonstrated that the VDRE in the CAMP gene originated from the exaptation of an AluSx SINE in the lineage leading to humans, apes, OWMs and NWMs and remained under purifying selection for the last 55-60 million years. We present convincing evidence of an evolutionarily fixed, Alu-mediated divergence in steroid hormone nuclear receptor gene regulation between humans/primates and other mammals. Evolutionary selection to place the primate CAMP gene under regulation of the vitamin D pathway potentiates the innate immune response and may counter the anti-inflammatory properties of vitamin D. Exaptation of an ancient Alu short interspersed element provides a highly conserved vitamin D-mediated innate immune response in humans and primates. Gombart AF, Saito T, Koeffler HP. BMC Genomics. 2009 Jul 16;10:321. PMID: 19607716 doi:10.1186/1471-2164-10-321

Use of vitamin D in clinical practice. Cannell JJ, Hollis BW. Altern Med Rev. 2008 Mar;13(1):6-20. PMID: 18377099 The recent discovery--from a meta-analysis of 18 randomized controlled trials--that supplemental cholecalciferol (vitamin D) significantly reduces all-cause mortality emphasizes the medical, ethical, and legal implications of promptly diagnosing and adequately treating vitamin D deficiency. Not only are such deficiencies common, and probably the rule, vitamin D deficiency is implicated in most of the diseases of civilization. Vitamin D's final metabolic product is a potent, pleiotropic, repair and maintenance, seco-steroid hormone that targets more than 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. One of the most important genes vitamin D up-regulates is for cathelicidin, a naturally occurring broad-spectrum antibiotic. Natural vitamin D levels, those found in humans living in a sun-rich environment, are between 40-70 ng per ml, levels obtained by few modern humans. Assessing serum 25-hydroxy-vitamin D (25(OH)D) is the only way to make the diagnosis and to assure treatment is adequate and safe. Three treatment modalities exist for vitamin D deficiency: sunlight, artificial ultraviolet B (UVB) radiation, and vitamin D3 supplementation. Treatment of vitamin D deficiency in otherwise healthy patients with 2,000-7,000 IU vitamin D per day should be sufficient to maintain year-round 25(OH)D levels between 40-70 ng per mL. In those with serious illnesses associated with vitamin D deficiency, such as cancer, heart disease, multiple sclerosis, diabetes, autism, and a host of other illnesses, doses should be sufficient to maintain year-round 25(OH)D levels between 55 -70 ng per mL. Vitamin D-deficient patients with serious illness should not only be supplemented more aggressively than the well, they should have more frequent monitoring of serum 25(OH)D and serum calcium. Vitamin D should always be

It seems not a single day passes that I don't learn something new about this unique hormone (mis)named "vitamin D." \nFrom its humble beginnings recognized only as the factor responsible for bone maturation (with deficiency leading to childhood rickets), vitamin D now commands a recognized role in almost every conceivable aspect of health and disease. \n

"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.

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

The role of Vitamin D3 metabolism in prostate cancer. Lou YR, Qiao S, Talonpoika R, Syvälä H, Tuohimaa P. J Steroid Biochem Mol Biol. 2004 Nov;92(4):317-25. Epub 2004 Dec 19. Review. PMID: 15663995 doi:10.1016/j.jsbmb.2004.10.007 In summary, the local metabolism of hormonal Vitamin D seems to play an important role in the development and progression of prostate cancer.

The bioavailability of vitamin D from fortified cheeses and supplements is equivalent in adults. Wagner D, Sidhom G, Whiting SJ, Rousseau D, Vieth R. J Nutr. 2008 Jul;138(7):1365-71. PMID: 18567762 Compared with baseline, serum parathyroid hormone decreased with both fortification (P = 0.003) and supplementation (P = 0.012). These data demonstrate that vitamin D is equally bioavailable from fortified hard cheeses and supplements, making cheese suitable for vitamin D fortification.

Bread fortified with cholecalciferol increases the serum 25-hydroxyvitamin D concentration in women as effectively as a cholecalciferol supplement. Natri AM, Salo P, Vikstedt T, Palssa A, Huttunen M, Kärkkäinen MU, Salovaara H, Piironen V, Jakobsen J, Lamberg-Allardt CJ. J Nutr. 2006 Jan;136(1):123-7. PMID: 16365070 Both fortified breads increased serum 25-hydroxyvitamin D concentration as effectively as the cholecalciferol supplement. Supplementation or fortification did not affect serum intact parathyroid hormone concentration or urinary calcium excretion. In conclusion, fortified bread is a safe and feasible way to improve vitamin D nutrition.

"Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone. In a national study in 1010 men, to be presented Nov. 15 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando, researchers say the new findings build on previous studies showing that deficiencies in vitamin D and low levels of estrogen, found naturally in differing amounts in men and women, were independent risk factors for hardened and narrowed arteries and weakened bones. Vitamin D is an essential part to keeping the body healthy, and can be obtained from fortified foods, such as milk and cereals, and by exposure to sunlight.

"Study Shows Vitamin D Supplements May Be Useful in Preventing Heart Disease Nov. 16, 2009 (Orlando, Fla.) -- Some men with low levels of vitamin D in their blood are at particularly high risk of developing heart disease and weakened bones that can lead to osteoporosis, researchers report. In a study of more than 1,000 men, those with low levels of both vitamin D and the sex hormone estrogen were at significantly increased risk of having cardiovascular disease, says study head Erin Michos, MD, a cardiologist at Johns Hopkins. "They were also at dramatically increased risk of osteopenia," or bone loss that can lead to osteoporosis, she says. "Our results suggest that vitamin D supplements, which are already prescribed to treat osteoporosis, may also be useful in preventing heart disease," Michos tells WebMD. Men with low levels of vitamin D and testosterone, on the other hand, were not at heightened risk for heart disease or osteopenia."

"Vitamin D is not just a sun-derived vitamin, but is a crucial steroid precursor that is transformed into one of the most potent hormones in the human body for strength, power, lung function and regulating gene expression in every organ system. Athletes need Vitamin D. Dr. Cannell has written quite extensively about the role of vitamin D in athletes"

A phase 2 trial exploring the effects of high-dose (10,000 IU/day) vitamin D(3) in breast cancer patients with bone metastases. Amir E, Simmons CE, Freedman OC, Dranitsaris G, Cole DE, Vieth R, Ooi WS, Clemons M. Cancer. 2009 Nov 13. [Epub ahead of print] PMID: 19918922 DOI: 10.1002/cncr.24749 METHODS: Patients with bone metastases treated with bisphosphonates were enrolled into this single-arm phase 2 study. Patients received 10,000 IU of vitamin D3 and 1000 mg of calcium supplementation each day for 4 months. The effect of this treatment on palliation, bone resorption markers, calcium metabolism, and toxicity were evaluated at baseline and monthly thereafter. CONCLUSIONS: Daily doses of 10,000 IU vitamin D3 for 4 months appear safe in patients without comorbid conditions causing hypersensitivity to vitamin D. Treatment reduced inappropriately elevated parathyroid hormone levels, presumably caused by long-term bisphosphonate use. There did not appear to be a significant palliative benefit nor any significant change in bone resorption. Cancer 2010. © 2009 American Cancer Society.