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Vitamin D deficiency is now recognized as a pandemic. The major cause of vitamin D deficiency is the lack of appreciation that sun exposure in moderation is the major source of vitamin D for most humans. Very few foods naturally contain vitamin D, and foods that are fortified with vitamin D are often inadequate to satisfy either a child's or an adult's vitamin D requirement. Vitamin D deficiency causes rickets in children and will precipitate and exacerbate osteopenia, osteoporosis, and fractures in adults. Vitamin D deficiency has been associated with increased risk of common cancers, autoimmune diseases, hypertension, and infectious diseases. A circulating level of 25-hydroxyvitamin D of >75 nmol/L, or 30 ng/mL, is required to maximize vitamin D's beneficial effects for health. In the absence of adequate sun exposure, at least 800-1000 IU vitamin D3/d may be needed to achieve this in children and adults. Vitamin D2 may be equally effective for maintaining circulating concentrations of 25-hydroxyvitamin D when given in physiologic concentrations.
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PMID:Vitamin D deficiency: a worldwide problem with health consequences. 1840 Jul 38

Vitamin D is known for its role in calcium homeostasis for optimal skeletal health. It was previously believed that only elderly or hospitalized patients were at risk for vitamin D insufficiency, but many people in the general US population have insufficient levels of 25-hydroxyvitamin D (25D). According to the Third National Health and Nutrition Examination Survey, 61% of white and 91% of black Americans suffer from vitamin D insufficiency (25D < 32 ng/mL). Recent studies have demonstrated that a minimum 25(OH)D level of 32 ng/mL is necessary for optimal protection from fracture and intestinal absorption of calcium. Recently, vitamin D has been recognized as important for extraskeletal functions such as immune function, cancer prevention, and hypertension prevention. We review the role of vitamin D in skeletal health and present data on vitamin D in other extraskeletal diseases, with special emphasis on the rheumatology patient.
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PMID:Calcium and vitamin D: skeletal and extraskeletal health. 1846 Feb 65

Vitamin D functions in the body through both an endocrine mechanism (regulation of calcium absorption) and an autocrine mechanism (facilitation of gene expression). The former acts through circulating calcitriol, whereas the latter, which accounts for more than 80% of the metabolic utilization of the vitamin each day, produces, uses, and degrades calcitriol exclusively intracellularly. In patients with end-stage kidney disease, the endocrine mechanism is effectively disabled; however, the autocrine mechanism is able to function normally so long as the patient has adequate serum levels of 25(OH)D, on which its function is absolutely dependent. For this reason, calcitriol and its analogs do not constitute adequate replacement in managing vitamin D needs of such patients. Optimal serum 25(OH)D levels are greater than 32 ng/mL (80 nmol/L). The consequences of low 25(OH)D status include increased risk of various chronic diseases, ranging from hypertension to diabetes to cancer. The safest and most economical way to ensure adequate vitamin D status is to use oral dosing of native vitamin D. (Both daily and intermittent regimens work well.) Serum 25(OH)D can be expected to rise by about 1 ng/mL (2.5 nmol/L) for every 100 IU of additional vitamin D each day. Recent data indicate that cholecalciferol (vitamin D(3)) is substantially more potent than ergocalciferol (vitamin D(2)) and that the safe upper intake level for vitamin D(3) is 10,000 IU/d.
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PMID:Vitamin D in health and disease. 1852 6

Experimental and epidemiological studies suggest that calcium and vitamin D supplements may lower blood pressure. We examined the effect of calcium plus vitamin D supplementation on blood pressure and the incidence of hypertension in postmenopausal women. The Women's Health Initiative Calcium/Vitamin D Trial randomly assigned 36 282 postmenopausal women to receive 1000 mg of elemental calcium plus 400 IU of vitamin D3 daily or placebo in a double-blind fashion. Change in blood pressure and the incidence of hypertension were ascertained. Over a median follow-up time of 7 years, there was no significant difference in the mean change over time in systolic blood pressure (0.22 mm Hg; 95% CI: -0.05 to 0.49 mm Hg) and diastolic blood pressure (0.11 mm Hg; 95% CI: -0.04 to 0.27 mm Hg) between the active and placebo treatment groups. This null result was robust in analyses accounting for nonadherence to study pills and in baseline subgroups of interest, including black subjects and women with hypertension or high levels of blood pressure, with low intakes of calcium and vitamin D or low serum levels of vitamin D. In 17 122 nonhypertensive participants at baseline, the hazard ratio for incident hypertension associated with calcium/vitamin D treatment was 1.01 (95% CI: 0.96 to 1.06.) In postmenopausal women, calcium plus vitamin D3 supplementation did not reduce either blood pressure or the risk of developing hypertension over 7 years of follow-up.
Hypertension 2008 Nov
PMID:Effect of calcium and vitamin D supplementation on blood pressure: the Women's Health Initiative Randomized Trial. 1882 61

Vitamin D deficiency is a highly prevalent condition, present in approximately 30% to 50% of the general population. A growing body of data suggests that low 25-hydroxyvitamin D levels may adversely affect cardiovascular health. Vitamin D deficiency activates the renin-angiotensin-aldosterone system and can predispose to hypertension and left ventricular hypertrophy. Additionally, vitamin D deficiency causes an increase in parathyroid hormone, which increases insulin resistance and is associated with diabetes, hypertension, inflammation, and increased cardiovascular risk. Epidemiologic studies have associated low 25-hydroxyvitamin D levels with coronary risk factors and adverse cardiovascular outcomes. Vitamin D supplementation is simple, safe, and inexpensive. Large randomized controlled trials are needed to firmly establish the relevance of vitamin D status to cardiovascular health. In the meanwhile, monitoring serum 25-hydroxyvitamin D levels and correction of vitamin D deficiency is indicated for optimization of musculoskeletal and general health.
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PMID:Vitamin D deficiency an important, common, and easily treatable cardiovascular risk factor? 1946 Jun 20

Vitamin D has a positive impact on our overall health. Also there are a few conditions with strong evidence for a protective effect of vitamin D, such as bone diseases, internal cancers, multiple sclerosis, hypertension and DM type 1. Skin is the major source of vitamin D through the action of UVB light on keratinocytes, although the biologically active form of vitamin D is not exclusively produced in the kidney but also in prostate, colon, skin and osteoblast where it acts as an autocrine or paracrine hormone. In the past decade raising incidence of skin cancers, especially melanoma and its connection with sun exposure lead to a sun protection policies and practices as part of the public health campaigns. The question is how much solar UV exposure is adequate to maintain the balance between the risk and the benefit. We as dermatologists have to raise public awareness of the potential health effects from excessive exposure to UV radiation but also we have to be aware that adequate blood level of vitamin D is necessary for optimal health. So future recommendation on sun protection have to balance between the risk and benefits of sun exposure, as well as to promote vitamin D supplementation as a safe alternatives in high risk population.
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PMID:Vitamin D--the true and the false about vitamin D. 1913 20

Extrarenal calcifications, particularly affecting the cardiovascular system, are common observations which can be a source of serious complications in patients with chronic renal disease, especially those on dialysis. In these patients, cardiovascular disease - myocardial infarction, arrhythmia, calcified valvulopathy, stroke, peripheral ischemic arteriopathy, calciphylaxy, etc. - is the leading cause of death (more than 50%). These complications are closely related to the presence of vascular calcifications (VC) which are much more frequent, severe, and progressive than in the general population. Previously, these calcifications were considered to arise via a passive process within the context of comorbid conditions without specific signs of gravity: high blood pressure, atherosclerosis, aging, diabetes, smoking, dyslipidemia, chronic micro-inflammation, hyperhomocysteinemia, disorders of calcium-phosphorus metabolism. It is now established that VC arise via a complex, probably regulated, active process analogous to the processes leading to bone formation and/or remodeling. New insight provided by a large body of work designed to ascertain the mechanisms underlying the onset of VC has enabled the development of new diagnostic and therapeutic approaches. It is now possible to identify factors clearly favoring the formation of VC: TNF-alpha (which stimulates cell necrosis/apoptosis), CRP, oxidized lipids, AGEs, leptin, inorganic phosphate, high calcium-phosphorus product (CaxPO(4)), calcium, 1,25-OH(2)D(3) and Vitamin D(3), PTHrP (via an intracrine pathway), cyclic AMP, TGF-beta, bone morphogenic protein 2 (BMP2) and factors protective against the formation of VC: magnesium, HDL, inorganic pyrophosphate, albumin, ahsg/fetuin A, osteopontin (OPN), osteoprotegerin (OPG), osteonectin (ON), bone morphogenic protein 7 (BMP7), klotho, PTHrP (via a paracrine pathway), matrix gla protein (MGP), PTH (via Msx2) and vitamin K. In conclusion, until recently, neglected disorders of calcium-phosphorus metabolism are currently recognized as the main actors in the process leading to vascular mediacalcosis in patients with chronic kidney failure.
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PMID:[Origin of the mediacalcosis in kidney failure]. 1934 26

It is the purpose of this comprehensive report to outline a revolutionary strategy to prevent vitamin D deficiency in our nation. Vitamin D is a unique vitamin. Its metabolic product, calcitriol, is a profound secosteroid hormone that has impact on over 1000 genes in the human body. Recent clinical research has implicated vitamin D deficiency as a major factor in the etiology of rickets, a wide variety of cancers, as well as hypertension, stroke, heart attack, diabetes, bone fractures, periodontal disease, and even multiple sclerosis. There are two forms of vitamin D utilized in the human body: D2 and D3. Measurement of 25(OH)D is the most reliable method of detecting vitamin D deficiency. Several methods, including high-performance liquid chromatography (HPLC), chemoluminescence, and radioimmunoassay (RIA), have been developed for the measurement of total 25(OH)D levels. Prevention and treatment of vitamin D deficiency is accomplished by regulated sun exposure as well as vitamin D, supplementation. This information describing our plan to prevent vitamin D deficiency in the patients and employees of Legacy Health System is a landmark accomplishment that should be replicated in every healthcare setting in our country to prevent vitamin D deficiency.
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PMID:Modern concepts in the diagnosis and treatment of vitamin D deficiency and its clinical consequences. 1939 50

Recent studies using genetically modified mice, such as FGF23-/- and Klotho-/- mice that exhibit altered mineral homeostasis due to a high vitamin D activity showed features of premature aging that include retarded growth, osteoporosis, atherosclerosis, ectopic calcification, immunological deficiency, skin and general organ atrophy, hypogonadism and short lifespan. The phenotype reversed by normalizing vitamin D and/or mineral homeostasis. Thus, hypervitaminosis D due to an increased 1alpha-hydroxylase activity seems to be a cause of the premature aging. In several studies, we have described that a complete or partial lack of vitamin D action (VDR-/- mice and CYP27B1-/-) show almost similar phenotype as FGF23-/- or Klotho-/- mice. VDR mutant mice have growth retardation, osteoporosis, kyphosis, skin thickening and wrinkling, alopecia, ectopic calcification, progressive loss of hearing and balance as well as short lifespan. CYP27B1-/- mice do not show alopecia nor balance deficit, which might be apoVDR-dependent or calcidiol-dependent. The features are typical to premature aging. The phenotype is resistant to a normalization of the mineral homeostasis by a rescue diet containing high calcium and phosphate. Taken together, aging shows a U-shaped dependency on hormonal forms of vitamin D suggesting that there is an optimal concentration of vitamin D in delaying aging phenomena. Our recent study shows that calcidiol is an active hormone. Since serum calcidiol but not calcitriol is fluctuating in physiological situations, calcidiol might determine the biological output of vitamin D action. Due to its high serum concentration and better uptake of calcidiol-DBP by the target cells through the cubilin-megalin system, calcidiol seems to be an important circulating hormone. Therefore, serum calcidiol might be associated with an increased risk of aging-related chronic diseases more directly than calcitriol. Aging and cancer seem to be tightly associated phenomena. Accumulation of damage on DNA and telomeres cause both aging and cancer, moreover the signalling pathways seem to converge on tumour suppressor protein, p53, which seems to be regulated by vitamin D. Also, the insulin-like growth factor signalling pathway (IGF-1, IGFBPs, IGFR) and fibroblast growth factor-23 (FGF-23) regulate growth, aging and cancer. Vitamin D can regulate these signalling pathways, too. Also NF-kappaB and telomerase reverse transcriptase (TERT) might be molecular mechanisms mediating vitamin D action in aging and cancer. Calcidiol serum concentrations show a U-shaped risk of prostate cancer suggesting an optimal serum concentration of 40-60 nmol/L for the lowest cancer risk. Therefore, it is necessary to study several common aging-associated diseases such as osteoporosis, hypertension and diabetes known to be vitamin D-dependent before any recommendations of an optimal serum concentration of calcidiol are given.
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PMID:Vitamin D and aging. 1944 37

Congestive heart failure is a chronic disease, whose incidence is especially growing in the subpopulation of elderly people. The majority of these patients have vitamin D levels in the insufficient range. Skin synthesis is the most important vitamin D source for humans. Congestive heart failure patients have relatively low outdoor activities. Consequently, a disease-related sedentary lifestyle is an important cause for the insufficient vitamin D status in patients. However, there is an accumulating body of evidence that vitamin D insufficiency plays a role in the etiology and pathogenesis of congestive heart failure. Vitamin D has direct effect on heart cells and indirect effect on the risk factors of the disease. Four major potential mechanisms may be important to explain the direct effects of vitamin D against congestive heart failure: the effect on myocardial contractile function, the regulation of natriuretic hormone secretion, the effect on extracellular matrix remodelling and the regulation of inflammation cytokines. It has been demonstrated that vitamin D has a high impact on congestive heart failure main risk factors as hypertension, renin-angiotensin system malfunction and atherosclerosis. In spite of the robust preclinical data only few clinical observations prove the positive effect of vitamin D on congestive heart failure.
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PMID:[The role of vitamin D in the development of cardiac failure]. 1959 34


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