Group items tagged

Pharmacokinetics of a single, large dose of cholecalciferol. Ilahi M, Armas LA, Heaney RP. Am J Clin Nutr. 2008 Mar;87(3):688-91. PMID: 1832660 Conclusions: Cholecalciferol (100 000 IU) is a safe, effective, and simple way to increase calcidiol concentrations. The dosing interval should be ≤2 mo to ensure continuous serum calcidiol concentrations above baseline. Our study highlights that 100 000 IU cholecalciferol is a safe, efficient, and cost-effective means to increase calcidiol concentrations in the elderly. From this study we can safely recommend 100 000 IU cholecalciferol dosed every 2 mo in persons with moderate baseline calcidiol concentrations. However, in those persons with baseline calcidiol concentrations < 20 ng/mL, even this large dose will not adequately raise their calcidiol concentrations.

Vitamin D, aging, and cancer. Tuohimaa P. Nutr Rev. 2008 Oct;66(10 Suppl 2):S147-52. Review. PMID: 18844842 DOI: 10.1111/j.1753-4887.2008.00095.x Deficiency of the prohormone calcidiol (25OH vitamin D3) seems to be associated with several aging-related chronic diseases including cancer. Our results suggest that calcidiol is mainly responsible for differentiation homeostasis, whereas calcitriol might be more involved in calcium homeostasis. Therefore, an imbalance of calcidiol rather than calcitriol is a risk factor for cancer and chronic diseases. Calcidiol insufficiency, as well as insufficient solar exposure, is associated with increased risk of several solid cancers. Both a vitamin D3 deficiency and a high concentration of calcidiol may increase cancer risk. Similarly, aging phenomena show a U-shaped association with vitamin D bioactivity. Therefore, the chronic diseases and cancers related to aging might be prevented by an optimal concentration of serum calcidiol, which remains to be determined.

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.

Vitamin D, nervous system and aging. P. Tuohimaa, T. Keisala, A. Minasyan, J. Cachat and A. Kalueff. . Psychoneuroendocrinology, Volume 34, Supplement 1, December 2009, Pages S278-S286 NEUROACTIVE STEROIDS: EFFECTS AND MECHANISMS OF ACTION doi:10.1016/j.psyneuen.2009.07.003 This is a mini-review of vitamin D3, its active metabolites and their functioning in the central nervous system (CNS), especially in relation to nervous system pathologies and aging. The vitamin D3 endocrine system consists of 3 active calcipherol hormones: calcidiol (25OHD3), 1α-calcitriol (1α,25(OH)2D3) and 24-calcitriol (24,25(OH)2D3). The impact of the calcipherol hormone system on aging, health and disease is discussed. Low serum calcidiol concentrations are associated with an increased risk of several chronic diseases including osteoporosis, cancer, diabetes, autoimmune disorders, hypertension, atherosclerosis and muscle weakness all of which can be considered aging-related diseases. The relationship of many of these diseases and aging-related changes in physiology show a U-shaped response curve to serum calcidiol concentrations. Clinical data suggest that vitamin D3 insufficiency is associated with an increased risk of several CNS diseases, including multiple sclerosis, Alzheimer's and Parkinson's disease, seasonal affective disorder and schizophrenia. In line with this, recent animal and human studies suggest that vitamin D insufficiency is associated with abnormal development and functioning of the CNS. Overall, imbalances in the calcipherol system appear to cause abnormal function, including premature aging, of the CNS.

Calcidiol and prostate cancer. Tuohimaa P, Golovko O, Kalueff A, Nazarova N, Qiao S, Syvälä H, Talonpoika R, Lou YR. J Steroid Biochem Mol Biol. 2005 Feb;93(2-5):183-90. Epub 2005 Jan 22. Review. PMID: 15860261

Heliotherapy improves vitamin D balance and atopic dermatitis. Vähävihu K, Ylianttila L, Salmelin R, Lamberg-Allardt C, Viljakainen H, Tuohimaa P, Reunala T, Snellman E. Br J Dermatol. 2008 Jun;158(6):1323-8. Epub 2008 Mar 20. PMID: 18363748 DOI: 10.1111/j.1365-2133.2008.08518.x CONCLUSIONS: A 2-week course of HT significantly improved vitamin D balance by increasing serum calcidiol concentration, and caused a marked healing of AD. These parallel positive responses should be taken into account when the benefits of HT are considered..

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.

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.

"Hypovitaminosis D is a deficiency of Vitamin D. It can result from: inadequate intake coupled with inadequate sunlight exposure (in particular sunlight with adequate ultra violet B rays), disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.[1] Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and contributes to osteoporosis.[1] Osteomalacia may also occur rarely as a side-effect of phenytoin use Hypovitaminosis D is typically diagnosed by measuring the concentration in blood of the compound 25-hydroxyvitamin D (calcidiol), which is a precursor to the active form 1,25-dihydroxyvitamin D (calcitriol).[6] One recent review has proposed the following four categories for hypovitaminosis D:[7] * Insufficient 50-100 nmol/L (20-40 ng/mL) * Mild 25-50 nmol/L (10-20 ng/mL) * Moderate 12.5-25.0 nmol/L (5-10 ng/mL) * Severe < 12.5 nmol/L (< 5 ng/mL) Note that 1.0 nmol/L = 0.4 ng/mL for this compound.[8] Other authors have suggested that a 25-hydroxyvitamin D level of 75-80 nmol/L (30-32 ng/mL) may be sufficient

Long-term effects of giving nursing home residents bread fortified with 125 {micro}g (5000 IU) vitamin D3 per daily serving. Mocanu V, Stitt PA, Costan AR, Voroniuc O, Zbranca E, Luca V, Vieth R. Am J Clin Nutr. 2009 Feb 25. [Epub ahead of print] PMID: 19244376

Why "Vitamin D" is not a hormone, and not a synonym for 1,25-dihydroxy-vitamin D, its analogs or deltanoids. Vieth R. J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):571-3. PMID: 15225841 doi:10.1016/j.jsbmb.2004.03.037

A nested case control study of plasma 25-hydroxyvitamin D concentrations and risk of colorectal cancer. Wu K, Feskanich D, Fuchs CS, Willett WC, Hollis BW, Giovannucci EL. J Natl Cancer Inst. 2007 Jul 18;99(14):1120-9. Epub 2007 Jul 10. PMID: 17623801

Dose response to vitamin D supplementation among postmenopausal African American women.\nTalwar SA, Aloia JF, Pollack S, Yeh JK.\nAm J Clin Nutr. 2007 Dec;86(6):1657-62.\nPMID: 18065583

Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease.\nEvatt ML, Delong MR, Khazai N, Rosen A, Triche S, Tangpricha V.\nArch Neurol. 2008 Oct;65(10):1348-52.\nPMID: 18852350

Vitamin D and prevention of colorectal adenoma: a meta-analysis.\nWei MY, Garland CF, Gorham ED, Mohr SB, Giovannucci E.\nCancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):2958-69.\nPMID: 18990737

Vitamin D status and its relationship to body fat, final height, and peak bone mass in young women.\nKremer R, Campbell PP, Reinhardt T, Gilsanz V.\nJ Clin Endocrinol Metab. 2009 Jan;94(1):67-73. Epub 2008 Nov 4.\nPMID: 18984659

A comparison of vitamin d levels in nondiabetic and diabetic patient populations.\nYoho RM, Frerichs J, Dodson NB, Greenhagan R, Geletta S.\nJ Am Podiatr Med Assoc. 2009 Jan-Feb;99(1):35-41.\nPMID: 19141720

Supplements of 20 microg/d cholecalciferol optimized serum 25-hydroxyvitamin D concentrations in 80% of premenopausal women in winter.\nNelson ML, Blum JM, Hollis BW, Rosen C, Sullivan SS.\nJ Nutr. 2009 Mar;139(3):540-6. Epub 2009 Jan 21.\nPMID: 19158226

Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis.\nHolick MF.\nAm J Clin Nutr. 2004 Mar;79(3):362-71. Review. Erratum in: Am J Clin Nutr. 2004 May;79(5):890.\nPMID: 14985208

Vitamin D and cardiovascular disease risk. Michos ED, Melamed ML. Curr Opin Clin Nutr Metab Care. 2008 Jan;11(1):7-12. Review. PMID: 18090651