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Clinical Responses to a Mega-dose of Vitamin D3 in Infants and Toddlers With Vitamin D Deficiency Rickets. Soliman AT, El-Dabbagh M, Adel A, Ali MA, Aziz Bedair EM, Elalaily RK. J Trop Pediatr. 2009 Jun 8. [Epub ahead of print] PMID: 19506025 doi:10.1093/tropej/fmp040 Conclusion: An IM injection of a mega dose of cholecalciferol is a safe and effective therapy for treatment of VDD rickets in infants and toddlers with normalization of all the biochemical parameters and healing of radiological manifestations. Measurement of serum 25(OH)D level is highly recommended in all short children with a clear need for a general vitamin D supplementation for all infants and young children in Qatar.

The effect of vitamin D2 and vitamin D3 on intestinal calcium absorption in Nigerian children with rickets. Thacher TD, Obadofin MO, O'Brien KO, Abrams SA. J Clin Endocrinol Metab. 2009 Sep;94(9):3314-21. Epub 2009 Jun 30. PMID: 19567516 Conclusions: Despite similar increases in 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D with vitamin D2 or vitamin D3, fractional calcium absorption did not increase, indicating that rickets in Nigerian children is not primarily due to vitamin D-deficient calcium malabsorption

Improved cholecalciferol nutrition in rats is noncalcemic, suppresses parathyroid hormone and increases responsiveness to 1, 25-dihydroxycholecalciferol. Vieth R, Milojevic S, Peltekova V. J Nutr. 2000 Mar;130(3):578-84. PMID: 10702588 We conclude suppression of 1,25(OH)(2)D and PTH, and higher renal VDR mRNA and 24-hydroxylase did not involve higher free 1,25(OH)(2)D concentration or a first pass effect at the gut. Thus, 25(OH)D or a metabolite other than 1,25(OH)(2)D is a physiological, transcriptionally and biochemically active, noncalcemic vitamin D metabolite. When viewed from a perspective that starts with higher vitamin D nutrition, the results indicate that low vitamin D nutrition may bring about a form of resistance to 1,25(OH)2D. This situation would explain why, in humans, nutritional rickets and osteomalacia are commonly associated with normal or increased levels of 1,25(OH)2D (Chesney et al. 1981Citation , Eastwood et al. 1979Citation , Garabedian et al. 1983Citation ,Rasmussen et al. 1980Citation )-these are not like the low hormone levels associated with any other endocrine-deficiency disorder. A connection between lower vitamin D nutrition and vitamin D resistance helps to explain why the supposedly inactive compound 25(OH)D is more relevant in diagnosing nutritional rickets than is the active hormone 1,25(OH)2D. If the features of improved vitamin D nutrition shown here were demonstrated for any newly synthesized compound, the compound would be classified as a noncalcemic 1,25(OH)2D analogue (Brown et al. 1989Citation , Finch et al. 1999Citation , Goff et al. 1993Citation , Koshizuka et al. 1999Citation ). Thus, we contend that 25(OH)D or a metabolite of it other than 1,25(OH)2D exists as a physiological and biologically-active noncalcemic vitamin D metabolite whose effects require further examination, particularly in relationship to studies involving the synthetic analogs of 1,25(OH)2D.

Prevention of rickets and vitamin D deficiency in infants, children, and adolescents.\nWagner CL, Greer FR; American Academy of Pediatrics Section on Breastfeeding; American Academy of Pediatrics Committee on Nutrition.\nPediatrics. 2008 Nov;122(5):1142-52. Erratum in: Pediatrics. 2009 Jan;123(1):197.\nPMID: 18977996

Effectiveness and safety of vitamin D in relation to bone health. Cranney A, Horsley T, O'Donnell S, Weiler H, Puil L, Ooi D, Atkinson S, Ward L, Moher D, Hanley D, Fang M, Yazdi F, Garritty C, Sampson M, Barrowman N, Tsertsvadze A, Mamaladze V. Evid Rep Technol Assess (Full Rep). 2007 Aug;(158):1-235. Review. PMID: 18088161 CONCLUSIONS: The results highlight the need for additional high quality studies in infants, children, premenopausal women, and diverse racial or ethnic groups. There was fair evidence from studies of an association between circulating 25(OH)D concentrations with some bone health outcomes (established rickets, PTH, falls, BMD). However, the evidence for an association was inconsistent for other outcomes (e.g., BMC in infants and fractures in adults). It was difficult to define specific thresholds of circulating 25(OH)D for optimal bone health due to the imprecision of different 25(OH)D assays. Standard reference preparations are needed so that serum 25(OH)D can be accurately and reliably measured, and validated. In most trials, the effects of vitamin D and calcium could not be separated. Vitamin D(3) (>700 IU/day) with calcium supplementation compared to placebo has a small beneficial effect on BMD, and reduces the risk of fractures and falls although benefit may be confined to specific subgroups. Vitamin D intake above current dietary reference intakes was not reported to be associated with an increased risk of adverse events. However, most trials of higher doses of vitamin D were not adequately designed to assess long-term harms.

Effectiveness and safety of vitamin D in relation to bone health. Cranney A, Horsley T, O'Donnell S, Weiler H, Puil L, Ooi D, Atkinson S, Ward L, Moher D, Hanley D, Fang M, Yazdi F, Garritty C, Sampson M, Barrowman N, Tsertsvadze A, Mamaladze V. Evid Rep Technol Assess (Full Rep). 2007 Aug;(158):1-235. Review. PMID: 18088161 CONCLUSIONS: The results highlight the need for additional high quality studies in infants, children, premenopausal women, and diverse racial or ethnic groups. There was fair evidence from studies of an association between circulating 25(OH)D concentrations with some bone health outcomes (established rickets, PTH, falls, BMD). However, the evidence for an association was inconsistent for other outcomes (e.g., BMC in infants and fractures in adults). It was difficult to define specific thresholds of circulating 25(OH)D for optimal bone health due to the imprecision of different 25(OH)D assays. Standard reference preparations are needed so that serum 25(OH)D can be accurately and reliably measured, and validated. In most trials, the effects of vitamin D and calcium could not be separated. Vitamin D(3) (>700 IU/day) with calcium supplementation compared to placebo has a small beneficial effect on BMD, and reduces the risk of fractures and falls although benefit may be confined to specific subgroups. Vitamin D intake above current dietary reference intakes was not reported to be associated with an increased risk of adverse events. However, most trials of higher doses of vitamin D were not adequately designed to assess long-term harms.

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.

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

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.

"We are fond of grumbling about Britain's grey skies, but there may be a good medical reason for doing so. It seems the dreary weather is bad for our hearts - worse, even, than raised cholesterol and an unhealthy diet. That's the controversial claim being made by Dr David Grimes, a gastroenterologist from Blackburn. He's been gazing at the sky for 20 years for clues about why his patients get more sick than those in the south of the country. And what he's found turns key assumptions about heart disease on their head. 'It's not diet or cholesterol levels that raise your risk of heart disease,' he claims. 'It's where you live. People in the north are more likely to be ill because they get less sunshine Basically they are suffering from 'latitude' sickness. The link is vitamin D. While we get some from our diet, the main source is the sun - sunlight converts a compound in the skin into vitamin D, so the amount you make is directly related to the amount of sunshine you get. In a new book Dr Grimes argues the higher the level of vitamin D in your blood, the lower your risk of heart disease and a range of other illnesses. If he's right, what we need is not diet and lifestyle advice, but food fortified with vitamin D. For years the vitamin was thought to be useful only for preventing rickets. So how does he treat them? 'You can do it with diet,' he says 'One Bangladeshi woman eats oily fish every day and now has a vitamin D blood level of 40. 'We give supplements of 1,000 international units (IU) a day or we can give an injection of 300,000 IU that lasts for a year. 'The patients respond well,' says Grimes 'but what's needed is a proper controlled, long-term trial and who is going to fund that? Not a drug company.'"

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.

"I discussed in my last post how Dr Vieth has a model of tissue 1,25(OH)2D synthesis and degradation in which the level of active substance is pretty well independent of blood vitamin D level, provided the level is either rising or stable. I think it is also worth pointing out that he is talking, hypothetically, about tissue 1,25(OH)2D, not plasma level... As we know, almost nothing is known about tissue 1,25(OH)2D control. By Vieth's hypothesis tissue 1,25(OH)2D is OK so long as there is at least SOME vitamin D present in plasma and the level dose not vary too much. Obviously there is a level below which you can have as much of the enzyme for converting vitamin D to the active form as you like, if there is no vitamin D in your blood you can't make any 1,25(OH)2D in your tissues, or in your kidneys for export to your blood to control calcium levels. At the lower extremes we have rickets and osteomalacia. These are clear cut, unarguable markers of vitamin D deficiency, in the absence of confounding factors (there are a few)."

"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

Prevalence and Associations of 25-Hydroxyvitamin D Deficiency in US Children: NHANES 2001-2004. Kumar J, Muntner P, Kaskel FJ, Hailpern SM, Melamed ML. Pediatrics. 2009 Aug 3. [Epub ahead of print] PMID: 19661054 CONCLUSIONS: 25(OH)D deficiency is common in the general US pediatric population and is associated with adverse cardiovascular risks.

Heaney RP. Functional indices of vitamin D status and ramifications of vitamin D deficiency.Am J Clin Nutr. 2004 Dec;80(6 Suppl):1706S-9S. Review.PMID: 15585791 [PubMed - indexed for MEDLINE]

McCollum Award Lecture, 1994: vitamin D--new horizons for the 21st century. Holick MF. Am J Clin Nutr. 1994 Oct;60(4):619-30. Review. PMID: 8092101

Vitamin D is a fat-soluble vitamin that is essential for maintaining normal calcium metabolism (1). Vitamin D3 (cholecalciferol) can be synthesized by humans in the skin upon exposure to ultraviolet-B (UVB) radiation from sunlight, or it can be obtained from the diet. Plants synthesize ergosterol, which is converted to vitamin D2 (ergocalciferol) by ultraviolet light. Vitamin D2 is less active in birds than vitamin D3 and may also be less active in humans (2). When exposure to UVB radiation is insufficient for the synthesis of adequate amounts of vitamin D3 in the skin, adequate intake of vitamin D from the diet is essential for health.

This critical nutrient builds bones, helps fight infection and may protect against some cancers. Do we get enough?