Holick MF. The vitamin D epidemic and its health consequences. J Nutr 135, 2739S-2748S

Boston University School of Medicine, Department of Medicine, Section of Endocrinology, Vitamin D Laboratory, Boston, MA 02118, USA.
Journal of Nutrition (Impact Factor: 3.88). 12/2005; 135(11):2739S-48S.
Source: PubMed


Vitamin D deficiency is now recognized as an epidemic in the United States. The major source of vitamin D for both children and adults is from sensible sun exposure. In the absence of sun exposure 1000 IU of cholecalciferol is required daily for both children and adults. Vitamin D deficiency causes poor mineralization of the collagen matrix in young children's bones leading to growth retardation and bone deformities known as rickets. In adults, vitamin D deficiency induces secondary hyperparathyroidism, which causes a loss of matrix and minerals, thus increasing the risk of osteoporosis and fractures. In addition, the poor mineralization of newly laid down bone matrix in adult bone results in the painful bone disease of osteomalacia. Vitamin D deficiency causes muscle weakness, increasing the risk of falling and fractures. Vitamin D deficiency also has other serious consequences on overall health and well-being. There is mounting scientific evidence that implicates vitamin D deficiency with an increased risk of type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common deadly cancers. Vigilance of one's vitamin D status by the yearly measurement of 25-hydroxyvitamin D should be part of an annual physical examination.

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    • "About 2/3 of the population in northern climates are considered deficient with average 25(OH)D 3 levels of 67 nmol/L [2], much below the 100–150 nmol/L level that has recently been associated with preferred health [3]. There are many papers emphasizing the benefits of supplemental vitamin D in order to achieve levels that are protective for many diseases [4] [5]. There has been recent concern expressed, however , that consumption of excessive doses of supplemental vitamin D may pose certain risks and potentially confer harm to individuals. "
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    ABSTRACT: In clinical medicine, increasing attention is being directed towards the important areas of nutritional biochemistry and toxicant bioaccumulation as they relate to human health and chronic disease. Optimal nutritional status, including healthy levels of vitamin D and essential minerals, is requisite for proper physiological function; conversely, accrual of toxic elements has the potential to impair normal physiology. It is evident that vitamin D intake can facilitate the absorption and assimilation of essential inorganic elements (such as calcium, magnesium, copper, zinc, iron, and selenium) but also the uptake of toxic elements (such as lead, arsenic, aluminum, cobalt, and strontium). Furthermore, sufficiency of essential minerals appears to resist the uptake of toxic metals. This paper explores the literature to determine a suitable clinical approach with regard to vitamin D and essential mineral intake to achieve optimal biological function and to avoid harm in order to prevent and overcome illness. It appears preferable to secure essential mineral status in conjunction with adequate vitamin D, as intake of vitamin D in the absence of mineral sufficiency may result in facilitation of toxic element absorption with potential adverse clinical outcomes.
    Full-text · Article · Jul 2015 · The Scientific World Journal
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    • "Deficiency of vitamin D is described as less than 50 nmol/L or 20 ng/mL, and its insufficient level lies in between 20 -32 ng/mL or 50 -80 nmol/L whereas optimum level is more than 40 ng/mL or 100 nmol/L. It is anticipated that the human body needs vitamin D 3000 to 5000 IU on a daily basis to congregate the requirements of body's all cells and tissues [13]. In vitamin D supplementation it has been observed in this study that lower levels of concentrations come out with greater response, so, upcoming studies may discover further considerable results by separating subjects into groups on the basis of their baseline 25-hydroxy vitamin D levels [14]. "

    Full-text · Article · Jan 2015
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    • "Studies in adults have demonstrated that parathyroid hormone concentrations are at their ideal physiologic concentrations when 25OHD concentrations are above 32 ng/mL [14,15]. Similar data in children are unavailable [16]. "
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    ABSTRACT: Neonatal late-onset hypocalcemia is defined as hypocalcemia developed after postnatal 3 days and associated with hypoparathyroidism, high phosphate diets and vitamin D deficiency. We experienced the increment of neonatal late onset hypocalcemia over 1 year. We tried to evaluate the relationship between late onset hypocalcemia and maternal hypovitaminosis D. The medical records in the neonates with late-onset hypocalcemia during January 2007 to July 2008 were retrospectively reviewed. Among those patients, 17 paired sera of mothers and neonates had collected. The levels of 25-OH vitamin D (25OHD) and intact parathyroid hormone (iPTH) were measured and were compared with neonate and the mother. The mean gestational age was 38(+1) weeks, and the mean body weight was 2,980 g. The onset time of hypocalcemia was 5.9 days of age. Most of them (88.2%) were feeding with formula and no one was only breast milk feeding. Of the 17 patients, 13 were born in spring or in winter. The median levels of calcium, phosphorus, alkaline phosphatase, iPTH and 25OHD were 7.0 mg/dL, 8.6 mg/dL, 191.0 U/L, 57.2 pg/mL and 24.0 ng/mL in neonates. The levels of 25OHD of 6 neonates were <20 ng/mL. A total of 16 mothers were considered vitamin D-deficient (<20 ng/mL), and vitamin D insufficient (20<25OHD<30 ng/mL). Neonatal late-onset hypocalcemia in our study seems to be influenced by maternal vitamin D deficiency and insufficiency. Sun tanning and vitamin D supplements from winter to spring would be helpful to prevent maternal vitamin D deficiency, one of the causes of neonatal late-onset hypocalcemia.
    Full-text · Article · Mar 2014
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