Bischoff-Ferrari HA, Giovannucci E, Willet WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr 84, 18-28

Department of Nutrition, Harvard School of Public Health, Boston, MA, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 08/2006; 84(1):18-28.
Source: PubMed


Recent evidence suggests that vitamin D intakes above current recommendations may be associated with better health outcomes. However, optimal serum concentrations of 25-hydroxyvitamin D [25(OH)D] have not been defined. This review summarizes evidence from studies that evaluated thresholds for serum 25(OH)D concentrations in relation to bone mineral density (BMD), lower-extremity function, dental health, and risk of falls, fractures, and colorectal cancer. For all endpoints, the most advantageous serum concentrations of 25(OH)D begin at 75 nmol/L (30 ng/mL), and the best are between 90 and 100 nmol/L (36-40 ng/mL). In most persons, these concentrations could not be reached with the currently recommended intakes of 200 and 600 IU vitamin D/d for younger and older adults, respectively. A comparison of vitamin D intakes with achieved serum concentrations of 25(OH)D for the purpose of estimating optimal intakes led us to suggest that, for bone health in younger adults and all studied outcomes in older adults, an increase in the currently recommended intake of vitamin D is warranted. An intake for all adults of > or =1000 IU (25 microg) [DOSAGE ERROR CORRECTED] vitamin D (cholecalciferol)/d is needed to bring vitamin D concentrations in no less than 50% of the population up to 75 nmol/L. The implications of higher doses for the entire adult population should be addressed in future studies.

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Available from: Thomas Dietrich, Oct 10, 2014
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    • "In contrast, AMI patients's mean levels were ~14 ng/mL, which falls in the range associated with higher likelihood of disease conditions. These authors also stated that an intake of vitamin D (cholecalciferol) ≥ 40 μg/day is needed to reach at least 50% of the aforementioned 25(OH)D optimal concentrations [18]. Given the low incidence of malnutrition in Western countries, there is a small possibility that diet deficiencies play a role in the 25(OH)D differences observed in our study. "

    International Journal of Cardiology 07/2015; 199. DOI:10.1016/j.ijcard.2015.07.082 · 4.04 Impact Factor
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    • "31 [28] [29] [30] [31] [32] [33] NS BMI (kg/m 2 ) 24.45 [22.68–28.91] 21.11 [20.44–24.77] "
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    ABSTRACT: Of many vitamin D extraskeletal functions, its modulatory role in insulin secretion and action is especially relevant for gestational diabetes mellitus (GDM). The aims of the present study were to determine midgestational and early postpartum vitamin D status in pregnant women with and without GDM and to describe the relationship between midgestational and postpartum vitamin D status and parallel changes of glucose tolerance. A total of 76 pregnant women (47 GDM and 29 healthy controls) were included in the study. Plasma levels of 25(OH)D were measured using an enzyme immunoassay. Vitamin D was not significantly decreased in GDM compared to controls during pregnancy; however, both groups of pregnant women exhibited high prevalence of vitamin D deficiency. Prevalence of postpartum 25(OH)D deficiency in post-GDM women remained significantly higher and their postpartum 25(OH)D levels were significantly lower compared to non-GDM counterparts. Finally, based on the oGTT repeated early postpartum persistent glucose abnormality was ascertained in 15% of post-GDM women; however, neither midgestational nor postpartum 25(OH)D levels significantly differed between subjects with GDM history and persistent postpartum glucose intolerance and those with normal glucose tolerance after delivery.
    05/2015; 2015:1-7. DOI:10.1155/2015/260624
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    • "Additionally, both these studies were for a long duration (1 year) and achieved a serum 25(OH)D >85 nmol/L. As suggested that for all endpoints, the most advantageous serum concentrations of 25(OH)D begin at 75 nmol/L (30 ng/mL), and the best are between 90 and 100 nmol/L (36e40 ng/mL) [23]. Whereas in our study after the supplementation of 6000 IU/day for 3 months we reached the s-25(OH)D of 77.2 ± 30.1 nmol/L, but the levels dropped on reducing the dose of vitamin D 3 in phase 2. A three month randomized clinical trial in overweight diabetic patients from Iran on supplementation of 300,000 IU vitamin D 3 (intramuscular) achieved mean S-25(OH)D Fig. 2. Mean serum 25(OH) vitamin D and plasma parathyroid hormone during the study period in intervention group. "
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    ABSTRACT: The co-existence of vitamin D deficiency with obesity and type 2 diabetes is highly prevalent in the United Arab Emirates. We do not have studies evaluating the vitamin D dose response and sufficiency, and if sufficient substitution dose during a longer period could decrease obesity or change fat distribution in obese type 2 diabetic vitamin D deficient Emiratis. A randomized double-blind clinical trial was conducted for 6 months followed by another 6 months of un-blinded follow up with 87 obese, type 2 diabetic participants. Serum 25-hydroxy vitamin D (S-25(OH)D), anthropometric data, and life-style factors such as diet and sunlight exposure were measured. The study was executed in 3 phases in two arms vitamin D arm (n = 45) and placebo arm (n = 42); in Phase 1 the vitamin D arm received 6000 IU vitamin D3/day (3 months) followed by Phase 2 with 3000 IU vitamin D3/day. During follow up (phase 3) both the arms were un-blinded and supplemented with 2200 IU vitamin D3/day for another 6 months. At the baseline a significant (p < 0.01) positive association between body fat mass and body weight (r = 0.97) muscle mass (r = 0.47), water mass (r = 0.54), waist circumference (r = 0.82) and serum PTH (r = 0.28) was observed. On supplementation no significant changes in anthropometric dimensions was observed. S-25(OH) D peaked in phase 1 (77.2 ± 30.1 vs 28.5 ± 9.2, p = 0.003) followed by a decrease in phase 2 (62.3 ± 20.8, p = 0.006) paralleled by a decrease in parathyroid hormone in phase 2 (5.9 ± 2.4 vs 4.5 ± 1.8, p < 0.01) compared to baseline in vitamin D group. This study shows no significant influence of vitamin D supplementation on weight, fat mass or waist circumference in type 2 diabetic obese vitamin D deficient participants of Arab ethnicity after one year. Despite a relatively high daily dose of vitamin D3 we did not achieve target levels of S-25(OH)D above 75 nmol/L in this population. However, supplementation was safe, improved s- 25 (OH)D also reducing the incidence of eucalcemic parathyroid hormone elevation. Clinical trial registry: Identifier: NCT02101151. Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
    Clinical nutrition (Edinburgh, Scotland) 03/2015; DOI:10.1016/j.clnu.2015.02.017 · 4.48 Impact Factor
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