Dose response to vitamin D supplementation among postmenopausal African American women

Bone Mineral Research Center, Winthrop University Hospital, Mineola, NY 11501, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 01/2008; 86(6):1657-62.
Source: PubMed


Reports on the dose response to vitamin D are conflicting, and most data were derived from white men and women.
The objective was to determine the response of serum 25-hydroxyvitamin D [25(OH)D] to oral vitamin D(3) supplementation in an African American population.
Healthy black postmenopausal women (n = 208) participated in a vitamin D(3) supplementation trial for a period of 3 y. Analyses were done in the vitamin D supplementation arm (n = 104) to quantify the response in serum 25-hydroxyvitamin D concentrations at a steady state vitamin D input. The participants received 20 microg/d (800 IU) oral vitamin D(3) for the initial 2 y and 50 microg/d (2000 IU) for the third year.
Supplementation with 20 microg/d (800 IU/d) vitamin D(3) raised the mean serum 25(OH)D concentration from a baseline of 46.9 +/- 20.6 nmol/L to 71.4 +/- 21.5 nmol/L at 3 mo. The mean (+/-SD) concentration of serum 25(OH)D was 87.3 +/- 27.0 nmol/L 3 mo after supplementation increased to 50 microg/d (2000 IU/d). All participants achieved a serum 25(OH)D concentration >35 nmol/L, 95% achieved a concentration >50 nmol/L, but only 60% achieved a concentration >75 nmol/L. All patients had concentrations <153 nmol/L. On the basis of our findings, an algorithm for prescribing vitamin D so that patients reach optimal serum concentrations was developed. The algorithm suggests a dose of 70 microg (2800 IU/d) for those with a concentration >45 nmol/L and a dose of 100 microg (4000 IU/d) for those with a concentration <45 nmol/L.
Supplementation with 50 microg/d (2000 IU/d) oral vitamin D(3) is sufficient to raise serum 25-hydroxyvitamin D concentrations to >50 nmol/L in almost all postmenopausal African American women. However, higher doses were needed to achieve concentrations >75 nmol/L in many women in this population.

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    • "37.7 ± 9.1 (0) 37.8 ± 10.8 (10) 32.5 (10) * 3.25 (10) at 12 months Islam et al. 2010 [22] 35.0 ± 9.4) (0) 37.1 ±12.1 (10) 31.6 (10) 3.16 (10) at 12 months Karkkaine et al. 2010 [23] 49.2 ± 17.7 (0) 50.1 ± 18.8 (20) 23.7 (20) 1.27 (20) at 36 months Nelson et al. 2009 [24] 61.9 ± 22.6 (0) 62.1 ± 24.0 (20) 25.5 (20) 1.28 (20) at 12 months Pfeifer et al. 2009 [25] 54 ± 18 (0) 55 ± 18 (20) 26 (20) 1.3 (20) at 12 months Pignotti et al. 2010 [26] 52.9 ± 21.4 (0) 46.7 ± 14.0 (10) 6.9 (10) 0.69 (10) At 3 months Smith et al. 2009 [27] 36 ± 17 (0) 44 ± 18 (10) 15 (10) 1.5 (10) at 6 months Talwar et al. 2007 [28] 43.2 ± 16.8 (0) 46.9 ± 20.6 (20) 29.6 (20) 1.48 (20) at 3 months Viljakainen et al. 2006 [29] 52.2 ± 19.9 (0) 46.0 ± 14.3 (5) 46.5 ± 10.2 (10) 44.1 ± 13.5 (20) 10.9 (5) 21.4 (10) 35.1 (20) 2.18 (5) 2.14 (10) 1.76 (20) at 12 weeks Bonjour et al. 2013 [30] 16.2 ± 0.6 (0) 19.2 ± 1.2 (10) 20.2 (10) 2.02 (10) at 8 weeks * as reported by authors. "
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    ABSTRACT: There is controversy surrounding the designation of vitamin D adequacy as defined by circulating levels of the metabolite 25-hydroxyvitamin D (25(OH)D). Depending on the cutoff level chosen, dietary intakes of vitamin D may or may not provide sufficient impact upon vitamin D status measured as improvement in serum levels of 25(OH)D. We sought to examine whether modest daily doses (5–20 μg) as found in fortified foods or multivitamin supplements had a measureable impact on vitamin D status, defined as moving from below to above 50 nmol/L, or from less than 30 nmol/L to above 30 nmol/L. Published literature was searched for relevant articles describing randomized controlled trials. Exclusion criteria were: studies not involving humans; review articles; studies lacking blood level data pre- and post-treatment; no control group; bolus treatments (weekly, monthly, yearly); vitamin D <5 μg or >20 μg; baseline 25(OH)D ≥75 nmol/L; subjects not defined as healthy; studies <8 weeks; and age <19 years. Of the 127 studies retrieved, 18 publications with 25 separate comparisons met criteria. The mean rate constant, defined as change in 25(OH)D in nmol/L per μg vitamin D administered, was calculated as 2.19 ± 0.97 nmol/L per μg. There was a significant negative correlation (r = −0.65, p = 0.0004) between rate constant and administered dose. To determine impact of the dose reflecting the Estimated Average Requirement (EAR) of 10 μg administered in nine studies (10 comparisons), in every case mean 25(OH)D status rose either from “insufficient” (30–50 nmol/L) to “sufficient” (>50 nmol/L) or from “deficient” (<30 nmol/L) to “insufficient” (>30 but <50 nmol/L). Our study shows that when baseline levels of groups were <75 nmol/L, for every microgram of vitamin D provided, 25(OH)D levels can be raised by 2 nmol/L; and further, when groups were deficient or insufficient in vitamin D, there was significant value in providing additional 10 μg per day of vitamin D.
    Nutrients 04/2015; 7(4):2311-2323. DOI:10.3390/nu7042311 · 3.27 Impact Factor
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    • "For EA adults, increasing vitamin D intake from supplementation or diet to more than 600 IU/day is necessary to keep serum 25(OH)D levels at 50 nmol/l (20 ng/ml), but maintaining levels ≥75 nmol/l (30 ng/ml) likely requires more than 1,500 IU/day of vitamin D (Holick et al. 2011; Institute of Medicine 2011; Ross et al. 2011). Administering 2,000 IU/day of vitamin D supplementation is shown to raise serum vitamin D to sufficient levels in AA populations (Dong et al. 2010; Talwar et al. 2007), and 4,000 IU/day of vitamin D supplement intake eliminated the differences in serum 25(OH)D levels between AA and EA men (Garrett-Mayer et al. 2012). These studies, however, observed a considerable variation in serum 25(OH)D levels, even after accounting for vitamin D supplement intake. "
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    ABSTRACT: Vitamin D deficiency is more common among African Americans (AAs) than among European Americans (EAs), and epidemiologic evidence links vitamin D status to many health outcomes. Two genome-wide association studies (GWAS) in European populations identified vitamin D pathway gene single-nucleotide polymorphisms (SNPs) associated with serum vitamin D [25(OH)D] levels, but a few of these SNPs have been replicated in AAs. Here, we investigated the associations of 39 SNPs in vitamin D pathway genes, including 19 GWAS-identified SNPs, with serum 25(OH)D concentrations in 652 AAs and 405 EAs. Linear and logistic regression analyses were performed adjusting for relevant environmental and biological factors. The pattern of SNP associations was distinct between AAs and EAs. In AAs, six GWAS-identified SNPs in GC, CYP2R1, and DHCR7/NADSYN1 were replicated, while nine GWAS SNPs in GC and CYP2R1 were replicated in EAs. A CYP2R1 SNP, rs12794714, exhibited the strongest signal of association in AAs. In EAs, however, a different CYP2R1 SNP, rs1993116, was the most strongly associated. Our models, which take into account genetic and environmental variables, accounted for 20 and 28 % of the variance in serum vitamin D levels in AAs and EAs, respectively. Electronic supplementary material The online version of this article (doi:10.1007/s00439-014-1472-y) contains supplementary material, which is available to authorized users.
    Human Genetics 08/2014; 133(11). DOI:10.1007/s00439-014-1472-y · 4.82 Impact Factor
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    • "Usually circulating 25(OH)D3 level is used to determine vitamin D nutritional status, because it is a predominant form of vitamin D in blood stream and has a much longer half life than that of 1,25(OH)2D3 (i.e., 15 days versus 15 hours) [19]. Importantly, its serum concentrations may be correlated with total vitamin D levels from both endogenous production and dietary uptakes [20–23]. However, 25(OH)D3 is by no means a perfect marker for active vitaminD3status.For example, it is questionable whether measuring 25(OH)D3 can represent the bioavailability of vitamin D2 (ergocalciferol, a vitamin D proform derived from fungus products) versus vitamin D3. "
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    ABSTRACT: Prostate cancer is the second common cancer in men worldwide. The prevention of prostate cancer remains a challenge to researchers and clinicians. Here, we review the relationship of vitamin D and sunlight to prostate cancer risk. Ultraviolet radiation of the sunlight is the main stimulator for vitamin D production in humans. Vitamin D's antiprostate cancer activities may be involved in the actions through the pathways mediated by vitamin D metabolites, vitamin D metabolizing enzymes, vitamin D receptor (VDR), and VDR-regulated genes. Although laboratory studies including the use of animal models have shown that vitamin D has antiprostate cancer properties, whether it can effectively prevent the development and/or progression of prostate cancer in humans remains to be inconclusive and an intensively studied subject. This review will provide up-to-date information regarding the recent outcomes of laboratory and epidemiology studies on the effects of vitamin D on prostate cancer prevention.
    06/2011; 2011:281863. DOI:10.4061/2011/281863
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