Abstract
Iron and vitamin D deficiencies are common during pregnancy. Our aim was to identify whether antenatal vitamin D3 supplementation affects iron status (via hepcidin suppression) and/or inflammation. Using a subset of the UK multicenter Maternal Vitamin D Osteoporosis Study (MAVIDOS)—a double-blinded, randomized, placebo-controlled trial (ISRCTN82927713; EudraCT2007-001716-23)—we performed a secondary laboratory analysis. Women with blood samples from early and late pregnancy (vitamin D3 (1000 IU/day from ~14 weeks gestation n = 93; placebo n = 102) who gave birth in the springtime (March–May) were selected as we anticipated seeing the greatest treatment group difference in change in 25-hydroxyvitamin D (25OHD) concentration. Outcomes were hepcidin, ferritin, C-reactive protein, and α1-acid glycoprotein concentration in late pregnancy (25OHD concentration was measured previously). By late pregnancy, 25OHD concentration increased by 17 nmol/L in the vitamin D3 group and decreased by 11 nmol/L in the placebo group; hepcidin, ferritin, and inflammatory markers decreased but no treatment group differences were seen. In late pregnancy, positive relationships between 25OHD and hepcidin and 25OHD and ferritin in the placebo group were observed but not in the treatment group (group × 25OHD interaction, p < 0.02). Vitamin D3 supplementation had no effect on hepcidin, ferritin, or inflammatory status suggesting no adjunctive value of vitamin D3 in reducing rates of antenatal iron deficiency.
Highlights
Vitamin D deficiency and anemia frequently coexist [1,2,3,4,5]
Through the mechanisms outlined above, adequate vitamin D status may be necessary for optimal hepcidin function and may help to provide protection against iron deficiency, potentially offering a complementary approach to combat anemia during pregnancy. The aim of this current study was to examine if daily vitamin D3 supplementation in pregnancy suppresses hepcidin concentration and/or affects iron body stores and inflammation (CRP and α1-acid glycoprotein (AGP)) compared to placebo
This was seen in late pregnancy where 79% of women with 25OHD 25 nmol/L
Summary
Vitamin D deficiency and anemia frequently coexist [1,2,3,4,5]. A number of mechanisms could explain this association [1] and recent data provide evidence for a direct role of vitamin D in the Nutrients 2019, 11, 190; doi:10.3390/nu11010190 www.mdpi.com/journal/nutrientsNutrients 2019, 11, 190 suppression of hepcidin: the primary regulator of systemic iron homeostasis. Vitamin D deficiency and anemia frequently coexist [1,2,3,4,5]. A number of mechanisms could explain this association [1] and recent data provide evidence for a direct role of vitamin D in the Nutrients 2019, 11, 190; doi:10.3390/nu11010190 www.mdpi.com/journal/nutrients. Hepcidin is suppressed when iron status is low to maximize dietary iron absorption and the release of iron from stores. Inflammation causes an increase in hepcidin concentration that reduces dietary iron absorption and the capacity for iron egress from cells, resulting in decreased hemoglobin concentrations [6]. In vitro work has shown a 1,25-dihydroxyvitamin D (1,25(OH) D; the active metabolite of vitamin
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