Journal
NUTRIENTS
Volume 11, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/nu11010190
Keywords
Vitamin D; C-reactive protein; hepcidin; ferritin; inflammation; pregnancy
Categories
Funding
- Arthritis Research UK
- Medical Research Council (MRC) [4050502589]
- Bupa Foundation
- National Institute for Health Research (NIHR) Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust
- NIHR Oxford Biomedical Research Centre, University of Oxford
- MRC [U105960371]
- European Union's Seventh Framework Programme (FP7/2007-2013) [289346, 613977]
- BBSRC [BB/P028179/1]
- ERA-Net on Biomarkers for Nutrition and Health (ERA HDHL), Horizon 2020 grant [696295]
- EPSRC [EP/J008192/1] Funding Source: UKRI
- MRC [MC_UU_12011/2, MC_U147585819, MC_U147585827, G0400491, MC_U105960371, MC_UP_A620_1015] Funding Source: UKRI
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Iron and vitamin D deficiencies are common during pregnancy. Our aim was to identify whether antenatal vitamin D-3 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 D-3 (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 alpha 1-acid glycoprotein concentration in late pregnancy (25OHD concentration was measured previously). By late pregnancy, 25OHD concentration increased by 17 nmol/L in the vitamin D-3 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 x 25OHD interaction, p < 0.02). Vitamin D-3 supplementation had no effect on hepcidin, ferritin, or inflammatory status suggesting no adjunctive value of vitamin D-3 in reducing rates of antenatal iron deficiency.
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