Abstract
BackgroundVitamin D regulates bone mineral metabolism and skeletal development. Some observational studies have suggested that prenatal vitamin D deficiency increases the risk of adverse pregnancy and/or birth outcomes; however, there is scant evidence from controlled trials, leading the World Health Organization to advise against routine vitamin D supplementation in pregnancy. Importantly, little is known about the effect of maternal vitamin D status on infant linear growth in communities in South Asia where stunting is highly prevalent and maternal-infant vitamin D status is commonly suboptimal.Methods/DesignThe Maternal Vitamin D for Infant Growth study is a randomized, placebo-controlled, dose-ranging trial of maternal vitamin D supplementation during pregnancy and lactation in Dhaka, Bangladesh. The primary aims are to estimate (1) the effect of maternal prenatal oral vitamin D3 supplementation (4200 IU/wk, 16,800 IU/wk, or 28,000 IU/wk, administered as weekly doses) versus placebo on infant length at 1 year of age and (2) the effect of maternal postpartum oral vitamin D3 supplementation (28,000 IU/wk) versus placebo on length at 1 year of age among infants born to women who received vitamin D 28,000 IU/wk during pregnancy. Generally healthy pregnant women (n = 1300) in the second trimester (17–24 weeks of gestation) are randomized to one of five parallel arms: placebo 4200 IU/wk, 16,800 IU/wk, or 28,000 IU/wk in the prenatal period and placebo in the postpartum period or 28,000 IU/wk in the prenatal period and 28,000 IU/wk in the postpartum period. Household- and clinic-based follow-up of mother-infant pairs is conducted weekly by trained personnel until 26 weeks postpartum and every 3 months thereafter. The primary trial outcome measure is length for age z-score at 1 year of age. Anthropometric measurements, clinical information, and biological specimens collected at scheduled intervals will enable the assessment of a range of maternal, perinatal, and infant outcomes.DiscussionThe role of vitamin D in maternal and infant health remains unresolved. This trial is expected to contribute unique insights into the effects of improving maternal-infant vitamin D status in a low-income setting where stunting and adverse perinatal outcomes represent significant public health burdens.Trial registrationClinicalTrials.gov identifier: NCT01924013. Registered on 13 August 2013Electronic supplementary materialThe online version of this article (doi:10.1186/s13063-015-0825-8) contains supplementary material, which is available to authorized users.
Highlights
Vitamin D regulates bone mineral metabolism and skeletal development
In South Asia, there is a high prevalence of biochemical vitamin D deficiency among women and young infants [15]; in Dhaka, we found that 34 % of pregnant women at 26–29 weeks gestation (N = 160) had serum 25-hydroxyvitamin D (25(OH)D) concentrations less than 30 nmol/L, and that 64 % had 25(OH)D levels less than 50 nmol/L [16], a threshold for sufficiency adopted by the Institute of Medicine (IOM) [17]
We observed an increase in length for age z-score (LAZ) of 0.44 at 1 year attributable to prenatal vitamin D supplementation, which corresponded to an increase of 1.1 cm, adjusted for sex [26]
Summary
Vitamin D regulates bone mineral metabolism and skeletal development. Some observational studies have suggested that prenatal vitamin D deficiency increases the risk of adverse pregnancy and/or birth outcomes; there is scant evidence from controlled trials, leading the World Health Organization to advise against routine vitamin D supplementation in pregnancy. Many low-income countries in Asia have experienced substantial recent reductions in mortality rates among children younger than 5 years of age [1]; for example, Bangladesh has met United Nations Millennium Development Goal 4—a two-thirds reduction in child mortality between 1990 and 2015. In Bangladesh, stunting (height or length less than 2 standard deviations below the standard median for age and sex) was estimated to affect 51 % of children younger than 5 years of age in 2004, but declined to 43 % in 2007 and to 41 % in 2011 according to national surveys [4]. Postnatal linear growth faltering—an abnormally slow velocity of length/ height gain that may eventually lead to stunting—often begins early in infancy in low-income settings (i.e., within the first 3 months of life [7]), suggesting an important contribution by prenatal determinants, including epigenetic and endocrine factors that regulate growth in the first months of life. The causal pathways implicated in early childhood stunting remain poorly understood [8, 9]
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