BACKGROUNDCauses of early infant growth restriction remain incompletely understood. Where vitamin D deficiency is common, vitamin D supplementation during pregnancy and lactation may improve fetal-infant growth and other birth outcomes.METHODSWe conducted a randomized, double-blind, placebo-controlled trial of maternal vitamin D supplementation from 17-24 weeks gestation until birth or 6 months postpartum. Participants were randomly allocated to five vitamin D and/or placebo supplementation groups: (A) 0 IU/week, (B) 4200 IU/week, (C) 16800 IU/week, or (D) 28000 IU/week in pregnancy, all with 0 IU/week postpartum; or, (E) 28000 IU/week in prenatal and postpartum periods. The primary outcome was length-for-age z-score at one year of age according to World Health Organization child growth standards.RESULTSAmong 1164 infants assessed at one year of age (90% of 1300 pregnancies), there were no differences across groups in length-for-age z-scores (mean ±standard deviation): A: -0.93 ±1.05, B: -1.11 ±1.12, C: -0.97 ±0.97, D: -1.06 ±1.07, E: -0.94 ±1.00 (p=0.23). Groups were similar with respect to other anthropometric measures, birth outcomes, and morbidity. Vitamin D had dose- dependent effects on maternal and infant serum 25-hydroxyvitamin D and calcium, maternal urinary calcium excretion, and maternal parathyroid hormone concentrations. No clinical adverse events were attributed to the vitamin D intervention. CONCLUSIONSIn a population with widespread prenatal vitamin D deficiency and fetal/infant growth restriction, maternal vitamin D supplementation from mid-pregnancy until birth or 6 months postpartum does not influence fetal or infant growth, and has no beneficial or harmful effects on numerous other birth and infant outcomes.

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SummaryBackgroundThe causes of early childhood linear growth faltering (known as stunting) in low-income and middle-income countries remain inadequately understood. We aimed to determine if the progressive postnatal decline in mean height-for-age Z score (HAZ) in low-income and middle-income countries is driven by relatively slow growth of certain high-risk children versus faltering of the entire population.MethodsDistributions of HAZ (based on WHO growth standards) were analysed in 3-month age intervals from 0 to 36 months of age in 179 Demographic and Health Surveys from 64 low-income and middle-income countries (1993–2015). Mean, standard deviation (SD), fifth percentiles, and 95th percentiles of the HAZ distribution were estimated for each age interval in each survey. Associations between mean HAZ and SD, fifth percentile, and 95th percentile were estimated using multilevel linear models. Stratified analyses were performed in consideration of potential modifiers (world region, national income, sample size, year, or mean HAZ in the 0–3 month age band). We also used Monte Carlo simulations to model the effects of subgroup versus whole-population faltering on the HAZ distribution.FindingsDeclines in mean HAZ from birth to 3 years of age were accompanied by declines in both the fifth and 95th percentiles, leading to nearly symmetrical narrowing of the HAZ distributions. Thus, children with relatively low HAZ were not more likely to have faltered than taller same-age peers. Inferences were unchanged in surveys regardless of world region, national income, sample size, year, or mean HAZ in the 0–3 month age band. Simulations showed that the narrowing of the HAZ distribution as mean HAZ declined could not be explained by faltering limited to a growth-restricted subgroup of children.InterpretationIn low-income and middle-income countries, declines in mean HAZ with age are due to a downward shift in the entire HAZ distribution, revealing that children across the HAZ spectrum experience slower growth compared to the international standard. Efforts to mitigate postnatal linear growth faltering in low-income and middle-income countries should prioritise action on community-level determinants of childhood HAZ trajectories.FundingBill & Melinda Gates Foundation.

Even with open enrollment and mandated purchase, incentives created by adverse selection may undermine the efficiency of service offerings by plans in the new health insurance Exchanges created by the Affordable Care Act. Using data on persons likely to participate in Exchanges drawn from five waves of the Medical Expenditure Panel Survey, we measure plan incentives in two ways. First, we construct predictive ratios, improving on current methods by taking into account the role of premiums in financing plans. Second, relying on an explicit model of plan profit maximization, we measure incentives based on the predictability and predictiveness of various medical diagnoses. Among the chronic diseases studied, plans have the greatest incentive to skimp on care for cancer, and mental health and substance abuse.