Maternal low-dose vitamin A or beta-carotene supplementation has no effect on fetal loss and early infant mortality: a randomized cluster trial in Nepal.
ABSTRACT The effect of vitamin A supplementation on the survival of infants aged <6 mo is unclear. Because most infant deaths occur in the first few month of life, maternal supplementation may improve infant survival.
The objective was to assess the effect of maternal vitamin A or beta-carotene supplementation on fetal loss and survival of infants <6 mo of age.
Married women of reproductive age in 270 wards of Sarlahi district, Nepal, were eligible to participate. Wards were randomly assigned to have women receive weekly doses of 7000 microg retinol equivalents as retinyl palmitate (vitamin A), 42 mg all-trans-beta-carotene, or placebo. Pregnancies were followed until miscarriage, stillbirth, maternal death, or live birth of one or more infants, who were followed through 24 wk of age.
A total of 43559 women were enrolled; 15832 contributed 17373 pregnancies and 15987 live born infants to the trial. The rate of fetal loss was 92.0/1000 pregnancies in the placebo group, comparable with rates in the vitamin A and beta-carotene groups, which had relative risks of 1.06 (95% CI: 0.91, 1.25) and 1.03 (95% CI: 0.87, 1.19), respectively. The 24-wk mortality rate was 70.8/1000 live births in the placebo group, comparable with rates in the vitamin A and beta-carotene groups, which had relative risks of 1.05 (95% CI: 0.87, 1.25) and 1.03 (95% CI: 0.86, 1.22), respectively.
Small weekly doses of vitamin A or beta-carotene given to women before conception, during pregnancy, and through 24 wk postpartum did not improve fetal or early infant survival in Nepal.
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ABSTRACT: To determine the effects of maternal vitamin A supplementation from preconception through postpartum on cognitive and motor development of children at 10-13 years of age in rural Nepal. Follow-up assessment of children born to women randomly assigned by a village to receive either supplemental vitamin A (7000 µg retinol equivalents) or placebo weekly during a continuous 3.5-year period from 1994-1997. The participants came from 12 wards, a subset of 270 wards in the original trial. Trained staff tested children for cognition by the Universal Nonverbal Intelligence Test (UNIT) and motor ability using four subtests from the Movement Assessment Battery for Children (MABC). Data on schooling, home environment and nutritional and socioeconomic status were also collected. Southern plains district of Sarlahi, Nepal. 390 Nepalese children 10-13 years of age. Raw scores on UNIT and square-root transformed scores on an abridged version of the MABC tests, expressed as cluster-summarised (mean±SD) values to account for the design of the original trial. There were no differences in UNIT (79.61±5.99 vs 80.69±6.71) or MABC (2.64±0.07 vs 2.49±0.09) test scores in children whose mothers were exposed to vitamin A vs placebo (mean differences: -1.07, 95% CI -7.10 to 9.26, p=0.78; 0.15, 95% CI 0.43 to -0.08, p=0.15), respectively. More children in the placebo group had repeated a grade in school (28% of placebo vs 16.7% of vitamin A, p=0.01). Preconceptional to postpartum maternal vitamin A supplementation, in an undernourished setting, does not improve cognition or motor development at ages 10-13 years.BMJ Open 01/2013; 3(5). · 1.58 Impact Factor
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ABSTRACT: Maternal and child malnutrition in low-income and middle-income countries encompasses both undernutrition and a growing problem with overweight and obesity. Low body-mass index, indicative of maternal undernutrition, has declined somewhat in the past two decades but continues to be prevalent in Asia and Africa. Prevalence of maternal overweight has had a steady increase since 1980 and exceeds that of underweight in all regions. Prevalence of stunting of linear growth of children younger than 5 years has decreased during the past two decades, but is higher in south Asia and sub-Saharan Africa than elsewhere and globally affected at least 165 million children in 2011; wasting affected at least 52 million children. Deficiencies of vitamin A and zinc result in deaths; deficiencies of iodine and iron, together with stunting, can contribute to children not reaching their developmental potential. Maternal undernutrition contributes to fetal growth restriction, which increases the risk of neonatal deaths and, for survivors, of stunting by 2 years of age. Suboptimum breastfeeding results in an increased risk for mortality in the first 2 years of life. We estimate that undernutrition in the aggregate-including fetal growth restriction, stunting, wasting, and deficiencies of vitamin A and zinc along with suboptimum breastfeeding-is a cause of 3·1 million child deaths annually or 45% of all child deaths in 2011. Maternal overweight and obesity result in increased maternal morbidity and infant mortality. Childhood overweight is becoming an increasingly important contributor to adult obesity, diabetes, and non-communicable diseases. The high present and future disease burden caused by malnutrition in women of reproductive age, pregnancy, and children in the first 2 years of life should lead to interventions focused on these groups.The Lancet 06/2013; · 39.06 Impact Factor
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ABSTRACT: Epigenetic events establish a particular gene expression signature for each cell type during differentiation and fertilization. Disruption of these epigenetic programs in response to environmental stimuli during prenatal exposure dysregulates the fetal epigenome, potentially impacting susceptibility to disease later in life (the fetal basis of adult disease). Maternal dietary modifications during gestation and lactation play a pivotal role in the period of fetal (re)programming. Recently, many studies have demonstrated the impact of maternal nutrition on the fetal epigenome. This review discusses the complex interplay among various environmental factors and epigenetic mechanisms that have been found to affect offspring in human and animal models. Further, it summarizes the impact of various dietary phytochemicals capable of modulating the epigenome with regard to diverse human cancers and childhood cancer, specifically those with potential environmental etiology through maternal consumption during pregnancy and lactation. Other dietary agents that are still untested as to their effectiveness in transplacental studies are also discussed. The recent developments discussed herein enhance current understanding of how chemopreventive agents act and their potential to impact the prenatal epigenome; they may also aid efforts to identify dietary interventions that can be beneficial in treating and preventing disease.Nutrition Reviews 07/2013; 71(7):441-57. · 4.60 Impact Factor