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Co-causation of reduced newborn size by maternal undernutrition, infections, and inflammation.

ABSTRACT: More than 20 million babies are born with low birthweight annually. Small newborns have an increased risk for mortality, growth failure, and other adverse outcomes. Numerous antenatal risk factors for small newborn size have been identified, but individual interventions addressing them have not markedly improved the health outcomes of interest. We tested a hypothesis that in low-income settings, newborn size is influenced jointly by multiple maternal exposures and characterized pathways associating these exposures with newborn size. This was a prospective cohort study of pregnant women and their offspring nested in an intervention trial in rural Malawi. We collected information on maternal and placental characteristics and used regression analyses, structural equation modelling, and random forest models to build pathway maps for direct and indirect associations between these characteristics and newborn weight-for-age Z-score and length-for-age Z-score. We used multiple imputation to infer values for any missing data. Among 1,179 pregnant women and their babies, newborn weight-for-age Z-score was directly predicted by maternal primiparity, body mass index, and plasma alpha-1-acid glycoprotein concentration before 20 weeks of gestation, gestational weight gain, duration of pregnancy, placental weight, and newborn length-for-age Z-score (p < .05). The latter 5 variables were interconnected and were predicted by several more distal determinants. In low-income conditions like rural Malawi, maternal infections, inflammation, nutrition, and certain constitutional factors jointly influence newborn size. Because of this complex network, comprehensive interventions that concurrently address multiple adverse exposures are more likely to increase mean newborn size than focused interventions targeting only maternal nutrition or specific infections.

SUBMITTER: Ashorn P

PROVIDER: S-EPMC6055652 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature

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Co-causation of reduced newborn size by maternal undernutrition, infections, and inflammation.

Ashorn Per P Hallamaa Lotta L Allen Lindsay H LH Ashorn Ulla U Chandrasiri Upeksha U Deitchler Megan M Doyle Ronan R Harjunmaa Ulla U Jorgensen Josh M JM Kamiza Steve S Klein Nigel N Maleta Kenneth K Nkhoma Minyanga M Oaks Brietta M BM Poelman Basho B Rogerson Stephen J SJ Stewart Christine P CP Zeilani Mamane M Dewey Kathryn G KG

Maternal & child nutrition 20180108 3

More than 20 million babies are born with low birthweight annually. Small newborns have an increased risk for mortality, growth failure, and other adverse outcomes. Numerous antenatal risk factors for small newborn size have been identified, but individual interventions addressing them have not markedly improved the health outcomes of interest. We tested a hypothesis that in low-income settings, newborn size is influenced jointly by multiple maternal exposures and characterized pathways associat ...[more]

PMID: 29316198

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Project description:BackgroundFetal growth restriction (FGR) has been associated with adverse perinatal outcomes and epigenetic modifications that impact gene expression leading to permanent changes of fetal metabolic pathways and thereby influence development of disease in childhood and adult life. In this study, we investigated the result of maternal food restriction on liver protein expression in Wistar male newborn pups.Materials & methodsTen (n = 10) timed pregnant Wistar rats on their 14th day of gestation were randomly assigned to either control (n = 4) or food restricted group (n = 6). The control group had ad libitum access to food. In the food restricted group, maternal diet was limited in a moderate fashion (50%) from day 15 of pregnancy until delivery. All rats delivered spontaneously on day 21 and newborn pups were immediately weighed. Pups born to normally nourished mothers were considered as controls, while pups born to food restricted mothers were subdivided into two groups, based on their birth weight: growth restricted (FGR) and appropriately grown (non-FGR). Rats were euthanized immediately after birth and liver tissues of 11 randomly selected male offspring (FGR n = 4, non-FGR n = 4, control n = 3) were collected and analyzed using quantitative proteomics.ResultsIn total 6,665 proteins were profiled. Of these, 451 and 751 were differentially expressed in FGR and non-FGR vs. control, respectively, whereas 229 proteins were commonly expressed. Bioinformatics analysis of the differentially expressed proteins (DEPs) in FGR vs. control revealed induction of the super-pathway of cholesterol biosynthesis and inhibition of thyroid hormone metabolism, fatty acid beta oxidation and apelin liver signaling pathway. Analysis of DEPs in non-FGR vs. control groups showed inhibition of thyroid hormone metabolism, fatty acid beta oxidation, and apelin liver signaling pathway.ConclusionThis study demonstrates the impact of prenatal food restriction on the proteomic liver profile of FGR and non-FGR offspring underlying the importance of both prenatal adversities and birth weight on liver-dependent postnatal disease.

Project description:Background and objectivesStudies in low-and middle-income countries where nutrition transition is underway provides mixed evidence of double burden of maternal overnutrition and child undernutrition among mother-child pairs. Shifting dietary pattern and rapid increase in overweight/obesity among adults with persistent child undernutrition indicate that India is experiencing nutrition transition and double burden of malnutrition. Hence, the study explores the presence of and the factors associated with mother-child dyads of over- and undernutrition in India.Methods and materialsThe study uses National Family Health Survey 2015-16 data. The analytic sample consists of 28,817 weighted mother-child pairs where an overweight/obese mother is paired with an undernourished child. The nutritional status of children is defined according to WHO 2006 child growth standards as underweight (i.e., low weight-for-age), stunting (i.e., low height-for-age) and wasting (i.e., low weight-for-height). Maternal overweight/obesity (i.e., BMI ≥ 25 kg/m2) is defined using adult BMI criterion. Descriptive, bivariate, and adjusted multivariable logistic regression analysis are conducted.ResultsOf the overweight/obese mothers, 21.3%, 26.5%, and 14% have underweight, stunted, and wasted children respectively. In adjusted models, maternal short stature (aOR: 2.94, 95% CI: 2.30-3.75), age of child (aOR: 3.29, 95% CI: 2.76-3.92), and poorest wealth status (aOR: 2.01, 95% CI: 1.59-2.54) are significant predictors of overweight/obese mothers and stunted child pairs. Similarly, poor wealth status (aOR: 1.68, 95% CI:1.32-2.14), maternal stature (aOR: 2.70, 95% CI: 2.08-3.52), and child aged 2-5 years (aOR: 1.77, 95% CI:1.51-2.08) are also significantly associated with higher occurrence of overweight/obese mother and-underweight child pairs.ConclusionFindings of the study are consistent with the phase of nutrition transition and double burden of malnutrition. The paper concludes with suggestions to improve the socioeconomic condition, more strategic nutrition specific investments and policy interventions to eliminate all forms of malnutrition for achieving SDGs.

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Co-causation of reduced newborn size by maternal undernutrition, infections, and inflammation.

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Co-causation of reduced newborn size by maternal undernutrition, infections, and inflammation.

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