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Association of Repeated Antibiotic Exposure Up to Age 4 Years With Body Mass at Age 4.5 Years.

ABSTRACT: Importance:Antibiotic exposures in early life may affect weight by altering gut microbiota, potentially increasing the likelihood of childhood obesity. Objective:To examine whether repeated antibiotic exposure by age 48 months is associated with higher body mass index (BMI) at age 54 months. Design, Setting, and Participants:This research was undertaken within a prospective cohort study in New Zealand (Growing Up in New Zealand) that recruited 6853 children antenatally during 2009 to 2010. At the 54-month follow-up, 5734 of 6156 children (93%) had their weight and height measured. Community pharmacy antibiotic dispensing data were obtained from the New Zealand Pharmaceutical Collection database for children whose parents consented to external data linkage. The analytic sample comprised singletons with 54-month weight and height measurements, community antibiotic dispensing and birth weight data, gestational age greater than 27 weeks, and no congenital anomalies. Data analysis took place from 2017 to 2018. Exposures:Antibiotic exposure (yes or no), the number of dispensings, age at first exposure, and timing (age) of exposures between birth and age 48 months. Main Outcomes and Measures:World Health Organization BMI-for-age z scores; and International Obesity Task Force overweight and obesity cutoff points that pass through adult BMI values of 25 and 30. Results:Of the 5128 singletons (2622 [51%] male; mean [SD] birth weight of 3527 [542] g), 4886 (95%) had an antibiotic prescription by age 48 months and 437 (9%) had obesity at age 54 months. Adjusted mean (SE) BMI-for-age z scores increased significantly with the number of antibiotic dispensings for 4 to 6, 7 to 9, and more than 9 dispensings (unexposed, 0.87 [0.09]; 1-3 exposures, 0.92 [0.06] [P = .57]; 4-6 exposures, 1.06 [0.06] [P = .02]; 7-9 exposures, 1.06 [0.06] [P = .02]; >9 exposures, 1.08 [0.05] [P = .01]). Additionally, receiving more than 9 dispensings was associated with greater likelihood of obesity compared with no exposure (adjusted odds ratio, 2.41; 95% CI, 1.07-5.41). Children whose exposure began in the first year of life had a higher adjusted mean (SD) BMI-for-age z score than those not exposed (1.06 [0.05] vs 0.89 [0.09]; P = .03), whereas those whose exposure commenced after the first year of life did not (1.02 [0.06] vs 0.89 [0.09]; P = .10). Conclusions and Relevance:In this study, repeated antibiotic exposure in early childhood was associated with higher mean BMI-for-age z score and an increased likelihood of obesity. Future research could examine whether interventions such as antibiotic stewardship programs, which are designed to reduce overprescribing of antibiotics, also reduce early childhood obesity.

SUBMITTER: Chelimo C

PROVIDER: S-EPMC6991235 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundPrenatal exposure to endocrine disruptors has been associated with increased risk of childhood obesity. However, epidemiologic studies on polybrominated diphenyl ethers (PBDEs) are limited despite animal studies indicating PBDEs' potential role as an obesogen.ObjectivesWe investigated whether maternal concentrations of BDEs 28, 47, 99, 100, 153, and ΣPBDEs during pregnancy were associated with anthropometric measures in children aged 1-8 years.MethodsWe examined 318 mother-child pairs in the Health Outcomes and Measures of the Environment (HOME) Study, a birth cohort enrolled from 2003 through 2006 (Cincinnati, OH). Serum PBDEs were measured at 16 ± 3 weeks gestation. We measured child height (1-8 years), weight (1-8 years), body mass index (BMI) (2-8 years), waist circumference (4-8 years), and body fat (8 years). To account for repeated measures, we used linear mixed models and generalized estimating equations to estimate associations between maternal PBDEs and child anthropometric measures.ResultsWe found no statistically significant associations between prenatal PBDEs and height or weight z-score. A 10-fold increase in maternal serum BDE-153 was associated with lower BMI z-score (β = -0.36; 95% CI: -0.60, -0.13) at 2-8 years, smaller waist circumference (β = -1.81 cm; 95% CI: -3.13, -0.50) at 4-8 years, and lower percent body fat (β = -2.37%; 95% CI: -4.21, -0.53) at 8 years. A decrease in waist circumference at 4-8 years was observed with a 10-fold increase in BDE-100 (β = -1.50 cm; 95% CI: -2.93, -0.08) and ΣPBDEs (β = -1.57 cm; 95% CI: -3.11, -0.02).ConclusionsReverse causality may have resulted in prenatal PBDEs, particularly BDE-153, and decreased BMI, waist circumference, and body fat. Citation: Vuong AM, Braun JM, Sjödin A, Webster GM, Yolton K, Lanphear BP, Chen A. 2016. Prenatal polybrominated diphenyl ether exposure and body mass index in children up to 8 years of age. Environ Health Perspect 124:1891-1897; http://dx.doi.org/10.1289/EHP139.

Project description:ImportancePast studies have showed associations between antibiotic exposure and child weight outcomes. Few, however, have documented alterations to body mass index (BMI) (calculated as weight in kilograms divided by height in meters squared) trajectory milestone patterns during childhood after early-life antibiotic exposure.ObjectiveTo examine the association of antibiotic use during the first 48 months of life with BMI trajectory milestones during childhood in a large cohort of children.Design, setting, and participantsThis retrospective cohort study used electronic health record data from 26 institutions participating in the National Patient-Centered Clinical Research Network from January 1, 2009, to December 31, 2016. Participant inclusion required at least 1 valid set of same-day height and weight measurements at each of the following age periods: 0 to 5, 6 to 11, 12 to 23, 24 to 59, and 60 to 131 months (183 444 children). Data were analyzed from June 1, 2019, to June 30, 2020.ExposuresAntibiotic use at 0 to 5, 6 to 11, 12 to 23, 24 to 35, and 36 to 47 months of age.Main outcomes and measuresAge and magnitude of BMI peak and BMI rebound.ResultsOf 183 444 children in the study (mean age, 3.3 years [range, 0-10.9 years]; 95 228 [51.9%] were boys; 80 043 [43.6%] were White individuals), 78.1% received any antibiotic, 51.0% had at least 1 episode of broad-spectrum antibiotic exposure, and 65.0% had at least 1 episode of narrow-spectrum antibiotic exposure at any time before 48 months of age. Exposure to any antibiotics at 0 to 5 months of age (vs no exposure) was associated with later age (β coefficient, 0.05 months [95% CI, 0.02-0.08 months]) and higher BMI (β coefficient, 0.09 [95% CI, 0.07-0.11]) at peak. Exposure to any antibiotics at 0 to 47 months of age (vs no exposure) was associated with an earlier age (-0.60 months [95% CI, -0.81 to -0.39 months]) and higher BMI at rebound (β coefficient, 0.02 [95% CI, 0.01-0.03]). These associations were strongest for children with at least 4 episodes of antibiotic exposure. Effect estimates for associations with age at BMI rebound were larger for those exposed to antibiotics at 24 to 35 months of age (β coefficient, -0.63 [95% CI, -0.83 to -0.43] months) or 36 to 47 (β coefficient, -0.52 [95% CI, -0.72 to -0.31] months) than for those exposed at 0 to 5 months of age (β coefficient, 0.26 [95% CI, 0.01-0.51] months) or 6 to 11 (β coefficient, 0.00 [95% CI, -0.20 to 0.20] months).Conclusions and relevanceIn this cohort study, antibiotic exposure was associated with statistically significant, but small, differences in BMI trajectory milestones in infancy and early childhood. The small risk of an altered BMI trajectory milestone pattern associated with early-life antibiotic exposure is unlikely to be a key factor during prescription decisions for children.

Project description:BackgroundMaternal seafood intake during pregnancy and prenatal mercury exposure may influence children's growth trajectories.MethodsThis study, based on the Norwegian Mother, Father and Child Cohort Study (MoBa), includes 51 952 mother-child pairs recruited in pregnancy during 2002-08 and a subsample (n = 2277) with maternal mercury concentrations in whole blood. Individual growth trajectories were computed by modelling based on child's reported weight and length/height from 1 month to 8 years. We used linear mixed-effects regression analysis and also conducted discordant-sibling analysis.ResultsMaternal lean fish was the main contributor to total seafood intake in pregnancy and was positively but weakly associated with child body mass index (BMI) growth trajectory. Higher prenatal mercury exposure (top decile) was associated with a reduction in child's weight growth trajectory, with the estimates ranging from -130 g [95% Confidence Intervals (CI) = -247, -12 g] at 18 months to -608 g (95% CI = -1.102, -113 g) at 8 years. Maternal fatty fish consumption was positively associated with child weight and BMI growth trajectory, but only in the higher mercury-exposed children (P-interaction = 0.045). Other seafood consumption during pregnancy was negatively associated with child weight growth compared with no intake, and this association was stronger for higher mercury-exposed children (P-interaction = 0.004). No association was observed between discordant maternal seafood intake and child growth in the sibling analysis.ConclusionsWithin a population with moderate seafood consumption and low mercury exposure, we found that maternal seafood consumption in pregnancy was associated with child growth trajectories, and the direction of the association varied by seafood type and level of prenatal mercury exposure. Prenatal mercury exposure was negatively associated with child growth. Our findings on maternal seafood intake are likely non-causal.

Project description:Importance:Although antibiotics are associated with obesity in animal models, the evidence in humans is conflicting. Objective:To assess whether antibiotic exposure during pregnancy and/or early childhood is associated with the development of childhood obesity, focusing particularly on siblings and twins. Design, Setting, and Participants:This cross-sectional national study included 284 211 participants (132 852 mothers and 151 359 children) in New Zealand. Data analyses were performed for 150 699 children for whom data were available, 30 696 siblings, and 4188 twins using covariate-adjusted analyses, and for 6249 siblings and 522 twins with discordant outcomes using fixed-effects analyses. Data analysis was performed November 2017 to March 2019. Exposure:Exposure to antibiotics during pregnancy and/or early childhood. Main Outcomes and Measures:The main outcome is odds of obesity at age 4 years. Anthropometric data from children born between July 2008 and June 2011 were obtained from the B4 School Check, a national health screening program that records the height and weight of 4-year-old children in New Zealand. These data were linked to antibiotics (pharmaceutical records) dispensed to women before conception and during all 3 trimesters of pregnancy and to their children from birth until age 2 years. Results:The overall study population consisted of 132 852 mothers and 151 359 children (77 610 [51.3%] boys) who were aged 4 to 5 years when their anthropometrical measurements were assessed. Antibiotic exposure was common, with at least 1 course dispensed to 35.7% of mothers during pregnancy and 82.3% of children during the first 2 years of life. Results from covariate-adjusted analyses showed that both prenatal and early childhood exposures to antibiotics were independently associated with obesity at age 4 years, in a dose-dependent manner. Every additional course of antibiotics dispensed to the mothers yielded an adjusted odds ratio (aOR) of obesity in their children (siblings) of 1.02 (95% CI, 0.99-1.06), which was similar to the odds across pregnancy for the whole population (aOR, 1.06; 95% CI, 1.04-1.07). For the child's exposure, the aOR for the association between antibiotic exposure and obesity was 1.04 (95% CI, 1.03-1.05) among siblings and 1.05 (95% CI, 1.02-1.09) among twins. However, fixed-effects analyses of siblings and twins showed no associations between antibiotic exposure and obesity, with aORs of 0.95 (95% CI, 0.90-1.00) for maternal exposure, 1.02 (95% CI, 0.99-1.04) for child's exposure, and 0.91 (95% CI, 0.81-1.02) for twins' exposure. Conclusions and Relevance:Although covariate-adjusted analyses demonstrated an association between antibiotic exposure and odds of obesity, further analyses of siblings and twins with discordant outcomes showed no associations. Thus, these discordant results likely reflect unmeasured confounding factors.

Project description:ImportanceHypoglycemia is common during neonatal transition and may cause permanent neurological impairment, but optimal intervention thresholds are unknown.ObjectiveTo test the hypothesis that neurodevelopment at 4.5 years is related to the severity and frequency of neonatal hypoglycemia.Design, setting, and participantsThe Children With Hypoglycemia and Their Later Development (CHYLD) Study is a prospective cohort investigation of moderate to late preterm and term infants born at risk of hypoglycemia. Clinicians were masked to neonatal interstitial glucose concentrations; outcome assessors were masked to neonatal glycemic status. The setting was a regional perinatal center in Hamilton, New Zealand. The study was conducted from December 2006 to November 2010. The dates of the follow-up were September 2011 to June 2015. Participants were 614 neonates born from 32 weeks' gestation with at least 1 risk factor for hypoglycemia, including diabetic mother, preterm, small, large, or acute illness. Blood and masked interstitial glucose concentrations were measured for up to 7 days after birth. Infants with hypoglycemia (whole-blood glucose concentration <47 mg/dL) were treated to maintain blood glucose concentration of at least 47 mg/dL.ExposuresNeonatal hypoglycemic episode, defined as at least 1 consecutive blood glucose concentration less than 47 mg/dL, a severe episode (<36 mg/dL), or recurrent (?3 episodes). An interstitial episode was defined as an interstitial glucose concentration less than 47 mg/dL for at least 10 minutes.Main outcomes and measuresCognitive function, executive function, visual function, and motor function were assessed at 4.5 years. The primary outcome was neurosensory impairment, defined as poor performance in one or more domains.ResultsIn total, 477 of 604 eligible children (79.0%) were assessed. Their mean (SD) age at the time of assessment was 4.5 (0.1) years, and 228 (47.8%) were female. Those exposed to neonatal hypoglycemia (280 [58.7%]) did not have increased risk of neurosensory impairment (risk difference [RD], 0.01; 95% CI, -0.07 to 0.10 and risk ratio [RR], 0.96; 95% CI, 0.77 to 1.21). However, hypoglycemia was associated with increased risk of low executive function (RD, 0.05; 95% CI, 0.01 to 0.10 and RR, 2.32; 95% CI, 1.17 to 4.59) and visual motor function (RD, 0.03; 95% CI, 0.01 to 0.06 and RR, 3.67; 95% CI, 1.15 to 11.69), with highest risk in children exposed to severe, recurrent, or clinically undetected (interstitial episodes only) hypoglycemia.Conclusions and relevanceNeonatal hypoglycemia was not associated with increased risk of combined neurosensory impairment at 4.5 years but was associated with a dose-dependent increased risk of poor executive function and visual motor function, even if not detected clinically, and may thus influence later learning. Randomized trials are needed to determine optimal screening and intervention thresholds based on assessment of neurodevelopment at least to school age.

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Association of Repeated Antibiotic Exposure Up to Age 4 Years With Body Mass at Age 4.5 Years.

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