Maternal obesity and gestational weight gain are risk factors for infant death.
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ABSTRACT:
SUBMITTER: Bodnar LM
PROVIDER: S-EPMC4731302 | biostudies-literature | 2016 Feb
REPOSITORIES: biostudies-literature
Publications
Maternal obesity and gestational weight gain are risk factors for infant death.
Bodnar Lisa M LM Siminerio Lara L LL Himes Katherine P KP Hutcheon Jennifer A JA Lash Timothy L TL Parisi Sara M SM Abrams Barbara B
Obesity (Silver Spring, Md.) 20151117 2
<h4>Objective</h4>Assessment of the joint and independent relationships of gestational weight gain and prepregnancy body mass index (BMI) on risk of infant mortality was performed.<h4>Methods</h4>This study used Pennsylvania linked birth-infant death records (2003-2011) from infants without anomalies born to mothers with prepregnancy BMI categorized as underweight (n = 58,973), normal weight (n = 610,118), overweight (n = 296,630), grade 1 obesity (n = 147,608), grade 2 obesity (n = 71,740), and ...[more]
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Project description:BackgroundMaternal metabolic abnormalities have been related to offspring obesity especially during childhood.ObjectivesWe analyzed whether the gestational diabetes mellitus (GDM)-associated melatonin receptor 1B (MTNR1B) genotype of mothers modified the relation between maternal gestational weight gain and childhood obesity.MethodsA total of 1114 Chinese mother-child pairs (mothers with or without prior GDM) were included. Mothers' MTNR1B rs10830962 genotype and gestational weight gain were assessed. Indicators of childhood obesity included BMI-for-age z-score, weight-for-age z-score, waist circumference, and body fat. Childhood overweight and obesity were also analyzed.ResultsWe found that the maternal MTNR1B genotype significantly interacted with gestational weight gain on indicators of offspring's obesity (all P for interaction < 0.05). After multivariable adjustment, BMI-for-age z-scores associated with 1-kg gestational weight gain were 0.009 (SE 0.018), 0.026 (SE 0.010), and 0.061 (SE 0.010) in children with the maternal MTNR1B genotype CC, CG, and GG, respectively (P-interaction = 0.012). Similar interactions were observed for weight-for-age z-score, waist circumference, and body fat (P-interaction = 0.001, 0.003, and 0.012, respectively). The associations remained consistently significant in women with and without GDM. We also found significant interactions between the maternal MTNR1B genotype and gestational weight gain on the offspring's childhood overweight and obesity (P-interaction = 0.005 and 0.026, respectively).ConclusionsThe maternal MTNR1B genotype might interact with gestational weight gain on offspring's obesity risk during childhood.
| S-EPMC6997086 | biostudies-literature
Project description:Background and objectiveEnvironmental or lifestyle exposures in utero may influence the development of childhood asthma. In this meta-analysis, we aimed to assess whether maternal obesity in pregnancy (MOP) or increased maternal gestational weight gain (GWG) increased the risk of asthma in offspring.MethodsWe included all observational studies published until October 2013 in PubMed, Embase, CINAHL, Scopus, The Cochrane Database, and Ovid. Random effects models with inverse variance weights were used to calculate pooled risk estimates.ResultsFourteen studies were included (N = 108 321 mother-child pairs). Twelve studies reported maternal obesity, and 5 reported GWG. Age of children was 14 months to 16 years. MOP was associated with higher odds of asthma or wheeze ever (OR = 1.31; 95% confidence interval [CI], 1.16-1.49) or current (OR = 1.21; 95% CI, 1.07-1.37); each 1-kg/m(2) increase in maternal BMI was associated with a 2% to 3% increase in the odds of childhood asthma. High GWG was associated with higher odds of asthma or wheeze ever (OR = 1.16; 95% CI, 1.001-1.34). Maternal underweight and low GWG were not associated with childhood asthma or wheeze. Meta-regression showed a negative association of borderline significance for maternal asthma history (P = .07). The significant heterogeneity among existing studies indicates a need for standardized approaches to future studies on the topic.ConclusionsMOP and high GWG are associated with an elevated risk of childhood asthma; this finding may be particularly significant for mothers without asthma history. Prospective randomized trials of maternal weight management are needed.
| S-EPMC4187236 | biostudies-literature
Project description:OBJECTIVES:Pregnancy characteristics may influence the infant fecal microbiota during early life. We aimed to examine associations of maternal gestational weight gain with infant fecal microbiota composition, bacterial community richness, and Shannon diversity index. METHODS:We analyzed data from a prospective cohort study of healthy infants. We collected prenatal data, including report of mother's gestational weight gain, and infant fecal samples from 84 infant-mother dyads. By applying 16S rRNA gene sequencing and an unbiased clustering by partitioning around medoids using Bray-Curtis distances, we identified 4 fecal microbiota profiles, and examined the associations of maternal gestational weight gain with the 4 fecal microbiota profiles, bacterial community richness, and Shannon diversity index. RESULTS:Overall, the median age of infants was 4.0 months and 43% were girls. The mothers of the 84 infants gained a mean of 14.2 kg (standard deviation, 5.4 kg) during pregnancy. We identified 4 distinct microbiota profiles: Bifidobacterium-dominant (42%), Enterobacter/Veillonella-dominant (23%), Bacteroides-dominant (19%), and Escherichia-dominant (17%). Infants whose mothers had higher gestational weight gain were less likely to have a Bacteroides-dominant profile, corresponding to a relative risk ratio of 0.83 (95% confidence interval, 0.71-0.96; P?=?0.01) per 1 kg increase in weight. In addition, higher gestational weight gain was also associated with lower bacterial community richness and Shannon diversity index (P?<?0.05). CONCLUSIONS:In this prospective cohort study of healthy infants, maternal gestational weight gain was associated with the infant fecal microbiota profiles, bacterial community richness, and Shannon diversity index.
| S-EPMC5589469 | biostudies-literature
Project description:ImportanceBoth low and high gestational weight gain have been associated with adverse maternal and infant outcomes, but optimal gestational weight gain remains uncertain and not well defined for all prepregnancy weight ranges.ObjectivesTo examine the association of ranges of gestational weight gain with risk of adverse maternal and infant outcomes and estimate optimal gestational weight gain ranges across prepregnancy body mass index categories.Design, setting, and participantsIndividual participant-level meta-analysis using data from 196 670 participants within 25 cohort studies from Europe and North America (main study sample). Optimal gestational weight gain ranges were estimated for each prepregnancy body mass index (BMI) category by selecting the range of gestational weight gain that was associated with lower risk for any adverse outcome. Individual participant-level data from 3505 participants within 4 separate hospital-based cohorts were used as a validation sample. Data were collected between 1989 and 2015. The final date of follow-up was December 2015.ExposuresGestational weight gain.Main outcomes and measuresThe main outcome termed any adverse outcome was defined as the presence of 1 or more of the following outcomes: preeclampsia, gestational hypertension, gestational diabetes, cesarean delivery, preterm birth, and small or large size for gestational age at birth.ResultsOf the 196 670 women (median age, 30.0 years [quartile 1 and 3, 27.0 and 33.0 years] and 40 937 were white) included in the main sample, 7809 (4.0%) were categorized at baseline as underweight (BMI <18.5); 133 788 (68.0%), normal weight (BMI, 18.5-24.9); 38 828 (19.7%), overweight (BMI, 25.0-29.9); 11 992 (6.1%), obesity grade 1 (BMI, 30.0-34.9); 3284 (1.7%), obesity grade 2 (BMI, 35.0-39.9); and 969 (0.5%), obesity grade 3 (BMI, ≥40.0). Overall, any adverse outcome occurred in 37.2% (n = 73 161) of women, ranging from 34.7% (2706 of 7809) among women categorized as underweight to 61.1% (592 of 969) among women categorized as obesity grade 3. Optimal gestational weight gain ranges were 14.0 kg to less than 16.0 kg for women categorized as underweight; 10.0 kg to less than 18.0 kg for normal weight; 2.0 kg to less than 16.0 kg for overweight; 2.0 kg to less than 6.0 kg for obesity grade 1; weight loss or gain of 0 kg to less than 4.0 kg for obesity grade 2; and weight gain of 0 kg to less than 6.0 kg for obesity grade 3. These gestational weight gain ranges were associated with low to moderate discrimination between those with and those without adverse outcomes (range for area under the receiver operating characteristic curve, 0.55-0.76). Results for discriminative performance in the validation sample were similar to the corresponding results in the main study sample (range for area under the receiver operating characteristic curve, 0.51-0.79).Conclusions and relevanceIn this meta-analysis of pooled individual participant data from 25 cohort studies, the risk for adverse maternal and infant outcomes varied by gestational weight gain and across the range of prepregnancy weights. The estimates of optimal gestational weight gain may inform prenatal counseling; however, the optimal gestational weight gain ranges had limited predictive value for the outcomes assessed.
| S-EPMC6506886 | biostudies-literature
Project description:BackgroundMaternal obesity may affect offspring asthma and atopic disease risk by altering fetal immune system development. However, few studies evaluate gestational weight gain (GWG).ObjectiveTo evaluate relationships between maternal body mass index (BMI), GWG, and persistent wheeze, eczema, allergy, and asthma risk in offspring through middle childhood.MethodsA total of 5939 children from Upstate KIDS, a population-based longitudinal cohort of children born in upstate New York (2008-2019) were included in the analysis. Persistent wheeze or asthma, eczema, and allergy were maternally reported at multiple study time points throughout early and middle childhood. Poisson regression models with robust SEs were used to estimate adjusted risk ratios (aRRs) and 95% confidence intervals (CIs) for offspring atopic outcomes by maternal prepregnancy BMI and GWG.ResultsPrepregnancy BMI was associated with increased risk of persistent wheeze by 3 years of age even after adjustments for maternal atopy (class I obesity: aRR, 1.58; 95% CI, 1.13-2.20; class II or III obesity: aRR, 1.69; 95% CI, 1.22-2.35). Associations with reported asthma in middle childhood did not reach statistical significance. Furthermore, no associations were found between prepregnancy BMI and atopic outcomes in either early or middle childhood. GWG was not associated with higher risk of early childhood persistent wheeze or middle childhood asthma.ConclusionMaternal prepregnancy BMI was associated with increased risk of offspring wheeze, whereas excessive GWG was generally not associated with childhood asthma or atopy.
| S-EPMC9329274 | biostudies-literature
Project description:Aims/hypothesisAccumulating evidence suggests an impact of gestational weight gain (GWG) on pregnancy outcomes; however, data on cardiometabolic risk factors later in life have not been comprehensively studied. This study aimed to evaluate the relationship between GWG and cardiometabolic risk in offspring aged 7 years.MethodsWe included a total of 905 mother-child pairs who enrolled in the follow-up visit of the multicentre Hyperglycemia and Adverse Pregnancy Outcome study, at the Hong Kong Centre. Women were classified as having gained weight below, within or exceeding the 2009 Institute of Medicine (IOM) guidelines. A standardised GWG according to pre-pregnancy BMI categories was calculated to explore for any quadratic relationship.ResultsIndependent of pre-pregnancy BMI, gestational hyperglycaemia and other confounders, women who gained more weight than the IOM recommendations had offspring with a larger body size and increased odds of adiposity, hypertension and insulin resistance (range of p values of all the traits: 4.6 × 10-9 < p < 0.0390) than women who were within the recommended range of weight gain during pregnancy. Meanwhile, women who gained less weight than outlined in the recommendations had offspring with increased risks of hypertension and insulin resistance, compared with those who gained weight within the recommended range (7.9 × 10-3 < p < 0.0477). Quadratic relationships for diastolic blood pressure, AUC for insulin, pancreatic beta cell function and insulin sensitivity index were confirmed in the analysis of standardised GWG (1.4 × 10-3 < pquadratic < 0.0282). Further adjustment for current BMI noticeably attenuated the observed associations.Conclusions/interpretationBoth excessive and inadequate GWG have independent and significant impacts on childhood adiposity, hypertension and insulin resistance. Our findings support the notion that adverse intrauterine exposures are associated with persistent cardiometabolic risk in the offspring.
| S-EPMC6223878 | biostudies-literature
Project description:IntroductionPre-pregnancy obesity, gestational diabetes mellitus (GDM), and gestational weight gain (GWG) are associated with each other. This is the first study to investigate whether genetic variants were associated with having GDM, and whether genetic variants-related GDM were associated with adiposity including pre-pregnancy obesity and excessive GWG in Turkish women.Patients and methodsWomen with GDM (n = 160) and without GDM (n = 145) were included in case-controlled study. Genotyping of the HNF1A gene (p.I27L rs1169288, p.98V rs1800574, p.S487N rs2464196), the VDR gene (p.BsmI rs1544410, p.ApaI rs7975232, p.TaqI rs731236, p.FokI rs2228570), and FTO gene (rs9939609) SNPs were performed by using RT-PCR.ResultsThe FTO AA genotype was associated with an increased risk of having GDM (AA vs. AT + TT, 24.4% vs. 12.4%, OR = 2.27, 95% CI [1.23-4.19], p = 0.007). The HNF1A p.I27L GT/TT genotype was associated with increased GDM risk (GT + TT vs. GG-wild, 79.4% vs. 65.5%, OR = 2.02, 95% CI 1.21-3.38], p = 0.007). However, all VDR gene SNPs and the HNF1A p.A98V, p.S487N were not associated with having GDM (p > 0.05). The FTO AA genotype was associated with an increased risk for pre-pregnancy overweight/obesity (OR = 1.43, 95% CI [1.25-3.4], p = 0.035), but not associated with excessive GWG after adjusting for pre-pregnancy weight (p > 0.05). Pre-pregnancy weight, weight at delivery, and GWG did not differ in both VDR and HNF1A gene carriers (p > 0.05). HOMA-IR and HbA1c were increased in both p.I27L TT and FTO AA genotype carriers (p < 0.05).ConclusionThe adiposity-related gene FTO is associated with GDM by the effect of FTO on pre-pregnancy obesity. The diabetes-related p.I27L gene is associated with GDM by increasing insulin resistance.
| S-EPMC6518700 | biostudies-literature
Project description:BackgroundSmall (SGA) and large (LGA) for gestational age infants have higher risks of infant morbidity when compared to those who are appropriate for gestational age (AGA). Increasing pre-pregnancy maternal BMI and gestational weight gain (GWG) are associated with higher risks of LGA and lower risks of SGA infants; however, their direct effects on infant morbidity are unknown. Therefore, we intended to 1) assess how maternal pre-pregnancy BMI, GWG, and birthweight (categorized as SGA, AGA or LGA) affect infant morbidity and 2) estimate at entry of care the risk of infant morbidity according to pre-pregnancy BMI and possible GWG.Methodswe used Consortium on Safe Labor data, a retrospective observational cohort study collecting pregnancy and birth data from 2002 to 2008 in 12 US centers. The association between maternal BMI, GWG and infant morbidity was estimated in singleton gestations delivering ≥ 37 weeks using binomial logistic regression. Hypoxic composite neonatal morbidity was defined as any the following: stillbirth, neonatal death, resuscitation at birth, NICU admission, intracranial hemorrhage, PVH grade III and IV, neonatal seizures, NEC, meconium aspiration, CPAP or mechanical ventilation, RDS, and sepsis. Traumatic composite neonatal morbidity included shoulder dystocia or birth injuries.ResultsIn this study of 110,594 mother-infant dyads, a total of 8,369 (7.6%) infants experienced hypoxic, while 2,134 (1.9%) developed traumatic morbidity. The risk of hypoxic morbidity among SGA, AGA and LGA infants increased when mothers were overweight (aOR 1.26 [95%CI 1.18-1.34]) or obese (class 1: aOR 1.3 [1.2-1.4]; class 2: aOR 1.7 [1.5-1.9]; class 3: aOR 1.8 [1.6-2]) as opposed to normal weight, and when GWG exceeded (aOR 1.08 [1.02-1.014]) rather than remained within recommendations. The risk of traumatic morbidity increased with maternal obesity (class 1: aOR 1.3 [1.1-1.5]), whilst it dropped with GWG below recommendations (aOR 0.7 [0.6-0.8]). The risk of hypoxic events estimated at entry of care increased with maternal overweight (aOR 1.27 [1.19-1.35]) or obesity (class 1: aOR 1.4 [1.2-1.5]; class 2: aOR 1.7 [1.5-1.9]; class 3: aOR 1.8 [1.6-2.1]), and with possible GWG above (aOR 1.09 [1.03-1.015]) recommendations. The risk of traumatic morbidity increased with overweight (aOR 1.1 [1-1.3]) or obesity (class 1: aOR 1.4 [1.2-1.6]; class 2: aOR 1.3 [1-1.6]), with possible GWG above (aOR 1.2 [1-1.3]), as opposed to below recommendations (aOR 0.7 [0.6-0.8]).ConclusionsWhile maternal pre-pregnancy BMI and GWG equally affected traumatic morbidity, the former had a greater impact on hypoxic complications. Therefore, weight control prior to pregnancy is at least as effective as avoiding excessive gestational weight gain to prevent neonatal morbidity.
| S-EPMC11302857 | biostudies-literature
Project description:Fatty acids (FAs) are fundamental for a foetus's growth, serving as an energy source, structural constituents of cellular membranes and precursors of bioactive molecules, as well as being essential for cell signalling. Long-chain polyunsaturated FAs (LC-PUFAs) are pivotal in brain and visual development. It is of interest to investigate whether and how specific pregnancy conditions, which alter fatty acid metabolism (excessive pre-pregnancy body mass index (BMI) or gestational weight gain (GWG)), affect lipid supply to the foetus. For this purpose, we evaluated the erythrocyte FAs of mothers and offspring (cord-blood) at birth, in relation to pre-pregnancy BMI and GWG. A total of 435 mothers and their offspring (237 males, 51%) were included in the study. Distribution of linoleic acid (LA) and α-linolenic acid (ALA), and their metabolites, arachidonic acid, dihomogamma linoleic (DGLA) and ecosapentanoic acid, was significantly different in maternal and foetal erythrocytes. Pre-pregnancy BMI was significantly associated with maternal percentage of MUFAs (Coeff: -0.112; p = 0.021), LA (Coeff: -0.033; p = 0.044) and DHA (Coeff. = 0.055; p = 0.0016); inadequate GWG with DPA (Coeff: 0.637; p = 0.001); excessive GWG with docosaexahenoic acid (DHA) (Coeff. = -0.714; p = 0.004). Moreover, pre-pregnancy BMI was associated with foetus percentage of PUFAs (Coeff: -0.172; p = 0.009), omega 6 (Coeff: -0.098; p = 0.015) and DHA (Coeff: -0.0285; p = 0.036), even after adjusting for maternal lipids. Our findings show that maternal GWG affects maternal but not foetal lipid profile, differently from pre-pregnancy BMI, which influences both.
| S-EPMC4924209 | biostudies-literature
Project description:BackgroundApproximately 17% of children in the U.S. are obese. Children that are overweight or obese are also more likely to be obese as adults and suffer from various chronic diseases and premature death. Maternal obesity can affect the weight status of her offspring through intrauterine mechanisms like excessive gestational weight gain (GWG). Current literature shows a positive association between maternal weight status and GWG on child obesity, yet the direct and indirect effects have not been decomposed or quantified. The purpose of this study was to estimate the effect of maternal obesity on child obesity, mediated by GWG, which is a modifiable risk factor.MethodsThe study participants were a birth cohort of offspring from women who received prenatal care in the Duke/Durham Regional health care system in Durham, NC between 2005 and 2009. Anthropomorphic data was collected via electronic medical records (EMRs) during each voluntary visit to a health care facility. The exposure of interest was maternal obesity, measured by pre-pregnancy body mass index, the mediator was GWG, dichotomized into excessive and not excessive based on maternal prenatal BMI, and the outcome was child obesity at age 4, measured as BMI z-scores from the last recorded height and weight. A counterfactual theory-based product method analysis estimated the mediated effects of GWG, adjusted for maternal race, socioeconomic status, and smoking status.ResultsOf the 766 children, 25% were overweight or obese, and among all mothers, 25 and 31% were overweight and obese, respectively. Maternal BMI was associated with an overall increase of 0.04 in offspring z-score. The proportion of the effect of maternal obesity on child age 4 obesity mediated by GWG was 8.1%.ConclusionGWG, in part, mediated the relationship between maternal BMI and childhood adiposity. Even when the mediator is fixed, children are at an increased risk of a higher BMI if the mother is obese. These findings highlight an important public health education opportunity to stress the impact of a pre-pregnancy weight and excessive GWG on the risk of child obesity for all mothers.
| S-EPMC6686549 | biostudies-literature