Increase In Prepregnancy Body Mass Index Research Articles

Effect of Maternal Pre-Pregnancy Body Mass Index on Longitudinal Fetal Growth and Mediating Role of Maternal Fasting Plasma Glucose: A Retrospective Cohort Study.

To assess the impact of maternal pre-pregnancy body mass index (BMI) on longitudinal fetal growth, and the potential mediation effect of the maternal fasting plasma glucose in first trimester. In this retrospective cohort study, we collected pre-pregnancy BMI data and ultrasound measurements during pregnancy of 3879 singleton pregnant women who underwent antenatal examinations and delivered at Peking Union Medical College Hospital. Generalized estimation equations, linear regression, and logistic regression were used to examine the association between pre-pregnancy BMI with fetal growth and adverse neonatal outcomes. Mediation analyses were also used to examine the mediating role of maternal fasting plasma glucose (FPG) in first trimester. A per 1 Kg/m² increase in pre-pregnancy BMI was associated with increase fetal body length Z-score (β 0.010, 95% CI 0.001, 0.019) and fetal body weight (β 0.017, 95% CI 0.008, 0.027). In mid pregnancy, pre-pregnancy BMI also correlated with an increase Z-score of fetal abdominal circumference, femur length (FL). Pre-pregnancy BMI was associated with an increased risk of large for gestational age and macrosomia. Mediation analysis indicated that the associations between pre-pregnancy BMI and fetal weight in mid and late pregnancy, and at birth were partially mediated by maternal FPG in first trimester (mediation proportion: 5.0%, 8.3%, 1.6%, respectively). Maternal pre-pregnancy BMI was associated with the longitudinal fetal growth, and the association was partly driven by maternal FPG in first trimester. The study emphasized the importance of identifying and managing mothers with higher pre-pregnancy BMI to prevent fetal overgrowth.

Maternal preconception BMI and gestational weight gain are associated with weight retention and maternal and child body fat at 6-7 years postpartum in the PRECONCEPT cohort.

There is limited evidence from prospective cohorts in low-resource settings on the long-term impact of pre-pregnancy body mass index (PPBMI) and gestational weight gain (GWG) on postpartum weight retention (PPWR) and maternal and child body composition. We examined the associations between PPBMI and timing of GWG on PPWR at 1, 2, and 6-7 years and maternal and child percent body fat at 6-7 years. We used data from the PRECONCEPT study (NCT01665378) that included prospectively collected data on 864 mother-child pairs from preconception through 6-7 years postpartum. The key outcomes were PPWR at 1, 2, and 6-7 years, and maternal and child percent body fat at 6-7 years that was measured using bioelectric impedance. Maternal conditional GWG (CGWG) was defined as window-specific weight gains (< 20wk, 21-29wk, and ≥ 30wk), uncorrelated with PPBMI and all prior body weights. PPBMI and CGWG were calculated as standardized z-scores to allow for relative comparisons of a 1 standard deviation (SD) increase in weight gain for each window. We used multivariable linear regressions to examine the associations, adjusting for baseline demographic characteristics, intervention, breastfeeding practices, diet and physical activity. Mean (SD) PPBMI and GWG were 19.7 (2.1) kg/m2 and 10.2 (4.0) kg, respectively. Average PPWR at 1, 2, and 6-7 years was 1.1, 1.5 and 4.3 kg, respectively. A one SD increase in PPBMI was associated with a decrease in PPWR at 1 year (β [95% CI]: -0.21 [-0.37, -0.04]) and 2 years (-0.20 [-0.39, -0.01]); while a one SD in total CGWG was associated with an increase in PPWR at 1 year (1.01 [0.85,1.18]), 2 years (0.95 [0.76, 1.15]) and 6-7 years (1.05 [0.76, 1.34]). Early CGWG (< 20 weeks) had the greatest association with PPWR at each time point as well as with maternal (0.67 [0.07, 0.87]) and child (0.42 [0.15, 0.69]) percent body fat at 6-7 years. Maternal nutrition before and during pregnancy may have long-term implications for PPWR and body composition. Interventions should consider targeting women preconception and early in pregnancy to optimize maternal and child health outcomes.

Maternal pre-pregnancy body mass index and the risk for gestational diabetes mellitus in women with twin pregnancy in South Korea

ObjectiveTo investigate the association between maternal pre-pregnancy body mass index (BMI) and the risk for gestational diabetes mellitus (GDM) in women with twin pregnancy in South Korea. Materials and methodsWe performed a single-center, retrospective cohort study involving 1028 women with twin pregnancy from January 2006 to December 2018 in South Korea. Pregnancies with monoamnionic twins, twin–twin transfusion syndrome, fetal death in utero before 24 weeks, pre-gestational diabetes mellitus, and unknown BMI or GDM status were excluded. Subjects were grouped into four groups based on pre-pregnancy BMI: underweight (<18.5 kg/m2), normal (18.5–22.9 kg/m2), overweight (23.0–24.9 kg/m2), and obese (≥25.0 kg/m2). ResultsAmong 1028 women who were included in the analysis, 169 (16.4%), 655 (63.7%), 111 (10.8%), and 93 (9.0%) women were underweight, normal, overweight, and obese, respectively, before pregnancy. The incidence of GDM was 8.9% in the total study population: 4.7%, 8.2%, 11.7%, and 17.2% in the underweight, normal, overweight, and obese group, respectively (p = 0.005). The incidence of GDM significantly increased according to the increase in pre-pregnancy BMI (p < 0.001). Women in the obese group were more likely to be affected by GDM compared to the normal group (adjusted odds ratio = 2.20, 95% confidence interval = 1.19–4.08) after controlling for maternal age, parity, type of conception, and chorionicity. ConclusionIn twin pregnancies in South Korea, the risk of GDM increased as maternal pre-pregnancy BMI increased and obese women before pregnancy were more likely to be affected by GDM.

Placental DNA methylation changes associated with maternal prepregnancy BMI and gestational weight gain.

BACKGROUNDMaternal obesity prior to or during pregnancy influences fetal growth, predisposing the offspring to increased risk for obesity across the life-course. Placental epigenetic mechanisms may underlie these associations. We conducted an epigenome-wide association study to identify placental DNA methylation changes associated with maternal pre-pregnancy body mass index (BMI) and rate of gestational weight gain at first (GWG1), second (GWG2) and third trimester (GWG3).METHODParticipants of the NICHD Fetal Growth Studies with genome-wide placental DNA methylation (n=301) and gene expression (n=75) data were included. Multivariable-adjusted regression models were used to test the associations of 1kg/m2 increase in pre-pregnancy BMI or 1kg/week increase in GWG with DNA methylation levels. Genes harboring top differentially methylated CpGs (FDR P<0.05) were evaluated for placental gene expression. We assessed whether DNA methylation sites known to be associated with BMI in child or adult tissues were also associated with maternal pre-pregnancy BMI in placenta.RESULTSPre-pregnancy BMI was associated with DNA methylation at cg14568196[EGFL7], cg15339142[VETZ] and cg02301019[AC092377.1] (FDR P<0.05, P ranging from 1.4×10−10 to 1.7×10−9). GWG1 or GWG2 was associated with DNA methylation at cg17918270[MYT1L], cg20735365[DLX5] and cg17451688[SLC35F3] (FDR P<0.05, P ranging from 6.4×10−10 to 1.2×10−8). Both pre-pregnancy BMI and DNA methylation at cg1456819 [EGFL7] were negatively correlated with EGFL7 expression in placenta (P<0.05). Several CpGs previously implicated in obesity traits in children and adults were associated with pre-pregnancy BMI in placenta. Functional annotations revealed that EGFL7 is highly expressed in placenta and the differentially methylated CpG sites near EGFL7 and VEZT were cis-meQTL targets in blood.CONCLUSIONSWe identified placental DNA methylation changes at novel loci associated with pre-pregnancy BMI and GWG. The overlap between CpGs associated with obesity traits in placenta and other tissues in children and adults suggests that epigenetic mechanisms in placenta may give insights to early origins of obesity.

253: Weight retention after pregnancies and risk of cesarean delivery in subsequent pregnancies

The impact of weight gain between pregnancies on subsequent pregnancies is not well studied. We sought to examine the rate of cesarean delivery according to weight gain between pregnancies. This was a retrospective cohort study of all women who had at least two pregnancies at 23 weeks’ gestation or greater between 2009 and 2018 at a single academic institution. Only the second pregnancy was analyzed. Women with a history of cesarean delivery, multiple gestation, placenta previa, fetal anomaly, and stillbirth were excluded. Weight retention was defined as an increase in prepregnancy BMI (body mass index kg/m2) between both pregnancies by at least 2 kg/m2. Our primary outcome was the rate of cesarean delivery. A multivariable logistic regression analysis was performed to calculate adjusted odds ratios (OR) and 95% confidence intervals (95%CI), controlling for predefined covariates (age, gestational age, and race/ethnicity). Secondary analyses were performed after limiting analyses to women with prepregnancy obesity (BMI >30 kg/m2) in the first pregnancy. Of 2,215 women, 736 (33%) women had weight retention after pregnancy. Women with weight retention compared with those without had higher odds of cesarean delivery (adjusted OR 1.41; 95%CI 1.01-1.98) and cesarean delivery for arrest of dilation or descent (3.1% vs. 1.2%; adjusted OR 2.47; 95%CI 1.31-4.65). After limiting analyses to obese women (BMI >30 kg/m2), those with weight retention compared to those without had almost twice the likelihood of having cesarean delivery (adjusted OR 1.91; 95%CI 1.05-3.50) but cesarean delivery for arrest of dilation or descent did not reach statistical significance. In our cohort of multiparous women without a history of cesarean delivery, a third of women had weight retention after the first pregnancy. Given increased odds of cesarean delivery associated with weight retention even in multiparous women, our data support the recommendations for weight loss before conception in obese women.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

The impact of maternal BMI, gestational weight gain, and breastfeeding on early childhood weight: Analysis of a statewide WIC dataset

Early childhood obesity is a persistent health concern with more frequent and significant impact on low-income families. Maternal weight factors impact offspring weight status, but evidence on whether breastfeeding protects against this impact is mixed. This analysis examined a model to predict early childhood obesity risk, simultaneously accounting for maternal pre-pregnancy body mass index (BMI), gestational weight gain, and breastfeeding. The team analyzed 27,016 unique maternal-child dyadic records collected via the Supplemental Nutrition Program for Wisconsin Women, Infants, and Children (WIC) between 2009 and 2011. Generalized Linear Modeling, specifically logistic regression, was used to predict a child's risk of obesity given the mother's pre-pregnancy BMI, gestational weight gain, and duration of breastfeeding. For each 1 kg/m2 increase in pre-pregnancy BMI, there was a 4.5% increase in risk of obesity compared to children with mothers of normal BMI. Children whose mothers had excessive gestational weight gain were 50% more likely to have obesity compared to those whose mothers had ideal weight gain. For each week of additional breastfeeding, there was a 1.9% increased risk of obesity. The risk models did not differ by race. In this model, accounting for pre-pregnancy weight, gestational weight gain, and breastfeeding among a diverse, low-income sample, women with pre-pregnancy overweight and obesity or who had excessive gestational weight gain had the highest risk of early childhood obesity. While breastfeeding is healthy for many reasons, providers should focus on maternal weight-related behaviors when counseling mothers about how to avoid risk of early childhood obesity.

Maternal body mass index is a better indicator of large-for-gestational-age infants compared with a 75-g oral glucose tolerance test in early pregnancy: The JAGS trial.

There is no previous study comparing the predictive ability of maternal pre-pregnancy body mass index (BMI) versus a 75-g oral glucose tolerance test (OGTT) in early pregnancy for large-for-gestational-age (LGA) infants. This multi-institutional prospective cohort study included 966 pregnant Japanese women. A multiple logistic regression model was applied to compare the effect size of pre-pregnancy BMI, fasting plasma glucose (PG), and 1- and 2-h PG levels after a 75-g OGTT performed before 22weeks gestation for LGA. After these variables were included separately into the model as per continuous variables 1 standard deviation (SD) increase, they were included simultaneously. When pre-pregnancy BMI, fasting PG, and 1- and 2-h PG after a 75-g OGTT were separately included in the model, the adjusted odds ratios (ORs) for LGA per 1 SD increase in pre-pregnancy BMI, fasting, and 1- and 2-h PG were 1.55 (95% confidence interval [CI]: 1.26-1.91), 1.26 (95% CI: 1.03-1.54), 0.99 (95% CI: 0.78-1.25), and 1.17 (95% CI: 0.93-1.49), respectively. When these variables were included simultaneously, the adjusted ORs per 1 SD increase in pre-pregnancy BMI, fasting, and 1- and 2-h PG were 1.52 (95% CI: 1.23-1.88), 1.19 (95% CI: 0.96-1.46), 0.77 (95% CI: 0.57-1.03), and 1.30 (95% CI: 0.96-1.76), respectively. Maternal pre-pregnancy BMI was more strongly associated with LGA compared with a 75-g OGTT in early pregnancy. Health-care providers should recognize that women with a higher pre-pregnancy BMI carry a higher risk for having LGA infants regardless of the results of a 75-g OGTT.

Maternal prepregnancy body mass index and offspring attention-deficit/hyperactivity disorder: aquasi-experimental sibling-comparison, population-based design.

High maternal prepregnancy body mass index (BMI) has been associated with increased risk of offspring attention-deficit/hyperactivity disorder (ADHD). However, whether this effect is attributable to maternal or familial level confounds has been little examined. The present study sought to examine these associations, utilizing data from the medical records of a health care system which treats 350,000 patients annually and a sibling-comparison design in a sample of 4,682 children born to 3,645 mothers. When examining the overall maternal effect, a linear association was observed between maternal prepregnancy BMI and child ADHD [b=0.04, 95% confidence interval (95% CI)=0.02-0.06, p=.0003], such that a one-unit (i.e. 1kg/m2 ) increase in prepregnancy BMI was associated with a 4% increase in the odds of ADHD (exp b=1.04). However, when the model was reparameterized to take full advantage of the sibling design to allow for the examination of both maternal and child-specific effects, the child-specific prepregnancy BMI effect was not reliably different from zero (b=-0.08, 95% CI=-0.23 to 0.06, p=.24). In contrast, at the maternal-level, average prepregnancy BMI was a reliably non-zero predictor of child ADHD (b=0.04, 95% CI=0.02-0.06, p<.0001) with each one-unit increase in maternal prepregnancy BMI associated with a 4.2% increase in the odds of ADHD (exp b=1.04, 95% CI=1.02-1.06). The association between maternal prepregnancy BMI and offspring ADHD may be better accounted for by familial or maternal confounds rather than a direct causal effect of BMI.

Maternal pre-pregnancy body mass index and newborn telomere length.

BackgroundNewborn telomere length sets telomere length for later life. At birth, telomere length is highly variable among newborns and the environmental factors during in utero life for this observation remain largely unidentified. Obesity during pregnancy might reflect an adverse nutritional status affecting pregnancy and offspring outcomes, but the association of maternal pre-pregnancy body mass index (BMI) with newborn telomere length, as a mechanism of maternal obesity, on the next generation has not been addressed.MethodsAverage relative telomere lengths were measured in cord blood (n = 743) and placental tissue (n = 702) samples using a quantitative real-time PCR method from newborns from the ENVIRONAGE birth cohort in Belgium. By using univariate and multivariable adjusted linear regression models we addressed the associations between pre-pregnancy BMI and cord blood and placental telomere lengths.ResultsMaternal age was 29.1 years (range, 17–44) and mean (SD) pre-pregnancy BMI was 24.1 (4.1) kg/m2. Decline in newborn telomere length occurred in parallel with higher maternal pre-pregnancy BMI. Independent of maternal and paternal age at birth, maternal education, gestational age, newborn gender, ethnicity, birthweight, maternal smoking status, parity, cesarean section, and pregnancy complications, each kg/m2 increase in pre-pregnancy BMI was associated with a −0.50 % (95 % CI, −0.83 to −0.17 %; P = 0.003) shorter cord blood telomere length and a −0.66 % (95 % CI, −1.06 to −0.25 %; P = 0.002) shorter placental telomere length.ConclusionsMaternal pre-pregnancy BMI is associated with shorter newborn telomere lengths as reflected by cord blood and placental telomeres. These findings support the benefits of a pre-pregnancy healthy weight for promoting molecular longevity from early life onwards.Electronic supplementary materialThe online version of this article (doi:10.1186/s12916-016-0689-0) contains supplementary material, which is available to authorized users.

Associations of maternal prepregnancy body mass index and gestational weight gain with cardio-metabolic risk factors in adolescent offspring: a prospective cohort study.

To assess the associations of maternal prepregnancy body mass index (BMI) and rates of early-pregnancy, mid-pregnancy and total gestational weight gain with adolescent body fat distribution and cardio-metabolic outcomes. Population-based prospective cohort study. Western Australia. Thousand three hundred and ninety-two mothers and their children. Maternal prepregnancy weight was assessed by questionnaire. Maternal weights at a mean of 16.5 ± 2.2 SD and 34.1 ± 1.5 SD weeks of gestation were obtained from medical records. Offspring adiposity and cardio-metabolic outcomes were assessed at a median age 17.0 years [95% confidence interval (CI) range: 16.7, 17.7]. Adolescent BMI, waist circumference (WC), waist-to-hip ratio (WHR), blood pressure, total and HDL-cholesterol, triglycerides, insulin, glucose and HOMA-IR. Higher prepregnancy BMI was associated with higher adolescent BMI, WC, WHR, systolic blood pressure, insulin, glucose and HOMA-IR levels (P-values <0.05). Adjustment for adolescent current BMI attenuated the associations of prepregnancy BMI with adolescent cardio-metabolic outcomes. Higher weight gain in early-pregnancy, but not mid-pregnancy, was associated with higher adolescent BMI, WC and WHR (P-values <0.05), but not with other cardio-metabolic risk factors. Total gestational weight gain was associated with adolescent BMI and WC (P-values <0.05). Higher prepregnancy BMI and early-pregnancy weight gain were associated with increased risks of the high-metabolic risk cluster in adolescents (OR 1.57, 95% CI 1.33, 1.85 and OR 1.23, 95% CI 1.03, 1.47 per SD increase in prepregnancy BMI and early-pregnancy weight gain, respectively). Higher maternal prepregnancy BMI and early-pregnancy weight gain rate are associated with an adverse adolescent cardio-metabolic profile. These associations are largely mediated by adolescent BMI.

Fetal Sex and Race Modify the Predictors of Fetal Growth

The objective of this study is unknown if fetal sex and race modify the impact of maternal pre-pregnancy body mass index (BMI), and smoking on fetal growth. The authors studied markers of fetal growth in singleton offspring of 8,801 primiparous, normotensive women, enrolled in the Collaborative Perinatal Project. The authors tested for departures from additivity between sex/race and each predictor. The head-to-chest circumference ratio (HCC) decreased more, while birthweight and ponderal index (PI) increased more for each 1kg/m(2) increase in pre-pregnancy BMI among term females versus males (P=0.07, P<0.01 and P=0.08, interaction respectively). For term offspring of White compared with Black women, smoking independent of "dose" was associated with larger reductions in growth (165g vs. 68g reduction in birthweight, P<0.01, interaction), greater reduction in fetal placental ratio (P<0.01, interaction), PI (P<0.01, interaction), and greater increase in HCC (P=0.02), respectively. The association of BMI and smoking with fetal size appeared to be reversed in term versus preterm infants. Our study provides evidence that the associations of pre-pregnancy BMI and smoking are not constant across sex and race. This finding may be relevant to sex and race differences in neonatal and long term health outcomes.