Increase In Maternal Body Mass Index Research Articles

Maternal body mass index and cerebral palsy in children: Asystematic review and dose-response meta-analysis.

Accumulating studies indicate that maternal obesity is associated with the risk of cerebral palsy (CP); however, their conclusions have been inconsistent. To quantitatively estimate the association between maternal body mass index (BMI) and CP in offspring. PubMed, Embase and Web of Science. Articles published up to 18 September 2022 were searched that reported the correlation between maternal BMI and CP in children. Two reviewers independently extracted data and critically assessed articles. Pooled relative risks (RR) and 95% confidence intervals (CI) were estimated by the random-effects model. Subgroup analysis and meta-regression were performed to explore sources of heterogeneity. In total, 11 articles (8,407,668 participants) were identified for inclusion in our meta-analysis. For maternal underweight, no significant association was found with CP risk (RR 1.11, 95% CI 0.90, 1.38). The risk of CP was increased by 25% (RR 1.25, 95% CI 1.06, 1.47), 38% (RR 1.38, 95% CI 1.18, 1.61) and 127% (RR 2.27, 95% CI 1.82, 2.83) for maternal overweight, obesity and obesity grade 3, respectively. In addition, we observed a positive linear dose-response relationship, with the pooled risk of cerebral palsy in offspring increasing by 3% with each unit increase in maternal BMI. This meta-analysis indicates that the risk of CP in offspring grew with maternal overweight or obesity grades increasing, and was positively correlated with maternal BMI.

Maternal Preconception Body Mass Index and Early Childhood Nutritional Risk

BackgroundRisk factors for problematic child eating behaviors and food preferences are thought to begin during the preconception period. It is unknown if maternal preconception body mass index (BMI) is associated with child nutritional risk factors (eg, poor dietary intake and eating behaviors). ObjectivesWe aimed to determine whether maternal preconception BMI was associated with child nutritional risk. MethodsIn this longitudinal cohort study, a secondary data analysis of children ages 18 mo to 5 y were recruited from The Applied Research Group for Kids (TARGet Kids!), a primary care practice-based research network in Canada. The primary exposure was maternal preconception BMI. The primary outcome was parent-reported child nutritional risk score, measured using the Nutrition Screening for Every Preschooler/Toddler (NutriSTEP), an age-appropriate validated questionnaire. Fitted linear mixed effects models analyzed associations between maternal preconception BMI and child nutritional risk after adjusting for covariates. ResultsThis study included 4733 children with 8611 repeated NutriSTEP observations obtained between ages 18 mo to 5 y. The mean (standard deviation [SD]) maternal preconception BMI was 23.6 (4.4), where 73.1% of mothers had a BMI ≤24.9 kg/m2, and 26.9% had a BMI ≥25 kg/m2. The mean (SD) NutriSTEP total score was 13.5 (6.2), with 86.6% at low risk (score <21) and 13.4% at high risk (score ≥21). Each 1 unit increase in maternal preconception BMI was associated with a 0.09 increase in NutriSTEP total score (95% confidence interval [CI]: 0.05, 0.12; P ≤ 0.001). After stratification, each 1 unit increase in maternal BMI was associated with a 0.06 increase in mean NutriSTEP total score (95% CI: 0.007, 0.11; P = 0.025) in toddlers and 0.11 increase in mean NutriSTEP total score (95% CI: 0.07, 0.15; P < 0.001) in preschoolers. ConclusionHigher maternal preconception BMI is associated with slightly higher NutriSTEP total scores. This provides evidence that the preconception period may be an important time to focus on for improving childhood nutrition.This study was registered at clinicaltrials.gov as NCT01869530.

Maternal body mass index, offspring body mass index, and blood pressure at 18 years: a causal mediation analysis.

Understanding the natural history of hypertension is key to identifying prevention strategies. Previous work suggests that in utero exposures and offspring anthropometrics may play a role. This study examined the relationship between maternal pre-pregnancy body mass index (BMI) and the mediating role of childhood and adolescent BMI on offspring blood pressure at 18 years. We performed multivariable regression and causal mediation analyses within 3217 mother - offspring pairs from the Avon Longitudinal Study of Parents and Children prospective birth cohort. The main exposure was maternal pre-pregnancy BMI, and the outcome was offspring blood pressure at 18 years of age categorized as normal or elevated. Latent trajectory analysis was used to quantify the mediator, offspring BMI trajectories, derived from multiple measurements throughout childhood and adolescence. Mediation analyses were repeated using current offspring BMI at 18 years as a continuous variable. Multivariable logistic regression revealed that for every 1 unit increase in maternal BMI, the risk of elevated blood pressure at 18 years of age increased by 5% (aOR: 1.05, 95% CI: 1.03-1.07; p < 0.001). The strength of this association was reduced after adjusting for offspring BMI trajectory (aOR: 1.03, 95% CI: 1.00-1.05; p = 0.017) and eliminated after adjusting for offspring BMI at 18 years (aOR: 1.00; 95% CI: 0.98-1.03; p = 0.70). Causal mediation analysis confirmed offspring BMI at 18 years as a mediator, where BMI trajectory accounted for 46% of the total effect of maternal BMI on elevated offspring blood pressure and current BMI account for nearly the entire effect. Maternal pre-pregnancy BMI is associated with an increased risk of elevated blood pressure in offspring at 18 years of age although it appears to be entirely mediated by offspring BMI.

Effect of body mass index on the assisted reproductive outcome of frozen-thawed embryo transfer in patients with polycystic ovary syndrome

Objective: To investigate the effect of body mass index (BMI) on clinical pregnancy and neonatal outcomes in patients with polycystic ovary syndrome (PCOS) during frozen-thawed embryo transfer. Methods: A total of 650 patients with PCOS who received routine in vitro fertilization or intracytoplasmic sperm injection treatment for frozen-thawed embryo transfer from June 2014 to June 2019 in Tianjin Central Hospital of Gynecology Obstetrics were retrospectively analyzed. According to BMI, PCOS patients were divided into group A (18.5≤BMI<23 kg/m2, n=253), group B (23≤BMI<25 kg/m2, n=167), and group C (BMI≥25 kg/m2, n=230). The general information, clinical pregnancy outcomes, pregnancy complications, the incidence of macrosomia and low-birth-weight infants were compared in the three groups, and the influencing factors of neonatal birth weight were analyzed. Results: The embryo implantation rate, clinical pregnancy rate, and ongoing pregnancy rate all showed downward trend with the increase of BMI, but the differences were not statistically significant (all P>0.05). The live birth rate in group C [47.0% (108/230)] was significantly lower than those in groups A and B, with statistical significance (χ²=7.43, P=0.024). The late miscarriage rate was higher in group C [9.4% (13/139)] than in groups A and B (χ²=7.66, P=0.022). The birth rates of macrosomia in groups B [22.2% (16/72)] and group C [21.1% (16/76)] were significantly higher than that in group A, and the difference was statistically significant (χ²=14.15, P=0.001). There was no statistically significant difference in the incidence of gestational diabetes between the three groups (χ²=3.81, P=0.149). The incidence of hypertension disorders complicating pregnancy increased with the increase of BMI, and the difference was not statistically significant (P>0.05). Regression analysis showed that macrosomia was significantly associated with maternal pre-pregnancy BMI and gestational weeks, and the risk of macrosomia increased by 15% (95%CI: 3%-28%) for every increase in maternal BMI. Conclusions: The embryo implantation rate, clinical pregnancy rate, and ongoing pregnancy rate of PCOS patients in frozen-thawed embryo transfer cycles show downward trend with the increase of BMI. Obese patients with PCOS have a significant increase in late miscarriage rate and a significant decrease in live birth rate. The incidence of hypertension disorders complicating pregnancy in PCOS patients in the obese group has an increasing trend, and the birth rate of macrosomia has increased significantly. Therefore, it is recommended that obese women with PCOS lose weight scientifically before pregnancy to improve pregnancy and neonatal outcomes.

Higher maternal BMI early in pregnancy is associated with overweight and obesity in young adult offspring in Thailand

BackgroundRates of overweight and obesity among women of reproductive age have been steadily increasing worldwide and in Thailand. There is mounting evidence that maternal obesity during pregnancy is associated with an increased risk of obesity and other adverse health outcomes in the offspring, but such data are lacking for Thailand. We examined the associations between maternal body mass index (BMI) and anthropometry (particularly the likelihood of obesity) and cardiometabolic parameters in young adult offspring.MethodsThis was a prospective follow-up study of a birth cohort in Chiang Mai (Thailand). Pregnant women carrying singletons were recruited at their first antenatal visit (< 24 weeks of gestation) and followed until delivery in 1989–1990. Participants were their young adult offspring followed up in 2010. Maternal BMI was recorded at the first antenatal visit. The offspring underwent clinical assessments, including anthropometry, lipid profile, insulin sensitivity (HOMA-IR), blood pressure, and carotid intima-media thickness. The primary outcome of interest was the likelihood of obesity in the offspring.ResultsWe assessed 628 young adults (54% were females) at 20.6 ± 0.5 years of age (range 19.1–22.1 years). The young adult offspring of mothers with overweight/obesity was 14.1 kg (95%CI 9.7, 18.5; p < 0.0001) and 9.4 kg (95% CI 6.1, 12.8; p < 0.0001) heavier than those born to mothers with underweight or normal weight, respectively, and had BMI 3.46 kg/m2 (95%CI 2.26, 4.67; p < 0.0001) and 5.27 kg/m2 (95%CI 3.67, 8.68; p < 0.0001) greater, respectively. For every 1-kg/m2 increase in maternal BMI, the adjusted odds ratio (aOR) of offspring obesity was 25% greater (95%CI 1.10, 1.42; p < 0.001). Thus, the aOR of obesity in offspring of mothers with overweight/obesity was 4.6 times greater (95%CI 1.86, 11.26; p < 0.001) and nearly 17-fold greater (95%CI 1.96, 146.4; p = 0.010) compared to young adults born to mothers with normal weight or underweight, respectively. There were no observed associations between maternal BMI status and offspring metabolism or blood pressure.DiscussionMaternal overweight/obesity early in pregnancy was associated with increased BMI and greater odds of obesity in their young adult offspring in Thailand. These findings highlight the public health importance of fostering healthier lifestyle choices among women of reproductive age.

Maternal Obesity Before Pregnancy Predicts Offspring Blood Pressure at 18 Years of Age – A Causal Mediation Analysis

Background: Hypertension is the second most common pediatric chronic disease in Westernized countries. Understanding the natural history of hypertension is key to identifying prevention strategies. The present study will examine the relationship between maternal pre-pregnancy body mass index (BMI) and the possible mediating role of growth throughout childhood and adolescence on offspring blood pressure at 18 years. Methods: We performed multivariable regression and causal mediation analyses within 3217 mother - offspring pairs from the Avon Longitudinal Study of Parents and Children (ALSAPC) prospective birth cohort. The main exposure was maternal pre-pregnancy BMI. Latent trajectory analysis (LTA) was used to quantify the mediating variable of offspring BMI Z scores from 7 to 18 years of age. The main outcome was offspring blood pressure at 18 years of age categorized as normal or elevated as per the 2017 American Academy of Pediatrics guidelines. Findings: At 18 years of age, among 3217 offspring, 676 (21%) were overweight or obese, 865 (27%) had elevated blood pressure, and 510 (16%) were hypertensive. LTA identified five distinct offspring BMI trajectories. Multivariable logistic regression revealed that for every 1 unit increase in maternal BMI the risk of elevated blood pressure at 18 years of age increased by 5% (aOR: 1.05, 95% CI: 1.03 – 1.07; p <0.001) and this effect was reduced after adjusting for offspring BMI trajectory (aOR: 1.03, 95% CI: 1.00 – 1.05; p = 0.017). Causal mediation analysis confirmed offspring BMI trajectory as a mediator, accounting for 46% of the total effect of maternal BMI on elevated offspring blood pressure (aOR 1.22; 95% CI: 1.07-1.39). Interpretation: Maternal BMI prior to pregnancy is associated with an increased risk of elevated blood pressure in offspring at 18 years of age and is largely mediated by offspring BMI trajectory throughout childhood and adolescence. Funding Statement: The UK Medical Research Council and Wellcome (Grant ref: 217065/Z/19/Z) and the University of Bristol provide core support for ALSPAC. A comprehensive list of grants funding is available on the ALSPAC website (http://www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf). JMM was supported by a Canadian Institute of Health Research (CIHR) Applied Public Health Chair, MBA holds a Tier 2 Canada Research Chair (CRC) in the Developmental Origins of Chronic Disease. JMM holds grants from the CIHR, Diabetes Canada, the Heart and Stroke Foundation (HSF), the Cosmopolitan Foundation, and the Lawson Foundation. AD currently has research funding from CIHR, Research Manitoba and CHRIM. MBA holds grants from the CIHR, The Bill and Melinda Gates Foundation, the Canada Foundation for Innovation, the Garfield G. Weston Foundation, Prolacta Biosciences, Mitacs, the Canadian Institutes for Advanced Research, the Children’s Hospital Foundation of Manitoba, and Research Manitoba; NB and Drs JMM, MBA and AD were also supported by a Research Manitoba grant to the DEVOTION research cluster. Declaration of Interests: None of the authors report potential or actual conflicts of interest. All authors have completed and submitted a Conflict of Interest Statement. Ethics Approval Statement: Ethical approval was obtained from the ALSPAC Law and Ethics Committee and the Biomedical Research Ethics Board at the University of Manitoba. Informed consent for the use of data collected via questionnaires and clinics was obtained from participants following the recommendations of the ALSPAC Ethics and Law Committee at the time.

In-hospital mortality and morbidity among extremely preterm infants in relation to maternal body mass index.

Objective:To compare in-hospital survival and survival without major morbidities in extremely preterm infants in relation to maternal body mass index (BMI).Methods:This retrospective cohort study included extremely preterm infants (gestational age 220/7-286/7 weeks). This study was conducted at National Institute of Child Health and Human Development Neonatal Research Network sites. Primary outcome was survival without any major morbidity.Results:Maternal BMI data were available for 2415 infants. Survival without any major morbidity was not different between groups: 30.8% in the underweight/normal, 28.1% in the overweight, and 28.5% in the obese (P=.65). However, survival was lower in the obese group (76.5%) compared with overweight group (83.2%) (P=.02). Each unit increase in maternal BMI was associated with decreased odds of infant survival (P<.01).Conclusion:Survival without any major morbidity was not associated with maternal obesity. An increase in maternal prepregnancy BMI was associated with decreased odds of infant survival.

Maternal Body Mass Index and Risk of Congenital Heart Defects in Infants: A Dose-Response Meta-Analysis.

Objective The exact shape of the dose-response relationship between maternal body mass index (BMI) and the risk of congenital heart defects (CHDs) in infants has not been clearly defined yet. This study aims to further clarify the relationship between maternal obesity and the risk of CHDs in infants by an overall and dose-response meta-analysis. Methods PubMed, Embase, and Web of Science databases were searched to identify all related studies. The studies were limited to human cohort or case-control studies in English language. Random-effect models and dose-response meta-analysis were used to synthesize the results. Heterogeneity, subgroup analysis, sensitivity analysis, and publication bias were also assessed. Results Nineteen studies with 2,416,546 participants were included in our meta-analysis. Compared with the mothers with normal weight, the pooled relative risks (RRs) of infants with CHDs were 1.08 (95% CI=1.03-1.13) in overweight and 1.23 (95% CI=1.17-1.29) in obese mothers. According to the findings from the linear meta-analysis, we observed an increased risk of infants with CHDs (RR=1.07, 95% CI=1.06-1.08) for each 5 kg/m2 increase in maternal BMI. A nonlinear relationship between maternal BMI and risk of infants with CHDs was also found (p=0.012). Conclusion The results from our meta-analysis indicate that increased maternal BMI is related to increased risk of CHDs in infants.

Predictors of Steroid Hormone Concentrations in Early Pregnancy: Results from a Multi-Center Cohort.

Objectives To identify factors predicting maternal sex steroid hormone concentrations in early pregnancy. Methods The Infant Development and the Environment Study recruited healthy pregnant women from academic medical centers in four US cities. Gold standard liquid chromatography-tandem mass spectrometry was used to measure maternal sex steroids concentrations (total testosterone [TT], free testosterone [FT], estrone [E1], estradiol [E2], and estriol [E3] concentrations) in serum samples from 548 women carrying singletons (median = 11.7 weeks gestation). Women completed questionnaires on demographic and lifestyle characteristics. Results In multivariable linear regression analyses, hormone concentrations varied in relation to maternal age, body mass index (BMI), race, and parity. Older mothers had significantly lower levels of most hormones; for every year increase in maternal age, there was a 1-2% decrease in E1, E2, TT, and FT. By contrast, each unit increase in maternal BMI was associated 1-2% lower estrogen (E1, E2, E3) levels, but 1-2% higher androgen (TT, FT) concentrations. Hormone concentrations were 4-18% lower among parous women, and for each year elapsed since last birth, TT and FT were 1-2% higher (no difference in estrogens). Androgen concentrations were 18-30% higher among Black women compared to women of other races. Fetal sex, maternal stress, and lifestyle factors (including alcohol and tobacco use) were not related to maternal steroid concentrations. Conclusions for Practice Maternal demographic factors predict sex steroid hormone concentrations during pregnancy, which is important given increasing evidence that the prenatal endocrine environment shapes future risk of chronic disease for both mother and offspring.

Length of inter-pregnancy interval and subsequent preconception adiposity: Findings from a population-based cohort in the South of England

Introduction Maternal obesity is a key predictor of adverse short- and long-term health outcomes for both mother and child. The aim was to investigate the association between duration of the inter-pregnancy interval between successive pregnancies and change in maternal body mass index (BMI) during that period to assess the optimal interval associated with the least likelihood of starting the following pregnancy with a higher body weight. Methods A regional population-based cohort of prospectively collected routine healthcare data for antenatal care between January 2003 and September 2017 at University Hospital Southampton was utilised. Records of women with two or more consecutive singleton pregnancies (up to five) were analysed. Information on previous births was used to categorise pregnancies as first to second, second to third, third to fourth and fourth to fifth. Inter-pregnancy interval was defined as timing between a live birth and the next conception calculated by subtracting gestational age according to dating ultrasound scan of the latter birth from the interval between births. BMI was treated as a continuous and categorical variable, which was defined as underweight (BMI Findings In total, 20,571 women of which 12,636 had first two, 2654 had first three, 530 had first four and 120 had first five pregnancies were included. Two-thirds of women had gained weight when first presenting to antenatal care for their subsequent pregnancy with 21–24% moving into a higher compared to 4–6% moving into a lower BMI category. A significant positive linear association was found between change in maternal BMI with each year of inter-pregnancy interval with the coefficient remaining similar across pregnancies (adjusted increase in maternal BMI per year of inter-pregnancy interval 0.25 kg/m2, 95% CI: 0.22 to 0.28) and increasing for the fourth to fifth pregnancy (adjusted increase in maternal BMI per year of inter-pregnancy interval 0.36 kg/m2, 95% CI: 0.25 to 0.47). Compared to an interval of 24–35 months, there is a significantly increased risk of starting the next pregnancy with a higher weight than the previous one with an interval of 36 months or more for the second, third and fourth pregnancies (adjusted OR: 1.43, 95% CI: 1.29 to 1.59, P Conclusions Birth spacing of 12–23 months appears most protective against starting the next pregnancy with a higher body weight, even when adjusting for maternal age. In high-income country settings, getting pregnant within 1–2 years of the previous birth and advising those anticipating longer intervals to limit weight gain could be simple preconception preventive measures in tackling maternal obesity and hence achieving better subsequent maternal and offspring health outcomes.

Maternal concerns and perceptions of elementary school-age children's weight status.

The purpose of this study was to identify characteristics associated with maternal concerns for her child becoming overweight, and how these concerns are related to her perceptions of her child's weight. A school-based sample of 55 children and their mothers from Houston, Texas, participated in a cross-sectional survey. Mothers reported on their concerns and perceptions regarding their child's weight. Child and mother height and weight were directly assessed to calculate body mass index (BMI). Covariate-adjusted logistic regression models were conducted. Over one-third of mothers misperceived their child's weight status [9% (n=5) overestimated; 27% (n=15) underestimated]. Mothers of sons were less accurate compared with mothers of daughters. For every one unit increase in maternal BMI, mothers had 13% higher odds of being concerned of their child becoming overweight. Concerned mothers had 82% lower odds of underestimating their child's weight. In order for school-based childhood obesity prevention and intervention programs to be successful, parents must accurately perceive their elementary school-age child's weight status. School nurses can be vital to these efforts through proper training and resources. Nurses can use the "School Nurse Childhood Obesity Toolkit" and motivational interviewing techniques to address parental concerns and perceptions prior to teaching behavior modification strategies to children/families.

Using Genetic Variation to Explore the Causal Effect of Maternal Pregnancy Adiposity on Future Offspring Adiposity: A Mendelian Randomisation Study.

BackgroundIt has been suggested that greater maternal adiposity during pregnancy affects lifelong risk of offspring fatness via intrauterine mechanisms. Our aim was to use Mendelian randomisation (MR) to investigate the causal effect of intrauterine exposure to greater maternal body mass index (BMI) on offspring BMI and fat mass from childhood to early adulthood.Methods and FindingsWe used maternal genetic variants as instrumental variables (IVs) to test the causal effect of maternal BMI in pregnancy on offspring fatness (BMI and dual-energy X-ray absorptiometry [DXA] determined fat mass index [FMI]) in a MR approach. This was investigated, with repeat measurements, from ages 7 to 18 in the Avon Longitudinal Study of Parents and Children (ALSPAC; n = 2,521 to 3,720 for different ages). We then sought to replicate findings with results for BMI at age 6 in Generation R (n = 2,337 for replication sample; n = 6,057 for total pooled sample).In confounder-adjusted multivariable regression in ALSPAC, a 1 standard deviation (SD, equivalent of 3.7 kg/m2) increase in maternal BMI was associated with a 0.25 SD (95% CI 0.21–0.29) increase in offspring BMI at age 7, with similar results at later ages and when FMI was used as the outcome.A weighted genetic risk score was generated from 32 genetic variants robustly associated with BMI (minimum F-statistic = 45 in ALSPAC). The MR results using this genetic risk score as an IV in ALSPAC were close to the null at all ages (e.g., 0.04 SD (95% CI -0.21–0.30) at age 7 and 0.03 SD (95% CI -0.26–0.32) at age 18 per SD increase in maternal BMI), which was similar when a 97 variant generic risk score was used in ALSPAC.When findings from age 7 in ALSPAC were meta-analysed with those from age 6 in Generation R, the pooled confounder-adjusted multivariable regression association was 0.22 SD (95% CI 0.19–0.25) per SD increase in maternal BMI and the pooled MR effect (pooling the 97 variant score results from ALSPAC with the 32 variant score results from Generation R) was 0.05 SD (95%CI -0.11–0.21) per SD increase in maternal BMI (p-value for difference between the two results = 0.05). A number of sensitivity analyses exploring violation of the MR results supported our main findings. However, power was limited for some of the sensitivity tests and further studies with relevant data on maternal, offspring, and paternal genotype are required to obtain more precise (and unbiased) causal estimates.ConclusionsOur findings provide little evidence to support a strong causal intrauterine effect of incrementally greater maternal BMI resulting in greater offspring adiposity.

Maternal Body Mass Index and the Risk of Fetal Death, Stillbirth, and Infant Death

Importance Evidence suggests that maternal obesity increases the risk of fetal death, stillbirth, and infant death; however, the optimal body mass index (BMI) for prevention is not known. Objective To conduct a systematic review and meta-analysis of cohort studies of maternal BMI and risk of fetal death, stillbirth, and infant death. Data Sources The PubMed and Embase databases were searched from inception to January 23, 2014. Study Selection Cohort studies reporting adjusted relative risk (RR) estimates for fetal death, stillbirth, or infant death by at least 3 categories of maternal BMI were included. Data Extraction Data were extracted by 1 reviewer and checked by the remaining reviewers for accuracy. Summary RRs were estimated using a random-effects model. Main Outcomes and Measures Fetal death, stillbirth, and neonatal, perinatal, and infant death. Results Thirty eight studies (44 publications) with more than 10 147 fetal deaths, more than 16 274 stillbirths, more than 4311 perinatal deaths, 11 294 neonatal deaths, and 4983 infant deaths were included. The summary RR per 5-unit increase in maternal BMI for fetal death was 1.21 (95% CI, 1.09-1.35; I2 = 77.6%; n = 7 studies); for stillbirth, 1.24 (95% CI, 1.18-1.30; I2 = 80%; n = 18 studies); for perinatal death, 1.16 (95% CI, 1.00-1.35; I2 = 93.7%; n = 11 studies); for neonatal death, 1.15 (95% CI, 1.07-1.23; I2 = 78.5%; n = 12 studies); and for infant death, 1.18 (95% CI, 1.09-1.28; I2 = 79%; n = 4 studies). The test for nonlinearity was significant in all analyses but was most pronounced for fetal death. For women with a BMI of 20 (reference standard for all outcomes), 25, and 30, absolute risks per 10 000 pregnancies for fetal death were 76, 82 (95% CI, 76-88), and 102 (95% CI, 93-112); for stillbirth, 40, 48 (95% CI, 46-51), and 59 (95% CI, 55-63); for perinatal death, 66, 73 (95% CI, 67-81), and 86 (95% CI, 76-98); for neonatal death, 20, 21 (95% CI, 19-23), and 24 (95% CI, 22-27); and for infant death, 33, 37 (95% CI, 34-39), and 43 (95% CI, 40-47), respectively. Conclusions and Relevance Even modest increases in maternal BMI were associated with increased risk of fetal death, stillbirth, and neonatal, perinatal, and infant death. Weight management guidelines for women who plan pregnancies should take these findings into consideration to reduce the burden of fetal death, stillbirth, and infant death.

Associations of maternal BMI and gestational weight gain with neonatal adiposity in the Healthy Start study

Maternal obesity and weight gain during pregnancy are risk factors for child obesity. Associations may be attributable to causal effects of the intrauterine environment or genetic and postnatal environmental factors. We estimated associations of maternal prepregnancy body mass index (BMI) and gestational weight gain (GWG) overall and in early pregnancy, midpregnancy, and late pregnancy with neonatal adiposity. Participants were 826 women enrolled in a Colorado prebirth cohort who delivered term infants (2010-2013). GWG to 39 wk of gestation was predicted by using mixed models, and early pregnancy, midpregnancy, and late pregnancy rates of GWG (0-17, 17-27, and 27 wk to delivery) were calculated from repeated weight measures. Neonatal body composition was measured by using air-displacement plethysmography ≤3 d after birth. Each1-kg/m(2) increase in maternal BMI was associated with increased neonatal fat mass (5.2 g; 95% CI: 3.5, 6.9 g), fat-free mass (7.7 g; 95% CI: 4.5, 10.9 g), and percentage of body fat (0.12%; 95% CI: 0.08%, 0.16%). Each 0.1-kg/wk increase in predicted GWG was associated with increased fat mass (24.0 g; 95% CI: 17.4, 30.5 g), fat-free mass (34.0 g; 95% CI: 21.4, 46.6 g), and percentage of body fat (0.55%; 95% CI: 0.37%, 0.72%). No interaction was detected between BMI and GWG in their effects on neonatal body composition. Early pregnancy, midpregnancy, and late pregnancy rates of GWG were independently associated with fat mass and percentage of body fat. Midpregnancy and late pregnancy GWGs were associated with fat-free mass. An observed GWG that exceeded recommendations was associated with higher neonatal fat mass and fat-free mass but not percentage of body fat relative to adequate GWG. Maternal prepregnancy BMI and GWG, including period-specific GWG, were positively and independently associated with neonatal adiposity. Associations of early and midpregnancy weight gain with neonatal adiposity support the hypothesis that greater maternal weight gain during pregnancy, regardless of prepregnancy BMI, is directly related to offspring adiposity at birth. The Healthy Start study was registered as an observational study at clinicaltrials.gov as NCT02273297.

Maternal Body Mass Index and the Risk of Fetal Death, Stillbirth, and Infant Death

Greater maternal body mass index (BMI) before or during early pregnancy is associated with an increased risk of fetal death, stillbirth, perinatal death, neonatal death, and infant death. This systematic review and meta-analysis of cohort studies was conducted to determine the strength of these associations, the shape of the dose-response relationship, potential confounding, and potential sources of heterogeneity. PubMed and EMBASE databases were searched for cohort studies that reported on maternal BMI before or in early pregnancy and risk of fetal death, miscarriage, stillbirth, and neonatal, perinatal, and infant death. Articles that provided adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for 3 or more categories of BMI (<18.5 or <20, <25, 30–<35, 35–<40, and 40–<45 kg/m2) were eligible. Summary RRs per 5 BMI units for the association between maternal BMI and fetal and infant death were calculated using the random effects model. Absolute risks were reported per 10,000 pregnancies for BMIs of 20, 25, and 30 kg/m2. Thirty-eight studies were included in the dose-response analysis. Seven studies investigated the association between BMI and fetal death. The summary RR was 1.21 (95% CI, 1.09–1.35). For BMIs of 20, 25, and 30 kg/m2, absolute risks were 76 (reference standard), 82 (95% CI, 76–88), and 102 (95% CI, 93–112), respectively. Five of these studies reported on BMI and miscarriages; the summary RR was 1.16 (95% CI, 1.07–1.26). Eighteen studies investigated BMI and stillbirth; the summary RR was 1.24 (95% CI, 1.18–1.30). For BMIs of 20, 25, and 30 kg/m2, absolute risks were 40 (reference standard), 48 (95% CI, 46–51), and 59 (95% CI, 55–63), respectively. Studies that reported results for antepartum and intrapartum stillbirths had summary RRs of 1.28 (95% CI, 1.15–1.43) and 0.90 (95% CI, 0.76–1.06), respectively. Eleven studies assessed BMI and perinatal death; the summary RR was 1.16 (95% CI, 1.00–1.35). For BMIs of 20, 25, and 30 kg/m2, absolute risks were 66 (reference standard), 73 (95% CI, 67–81), and 86 (95% CI, 76–98), respectively. Twelve studies analyzed BMI and neonatal death; the summary RR was 1.15 (95% CI, 1.07–1.23). For BMIs of 20, 25, and 30 kg/m2, absolute risks were 20 (reference standard), 21 (95% CI, 19–23), and 24 (95% CI, 22–27), respectively. For early and postneonatal deaths, the summary RRs were 1.31 (95% CI, 1.22–1.41) and 1.14 (95% CI, 1.06–1.22). Four studies analyzed maternal BMI and infant death; the summary RR was 1.18 (95% CI, 1.09–1.28). For BMIs of 20, 25, and 30 kg/m2, absolute risks were 33 (reference standard), 37 (95% CI, 34–39), and 43 (95% CI, 40–47), respectively. Even small increases in maternal BMI were associated with increased risks of adverse pregnancy outcomes. Weight management guidelines for women who plan pregnancies should consider these findings to reduce the incidence of adverse outcomes.

Maternal body mass index and the risk of fetal death, stillbirth, and infant death: a systematic review and meta-analysis.

Evidence suggests that maternal obesity increases the risk of fetal death, stillbirth, and infant death; however, the optimal body mass index (BMI) for prevention is not known. To conduct a systematic review and meta-analysis of cohort studies of maternal BMI and risk of fetal death, stillbirth, and infant death. The PubMed and Embase databases were searched from inception to January 23, 2014. Cohort studies reporting adjusted relative risk (RR) estimates for fetal death, stillbirth, or infant death by at least 3 categories of maternal BMI were included. Data were extracted by 1 reviewer and checked by the remaining reviewers for accuracy. Summary RRs were estimated using a random-effects model. Fetal death, stillbirth, and neonatal, perinatal, and infant death. Thirty eight studies (44 publications) with more than 10,147 fetal deaths, more than 16,274 stillbirths, more than 4311 perinatal deaths, 11,294 neonatal deaths, and 4983 infant deaths were included. The summary RR per 5-unit increase in maternal BMI for fetal death was 1.21 (95% CI, 1.09-1.35; I2 = 77.6%; n = 7 studies); for stillbirth, 1.24 (95% CI, 1.18-1.30; I2 = 80%; n = 18 studies); for perinatal death, 1.16 (95% CI, 1.00-1.35; I2 = 93.7%; n = 11 studies); for neonatal death, 1.15 (95% CI, 1.07-1.23; I2 = 78.5%; n = 12 studies); and for infant death, 1.18 (95% CI, 1.09-1.28; I2 = 79%; n = 4 studies). The test for nonlinearity was significant in all analyses but was most pronounced for fetal death. For women with a BMI of 20 (reference standard for all outcomes), 25, and 30, absolute risks per 10,000 pregnancies for fetal death were 76, 82 (95% CI, 76-88), and 102 (95% CI, 93-112); for stillbirth, 40, 48 (95% CI, 46-51), and 59 (95% CI, 55-63); for perinatal death, 66, 73 (95% CI, 67-81), and 86 (95% CI, 76-98); for neonatal death, 20, 21 (95% CI, 19-23), and 24 (95% CI, 22-27); and for infant death, 33, 37 (95% CI, 34-39), and 43 (95% CI, 40-47), respectively. Even modest increases in maternal BMI were associated with increased risk of fetal death, stillbirth, and neonatal, perinatal, and infant death. Weight management guidelines for women who plan pregnancies should take these findings into consideration to reduce the burden of fetal death, stillbirth, and infant death.

Parent-Offspring Body Mass Index Associations in the Norwegian Mother and Child Cohort Study: A Family-based Approach to Studying the Role of the Intrauterine Environment in Childhood Adiposity

In the present study, the authors investigated the role of the intrauterine environment in childhood adiposity by comparing the maternal-offspring body mass index (BMI) association with the paternal-offspring BMI association when the offspring were 3 years of age, using parental prepregnancy BMI (measured as weight in kilograms divided by height in meters squared). The parent-offspring trios (n = 29,216) were recruited during pregnancy from 2001 to 2008 into the Norwegian Mother and Child Cohort Study conducted by The Norwegian Institute of Public Health. Data from self-administered questionnaires were used in linear regression analyses. Crude analyses showed similar parental-offspring BMI associations; the mean difference in offspring BMI was 0.15 (95% confidence interval: 0.13, 0.16) per each 1-standard-deviation increase in maternal BMI and 0.15 (95% confidence interval: 0.13, 0.17) per each 1-standard-deviation increase in paternal BMI. After all adjustments, the mean difference in offspring BMI per each 1-standard-deviation increment of maternal BMI was 0.12, and the mean difference in offspring BMI per each 1-standard-deviation increment of paternal BMI was 0.13. There was no strong support for heterogeneity between the associations (P > 0.6). In conclusion, results from the present large population-based study showed similar parental-offspring BMI associations when the offspring were 3 years of age, which indicates that the maternal-offspring association may be explained by shared familial (environmental and genetic) risk factors rather than by the intrauterine environment.

54 Impact of Maternal Body Mass Index on Offspring Liver Lipid Depends on Mode of Delivery

Background: Maternal overweight/obesity is associated with increased risk of Caesarean Section (CS) and offspring metabolic syndrome, though the mediating biological pathway is unknown. In an animal model pre-labour CS in comparison with vaginal delivery (VD), is associated with significantly higher offspring intrahepatocellular lipid (IHCL), a central component of the metabolic syndrome (Hyde MJ, 2010).Aim: To examine the effects of maternal Body Mass Index (BMI) and mode of delivery on neonatal IHCL.Methods: With research ethics approval and informed written parent consent we employed 1H Magnetic Resonance Spectroscopy of liver during natural sleep in healthy term neonates (Thomas EL, 2008). We used analysis of covariance to explore the effect of maternal BMI, diabetes and mode of delivery, and infant gender, birth weight and postnatal age and their interactions on IHCL (presented as the ratio of lipid CH2/water).Results: To date we have studied 57 infants (45 VD, 12 pre-labour CS). IHCL ranged from 0 to 5.5, and maternal BMI from 17 to 35 kg/m2. There was a significant interaction between maternal BMI and mode of delivery (p=0.010). In neonates born by pre-labour CS, IHCL increased by a mean of 29% [95%CI 9-54%] per unit increase in maternal BMI (p=0.004). Maternal BMI had no impact on IHCL in VD infants (p=0.81).Conclusion: VD may activate pathways that protect against liver lipid accumulation in the presence of increasing maternal BMI. Pre-labour CS may pose an added risk for the development of the metabolic syndrome in offspring of overweight/ obese mothers.

Percentage Change in Antenatal Body Mass Index as a Predictor of Neonatal Macrosomia

We wanted to evaluate the predictive value of percentage change in antenatal maternal body mass index (BMI) as it relates to macrosomia, as well as to compare change in pregnancy BMI with existing weight gain guidelines. We analyzed data from 6 months of consecutive deliveries, focusing on first visit (first trimester) BMI, last visit (37 weeks or later) BMI, and fetal birth weight. Using regression and chi(2) analyses, we evaluated the relationship between change in BMI and macrosomia. Of the 238 consecutive deliveries, we were able to analyze data from 186, of which 15.6% (n = 29) of the infants were macrosomic. Among macrosomic infants, 86.2% (25/29) of their mothers had a 25% or greater increase in BMI compared with 6.6% (10/157) of mothers of normal-weight infants (P <.001), for a relative risk 13.5% (95% confidence interval [CI], 7.3%-25.1%). Percentage change in BMI of 25% or greater had a sensitivity of 86.2% (95% CI, 68.3%-96.1%), a specificity of 93.6% (95% CI, 88.6%-96.9%), a positive predictive value of 71.4% (95% CI, 53.7%-85.4%), and a negative predictive value 97.4% (95% CI, 93.4%-99.3%) for macrosomia. Logistic regression adjusted for maternal age, race, parity, and gravidity showed that those women whose BMI increased 25% or greater were more than 200 times more likely (odds ratio [OR] = 219.3; 95% CI, 38.8-1,238.6; P <.001) to give birth to a macrosomic infant. Further adjusting for initial BMI strengthened the association (OR=1,062.4; 95% CI, 83.2-13,572.2; P < 001). Regardless of weight gain, when compared with Institute of Medicine weight gain recommendations, change in BMI or 25% or greater was associated with macrosomia (P <.001). Independent of initial pregnancy BMI or absolute weight gain, an increase in maternal BMI of 25% or greater during pregnancy is highly predictive of macrosomia.

Multiple sexual partners and early menarche are risk factors for preeclampsia in an African population

ISRAEL HENDLER, SEAN BLACKWELL, SHOBHA MEHTA, JANICE WHITTY, EVIE RUSSELL, YORAM SOROKIN, DAVID COTTON, Wayne State University, Obstetrics and Gynecology, Detroit, Michigan OBJECTIVE: Adipose tissue derived proteins (adipokines) have been suggested to play a role in the pathogenesis of preeclampsia in obese and non obese women. The objective was to compare the levels of different Adipokines between women with and without preeclampsia based on maternal body mass index (BMI). STUDY DESIGN: This was a prospective nested case control study among third trimester singleton pregnancies with severe or mild preeclampsia (PIH) (n = 85) compared to normotensive controls (n = 23). Women with chronic hypertension or gestational diabetes mellitus were excluded. Severe and mild preeclampsia was defined according to standard criteria. Levels of adiponectin, leptin and resistin were measured in serum prior to delivery by radioimmunoassay or ELISA and were analyzed with non parametric tests. RESULTS: Adipokines levels were available for 20 (mean gestational age 38.3 G 1.7 wks) normotensive and 75 mPIH and sPIH women. (37.3 G 2.8 weeks). The rate of obesity (BMI R30 kg/m) was 43.5 and 65.9%, respectively, P = .04). Leptin levels gradually increased with maternal BMI; (!30 kg/m), class I and II obesity (30-39.9 kg/m) and extreme obesity (R40 kg/m), (19.2; 2.2-38.8, 27.5; 13-54.9, and 38.0; 9.2-66.0 ng/mL, P ! .05). After adjustment for maternal BMI, leptin was not associated with preeclampsia (OR1.03, 95%CI 0.99-1.08). Adiponectin and resistin levels were not correlated (Spearman’s rho0.85, P = .41) and there was no difference in their levels when compared between obese and non obese patients (9.2; 1.8-31.1 vs. 9.0; 2.6-30.4ug/mL, P = .11 and 1.5; 0.5-5.4 vs. 2.0; 0.7-7.9 ng/mL, P = .50 respectively), or between patients with and without preeclampsia. Leptin, adiponectin and resistin levels did not diverge between obese or non obese patients with and without preeclampsia. CONCLUSION: Increase in maternal BMI is associated with increased serum leptin levels. In this study, there was no association between leptin, adiponectin or resistin levels and preeclampsia both in obese and non obese women.