The Ibadan Pregnancy Cohort Study (IbPCS), a Prospective Cohort Study Protocol

Maternal obesity during pregnancy as a risk for early-life asthma

Background and aims: Parental obesity is one of the important factors that is strongly linked with the development of offspring obesity. When both parents are obese, the risk of offspring being obese is greater than when one parent is obese. Irrespective of the exposure time of parental overweight and obesity, studies have consistently found that parental overweight and obesity is positively associated with offspring overweight and obesity. Few longitudinal birth-cohort studies have examined pre-pregnancy parental overweight or obesity and whether it is positively associated with offspring overweight and obesity in the long term. Additionally, there are limited studies reporting on the association of prenatal parental obesity with offspring body mass index (BMI) change, and even less is known about the association between long-term post-partum parental BMI change and the risk of offspring obesity. The aim of the current study is to investigate the association between parental obesity and offspring obesity over the life course, using data from birth-cohort studies. This study examines the longitudinal association between prenatal parental BMI and offspring BMI and adiposity in infancy, childhood, adolescence and adulthood. This study also investigates the association between prenatal parental BMI and offspring BMI change in childhood, adolescence and adulthood. Finally, this study adds to research examining the association between 21 years maternal post-partum weight change (PPWC) and the risk of adulthood obesity in offspring. Methods: Data are from two cohorts-Universiti Sains Malaysia Pregnancy Cohort which consists of 145 respondents who provided details of pre-pregnancy parental weight and height and weight and length of offspring at the 12-month follow-up; and the Mater-University of Queensland Study of Pregnancy (MUSP) which consists of 1494 participants with complete weight and height for pre-pregnancy paternal–maternal and offspring weight and height at 5, 14 and 21 years. A series of models were used to test the association between prenatal parental BMI and offspring outcomes to adjust the potential covariates obtained from either cohorts (e.g. maternal factors: gestational weight gain; offspring factors: birth weight, TV watching hours at 14 years). Multiple linear regression, logistic regression and multinomial regression were used (continuous or categorical predictors) to examine the association between pre-pregnancy parental BMI and its categories, and offspring BMI and its categories. Multiple imputation was used to address the issue of missing values in covariates. Generalized estimating equation models were used to examine the longitudinal parental–offspring BMI association in infants and were again used to determine the differential effect size of prenatal parental BMI on childhood, adolescence and adulthood. Finally, we analysed the association between 21 years maternal postpartum BMI change and offspring BMI and waist circumference (WC at 21 years using multiple linear regression and multinomial logistic regression. Results: Major findings are as follows: 1) A significant association was found between maternal BMI and child’s weight for age z-score (WAZ), weight for height z-score (WHZ) and BMI for age z-score (BAZ) at 12 months; although it was attenuated in the fully adjusted model. 2) After adjustment for confounders, for each unit increase in paternal and maternal BMI, the BMI of young adult offspring increased by 0.33 kg/m2 and 0.35 kg/m2, and the waist circumference (WC) increased by 0.76 cm and 0.62 cm, respectively. Offspring at 21 years were at six times more at risk of being overweight/obese (OW/OB) when both parents were OW/OB, compared to offspring of normal-weight parents. 3) A total of 14.7% of the offspring experienced BMI change from normal at 5 years to OW/OB at 14 years, 15.3% from normal at 14 years to OW/OB at 21 years. Overall, the strength of the association of parental BMI with offspring BMI was stronger as offspring became older. When both parents were OW/OB, these associations were stronger than when one parent was OW/OB. 4) In two decades, mothers who had highest weight change were associated with adult offspring’s risk of OW/OB and abdominal obesity with odds of 1.47 (95%CI: 1.08–2.00) and 1.50 (95%CI: 1.10–2.02), respectively. Conclusions: These findings suggest that parental BMI before pregnancy has a long-term association with offspring BMI from early childhood to adulthood. We found mother–offspring and father–offspring associations were of similar strength and direction. There was no offspring male–female differential association. Our study further demonstrated that parental pre-pregnancy nutritional status is an important predictor in early life that influences offspring overweight and obesity throughout life. Intervening to reduce the prevalence of overweight or obesity in early life by targeting parents may have potential benefits. Encouraging adults to maintain a healthy lifestyle in this challenging obesogenic environment may benefit both themselves and subsequent generations. Studies are warranted to further explore parental lifestyle (dietary and physical activities) before pregnancy and the impact of intervention to improve parental lifestyle on offspring outcomes in the long term.

Care of Women with Obesity in Pregnancy

Purpose: Obesity often aggregates within families and parental obesity has been identified as a risk factor. To examine the different effects of maternal and paternal body mass index on the prevalence rate and risk of overweight in children. Materials and Methods: A total of 1418 students, aged 12 or 13 years, were recruited for analysis. Children's body height, weight and waist and hip circumferences were obtained. Self-reported body height and weight of their parents were collected. The 85th percentile of body mass index (BMI) was used as cutoff points to identify the children being overweight. Spearman's correlation and logistic regression analysis were used to examine the parent-offspring BMI relationship. Paternal and maternal BMI were classified into four groups using the quartile categories to examine their different effects on the prevalence rate and risk of children overweight. Results: The association of children's BMI with parents' BMI was the strongest, closely followed by children's waist circumference whereas waist-hip ratio barely had any association. The Spearman's correlation coefficient of the mother-daughter association was the highest among all the parent-offspring association. Among the boys, the prevalence rate for being overweight increased significantly from 9.2% in the lowest quartile to 21.3% in the highest quartile of paternal BMI (p trend＜0.005). The effect of maternal BMI on the prevalence rate for being overweight was also noted (p trend＜0.0001). Among the girls, an increasing rate of being overweight for the increasing quartile of paternal and maternal BMI was also noted (p trend＜0.0001). Multiple logistic regression analysis revealed that maternal BMI was significantly associated with boys' overweight with the odds ratios increased from 1.0 in the lowest quartile to 2.33 in the highest quartile of maternal BMI (p＜0.001). However, the association between paternal BMI and boys' overweight was marginally significant (p=0.055). Among the girls, both maternal and paternal BMI were significantly associated with girls' overweight (p＜0.001 and p=0.001, respectively). Conclusion: Maternal BMI was an independent risk factor of overweight in both boys and girls. Paternal BMI was also associated with girls' overweight.

We investigated the association between maternal early pregnancy body mass index (BMI) and offspring sleep apnea diagnosis. We conducted a nationwide cohort study among 3,281,803 singleton live births in Sweden born 1983-2015. Using national registers with prospectively recorded information, we followed participants for a sleep apnea diagnosis from 2 to up to 35 years of age. We compared sleep apnea risks by early pregnancy BMI categories using hazard ratios with 95% confidence intervals from adjusted Cox models. To address confounding by factors shared within families, we conducted sibling-controlled analyses and studied the relation of siblings' maternal BMI with index offspring's sleep apnea risk. There were 17,830 sleep apnea diagnoses. Maternal early pregnancy BMI was positively associated with offspring sleep apnea risk; compared with women with normal BMI (18.5-24.9), adjusted hazard ratios (95% confidence intervals) of offspring sleep apnea for maternal BMI categories 25.0-29.9 (overweight), 30.0-34.9 (obesity class I), and ≥35.0 (obesity class II or III) were, respectively, 1.14 (1.09, 1.19), 1.28 (1.20, 1.36), and 1.40 (1.27, 1.54). Corresponding hazard ratios from sibling-controlled analyses representing risk change for maternal BMI differences between pregnancies were, respectively, 1.13 (1.01, 1.26), 1.17 (0.97, 1.42), and 1.32 (0.97, 1.80). Hazard ratios by siblings' maternal BMI were attenuated, suggesting a weak role for shared familial factors. Other pregnancy, birth, and neonatal complications were associated with offspring sleep apnea risk but did not substantially mediate the association with maternal obesity. Maternal overweight and obesity are associated with offspring sleep apnea risk in a dose-response manner. Zhu MQ, Cnattingius S, O'Brien LM, Villamor E. Maternal early pregnancy body mass index and risk of sleep apnea in the offspring. J Clin Sleep Med. 2024;20(10):1675-1684.

BackgroundA causal relationship between maternal obesity and offspring asthma is hypothesized to begin during early development, but no underlying mechanism for the found association is identified. We quantitatively examined mediation by offspring body mass index (BMI) in the association of maternal pre-pregnancy BMI on risk of asthma and wheezing during the first 7–8 years of life in a large Amsterdam born birth cohort.MethodsFor 3185 mother-child pairs, mothers reported maternal pre-pregnancy BMI and offspring outcomes “ever being diagnosed with asthma” and “wheezing in the past 12 months” on questionnaires. We measured offspring height and weight at age 5–6 years. We performed a multivariate log linear regression comparing outcomes in offspring of mothers with different BMI categories. For each category we quantified and tested mediation by offspring BMI and also investigated interaction by parental asthma.ResultsAt the age of 7–8 years, 8% of the offspring ever had asthma and 7% had current wheezing. Maternal pre-pregnancy obesity was associated with higher risks of asthma (adjusted RR 2.32 (95% CI: 1.49–3.61) and wheezing (adjusted RR 2.16 (95% CI: 1.28–3.64). Offspring BMI was a mediator in the association between maternal BMI and offspring wheezing, but not for asthma. There was no interaction by parental asthma.ConclusionsMaternal pre-pregnancy obesity was associated with higher risks of offspring asthma and wheezing. The association between maternal obesity and offspring wheezing was both direct and indirect (mediated) through the child’s own BMI.

Excessive early childhood adiposity is a prevalent and increasing concern in many parts of the world. Parental obesity is one of the several factors previously associated with infant and early childhood weight, length and adiposity. Parental obesity represents a surrogate marker of the complex interplay among genetic, epigenetic and shared environmental factors, and is potentially modifiable. The relative contributions of maternal and paternal body mass index (BMI) to infant and early childhood growth, as well as the timing of such effects, have not been firmly established. Utilizing serial infant measurements and growth curve modelling, this is the largest study to fully characterize and formally compare associations between maternal and paternal BMI and offspring growth across the entire infancy and early childhood period. Maternal obesity is a stronger determinant of offspring BMI than paternal obesity at birth and from 2 to 3 years of age, suggesting that prevention efforts focused particularly on maternal lifestyle and BMI may be important in reducing excess infant BMI. The observation that maternal BMI effects are not constant, but rather present at birth, wane and re-emerge during late infancy, suggests that there is a window of opportunity in early infancy when targeted interventions on children of obese mothers may be most effective. Parental obesity influences infant body size. To fully characterize their relative effects on infant adiposity, associations between maternal and paternal body mass index (BMI) category (normal: ≤25 kg m(-2) , overweight: 25 - <30 kg m(-2) , obese: ≥30 kg m(-2) ) and infant BMI were compared in Fels Longitudinal Study participants. A median of 9 serial weight and length measures from birth to 3.5 years were obtained from 912 European American children born in 1928-2008. Using multivariable mixed effects regression, contributions of maternal vs. paternal BMI status to infant BMI growth curves were evaluated. Cubic spline models also included parental covariates, infant sex, age and birth variables, and interactions with child's age. Infant BMI curves were significantly different across the three maternal BMI categories (Poverall < 0.0001), and offspring of obese mothers had greater mean BMI at birth and between 1.5 and 3.5 years than those of over- and normal weight mothers (P ≤ 0.02). Average differences between offspring of obese and normal weight mothers were similar at birth (0.8 kg m(-2) , P = 0.0009) and between 2 and 3.5 years (0.7-0.8 kg m(-2) , P < 0.0001). Infants of obese fathers also had BMI growth curves distinct from those of normal weight fathers (P = 0.02). Infant BMI was more strongly associated with maternal than paternal obesity overall (P < 0.0001); significant differences were observed at birth (1.11 kg m(-2) , P = 0.006) and from 2 to 3 years (0.62 kg m(-2) , P3 years = 0.02). At birth and in later infancy, maternal BMI has a stronger influence on BMI growth than paternal BMI, suggesting weight control in reproductive age women may be of particular benefit for preventing excess infant BMI.

Maternal underweight and obesity are prevalent conditions, associated with chronic, low-grade inflammation, poor fetal development, and long-term adverse outcomes for the child. The placenta senses and adapts to the pregnancy environment in an effort to support optimal fetal development. However, the mechanisms driving these adaptations, and the resulting placental phenotypes, are poorly understood. We hypothesised that maternal underweight and obesity would be associated with increased prevalence of placental pathologies in term and preterm pregnancies. Data from 12,154 pregnancies were obtained from the Collaborative Perinatal Project, a prospective cohort study conducted from 1959 to 1974. Macro- and microscopic placental pathologies were analysed across maternal prepregnancy body mass index (BMI) to assess differences in the presence of pathologies among underweight, overweight, and obese BMI groups compared to normal weight reference BMI at term and preterm. Placental pathologies were also assessed across fetal sex. Pregnancies complicated by maternalobesity had placentae with increased fetal inflammation at preterm, and increased inflammation of maternal gestational tissues at term. In term pregnancies, increasing maternal BMI associated with increased maternal vascular malperfusion (MVM), odds of an appropriately mature placenta for gestational age, and placental weight, and decreased placental efficiency. Male placentae, independent of maternal BMI, had increased inflammation, MVM, and placental efficiency than female placentae, particularly at term. Maternal underweight and obesity are not inert conditions for the placenta, and the histomorphological changes driven by suboptimal maternal BMI may serve as indicators of adversities experienced in utero and potential predictors of future health trajectories.

Maternal obesity, pregestational type 1 diabetes, and gestational diabetes have been reported to increase the risks for large birth weight and preterm birth in offspring. However, the associations for insulin-treated diabetes and non-insulin-treated type 2 diabetes, as well as the associations for joint diabetes disorders and maternal body mass index, with these outcomes are less well documented. To examine associations of maternal diabetes disorders, separately and together with maternal underweight or obesity, with the offspring being large for gestational age and/or preterm at birth. This population-based cohort study used nationwide registries to examine all live births (n = 649 043) between January 1, 2004, and December 31, 2014, in Finland. The study and data analysis were conducted from April 1, 2018, to October 10, 2018. Maternal prepregnancy body mass index, pregestational diabetes with insulin treatment, pregestational type 2 diabetes without insulin treatment, and gestational diabetes. Offspring large for gestational age (LGA) at birth and preterm delivery. Logistic regression models were adjusted for offspring birth year; parity; and maternal age, country of birth, and smoking status. Of the 649 043 births, 4000 (0.62%) were delivered by mothers who had insulin-treated diabetes, 3740 (0.57%) by mothers who had type 2 diabetes, and 98 568 (15.2%) by mothers who had gestational diabetes. The mean (SD) age of mothers was 30.15 (5.37) years, and 588 100 mothers (90.6%) were born in Finland. Statistically significant interactions existed between maternal body mass index and diabetes on offspring LGA and prematurity (insulin-treated diabetes: LGA F = 3489.0 and prematurity F = 1316.4 [P < .001]; type 2 diabetes: LGA F = 147.3 and prematurity F = 21.9 [P < .001]; gestational diabetes: LGA F = 1374.6 and prematurity F = 434.3 [P < .001]). Maternal moderate obesity, compared with normal-weight mothers with no diabetes, was associated with a mildly increased risk of having an offspring LGA (1069 [3.5%] vs 5151 [1.5%]; adjusted odds ratio [aOR], 2.45; 95% CI, 2.29-2.62), and mothers with insulin-treated diabetes had markedly elevated risks of having an offspring LGA (1585 [39.6%] vs 5151 [1.5%]; aOR, 43.80; 95% CI, 40.88-46.93) and a preterm birth (1483 [37.1%] vs 17 481 [5.0%]; aOR, 11.17; 95% CI, 10.46-11.93). Mothers who were moderately obese with type 2 diabetes were at increased risks of LGA (132 [16.4%] vs 5151 [1.5%]; aOR, 12.44; 95% CI, 10.29-15.03) and prematurity (83 [10.3%] vs 17 481 [5.0%]; aOR, 2.14; 95% CI, 1.70-2.69). Mothers who were moderately obese with gestational diabetes had a milder risk of LGA (1195 [6.7%] vs 5151 [1.5%]; aOR, 4.72; 95% CI, 4.42-5.04). Among spontaneous deliveries, the risks were strongest for moderately preterm births, but insulin-treated diabetes was associated with an increased risk also for very and extremely preterm births. Maternal insulin-treated diabetes appeared to be associated with markedly increased risks for LGA and preterm births, whereas obesity in mothers with type 2 diabetes had mild to moderately increased risks; these findings may have implications for counseling and managing pregnancies.

Prenatal experiences can influence fetal brain development. To examine associations of maternal prenatal body mass index (BMI) with cognition and behavior of offspring born full-term. This cohort study examined follow-up data from a breastfeeding promotion intervention at 31 hospitals and affiliated polyclinics in the Republic of Belarus. Participants included 11 276 children who were evaluated from birth (1996-1997) to adolescence (2017-2019), with maternal BMI information available in prenatal medical records. Maternal BMI, calculated as weight in kilograms divided by height in meters squared, after 35 weeks gestation; secondary analyses examined maternal BMI at other time points and paternal BMI. Trained pediatricians assessed child cognition with the Wechsler Abbreviated Scales of Intelligence (WASI) at 6.5 years and the computerized self-administered NeuroTrax battery at 16 years, both with an approximate mean (SD) of 100 (15). Parents and teachers rated behaviors at 6.5 years using the Strengths and Difficulties Questionnaire (SDQ, range 0-40). Mixed-effects linear regression analyses corrected for clustering, adjusted for the randomized intervention group and baseline parental sociodemographic characteristics, and were considered mediation by child BMI. Among 11 276 participants, 9355 women (83%) were aged 20 to 34 years, 10 128 (89.8%) were married, and 11 050 (98.0%) did not smoke during pregnancy. Each 5-unit increase in of maternal late-pregnancy BMI (mean [SD], 27.2 [3.8]) was associated with lower offspring WASI performance intelligence quotient (IQ) (-0.52 points; 95% CI, -0.87 to -0.17 points) at 6.5 years and lower scores on 5 of 7 NeuroTrax subscales and the global cognitive score at 16 years (-0.67 points; 95% CI, -1.06 to -0.29 points). Results were similar after adjustment for sociodemographic characteristics, pregnancy complications, and paternal BMI and were not mediated by child weight. Higher late pregnancy maternal BMI was also associated with more behavioral problems reported on the SDQ by teachers but not associated with parent-reported behaviors (externalizing behaviors: 0.13 points; 95% CI, 0.02 to 0.24 points; and total difficulties: 0.14 points, 95% CI, -0.02 to 0.30 points). Results were similar for maternal BMI measured in the first trimester or postpartum. In contrast, higher 6.5-year paternal BMI was associated with slightly better child cognition (WASI verbal IQ: 0.42 points; 95% CI, 0.02 to 0.82 points; NeuroTrax executive function score: 0.68 points; 95% CI, 0.24 to 1.12 points) and fewer teacher-reported behavioral problems (total difficulties: -0.29 points; 95% CI, -0.46 to -0.11 points). This cohort study supports findings from animal experiments and human observational studies in settings with higher maternal BMI and obesity rates. Higher maternal prenatal BMI may be associated with poorer offspring brain development, although residual confounding cannot be excluded.

BackgroundThere is a global obesity crisis, particularly among women and disadvantaged populations. Early-life intervention to prevent childhood obesity is a priority for public health, global health, and clinical practice. Understanding the association between childhood obesity and maternal pre-pregnancy weight status would inform policy and practice by allowing one to estimate the potential for offspring health gain through channelling resources into intervention. This systematic review and meta-analysis aimed to examine the dose–response association between maternal body mass index (BMI) and childhood obesity in the offspring.Methods and findingsSearches in MEDLINE, Child Development & Adolescent Studies, CINAHL, Embase, and PsycInfo were carried out in August 2017 and updated in March 2019. Supplementary searches included hand-searching reference lists, performing citation searching, and contacting authors. Two researchers carried out independent screening, data extraction, and quality assessment. Observational studies published in English and reporting associations between continuous and/or categorical maternal and child BMI or z-score were included. Categorical outcomes were child obesity (≥95th percentile, primary outcome), overweight/obesity (≥85th percentile), and overweight (85th to 95th percentile). Linear and nonlinear dose–response meta-analyses were conducted using random effects models. Studies that could not be included in meta-analyses were summarised narratively. Seventy-nine of 41,301 studies identified met the inclusion criteria (n = 59 cohorts). Meta-analyses of child obesity included 20 studies (n = 88,872); child overweight/obesity, 22 studies (n = 181,800); and overweight, 10 studies (n = 53,238). Associations were nonlinear and there were significantly increased odds of child obesity with maternal obesity (odds ratio [OR] 3.64, 95% CI 2.68–4.95) and maternal overweight (OR 1.89, 95% CI 1.62–2.19). Significantly increased odds were observed for child overweight/obesity (OR 2.69, 95% CI 2.10–3.46) and for child overweight (OR 1.80, 95% CI 1.25, 2.59) with maternal obesity. A limitation of this research is that the included studies did not always report the data in a format that enabled inclusion in this complex meta-analysis.ConclusionsThis research has identified a 264% increase in the odds of child obesity when mothers have obesity before conception. This study provides substantial evidence for the need to develop interventions that commence prior to conception, to support women of childbearing age with weight management in order to halt intergenerational obesity.

BackgroundMaternal pre-pregnancy obesity is an established risk factor for childhood obesity. Investigating epigenetic alterations induced by maternal obesity during fetal development could gain mechanistic insight into the developmental origins of childhood obesity. While obesity disproportionately affects underrepresented racial and ethnic mothers and children in the USA, few studies investigated the role of prenatal epigenetic programming in intergenerational obesity of these high-risk populations.MethodsThis study included 903 mother–child pairs from the Boston Birth Cohort, a predominantly urban, low-income minority birth cohort. Mother-infant dyads were enrolled at birth and the children were followed prospectively to age 18 years. Infinium Methylation EPIC BeadChip was used to measure epigenome-wide methylation level of cord blood. We performed an epigenome-wide association study of maternal pre-pregnancy body mass index (BMI) and cord blood DNA methylation (DNAm). To quantify the degree to which cord blood DNAm mediates the maternal BMI-childhood obesity, we further investigated whether maternal BMI-associated DNAm sites impact birthweight or childhood overweight or obesity (OWO) from age 1 to age 18 and performed corresponding mediation analyses.ResultsThe study sample contained 52.8% maternal pre-pregnancy OWO and 63.2% offspring OWO at age 1–18 years. Maternal BMI was associated with cord blood DNAm at 8 CpG sites (genome-wide false discovery rate [FDR] < 0.05). After accounting for the possible interplay of maternal BMI and smoking, 481 CpG sites were discovered for association with maternal BMI. Among them 123 CpGs were associated with childhood OWO, ranging from 42% decrease to 87% increase in OWO risk for each SD increase in DNAm. A total of 14 identified CpG sites showed a significant mediation effect on the maternal BMI-child OWO association (FDR < 0.05), with mediating proportion ranging from 3.99% to 25.21%. Several of these 14 CpGs were mapped to genes in association with energy balance and metabolism (AKAP7) and adulthood metabolic syndrome (CAMK2B).ConclusionsThis prospective birth cohort study in a high-risk yet understudied US population found that maternal pre-pregnancy OWO significantly altered DNAm in newborn cord blood and provided suggestive evidence of epigenetic involvement in the intergenerational risk of obesity.

Maternal obesity in pregnancy predicts offspring psychopathology risk in childhood but it remains unclear whether maternal obesity or underweight associate with adult offspring mental disorders. We examined longitudinally whether maternal body mass index (BMI) in pregnancy predicted mental disorders in her offspring and whether the associations differed by offspring birth year among 68,571 mother–child dyads of Aberdeen Maternity and Neonatal Databank, Scotland. The offspring were born 1950–1999. Maternal BMI was measured at a mean 15.7 gestational weeks and classified into underweight, normal weight, overweight, moderate obesity and severe obesity. Mental disorders were identified from nationwide registers carrying diagnoses of all hospitalizations and deaths in Scotland in 1996–2017. We found that maternal BMI in pregnancy was associated with offspring mental disorders in a time-dependent manner: In offspring born 1950–1974, maternal underweight predicted an increased hazard of mental disorders [Hazard Ratio (HR) = 1.74; 95% Confidence Interval (CI) = 1.01–3.00)]. In offspring born 1975–1999, maternal severe obesity predicted increased hazards of any mental (HR 1.60; 95% CI 1.08–2.38) substance use (HR 1.91; 95% CI 1.03–3.57) and schizophrenia spectrum (HR 2.80; 95% CI 1.40–5.63) disorders. Our findings of time-specific associations between maternal prenatal BMI and adult offspring mental disorders may carry important public health implications by underlining possible lifelong effects of maternal BMI on offspring psychopathology.

Maternal obesity and excessive gestational weight gain are associated with an increased risk of obesity in offspring. It remains unclear whether maternal adiposity also affects organ fat, which has important adverse cardiometabolic health consequences and whether the associations reflect intrauterine causal mechanisms. We examined the associations of parental pre-pregnancy body mass index (BMI) and gestational weight gain with general, abdominal, pericardial, and liver fat in 10-year-old children. In a population-based prospective cohort study among 2354 parents and their children, we obtained pre-pregnancy maternal and paternal BMI and gestational weight gain and offspring BMI, fat mass index (total fat/height4) by dual-energy X-ray absorptiometry, and subcutaneous fat index (subcutaneous fat/height4), visceral fat index (visceral fat/height3), pericardial fat index (pericardial fat/height3), and liver fat fraction by magnetic resonance imaging (MRI) at 10 years. A 1-standard deviation score (SDS) higher maternal pre-pregnancy BMI was associated with higher childhood BMI (difference 0.32 (95% confidence interval (CI) 0.28, 0.36) SDS), fat mass index (difference 0.28 (95% CI 0.24, 0.31) SDS), subcutaneous fat index (difference 0.26 (95% CI 0.22, 0.30) SDS), visceral fat index (difference 0.24 (95% CI 0.20, 0.28) SDS), pericardial fat index (difference 0.12 (95% CI 0.08, 0.16) SDS), and liver fat fraction (difference 0.15 (95% CI 0.11, 0.19) SDS). After conditioning each MRI adiposity measure on BMI at 10 years, higher maternal pre-pregnancy BMI remained associated with higher childhood subcutaneous and visceral fat indices. Smaller but not statistically different effect estimates were observed for paternal BMI. Gestational weight gain was not consistently associated with organ fat. Higher maternal pre-pregnancy BMI, but not gestational weight gain, was associated with higher general and organ fat. Similar associations of pre-pregnancy maternal and paternal BMI with offspring adiposity suggest a role of family shared lifestyle factors and genetics.

Background: Maternal pre-pregnancy BMI is well established to be a detrimental factor for prenatal development and neonatal anthropometric measures. Objectives of the study was to study the association between maternal pre-pregnancy Body Mass Index (BMI) and the anthropometry of the newborn.Methods: A hospital based cross-sectional, observational study was conducted that included 236 normal newborns and their mothers. A pre-designed questionnaire was used to collect relevant socio-demographic data and obstetric history. Details regarding maternal pre-pregnancy weight was collected from antenatal records at first antenatal visit, maternal height was measured and BMI was calculated. Neonatal anthropometric measurements including birth weight, recumbent length, head circumference, chest circumference and the mid arm circumference was measured.Results: In this study 49.6% of the women were in the age group of 21-25 years, 52.5% of them were multi-gravida and 56.4% had normal vaginal delivery. Among the newborns included in the study 25.8% had low birth weight. We saw a significant positive correlation between BMI and age, BMI and birth weight, BMI and chest circumference that is with increase in BMI there was significant increase in the age, birth weight and chest circumference and vice versa. There was no association between maternal BMI and mid-arm circumference or head circumference of the newborn.Conclusions: Study showed the association between maternal BMI and anthropometry of the newborn especially with respect to the BMI and birth weight, BMI and chest circumference. Thereby, establishing that interventions aimed at improving the nutritional status of the mother have a direct impact on the fetal growth outcomes.