Parental Pre-pregnancy Body Mass Index Research Articles

Body mass index growth trajectories and body composition influencing factors: An ambidirectional preschooler cohort

ObjectivesThe purpose of the present study was to explore the latent growth trajectory of body mass index (BMI) from birth to 24 months and comprehensively analyze body composition development influencing factor in preschool children. MethodsThis ambidirectional cohort study was conducted in Tianjin, China, from 2017 to 2020, and children's regular medical check-up data from birth to 24 months were retrospectively collected. The growth models were used to fit BMI z-score trajectories for children aged 0–24 months. Crossover analysis and interaction model were used to explore the interaction of influencing factors. ResultsWe analyzed the growth trajectories of 3217 children, of these, 1493 children with complete follow-up data were included in the influencing factors analysis. Trajectories and parental prepregnancy BMI (ppBMI) were independent factors influencing children's body composition. When paternal ppBMI ≥24 kg/m2, regardless of maternal ppBMI, the risk of overweight and obesity in senior-class children was increased. The high trajectories played a partial mediating role in the association between paternal ppBMI and body composition in preschool children. ConclusionsBMI growth in children aged 0–24 months can be divided into three latent trajectories: low, middle, and high. These trajectories and parental ppBMI were independent and interactive factors influencing children's body composition. The high trajectories played a partial mediating role in the association between paternal ppBMI and body composition in preschool children. It is necessary to pay attention to the BMI growth level of children aged 0–24 months, which plays an important role in the development of body fat in the future.

Parental pre-pregnancy body mass index and risk of low birth weight in offspring: A prospective cohort study in central China.

Low birth weight (LBW) is one of the most common adverse pregnancy outcomes. Previous studies have consistently shown that maternal body mass index (BMI) status before and during pregnancy is associated with LBW. However, previous studies lacked an association between paternal BMI and the conjunction effect of a couple's BMI and LBW in the offspring. Therefore, we established a cohort of pre-pregnancy couples to prospectively assess the relationship between maternal and paternal pre-pregnancy BMI and offspring LBW, very low birth weight (VLBW), and extremely low birth weight (ELBW). A prospective cohort study was established in Central China. A total of 34,104 pregnant women with singleton pregnancies at 8-14 gestational weeks and their husbands were finally enrolled and followed to 3 months postpartum. The multivariate logistic regression and restrictive cubic spline model were used to explore the relationship between parental pre-pregnancy BMI and the risk of LBW, VLBW, and ELBW in offspring. Of the 34,104 participants, maternal pre-pregnancy overweight and obesity were associated with a higher risk of LBW (overweight: OR = 1.720, 95% CI = 1.533 ~ 1.930; obesity: OR = 1.710, 95% CI = 1.360 ~ 2.151), VLBW (overweight: OR = 2.283, 95% CI = 1.839 ~ 2.834; obesity: OR = 4.023, 95% CI = 2.855 ~ 5.670), and ELBW (overweight: OR = 3.292, 95% CI = 2.151 ~ 5.036; obesity: OR = 3.467, 95% CI = 1.481 ~ 8.115), while underweight was associated with a higher risk of LBW (OR = 1.438, 95% CI = 1.294 ~ 1.599) and a lower risk of ELBW (OR = 0.473, 95% CI = 0.236 ~ 0.946). Paternal pre-pregnancy overweight and obesity were associated with a higher risk of LBW (overweight: OR = 1.637, 95% CI = 1.501 ~ 1.784; obesity: OR = 1.454, 95% CI = 1.289 ~ 1.641) and VLBW (overweight: OR = 1.310, 95% CI = 1.097 ~ 1.564; obesity: OR = 1.320, 95% CI = 1.037 ~ 1.681), while underweight was associated with a lower risk of LBW (OR = 0.660, 95% CI = 0.519 ~ 0.839). Parents who were both excessive-weights in pre-pregnancy BMI, as well as overweight mothers and normal-weight fathers before pre-pregnancy, were more likely to have offspring with LBW, VLBW, and ELBW. Dose-response relationship existed between parental pre-pregnancy and LBW, VLBW, and ELBW, except for paternal BMI and ELBW. Parental pre-pregnancy BMI was associated with the risk of LBW in offspring. Management of weight before pregnancy for couples might help reduce their adverse pregnancy outcomes in future intervention studies.

Protective Effect of Maternal First-Trimester Low Body Mass Index Against Macrosomia: A 10-Year Cross-Sectional Study.

ObjectiveWe aimed to assess whether maternal first-trimester low body mass index (BMI) has a protective effect against macrosomia.MethodsThis was a cross-sectional study from January 1, 2011, to June 30, 2021, and 84,900 participants were included. The predictive performance of maternal first-trimester and parental pre-pregnancy BMI for macrosomia was assessed using the area under the receiver-operating characteristics curve (AUC). Multivariate logistic regression analyses were performed to evaluate the independent effect of maternal first-trimester low BMI on macrosomia. Interactions were investigated to evaluate the potential variation of the effect of first-trimester low BMI across different groups. Furthermore, interactions were also examined across groups determined by multiple factors jointly: a) gestational diabetes mellitus (GDM)/GDM history status, parity, and maternal age; and b) GDM/GDM history status, fetal sex, and season of delivery.ResultsThe proportion of macrosomia was 6.14% (5,215 of 84,900). Maternal first-trimester BMI showed the best discrimination of macrosomia (all Delong tests: P < 0.001). The protective effect of maternal first-trimester low BMI against macrosomia remained significant after adjusting for all confounders of this study [adjusted odds ratios (aOR) = 0.37, 95% CI: 0.32–0.43]. Maternal first-trimester low BMI was inversely associated with macrosomia, irrespective of parity, fetal sex, season of delivery, maternal age, and GDM/GDM history status. The protective effect was most pronounced among pregnant women without GDM/GDM history aged 25 to 29 years old, irrespective of parity (multipara: aOR = 0.32, 95% CI: 0.22–0.47; nullipara: aOR = 0.32, 95% CI: 0.24–0.43). In multipara with GDM/GDM history, the protective effect of low BMI was only observed in the 30- to 34-year-old group (aOR = 0.12, 95% CI: 0.02–0.86). For pregnant women without GDM/GDM history, the protective effect of maternal first-trimester low BMI against macrosomia was the weakest in infants born in winter, irrespective of fetal sex (female: aOR = 0.45, 95% CI: 0.29–0.69; male: aOR = 0.39, 95% CI: 0.28–0.55).ConclusionMaternal first-trimester low BMI was inversely associated with macrosomia, and the protective effect was most pronounced among 25- to 29-year-old pregnant women without GDM/GDM history and was only found among 30- to 34-year-old multipara with GDM/GDM history. The protective effect of maternal first-trimester low BMI against macrosomia was the weakest in winter among mothers without GDM/GDM history.

Maternal overweight but not paternal overweight before pregnancy is associated with shorter newborn telomere length: evidence from Guangxi Zhuang birth cohort in China

BackgroundTelomere length (TL) is variable at birth and is inversely associated with body mass index (BMI) in adulthood. A growing number of evidences suggested that a higher maternal pre-pregnancy BMI results in adverse offspring health outcomes, especially shorter newborn TL. However, a newborn’s genetic endowment is equally derived from both parents, the association between parental pre-pregnancy BMI and newborn TL has been rarely discussed. We aimed to determine the association between parental pre-pregnancy BMI and newborn TL.MethodsA total of 1082 parent-newborn pairs were recruited from the Guangxi Zhuang Birth Cohort (GZBC). TL in cord blood was measured using quantitative real-time polymerase chain reaction (qPCR) and expressed as the ratio of telomere copy number to single-copy gene number (T/S). A series of linear regressions were performed to assess the associations between parental pre-pregnancy BMI and newborn TL.ResultsMothers who were overweight before pregnancy had significantly shorter cord blood telomere length in their newborns than those who were normal weight before pregnancy [percentage change: − 7.96% (95% CI: − 14.49 to − 0.69%; P = 0.032)]. Further analysis of the combined effects of parental weight status on newborn TL showed that TL was significantly shortened among newborns whose mothers were overweight and fathers were of healthy weight when compared with those whose mothers and fathers were both of normal weight [percentage change: − 8.38% (95% CI: − 15.47 to − 0.92%; P = 0.028)]. Subgroup analysis indicated these effects were more pronounced among male newborns and those whose paternal age < 31 years or maternal age ≥ 28 years at delivery.ConclusionsMaternal pre-pregnancy overweight, but not paternal pre-pregnancy overweight is associated with shorter newborn TL. Weight control in reproductive women and effective healthy weight management before pregnancy may be of particular benefit for improving longevity and life quality of offspring.

Premature Birth is an Independent Risk Factor for Early Adiposity Rebound: Longitudinal Analysis of BMI Data from Birth to 7 Years.

Adiposity rebound (AR) refers to the second rise of the body mass index (BMI) curve that usually occurs physiologically between five and seven years of age. AR timing has a great impact on patients’ health, since early adiposity rebound (EAR) is associated with the development of metabolic syndrome later in life. We aimed to investigate the prevalence of EAR in a cohort of inborn preterm infants admitted to the Neonatal Intensive Care Section of the Policlinico University Hospital of Bari, Italy. Secondarily, we assessed whether some determinants such as (1) gender; (2) delivery mode; (3) birth weight and classification into small, normal, or large for gestational age; (4) type of feeding; (5) breastfeeding duration; (6) timing of introduction of solid food; (7) parental education; and (8) parental pre-pregnancy body mass index (BMI) influenced EAR in this cohort. The tertiary aim was to evaluate the prevalence of obesity or being overweight at seven years of age in children according to early versus timely AR. This is a prospective, population-based longitudinal study conducted at the Neonatal Intensive Care Section of the Policlinico University Hospital of Bari, Italy. Inborn preterm infants admitted to the neonatal ward between 2009 and 2011 were eligible. Enrolled preterm infants were evaluated at birth and at 1, 3, 6, 9, 12, 15, 18, and 24 months and 3, 4, 5, 6, and 7 years of age. Weight and height data were analyzed, and BMI was calculated. AR was assessed in the growth trajectory in a body mass index (BMI) plot. Of the 250 preterm newborns included, 100 completed the seven-year follow-up and entered the final analysis, 138 were lost during the seven-year follow-up, and in 12 cases parents withdrew over the course of the study. The prevalence of EAR in our cohort of preterm newborns was 54% at seven years of age. Early adiposity rebound was associated with being large for gestational age (LGA) at birth. No other factors were associated with EAR. Early adiposity rebounders had a significantly higher BMI at seven years compared to children with timely AR (17.2 ± 2.7 vs. 15.6 ± 2.05, p = 0.021). No significant differences were found in the prevalence of obesity or being overweight at seven years of age in children with early or timely AR (29% vs. 14%, p = 0.202). Ex-preterm infants have an increased risk of EAR. Since EAR may lead to long-term detrimental health effects with the onset of various chronic diseases (e.g., obesity, metabolic syndrome, etc.), healthcare providers should be prepared to counteract its occurrence, especially in delicate sub-populations of infants.

Pre-pregnancy parental BMI and offspring blood pressure in infancy.

AimsA growing body of evidence suggests that a higher maternal pre-pregnancy body mass index results in higher offspring’s blood pressure, but there is inconsistency about the impact of father’s body mass index. Furthermore, evidence is limited with regard to low and middle income countries. We aimed to determine the association between parental pre-pregnancy body mass index and offspring’s blood pressure during the first year of life.MethodsIn 587 infants of the BReastfeeding Attitude and Volume Optimization (BRAVO) trial systolic and diastolic blood pressure were measured twice at the right leg in a supine position, using an automatic oscillometric device at day 7, month 1, 2, 4, 6, 9 and 12. Parental pre-pregnancy body mass index was based on self-reported weight and height. Linear mixed models were performed to investigate the associations between parental pre-pregnancy body mass index and offspring blood pressure patterns.ResultsEach unit increase in maternal body mass index was associated with 0.24 mmHg (95% confidence interval 0.05; 0.44) and 0.13 mmHg (0.01; 0.25) higher offspring’s mean systolic and diastolic blood pressure, respectively, during the first year of life. A higher offspring blood pressure with increased maternal pre-pregnancy body mass index was seen at birth and remained higher during the first year of life. The association with systolic blood pressure remained similar after including birth size and offspring’s weight and height over time. The association with diastolic blood pressure attenuated slightly to a non-significant result after including these variables. Paternal body mass index was not associated with offspring’s blood pressure.ConclusionHigher maternal pre-pregnancy body mass index, but not paternal pre-pregnancy body mass index, is associated with higher offspring blood pressure already from birth onwards.

Maternal body mass index, gestational weight gain, and childhood abdominal, pericardial, and liver fat assessed by magnetic resonance imaging.

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.

Association of pre-pregnancy body mass index with offspring metabolic profile: Analyses of 3 European prospective birth cohorts.

BackgroundA high proportion of women start pregnancy overweight or obese. According to the developmental overnutrition hypothesis, this could lead offspring to have metabolic disruption throughout their lives and thus perpetuate the obesity epidemic across generations. Concerns about this hypothesis are influencing antenatal care. However, it is unknown whether maternal pregnancy adiposity is associated with long-term risk of adverse metabolic profiles in offspring, and if so, whether this association is causal, via intrauterine mechanisms, or explained by shared familial (genetic, lifestyle, socioeconomic) characteristics. We aimed to determine if associations between maternal body mass index (BMI) and offspring systemic cardio-metabolic profile are causal, via intrauterine mechanisms, or due to shared familial factors.Methods and findingsWe used 1- and 2-stage individual participant data (IPD) meta-analysis, and a negative-control (paternal BMI) to examine the association between maternal pre-pregnancy BMI and offspring serum metabolome from 3 European birth cohorts (offspring age at blood collection: 16, 17, and 31 years). Circulating metabolic traits were quantified by high-throughput nuclear magnetic resonance metabolomics. Results from 1-stage IPD meta-analysis (N = 5327 to 5377 mother-father-offspring trios) showed that increasing maternal and paternal BMI was associated with an adverse cardio-metabolic profile in offspring. We observed strong positive associations with very-low-density lipoprotein (VLDL)-lipoproteins, VLDL-cholesterol (C), VLDL-triglycerides, VLDL-diameter, branched/aromatic amino acids, glycoprotein acetyls, and triglycerides, and strong negative associations with high-density lipoprotein (HDL), HDL-diameter, HDL-C, HDL2-C, and HDL3-C (all P < 0.003). Slightly stronger magnitudes of associations were present for maternal compared with paternal BMI across these associations; however, there was no strong statistical evidence for heterogeneity between them (all bootstrap P > 0.003, equivalent to P > 0.05 after accounting for multiple testing). Results were similar in each individual cohort, and in the 2-stage analysis. Offspring BMI showed similar patterns of cross-sectional association with metabolic profile as for parental pre-pregnancy BMI associations but with greater magnitudes. Adjustment of parental BMI–offspring metabolic traits associations for offspring BMI suggested the parental associations were largely due to the association of parental BMI with offspring BMI. Limitations of this study are that inferences cannot be drawn about the role of circulating maternal fetal fuels (i.e., glucose, lipids, fatty acids, and amino acids) on later offspring metabolic profile. In addition, BMI may not reflect potential effects of maternal pregnancy fat distribution.ConclusionOur findings suggest that maternal BMI–offspring metabolome associations are likely to be largely due to shared genetic or familial lifestyle confounding rather than to intrauterine mechanisms.

Parental pre-pregnancy obesity and the risk of offspring weight and body mass index change from childhood to adulthood.

The purpose of this study was to examine the association of parental pre-pregnancy weight and body mass index (BMI) on offspring weight and BMI change from childhood to adulthood. We analysed BMI data from a subsample of parents (n = 1494) from the Mater-University of Queensland Study of Pregnancy cohort that started in the early 1980s in Brisbane, Australia: data were collected at pre-pregnancy and then also for offspring at 5, 14 and 21-year follow-ups. Multiple regression for continuous outcomes and multinomial regression for categorical outcomes were performed. A total of 14.7% of offspring experienced BMI change from normal at 5 years to overweight or obese (OW/OB) at 14 years, 15.3% of normal at 14 years to OW/OB at 21 years and 22.8% from normal at 5 years to OW/OB at 21 years. Overall, the strength of the association of parental BMI with offspring BMI was stronger as offspring become older. Pre-pregnancy parental BMI differentially impacts offspring OW/OB across the life course. For every unit increase in paternal and maternal BMI z-score, offspring BMI z-score increased, on average, by between 0.15% (kg m-2 ) and 0.24% (kg m-2 ) throughout all three stages of life when both parents were OW/OB; these associations were stronger than with one parent. Parental pre-pregnancy BMI and OW/OB is a strong predictor of offspring weight and BMI change from early life to adulthood.

Parental pre-pregnancy BMI is a dominant early-life risk factor influencing BMI of offspring in adulthood.

SummaryObjectiveWe examined parental and early‐life variables in order to identify risk factors for adulthood overweight and obesity in offspring. We report here on the longitudinal prevalence of overweight and obesity in Australian children born between 1989 and 1991 and followed from birth to age 22.MethodsData were analysed on 1355 participants from the Western Australian Pregnancy Cohort (Raine) Study, with anthropometry collected during pregnancy, at birth, one year and at three yearly intervals thereafter. Multivariate analyses and cross‐sectional logistic regression quantified the timing and contribution of early‐life risk factors for overweight and obesity in young‐adulthood.ResultsAt five years of age 12.6% of children were overweight and 5.2% were obese. By early adulthood, the prevalence of obesity had increased to 12.8%, whilst overweight remained relatively stable at 14.2% (range from early childhood to adulthood 11–16%). Parental pre‐pregnancy body mass index (BMI) was the strongest determinant of adult offspring BMI. Although rapid first year weight gain was associated with increased offspring BMI, the impact of first year weight‐gain diminished over childhood, whilst the impact of parental BMI increased over time.ConclusionsParental pre‐pregnancy BMI and rapid early‐life weight gain predispose offspring to obesity in adulthood.

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.

Intergenerational transmission of overweight among Finnish adolescents and their parents: a 16-year follow-up study

Previous studies have shown strong parental influences on adolescent overweight. However, longitudinal data is scarce on gender-specific effects of parental body mass index (BMI) on offspring overweight. The objective of this study was to examine the associations of parental pre-pregnancy BMI, weight change, BMI and BMI class transition 16 years after pregnancy with the BMI of their 16-year-old children. The study population was derived from the general population-based Northern Finland Birth Cohort 1986. A total of 4788 child-mother-father trios (2325 boys, 2463 girls) were analysed. Weight and height of the adolescents were measured and overweight and obesity defined according to the International Obesity Task Force. For the parents, self-reported data were obtained and overweight and obesity defined according to the World Health Organization. Associations of parental BMI status and weight change with offspring BMI were assessed using binary logistic regression analyses stratified by gender and adjusted for parental age and education. Children whose both parents were overweight or obese both before pregnancy and after 16-year follow-up had a strikingly high risk of overweight at age 16 years (boys odds ratio (OR) 5.66 95% confidence interval (CI) 3.12, 10.27; girls OR 14.84 95% CI 7.41, 29.73). Parental pre-pregnancy obesity strongly predicted offspring overweight (mother-son OR 4.36 95% CI 2.50, 7.59; mother-daughter OR 3.95 95% CI 2.34, 6.68; father-son OR 3.17 95% CI 1.70, 5.92; father-daughter OR 5.58 95% CI 3.09, 10.07). Parental overweight conveys a major risk for overweight in children for which both parents' long-term overweight (BMI ≥25 kg m(-2) before pregnancy and after 16-year follow-up) was the strongest single predictor. Preventing intergenerational transmission of obesity by helping parents to maintain a healthy weight is an essential target for public health.

Epidemiologic Evidence for the Fetal Overnutrition Hypothesis: Findings from the Mater-University Study of Pregnancy and Its Outcomes

The fetal overnutrition hypothesis proposes that greater maternal adiposity results in increased obesity throughout life in the offspring. The authors examined the associations between parental prepregnancy body mass index (BMI; weight (kg)/height (m)(2)), based on height and weight reported by the mother at her first antenatal clinic visit, and offspring BMI (height and weight measured at age 14 years) in 3,340 parent-offspring trios from a birth cohort based in Brisbane, Australia (mothers were recruited in 1981-1984). The maternal-offspring BMI association was stronger than the paternal-offspring BMI association. In the fully adjusted model, the increase in standardized offspring BMI at age 14 for a one-standard-deviation (SD) increase in maternal BMI was 0.362 SD (95% confidence interval: 0.323, 0.402), and the corresponding result for a one-SD increase in paternal BMI was 0.239 SD (95% confidence interval: 0.197, 0.282). There was statistical support for a difference in the magnitude of the association between maternal-offspring BMI and paternal-offspring BMI in all confounder-adjusted models tested (all p's < 0.0001). In sensitivity analyses taking account of different plausible levels of nonpaternity (up to 15%), the greater maternal effect remained. These findings provide some support for the fetal overnutrition hypothesis.