OBJECTIVE: To provide an updated birth weight–for–gestational age (BW-for-GA) reference in the United States by using the most recent, nationally representative birth data with obstetric estimates of gestational age (GA).METHODS: We abstracted 3 285 552 singleton births between 22 and 42 weeks’ gestation with nonmissing race and/or ethnicity, infant sex, parity, birth weight, and obstetric estimate of GA from the 2017 US natality files. We used 2 techniques (nonlinear, resistant smoothing [4253H] and lambda-mu-sigma) to derive smoothed BW-for-GA curves and compared resulting BW-for-GA cut-points at the third, 10th, 90th, and 97th percentiles with US references from 1999 to 2009.RESULTS: The smoothed BW-for-GA curves from both techniques overlapped considerably with each other, with strong agreements seen between the 2 techniques (>99% agreement; κ-statistic >0.9) for BW-for-GA cut-points at the third, 10th, 90th, and 97th percentiles across all GAs. Cut-points from 2017 using the lambda-mu-sigma method captured 9.8% to 10.2% of births 90th percentiles and 2.6% to 3.3% of births below the third and above the 97th percentile across all GAs. However, cut-points from US references in 1999 and 2009 (when GA was based on last menstrual period) captured a much larger range of proportions of 2017 births at these thresholds, especially among preterm and postterm GA categories.CONCLUSIONS: We have provided an updated BW-for-GA reference in the United States using the most recent births with obstetric estimates of GA and information to calculate continuous measures of birth size that are sex or parity specific.

The quality of neighborhoods in which children reside has been increasingly recognized as an important factor associated with health across the lifecourse.^1,2 Compared with adults, children may be particularly vulnerable to adverse neighborhood conditions, with consequences for lifelong health. For example, residence in a neighborhood with high rates of poverty and/or crime has been associated with increased risk of high body mass index (BMI) or obesity in childhood,^3,4 which is a risk factor for chronic disease, such as type 2 diabetes, in adulthood.⁵ Such studies highlight the potential importance of neighborhood contexts as factors associated with high childhood BMI. However, most studies examining these questions have been cross-sectional in study design or focused on singular socioeconomic indicators of neighborhood disadvantage, such as rates of low household income or unemployment.^6-8 Moreover, few studies have examined the extent to which neighborhood conditions during early life—at birth, in infancy, or in early childhood, which are key life stages that lay the foundation for long-term health outcomes⁹—are associated with BMI from childhood to adolescence. Even fewer studies have attempted to ascertain the sensitive periods of exposure to neighborhood conditions by comparing the consequences of exposures during multiple life stages.

Obesity is an escalating health problem worldwide, and hence the causes underlying its development are of primary importance to public health. There is growing evidence that suboptimal intrauterine environment can perturb the metabolic programing of the growing fetus, thereby increasing the risk of developing obesity in later life. However, the link between early exposures in the womb, genetic susceptibility, and perturbed epigenome on metabolic health is not well understood. In this study, we shed more light on this aspect by performing a comprehensive analysis on the effects of variation in prenatal environment, neonatal methylome, and genotype on birth weight and adiposity in early childhood. In a prospective mother-offspring cohort (N = 987), we interrogated the effects of 30 variables that influence the prenatal environment, umbilical cord DNA methylation, and genotype on offspring weight and adiposity, over the period from birth to 48 months. This is an interim analysis on an ongoing cohort study. Eleven of 30 prenatal environments, including maternal adiposity, smoking, blood glucose and plasma unsaturated fatty acid levels, were associated with birth weight. Polygenic risk scores derived from genetic association studies on adult adiposity were also associated with birth weight and child adiposity, indicating an overlap between the genetic pathways influencing metabolic health in early and later life. Neonatal methylation markers from seven gene loci (ANK3, CDKN2B, CACNA1G, IGDCC4, P4HA3, ZNF423 and MIRLET7BHG) were significantly associated with birth weight, with a subset of these in genes previously implicated in metabolic pathways in humans and in animal models. Methylation levels at three of seven birth weight-linked loci showed significant association with prenatal environment, but none were affected by polygenic risk score. Six of these birth weight-linked loci continued to show a longitudinal association with offspring size and/or adiposity in early childhood. This study provides further evidence that developmental pathways to adiposity begin before birth and are influenced by environmental, genetic and epigenetic factors. These pathways can have a lasting effect on offspring size, adiposity and future metabolic outcomes, and offer new opportunities for risk stratification and prevention of obesity. This birth cohort is a prospective observational study, designed to study the developmental origins of health and disease, and was retrospectively registered on 1 July 2010 under the identifier NCT01174875 .

Video Abstract Video Abstract The Child Opportunity Index (ChOI) is a publicly available surveillance tool that incorporates traditional and novel attributes of neighborhood conditions that may promote or inhibit healthy child development. The extent to which ChOI relates to individual-level cardiometabolic risk remains unclear. We geocoded residential addresses obtained from 743 participants in midchildhood (mean age 7.9 years) in Project Viva, a prebirth cohort from eastern Massachusetts, and linked each location with census tract-level ChOI data. We measured adiposity and cardiometabolic outcomes in midchildhood and early adolescence (mean age 13.1 years) and analyzed their associations with neighborhood-level ChOI in midchildhood using mixed-effects models, adjusting for individual and family sociodemographics. On the basis of nationwide distributions of ChOI, 11.2% (n = 83) of children resided in areas of very low overall opportunity (ChOI score <20 U) and 55.3% (n = 411) resided in areas of very high (ChOI score ≥80 U) overall opportunity. Children who resided in areas with higher overall opportunity in midchildhood had persistently lower levels of C-reactive protein from midchildhood to early adolescence (per 25-U increase in ChOI score: β = .14 mg/L; 95% confidence interval, .28 to .00). Additionally, certain ChOI indicators, such as greater number of high-quality childhood education centers, greater access to healthy food, and greater proximity to employment in midchildhood, were associated with persistently lower adiposity, C-reactive protein levels, insulin resistance, and metabolic risk z scores from midchildhood to early adolescence. Our findings suggest more favorable neighborhood opportunities in midchildhood predict better cardiometabolic health from midchildhood to early adolescence.

Background: Infant body mass index (BMI) peak characteristics and early childhood BMI are emerging markers of future obesity and cardiometabolic disease risk, but little is known about their maternal nutritional determinants.

Appetitive traits in childhood such as food responsiveness and enjoyment of food have been associated with body mass index (BMI) in later childhood. However, data on appetitive traits during infancy in relation to BMI in later childhood are sparse. We aimed to relate appetitive traits in infancy to subsequent BMI and weight gain up to 24 months of age. Data of 210 infants from the Singapore GUSTO mother-offspring cohort was obtained. The Baby Eating Behavior Questionnaire (BEBQ) and the Child Eating Behavior Questionnaire (CEBQ) were administered to mothers when their offspring were aged 3 and 12 months respectively. Height and weight of offspring were measured at ages 3, 6, 9,12,15,18 and 24 months. The association of appetitive traits with both BMI z-score and weight gain were evaluated using multivariate linear regression. Food responsiveness at 3 months was associated with higher BMI from 6 months up to 15 months of age (p < 0.01) and with greater weight gain between 3 and 6 months of age (p = 0.012). Slowness in eating and satiety responsiveness at 3 months was significantly associated with lower BMI at 6 months (p < 0.01) and with less weight gain between 3 to 6 months of age (p = 0.034). None of the appetitive traits at 12 months were significantly associated with BMI or weight gain over any time period. Early assessment of appetitive traits at 3 months of age but not at 12 months of age was associated with BMI and weight gain over the first two years of life. Clinical Trials identifier NCT01174875