Pre-pregnancy maternal obesity is associated with adverse offspring outcomes at birth and later in life. Individual studies have shown that epigenetic modifications such as DNA methylation could contribute. Within the Pregnancy and Childhood Epigenetics (PACE) Consortium, we meta-analysed the association between pre-pregnancy maternal BMI and methylation at over 450,000 sites in newborn blood DNA, across 19 cohorts (9,340 mother-newborn pairs). We attempted to infer causality by comparing the effects of maternal versus paternal BMI and incorporating genetic variation. In four additional cohorts (1,817 mother-child pairs), we meta-analysed the association between maternal BMI at the start of pregnancy and blood methylation in adolescents. In newborns, maternal BMI was associated with small (<0.2% per BMI unit (1 kg/m2), P < 1.06 × 10−7) methylation variation at 9,044 sites throughout the genome. Adjustment for estimated cell proportions greatly attenuated the number of significant CpGs to 104, including 86 sites common to the unadjusted model. At 72/86 sites, the direction of the association was the same in newborns and adolescents, suggesting persistence of signals. However, we found evidence for a6causal intrauterine effect of maternal BMI on newborn methylation at just 8/86 sites. In conclusion, this well-powered analysis identified robust associations between maternal adiposity and variations in newborn blood DNA methylation, but these small effects may be better explained by genetic or lifestyle factors than a causal intrauterine mechanism. This highlights the need for large-scale collaborative approaches and the application of causal inference techniques in epigenetic epidemiology.

Background: Diverse environmental factors are associated with physical activity (PA) and healthy eating (HE) among youth. However, no study has created a comprehensive obesogenic environment index for children that can be applied at a large geographic scale. The purpose of this study was to describe the development of a childhood obesogenic environment index (COEI) at the county level across the United States. Methods: A comprehensive search of review articles (n = 20) and input from experts (n = 12) were used to identify community-level variables associated with youth PA, HE, or overweight/obesity for potential inclusion in the index. Based on strength of associations in the literature, expert ratings, expertise of team members, and data source availability, 10 key variables were identifiedsix related to HE (# per 1000 residents for grocery/superstores, farmers markets, fast food restaurants, full-service restaurants, and convenience stores; as well as percentage of births at baby (breastfeeding)-friendly facilities) and four related to PA (percentage of population living close to exercise opportunities, percentage of population < 1 mile from a school, a composite walkability index, and number of violent crimes per 1000 residents). Data for each variable for all counties in the U.S. (n = 3142) were collected from publicly available sources. For each variable, all counties were ranked and assigned percentiles ranging from 0 to 100. Positive environmental variables (e.g., grocery stores, exercise opportunities) were reverse scored such that higher values for all variables indicated a more obesogenic environment. Finally, for each county, a total obesogenic environment index score was generated by calculating the average percentile for all 10 variables.

Background Approximately 17% of children in the U.S. are obese. Children that are overweight or obese are also more likely to be obese as adults and suffer from various chronic diseases and premature death. Maternal obesity can affect the weight status of her offspring through intrauterine mechanisms like excessive gestational weight gain (GWG). Current literature shows a positive association between maternal weight status and GWG on child obesity, yet the direct and indirect effects have not been decomposed or quantified. The purpose of this study was to estimate the effect of maternal obesity on child obesity, mediated by GWG, which is a modifiable risk factor. Methods The study participants were a birth cohort of offspring from women who received prenatal care in the Duke/Durham Regional health care system in Durham, NC between 2005 and 2009. Anthropomorphic data was collected via electronic medical records (EMRs) during each voluntary visit to a health care facility. The exposure of interest was maternal obesity, measured by pre-pregnancy body mass index, the mediator was GWG, dichotomized into excessive and not excessive based on maternal prenatal BMI, and the outcome was child obesity at age 4, measured as BMI z-scores from the last recorded height and weight. A counterfactual theory-based product method analysis estimated the mediated effects of GWG, adjusted for maternal race, socioeconomic status, and smoking status. Results Of the 766 children, 25% were overweight or obese, and among all mothers, 25 and 31% were overweight and obese, respectively. Maternal BMI was associated with an overall increase of 0.04 in offspring z-score. The proportion of the effect of maternal obesity on child age 4 obesity mediated by GWG was 8.1%. Conclusion GWG, in part, mediated the relationship between maternal BMI and childhood adiposity. Even when the mediator is fixed, children are at an increased risk of a higher BMI if the mother is obese. These findings highlight an important public health education opportunity to stress the impact of a pre-pregnancy weight and excessive GWG on the risk of child obesity for all mothers. Electronic supplementary material The online version of this article (10.1186/s12889-019-7349-1) contains supplementary material, which is available to authorized users.