Maternal smoking during pregnancy and childhood obesity: results from the CESAR Study.

Childhood obesity is a worldwide public health concern. Recent studies from high income countries have demonstrated associations between maternal smoking during pregnancy and children's excess body weight. We examine associations between maternal smoking during pregnancy and children's overweight or obesity, in six countries in the less affluent Central/Eastern European region. Questionnaire data were analysed, for 8,926 singleton children aged 9-12 years. Country-specific odds ratios for effects of maternal smoking during pregnancy on being overweight, and on obesity, were estimated using logistic regression. Heterogeneity between country-specific results, and mean effects (allowing for heterogeneity) were estimated. Positive associations between maternal smoking and overweight were seen in all countries but Romania. While not individually statistically significant, the mean odds ratio was 1.26 (95% CI 1.03-1.55), with no evidence of between-country heterogeneity. Obese children were few (2.7%), and associations between obesity and maternal smoking during pregnancy were more heterogeneous, with odds ratios ranging from 0.71 (0.32-1.57) in Poland to 5.49 (2.11-14.30) in Slovakia. Between-country heterogeneity was strongly related to average persons-per-room, a possible socioeconomic indicator, with stronger associations where households were less crowded. Estimates of dose-response relationships tended to be small and non-significant, even when pooled. Our results provide evidence of a link between maternal smoking in pregnancy and childhood overweight. Associations with obesity, though strong in some countries, were less consistent. Maternal smoking may confer an addition to a child's potential for obesity, which is more likely to be realised in affluent conditions

Maternal awareness of health promotion, parental and preschool childhood obesity

Aim: To investigate the association between parental and preschool childhood obesity, as well as maternal awareness of public health promotion on healthy eating with parental and preschool childhood obesity. Methods: Data were collected by measuring the height and weight of two hundred randomly selected three-year old children and their parents. Details of the early feeding and dietary styles and level of health promotion awareness were assessed in faceto-face structured health interviews with the parents. Results: There were statistically significant relationships between childhood obesity and parents’ obesity (r=0.2; p<0.001). A higher proportion of overweight and obese preschool children showed that their mothers lacked awareness of health promotion as compared to children with normally accepted weight (χ2 (6, n=200)=17.32, p=0.008). Maternal awareness of health promotion on healthy eating appeared to have a protective effect against overweight/obesity in three year old children (odds ratio=0.38, 95% CI=0.20 to 0.70). Furthermore, a higher proportion of overweight/obesity mothers had no awareness of health promotion as compared to mothers with normally accepted weight (χ 2 (4, n=200)=13.29, p=0.01). Maternal awareness of health promotion appeared to also have a protective effect against overweight/obesity in mothers (odds ratio=0.51, 95% CI=0.28 to 0.95). Conclusions: This study showed the protective effect of maternal awareness of health promotion on maternal and preschool childhood obesity. Additionally, this study showed that overweight and obese preschool children had parents who were also overweight and obese.peer-reviewe

The impact of maternal BMI, gestational weight gain, and breastfeeding on early childhood weight: Analysis of a statewide WIC dataset

Early childhood obesity is a persistent health concern with more frequent and significant impact on low-income families. Maternal weight factors impact offspring weight status, but evidence on whether breastfeeding protects against this impact is mixed. This analysis examined a model to predict early childhood obesity risk, simultaneously accounting for maternal pre-pregnancy body mass index (BMI), gestational weight gain, and breastfeeding. The team analyzed 27,016 unique maternal-child dyadic records collected via the Supplemental Nutrition Program for Wisconsin Women, Infants, and Children (WIC) between 2009 and 2011. Generalized Linear Modeling, specifically logistic regression, was used to predict a child\u27s risk of obesity given the mother\u27s pre-pregnancy BMI, gestational weight gain, and duration of breastfeeding. For each 1 kg/m2 increase in pre-pregnancy BMI, there was a 4.5% increase in risk of obesity compared to children with mothers of normal BMI. Children whose mothers had excessive gestational weight gain were 50% more likely to have obesity compared to those whose mothers had ideal weight gain. For each week of additional breastfeeding, there was a 1.9% increased risk of obesity. The risk models did not differ by race. In this model, accounting for pre-pregnancy weight, gestational weight gain, and breastfeeding among a diverse, low-income sample, women with pre-pregnancy overweight and obesity or who had excessive gestational weight gain had the highest risk of early childhood obesity. While breastfeeding is healthy for many reasons, providers should focus on maternal weight-related behaviors when counseling mothers about how to avoid risk of early childhood obesity

Maternal obesity has little effect on the immediate offspring but impacts on the next generation

Maternal obesity during pregnancy has been linked to an increased risk of obesity and cardiometabolic disease in the offspring, a phenomenon attributed to developmental programming. Programming effects may be transmissible across generations through both maternal and paternal inheritance, although the mechanisms remain unclear. Using a mouse model, we explored the effects of moderate maternal diet-induced obesity (DIO) on weight gain and glucose-insulin homeostasis in first-generation (F1) and second-generation offspring. DIO was associated with insulin resistance, hyperglycemia and dyslipidemia before pregnancy. Birth weight was reduced in female offspring of DIO mothers (by 6%, P = .039), and DIO offspring were heavier than controls at weaning (males by 47%, females by 27%), however there were no differences in glucose tolerance, plasma lipids, or hepatic gene expression at 6 months. Despite the relative lack of effects in the F1, we found clear fetal growth restriction and persistent metabolic changes in otherwise unmanipulated second-generation offspring with effects on birth weight, insulin levels, and hepatic gene expression that were transmitted through both maternal and paternal lines. This suggests that the consequences of the current dietary obesity epidemic may also have an impact on the descendants of obese individuals, even when the phenotype of the F1 appears largely unaffected

Maternal short stature does not predict their children's fatness indicators in a nutritional dual-burden sample of urban Mexican Maya.

The co-existence of very short stature due to poor chronic environment in early life and obesity is becoming a public health concern in rapidly transitioning populations with high levels of poverty. Individuals who have very short stature seem to be at an increased risk of obesity in times of relative caloric abundance. Increasing evidence shows that an individual is influenced by exposures in previous generations. This study assesses whether maternal poor early life environment predicts her child's adiposity using cross sectional design on Maya schoolchildren aged 7-9 and their mothers (n = 57 pairs). We compared maternal chronic early life environment (stature) with her child's adiposity (body mass index [BMI] z-score, waist circumference z-score, and percentage body fat) using multiple linear regression, controlling for the child's own environmental exposures (household sanitation and maternal parity). The research was performed in the south of Merida, Yucatan, Mexico, a low socioeconomic urban area in an upper middle income country. The Maya mothers were very short, with a mean stature of 147 cm. The children had fairly high adiposity levels, with BMI and waist circumference z-scores above the reference median. Maternal stature did not significantly predict any child adiposity indicator. There does not appear to be an intergenerational component of maternal early life chronic under-nutrition on her child's obesity risk within this free living population living in poverty. These results suggest that the co-existence of very short stature and obesity appears to be primarily due to exposures and experiences within a generation rather than across generations

The Influence Of Maternal Obesity On Adolescent Obesity In Santiago, Chile

Objective: To examine the relationship between adolescent obesity and associated maternal obesity variables of interest, specifically maternal pre-pregnancy obesity and maternal obesity 10 years postpartum. Design: Secondary data analysis of a longitudinal study in Santiago, Chile (N=786 adolescents). Variables were extracted from multiple waves of data collection. The maternal obesity variables of interest and covariates were stratified by gender and associations of interest examined using univariate logistic regression analyses and multivariate logistic regression models with missing data imputation. Covariates included were birth weight percentile, breastfeeding for 6 months, father\u27s presence, maternal age, and maternal education. Results: Adolescent obesity was associated with maternal obesity in both males and females. Female obese adolescents had a positive association with maternal obesity at 10 years postpartum (OR= 3.65, CI= 1.19, 11.14) and a negative association with father\u27s presence in the household (OR= 0.236, CI= 0.07, 0.76). Among male adolescents obesity was positively associated with maternal pre-pregnancy obesity (OR= 9.59, CI= 1.25, 73.31). Conclusions: Maternal obesity status is an important predictor of adolescent obesity. Maternal obesity was a significant predictor of obesity among males and females but at chronologically different periods of the child\u27s development. This may be attributed to gender related differences in genetic, behavioral, and/or environmental factors. Adolescent obesity intervention programs should provide varied approaches that cater to the different needs of males and females. Future research on maternal and other influences of adolescent obesity should focus on quantitative collection of parental and peer-related measures of anthropometrics, physical activity, dietary habits, as well as other sociobehavioral determinants of health

The Connection Between Maternal Employment and Childhood Obesity: Inspecting the Mechanisms

This paper investigates the channels through which maternal employment affects childhood obesity. We use time diaries and interview responses from the Child Development Supplement of the Panel Study of Income Dynamics which combine information on children’s time allocation and mother’s labor force participation. Our empirical strategy involves estimating the effect of children’s activities and meal routines on BMI, estimating the effect of maternal employment on these activities and routines and then combining these two estimates. We find that maternal employment affects child weight through two main mechanisms – supervision and nutrition, however, the particular channels vary by mother’s education.Childhood Obesity, Labor Supply, Time Allocations

Maternal Obesity Promotes Diabetic Nephropathy in Rodent Offspring

Maternal obesity is known to increase the risk of obesity and diabetes in offspring. Though diabetes is a key risk factor for the development of chronic kidney disease (CKD), the relationship between maternal obesity and CKD has not been clearly defined. In this study, a mouse model of maternal obesity was employed to determine the impact of maternal obesity on development of diabetic nephropathy in offspring. Female C57BL/6 mice were fed high-fat diet (HFD) for six weeks prior to mating, during gestation and lactation. Male offspring were weaned to normal chow diet. At postnatal Week 8, offspring were randomly administered low dose streptozotocin (STZ, 55 mg/kg/day for five days) to induce diabetes. Assessment of renal damage took place at postnatal Week 32. We found that offspring of obese mothers had increased renal fibrosis, inflammation and oxidative stress. Importantly, offspring exposed to maternal obesity had increased susceptibility to renal damage when an additional insult, such as STZ-induced diabetes, was imposed. Specifically, renal inflammation and oxidative stress induced by diabetes was augmented by maternal obesity. Our findings suggest that developmental programming induced by maternal obesity has implications for renal health in offspring. Maternal obesity should be considered a risk factor for CKD