BackgroundEpstein-Barr virus (EBV) is a common herpesvirus linked to infectious mononucleosis and multiple cancers. There are no national estimates of EBV seroprevalence in the United States. Our objective was to estimate the overall prevalence and sociodemographic predictors of EBV among U.S. children and adolescents aged 6–19.MethodsWe calculated prevalence estimates and prevalence ratios for EBV seroprevalence using data from the 2003–2010 U.S. National Health and Nutrition Examination Survey (NHANES) for children aged 6–19 (n = 8417). Poisson regression was used to calculate multivariable-adjusted prevalence ratios across subgroup categories (sex, race/ethnicity, parental education, household income, household size, foreign-born, BMI, and household smoking).FindingsOverall EBV seroprevalence was 66.5% (95% CI 64.3%–68.7%.). Seroprevalence increased with age, ranging from 54.1% (95% CI 50.2%–57.9%) for 6–8 year olds to 82.9% (95% CI 80.0%–85.9%) for 18–19 year olds. Females had slightly higher seroprevalence (68.9%, 95% CI 66.3%–71.6%) compared to males (64.2%, 95% CI 61.7%–66.8%). Seroprevalence was substantially higher for Mexican-Americans (85.4%, 95% CI 83.1%–87.8%) and Non-Hispanic Blacks (83.1%, 95% CI 81.1%–85.1%) than Non-Hispanic Whites (56.9%, 95% CI 54.1%–59.8%). Large differences were also seen by family income, with children in the lowest income quartile having 81.0% (95% CI 77.6%–84.5%) seroprevalence compared to 53.9% (95% CI 50.5%–57.3%) in the highest income quartile, with similar results for parental education level. These results were not explained by household size, BMI, or parental smoking. Among those who were seropositive, EBV antibody titers were significantly higher for females, Non-Hispanic Blacks and Mexican-Americans, with no association found for socioeconomic factors.ConclusionsIn the first nationally representative U.S. estimates, we found substantial socioeconomic and race/ethnic differences in the seroprevalence of EBV across all ages for U.S. children and adolescents. These estimates can help researchers and clinicians identify groups most at risk, inform research on EBV-cancer etiology, and motivate potential vaccine development.

ObjectiveObesity is a risk factor for congenital heart defects (CHD), but whether risk is independent of abnormal glucose metabolism is unknown. Data on whether overweight status increases risk is also conflicting.Research Design and MethodsWe included 121815 deliveries from a cohort study, the Consortium on Safe Labor, after excluding women with pregestational diabetes as recorded in the electronic medical record. CHD were identified via medical record discharge summaries. Adjusted odds ratios (OR) for any CHD were calculated for prepregnancy body mass index (BMI) categories of overweight (25 to <30 kg/m2), obese (30 to <40 kg/m2), and morbidly obese (≥40 kg/m2) compared to normal weight (18.5 to <25 kg/m2) women, and for specific CHD with obese groups combined (≥30 kg/m2). A sub-analysis adjusting for oral glucose tolerance test (OGTT) results where available was performed as a proxy for potential abnormal glucose metabolism present at the time of organogenesis.ResultsThere were 1388 (1%) infants with CHD. Overweight (OR=1.15 95% CI: 1.01–1.32), obese (OR=1.26 95% CI: 1.09, 1.44), and morbidly obese (OR=1.34 95% CI: 1.02–1.76) women had greater odds of having a neonate with CHD than normal weight women (P< 0.001 for trend). Obese women (BMI ≥30 kg/m2) had higher odds of having an infant with conotruncal defects (OR=1.34 95%CI: 1.04–1.72), atrial septal defects (OR =1.22 95% CI: 1.04–1.43), and ventricular septal defects (OR=1.38 95% CI: 1.06–1.79). Being obese remained a significant predictor of CHD risk after adjusting for OGTT.ConclusionIncreasing maternal weight class was associated with increased risk for CHD. In obese women, abnormal glucose metabolism did not completely explain the increased risk for CHD; the possibility that other obesity-related factors are teratogenic requires further investigation.

Aims/hypothesis The escalating rate of childhood obesity is a public health concern worldwide, with children in certain ethnic groups being disproportionately affected. Our objective was to examine the joint effects of pre-pregnancy adiposity, pregnancy weight gain and gestational diabetes (GDM) in relation to excess fetal growth and to identify susceptible races or ethnic populations. Methods The risk for delivery of a large-for-gestational-age (LGA) infant, specific to race and fetal sex, was evaluated in 105,985 pregnancies in the Consortium on Safe Labor from [2002][2003][2004][2005][2006][2007][2008]. Generalised estimating equations were used to estimate the risk for delivery of LGA infants. Joint effects were employed to evaluate the interplay of three risk factors.Models were stratified by racial group considering one, two or three factors (i.e. pre-pregnancy adiposity, pregnancy weight gain and GDM, with 0 factors as the reference group). Results Greater pre-pregnancy adiposity, pregnancy weight gain and GDM were independently associated with increased risk of giving birth to an LGA infant across all races (except GDM among non-Hispanic whites), in both underweight and normal-weight women. Among non-Hispanic white, non-Hispanic black and Hispanic women, the threefactor joint effect was associated with substantially increased odds of LGA (OR [95% CI] 11. 27 [8.40, 15.11], 7.09 [4.81, 10.45] and 10.19 [6.84, 15.19], respectively). However, for Asian women the joint effect of all three factors (OR [95% CI] 5.14 [2.11, 12.50]) was approximately the same as any of the two factors. Conclusions/interpretation GDM, pre-pregnancy obesity and excessive pregnancy weight gain were jointly associated with elevated risk of giving birth to an LGA infant and the effects varied by race. This suggests that those involved in public health efforts aimed at preventing LGA deliveries should consider variations in racial groups when devising effective strategies.