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Background: Most studies of the effects of prenatal alcohol exposure (PAE) on cognitive function have assumed that the dose-response curve is linear. However, data from a few animal and human studies suggest that there may be an inflection point in the dose-response curve above which PAE effects are markedly stronger and that there may be differences associated with pattern of exposure, assessed in terms of alcohol dose per drinking occasion and drinking frequency. Methods: We performed second-order confirmatory factor analysis on data obtained at school age, adolescence, and early adulthood from 2227 participants in six US longitudinal cohorts to derive a composite measure of cognitive function. Regression models were constructed to examine effects of PAE on cognitive function, adjusted for propensity scores. Analyses based on a single predictor (absolute alcohol (AA)/day) were compared with analyses based on two predictors (dose/occasion and drinking frequency), using (1) linear models and (2) nonparametric general additive models (GAM) that allow for both linear and nonlinear effects. Results: The single-predictor GAM model showed virtually no nonlinearity in the effect of AA/day on cognitive function. However, the two-predictor GAM model revealed differential effects of maternal drinking pattern. Among offspring of infrequent drinkers, PAE effects on cognitive function were markedly stronger in those whose mothers drank more than ~3 drinks/occasion, and the effect of dose/occasion was strongest among the very frequent drinkers. Frequency of drinking did not appear to alter the PAE effect on cognitive function among participants born to mothers who limited their drinking to ~1 drink/occasion or less. Conclusions: These findings suggest that linear models based on total AA/day are appropriate for assessing whether PAE affects a given cognitive outcome. However, examination of alcohol dose/occasion and drinking frequency is needed to fully characterize the impact of different levels of alcohol intake on cognitive impairment. [ABSTRACT FROM AUTHOR]

Purpose: A longitudinal cohort of adolescents who initiated drinking before age 15 were studied to determine which factors distinguished between early initiators who continued to drink (persisters) from those who stopped drinking (desisters). There were 308 early initiators in the total sample (n = 917); 247 were persisters, and 61 were desisters. Method: A stepwise discriminant analysis identified differences between the two groups. Considered risk/protective factors were parenting practices, peer drinking, child and maternal depression, child behavior, prenatal alcohol exposure, home environment, and demographic factors. Results: Desistence was significantly related to African American race and more parental strictness. Exposure to =1 drink/day during pregnancy and high levels of autonomy from parents were significant predictors of persistent drinking. Conclusions: Early initiation places adolescents at risk for continued and heavier drinking. Identifying characteristics of those who start early but do or do not continue drinking can inform education programs to better target the most appropriate adolescents.

Summary: High levels of prenatal alcohol exposure (PAE) result in significant cognitive deficits in children, but the exact nature of the dose‐response relationship is less well understood. To investigate this relationship, data were assembled from six longitudinal birth cohort studies examining the effects of PAE on cognitive outcomes from early school age through adolescence. Structural equation models (SEMs) are a natural approach to consider, because of the way they conceptualise multiple observed outcomes as relating to an underlying latent variable of interest, which can then be modelled as a function of exposure and other predictors of interest. However, conventional SEMs could not be fitted in this context because slightly different outcome measures were used in the six studies. In this paper we propose a multi‐group Bayesian SEM that maps the unobserved cognition variable to a broad range of observed outcomes. The relation between these variables and PAE is then examined while controlling for potential confounders via propensity score adjustment. By examining different possible dose‐response functions, the proposed framework is used to investigate whether there is a threshold PAE level that results in minimal cognitive deficit. [ABSTRACT FROM AUTHOR]

To test the feasibility of conducting a pragmatic randomized controlled trial (RCT) comparing the International Association of Diabetes in Pregnancy Study Groups (IADPSG) versus Carpenter-Coustan diagnostic criteria for gestational diabetes (GDM), and to examine patient and provider views on GDM screening. A single-blinded pragmatic pilot RCT. Participants with a singleton pregnancy between 24 and 28 weeks gestation received a 50 g oral glucose challenge test and if the value was, Author(s): Christina M. Scifres[sup.1] , Kaleab Z. Abebe[sup.2] , Kelley A. Jones[sup.3] , Diane M. Comer[sup.2] , Tina Costacou[sup.3] , Matthew S. Freiberg[sup.2] , Hyagriv N. Simhan[sup.1] , Nancy L. [...]

The objective of this study was to estimate whether maternal history of childhood maltreatment was associated with pre‐pregnancy obesity or excessive gestational weight gain. Pregnant women (n = 472) reported pre‐pregnancy weight and height and gestational weight gain and were followed up to 16 years post‐partum when they reported maltreatment on the Childhood Trauma Questionnaire (CTQ). CTQ score ranged from no maltreatment (25) to severe maltreatment (125). Prenatal mental health modified the association between CTQ score and maternal weight (P < 0.15), and thus stratified models are presented. After adjusting for race, prenatal tobacco, marijuana and alcohol use, a one standard deviation (1 SD) increase in CTQ score was associated with a 45% increase in the risk of pre‐pregnancy obesity among the 141 women with elevated anxiety (≥75th percentile on the State Trait Anxiety Inventory) [relative risk, RR (95% confidence interval, CI): 1.45 (1.12, 1.88)], but was not associated among less anxious (<75th percentile) women [RR (95% CI): 1.10 (0.81, 1.51)]. Risk of excessive gestational weight gain was higher [adjusted RR (95% CI): 1.21 (1.07, 1.37)] with every 1 SD increase in CTQ score for anxious women. No association was observed for less anxious women [adjusted RR (95% CI): 0.89 (0.78, 1.02)]. Prenatal depression similarly modified the association between maltreatment and weight gain. Factors such as psychological status and traumatic experiences in early childhood may contribute to pre‐pregnancy obesity and excessive gestational weight gain. [ABSTRACT FROM AUTHOR]

Evidence from animal models and epidemiological studies has linked prenatal alcohol exposure (PAE) to a broad range of long-term cognitive and behavioural deficits. However, there is a paucity of evidence regarding the nature and levels of PAE associated with increased risk of clinically significant cognitive deficits. To derive robust and efficient estimates of the effects of PAE on cognitive function, we have developed a hierarchical meta-analysis approach to synthesize information regarding the effects of PAE on cognition, integrating data on multiple outcomes from six U.S. Iongitudinal cohort studies. A key assumption of standard methods of meta-analysis, effect sizes are independent, is violated when multiple intercorrelated outcomes are synthesized across studies. Our approach involves estimating the dose-response coefficients for each outcome and then pooling these correlated dose-response coefficients to obtain an estimated "global" effect of exposure on cognition. In the first stage, we use individual participant data to derive estimates of the effects of PAE by fitting regression models that adjust for potential confounding variables using propensity scores. The correlation matrix characterizing the dependence between the outcome-specific dose-response coefficients estimated within each cohort is then run, while accommodating incomplete information on some outcome. We also compare inferences based on the proposed approach to inferences based on a full multivariate analysis.