Objective To assess offspring attention-deficit hyperactivity disorder (ADHD) symptoms and emotional/behavioral impairments at age 10 in relation to maternal gestational weight gain (GWG) and pre-pregnancy body mass index (BMI). Design and Setting Longitudinal birth cohort from Magee-Womens Hospital, Pittsburgh, Pennsylvania (enrolled 1983-1986). Population Mother-infant dyads (n=511) were followed through pregnancy to 10 years. Methods Self-reported total GWG was converted to gestational-age-standardised z-scores. Multivariable linear and negative binomial regressions were used to estimate effects of GWG and BMI on outcomes. Main outcome measures Child ADHD symptoms were assessed with the Conners’ Continuous Performance Test. Child behavior was assessed by parent and teacher ratings on the Child Behavior Checklist (CBCL) and Teacher Report Form, respectively. Results The mean(SD) total GWG(kg) was 14.5(5.9), and 10% of women had a pregravid BMI ≥30. Pre-pregnancy obesity (BMI of 30kg/m2) was associated with increased offspring problem behaviors including internalizing behaviors (adjusted β: 3.3 points, 95% CI: 1.7, 4.9), externalizing behaviors (adjusted β: 2.9 points, 95% CI: 1.4, 4.6), and attention problems (adjusted β: 2.3 points, 95% CI: 1.1, 3.4) on the CBCL, compared with normal weight mothers (BMI of 22 kg/m2). There were non-significant trends towards increased offspring impulsivity with low GWG among lean mothers (adjusted IRR: 1.2, 95% CI: 0.9, 1.5) and high GWG among overweight mothers (adjusted IRR: 1.7, 95% CI: 0.9, 2.8), but additional outcomes did not differ by GWG z-score. Results were not meaningful different after excluding high-substance users. Conclusions In a low-income and high-risk sample, we observed a small increase in child behavior problems among children of obese mothers, which could have an impact on child behavior in the population.

ObjectiveTo study the association between total and early pregnancy (<22 completed weeks) weight gain and risk of stillbirth, stratified by early‐pregnancy body mass index (BMI).DesignPopulation‐based cohort study.SettingStockholm‐Gotland Region, Sweden.PopulationPregnant women with singleton births (n = 160 560).MethodsPregnancy weight gain was standardised into gestational age‐specific z‐scores. For analyses of total pregnancy weight gain, a matched design with an incidence density sampling approach was used. Findings were also contrasted with current Institute of Medicine (IOM) weight gain recommendations.Main outcome measuresStillbirth defined as fetal death at ≥22 completed weeks of gestation.ResultsFor all BMI categories, there was no statistical association between total or early pregnancy weight gain and stillbirth within the range of a weight gain z‐score of −2.0 SD to +2.0 SD. Among normal‐weight women, the adjusted odds ratio of stillbirth for lower (−2.0 to −1.0 SD) and higher (+1.0 to +1.9 SD) total weight gain was 0.85 (95% CI; 0.48–1.49) and 1.03 (0.60–1.77), respectively, as compared with the reference category. Further, there were no associations between total or early pregnancy weight gain and stillbirth within the range of weight gain currently recommended by the IOM. For the majority of the BMI categories, the point estimates at the extremes of weight gain values (<−2.0SD and ≥2.0 SD) suggested protective effects of low weight gain and increased risks of high weight gain, but estimates were imprecise and not statistically significant.ConclusionWe found no associations between total or early pregnancy weight gain and stillbirth across the range of weight gain experienced by most women.Tweetable abstractThere was no association between weight gain during pregnancy and stillbirth among most women.

Aims To estimate the association between serum 25-hydroxyvitamin D concentrations and maternal hyperglycaemia (post-load glucose concentration ≥ 7.5 mmol/l). Methods Pregnant women (n = 429; 61% black, 36% obese, 45% smokers) enrolled in a cohort study at <16 weeks gestation. Non-fasting blood samples were assayed for serum 25-hydroxyvitamin D at enrolment. At 24–28 weeks gestation, maternal hyperglycaemia was determined using a 50-g 1-h oral glucose challenge test. Results A total of 67% of women had 25-hydroxyvitamin D concentrations < 50 nmol/l and 11% had maternal hyperglycaemia. Among smokers, each 23-nmol/l increase in serum 25-hydroxyvitamin D was associated with a reduction in the odds of maternal hyperglycaemia [odds ratio: 0.30 (95% CI: 0.13, 0.68)] after adjustment for parity, race/ethnicity, age, pre-pregnancy BMI, marital status, income, family history of diabetes, and gestational age of gestational diabetes mellitus screening. Among non-smokers, we found no association between early pregnancy vitamin D status and maternal hyperglycaemia. Conclusions Smoking status may modify the relationship between poor maternal vitamin D status and maternal hyperglycaemia.

Vitamin D is inversely related to risk of pre-eclampsia and preterm birth at <35 weeks in high-risk pregnancies.

Previous reports have implicated that pituitary-derived prolactin (PRL) is secreted from two distinct zones of mammotropes within the anterior lobe (AL). The inner zone (AL-IZ), located adjacent to the neuro-intermediate lobe (NIL), is supposed to be involved in the rapid and massive discharge of PRL from the pituitary gland due to suckling stimulus. Whereas the outer-zone (AL-OZ) gives the basal secretion and it does not play a role in the acute secretory response during nursing. Anatomically, the AL-IZ has an intimate contact with the NIL because the blood passing through the short portal vessels (SPV) bathes it first. Based on this fact it would be hypothesized that locally released and/or produced compounds, like OXY and alpha-MSH, can be delivered to the AL-IZ. In conjunction, OXY and alpha-MSH have already been implicated to play a role in the regulation of PRL release during suckling. Therefore, the purpose of this study was to examine the possible local transportation of these hormones into the median eminence and various regions of the pituitary gland of lactating rats. We have measured the concentrations of OXY and alpha-MSH from tissue samples of nonsuckled (NS) and 10 or 30 min after suckling (S) was initiated using specific RIAs. It has been shown that there are no changes in the concentration of OXY and alpha-MSH in theAL-IZ and AL-OZ due to suckling stimulus. In contrast, our data provide compelling evidence that OXY is transported into the IL, which can be further increased by suckling stimulus. These data suggest that blood transfusing NL passes through the IL before it is drained into the cavernous sinus, which opens the road for OXY into the general circulation. In addition, our data have unequivocally shown a lack of local delivery of either alpha MSH or OXY into the AL that raises serious doubt about their possible role in PRL secretion during suckling stimulus.