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BACKGROUND: Maternal obesity and high gestational weight gain (GWG) disproportionally affect low-income populations and may be associated with child neurodevelopment in a sex-specific manner. We examined sex-specific associations between prepregnancy BMI, GWG, and child neurodevelopment at age 7. METHODS: Data are from a prospective low-income cohort of African American and Dominican women (n = 368; 44.8% male offspring) enrolled during the second half of pregnancy from 1998 to 2006. Neurodevelopment was measured using the Wechsler Intelligence Scale for Children (WISC-IV) at approximately child age 7. Linear regression estimated associations between prepregnancy BMI, GWG, and child outcomes, adjusting for race/ethnicity, marital status, gestational age at delivery, maternal education, maternal IQ and child age. RESULTS: Overweight affected 23.9% of mothers and obesity affected 22.6%. At age 7, full-scale IQ was higher among girls (99.7 ± 11.6) compared to boys (96.9 ± 13.3). Among boys, but not girls, prepregnancy overweight and obesity were associated with lower full-scale IQ scores [overweight ß: - 7.1, 95% CI: (- 12.1, - 2.0); obesity ß: - 5.7, 95% CI: (- 10.7, - 0.7)]. GWG was not associated with full-scale IQ in either sex. CONCLUSIONS: Prepregnancy overweight and obesity were associated with lower IQ among boys, but not girls, at 7 years. These findings are important considering overweight and obesity prevalence and the long-term implications of early cognitive development.

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OBJECTIVES: This study aimed to evaluate the association between nightly, napping, and 24-h sleep duration throughout pregnancy and birth weight z-score among nulli- and multiparous women. METHODS: Nightly,napping, and 24-h sleep duration and birth weight z-score (calculated on thebasis of the International Fetal and Newborn Growth Consortium for the 21st century standards) were studied in a cohort of 176 pregnant women from Brazil. Linear mixed-effect analyses were performed to assess the longitudinal evolution of sleep duration and the best unbiased linear predictors of the random coefficients were estimated. The best unbiased linear predictor estimates of sleep duration intercept and slope were included in the linear regression models with birth weight z-score as the outcome. RESULTS: The mean hours of nightly sleep decreased during pregnancy in nulliparous women (ß = -0.55; 95% confidence interval [CI], -0.83 to -0.27) but the decrease was not statistically significant in multiparous women (ß = -0.19; 95% CI, -0.30 to 0.01). Twenty-four hour sleep duration decreased during pregnancy in both multiparous (ß = -0.50; 95% CI, -0.76 to -0.25) and nulliparous women (ß = 0.77; 95% CI, -1.06 to -0.48). Napping sleep duration did not change in either group. Among the nulliparous women, both first-trimester 24-h sleep duration and its change throughout pregnancy were inversely associated with birth weight (ß = -0.44; 95% CI, -0.68 to -0.21; ß = -1.75; 95% CI, -3.17 to -0.30, respectively). No associations were detected in multiparous women for nightly and napping sleep duration. CONCLUSIONS: Nulliparous women with greater decreases in sleep duration throughout their pregnancy gave birth to newborns with lower birth weight z-scores.

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OBJECTIVE: The aim of this study was to investigate whether serum concentrations of total saturated fatty acids (SFAs), polyunsaturated fatty acids (PUFAs), and their fractions are associated with plasma adiponectin and leptin concentrations throughout pregnancy. METHODS: A prospective cohort of 201 pregnant women was followed from gestational weeks 5 to 13, 20 to 26, and 30 to 36. Blood samples were collected at the three visits after 12 h of fasting. Fatty acid concentrations were determined using fast gas-liquid chromatography. Plasma adiponectin (µg/mL) and leptin (ng/dL) concentrations were evaluated using enzyme-linked immunosorbent assay kits. Statistical analyses included median adipokine concentrations according to the tertiles of fatty acid distribution and multiple linear mixed-effect models adjusted for body mass index, gestational age, total energy intake, alcohol consumption, and smoking. RESULTS: Women classified in the third SFA concentration tertile had lower median values of adiponectin compared with those in the first tertile ([first trimester: first tertile = 5.36; third tertile = 5.00]; [second trimester: first tertile = 6.39; third tertile = 4.47]; [third trimester: first tertile = 6.46; third tertile = 4.60]). Similar trends were observed for the 14:0, 16:0 and 18:0 fractions. In the multiple longitudinal models, total SFA (ß = -41.039; P = 0.008) and 16:0 were negatively associated with plasma adiponectin (16:0, ß = -0.511; P = 0.001). Total PUFA ω-6 (ß = 28.961; P = 0.002) and 18:2 ω-6 (ß = 0.259, P = 0.006) were positively associated with the adiponectin. Total SFA (ß = 0.110, P = 0.007), 14:0 (ß = 0.072, P = 0.011), and 20:3 ω-6 (ß = 0.039; P = 0.035) were positively associated with plasma leptin. CONCLUSIONS: Total serum SFA and the 16:0 fraction were negatively associated with plasma adiponectin and positively associated with leptin concentrations. Total ω-6 PUFA was positively associated only with plasma adiponectin concentrations throughout pregnancy.

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OBJECTIVE: To understand phenotypic and molecular characteristics of patients with clinically "definite" primary lateral sclerosis (PLS) in a prospective study. METHODS: Six sites enrolled 41 patients who had pure upper motor neuron dysfunction, bulbar symptoms, a normal EMG done within 12 months of enrollment, and onset of symptoms ≥5 years before enrollment. For phenotypic analyses, 27 demographic, clinical, and cognitive variables were analyzed using the k-means clustering method. For molecular studies, 34 available DNA samples were tested for the C9ORF72 mutation, and exome sequencing was performed to exclude other neurologic diseases with known genetic cause. RESULTS: K-means clustering using the 25 patients with complete datasets suggested that patients with PLS can be classified into 2 groups based on clinical variables, namely dysphagia, objective bulbar signs, and urinary urgency. Secondary analyses performed in all 41 patients and including only variables with complete data corroborated the results from the primary analysis. We found no evidence that neurocognitive variables are important in classifying patients with PLS. Molecular studies identified C9ORF72 expansion in one patient. Well-characterized pathogenic mutations were identified in SPG7, DCTN1, and PARK2. Most cases showed no known relevant mutations. CONCLUSIONS: Cluster analyses based on clinical variables indicated at least 2 subgroups of clinically definite PLS. Molecular analyses further identified 4 cases with mutations associated with amyotrophic lateral sclerosis, Parkinson disease, and possibly hereditary spastic paraplegia. Phenotypic and molecular characterization is the first step in investigating biological clues toward the definition of PLS. Further studies with larger numbers of patients are essential.