Alcohol Exposure In Utero and Child Academic Achievement.
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ABSTRACT:
SUBMITTER: von Hinke Kessler Scholder S
PROVIDER: S-EPMC4243528 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Our understanding of health and social stratification can be enriched by testing tenets of cumulative inequality theory that emphasize how the accumulation of inequality is dependent on the developmental stage being considered, the duration and stability of poor health, and the family resources available to children. I analyze longitudinal data from the British National Child Development Study (N = 9,252) to ask: (1) if child health is a source of cumulative inequality in academic achievement, (2) whether this relationship depends on the timing and duration of poor health, and (3) whether trajectories are sensitive to levels of family capital. The results suggest that the relationship between health and academic achievement emerges very early in life and persists and that whether we observe shrinking or widening inequality as children age depends on when we measure their health and whether children have access to compensatory resources.
| S-EPMC4631384 | biostudies-literature
Project description:IMPORTANCE:Children living in poverty generally perform poorly in school, with markedly lower standardized test scores and lower educational attainment. The longer children live in poverty, the greater their academic deficits. These patterns persist to adulthood, contributing to lifetime-reduced occupational attainment. OBJECTIVE:To determine whether atypical patterns of structural brain development mediate the relationship between household poverty and impaired academic performance. DESIGN, SETTING, AND PARTICIPANTS:Longitudinal cohort study analyzing 823 magnetic resonance imaging scans of 389 typically developing children and adolescents aged 4 to 22 years from the National Institutes of Health Magnetic Resonance Imaging Study of Normal Brain Development with complete sociodemographic and neuroimaging data. Data collection began in November 2001 and ended in August 2007. Participants were screened for a variety of factors suspected to adversely affect brain development, recruited at 6 data collection sites across the United States, assessed at baseline, and followed up at 24-month intervals for a total of 3 periods. Each study center used community-based sampling to reflect regional and overall US demographics of income, race, and ethnicity based on the US Department of Housing and Urban Development definitions of area income. One-quarter of sample households reported the total family income below 200% of the federal poverty level. Repeated observations were available for 301 participants. EXPOSURE:Household poverty measured by family income and adjusted for family size as a percentage of the federal poverty level. MAIN OUTCOMES AND MEASURES:Children's scores on cognitive and academic achievement assessments and brain tissue, including gray matter of the total brain, frontal lobe, temporal lobe, and hippocampus. RESULTS:Poverty is tied to structural differences in several areas of the brain associated with school readiness skills, with the largest influence observed among children from the poorest households. Regional gray matter volumes of children below 1.5 times the federal poverty level were 3 to 4 percentage points below the developmental norm (P?<?.05). A larger gap of 8 to 10 percentage points was observed for children below the federal poverty level (P?<?.05). These developmental differences had consequences for children's academic achievement. On average, children from low-income households scored 4 to 7 points lower on standardized tests (P?<?.05). As much as 20% of the gap in test scores could be explained by maturational lags in the frontal and temporal lobes. CONCLUSIONS AND RELEVANCE:The influence of poverty on children's learning and achievement is mediated by structural brain development. To avoid long-term costs of impaired academic functioning, households below 150% of the federal poverty level should be targeted for additional resources aimed at remediating early childhood environments.
| S-EPMC4687959 | biostudies-literature
Project description:BackgroundRecent data suggest that children of mothers who are obese before pregnancy, or who gain too much weight during pregnancy, may be at an increased risk of cognitive impairments.MethodsMother-infant dyads enrolled in a birth cohort study in Pittsburgh, Pennsylvania (1983-1986), were followed from early pregnancy to 14 years postpartum (n=574). Math, reading and spelling achievements were assessed at ages 6 and 10 years using the Wide Range Achievement Test-Revised, and at age 14 years using the Wechsler Individual Achievement Test Screener. Self-reported total GWG was converted to gestational age-standardised z-scores. Generalised estimating equations were used to estimate the effects of GWG and pre-pregnancy body mass index (BMI) on academic achievement at 6, 10 and 14 years, while adjusting for maternal race, child sex, parity, employment, family income, maternal intelligence, maternal depression, pre-pregnancy BMI (in GWG models only) and the home environment.ResultsThe mean (SD) BMI was 23.4 (5.7) kg/m(2) and the mean (SD) GWG reported at delivery was 14.4 (5.9) kg. There was a significant non-linear association between pre-pregnancy BMI and an offspring's academic achievement. At 6, 10 and 14 years, an offspring's academic scores were inversely associated with pre-pregnancy BMI beyond 22 kg/m(2). High GWG (>1 SD) was associated with approximately 4-point lower reading (adjusted β (adjβ) -3.75, 95% CI -7.1 to -0.4) and spelling scores (adjβ -3.90, 95% CI -7.8 to -0.2), compared with GWG -1 to +1 SD.ConclusionsFuture studies in larger and socioeconomically diverse populations are needed to confirm maternal weight and weight gain as causal determinants of a child's academic skills, and whether this effect persists into adulthood.
| S-EPMC4865436 | biostudies-literature
Project description:Prior research suggests a link between academic performance and alcohol use during adolescence, but the degree to which this association reflects actual protective effects continues to be debated. We investigated the role of genetic factors in the association between academic achievement and adolescent alcohol use and whether achievement might constrain the translation of genetic influences on drinking into actual behavior (a Gene × Environment interaction). Analysis of twin data from Add Health (n = 399 monozygotic and dizygotic twin pairs) revealed not only common genetic factors underlying the association between achievement and alcohol consumption but also evidence for a gene-environment interaction. Specifically, the protective effect of achievement operated by moderating heritability of alcohol use, which was particularly salient for adolescents at high genetic risk for alcohol use.
| S-EPMC5553450 | biostudies-other
Project description:Deficits in behavioral flexibility are a hallmark of multiple psychiatric, neurological, and substance use disorders. These deficits are often marked by decreased function of the prefrontal cortex (PFC); however, the genesis of such executive deficits remains understudied. Here we report how the most preventable cause of developmental disability, in utero exposure to alcohol, alters cortico-striatal circuit activity leading to impairments in behavioral flexibility in adulthood. We utilized a translational touch-screen task coupled with in vivo electrophysiology in adult mice to examine single unit and coordinated activity of the lateral orbital frontal cortex (OFC) and dorsolateral striatum (DS) during flexible behavior. Prenatal alcohol exposure (PAE) decreased OFC, and increased DS, single unit activity during reversal learning and altered the number of choice responsive neurons in both regions. PAE also decreased coordinated activity within the OFC and DS as measured by oscillatory field activity and altered spike-field coupling. Furthermore, PAE led to sustained connectivity between regions past what was seen in control animals. These findings suggest that PAE causes altered coordination within and between the OFC and DS, promoting maladaptive perseveration. Our model suggests that in optimally functioning mice OFC disengages the DS and updates the newly changed reward contingency, whereas in PAE animals, aberrant and persistent OFC to DS signaling drives behavioral inflexibility during early reversal sessions. Together, these findings demonstrate how developmental exposure alters circuit-level activity leading to behavioral deficits and suggest a critical role for coordination of neural timing during behaviors requiring executive function.
| S-EPMC6899166 | biostudies-literature
Project description:Using a longitudinal mediation framework and a low-income sample, this study had 2 aims: (a) to model bidirectional associations between parent academic expectations and child academic outcomes from first through fifth grade, and (b) to explore 3 mediators of parental influence: parent involvement in child schooling, child learning behaviors, and child perceived academic competence. Participants included 356 children and their caregivers (89% mothers) recruited from Head Start centers (58% European American, 25% African American, 17% Latino). At each time point (grades 1, 2, 3, 5), parents rated their academic expectations, teachers rated parent involvement and child learning behaviors, and children rated their self-perceptions of their academic competence. Bidirectional longitudinal associations emerged between parent academic expectations and child academic outcomes. Child learning behaviors mediated this association from first to third grade, whereas child perceived academic competence mediated from second to fifth grade. Parallel cross-lagged models replicated these findings with child academic outcomes assessed using a test of reading achievement and teacher ratings of academic performance. (PsycINFO Database Record
| S-EPMC5565683 | biostudies-literature
Project description:Epidemiological studies have raised concerns about the reproductive consequences of in utero exposure to alcohol. Maternal lifestyle factors have been associated with altered pubertal development, but the impact of prenatal alcohol exposure on male puberty is unknown. Thus, the objective was to explore whether prenatal alcohol exposure alters pubertal development in boys.Follow-up of a Danish pregnancy cohort.Sons (N=2522) of women who were enrolled in a Danish pregnancy cohort between 1984 and 1987.Indicators of pubertal development, assessed by age at first nocturnal emission, voice break, acne and regular shaving.We found a tendency towards a later age at first nocturnal emission and voice break following in utero exposure to binge drinking. Boys exposed to ?5 binge drinking episodes during pregnancy experienced their first nocturnal emission 7.3?months (95% CI -2.8 to 17.4) later and voice break 4.9?months (95% CI -0.6 to 10.4) later than the unexposed boys. Results for average weekly alcohol consumption were in the same direction, but differences were smaller and not statistically significant.We found no strong support for the hypothesis that in utero exposure to weekly alcohol consumption is a risk factor for altered pubertal development, but a tendency towards delayed pubertal development among boys exposed to binge drinking during fetal life was observed. Longitudinal studies, with data collected as children go through puberty, are needed to explore this further.
| S-EPMC4067820 | biostudies-literature
Project description:Most children with in utero alcohol exposure do not exhibit all features of fetal alcohol syndrome (FAS), and a challenge for clinicians is to make an early diagnosis of fetal alcohol spectrum disorders (FASD) to avoid lost opportunities for care. In brain, correct neurodevelopment requires proper angiogenesis. Since alcohol alters brain angiogenesis and the placenta is a major source of angiogenic factors, we hypothesized that it is involved in alcohol-induced brain vascular defects. In mouse, using in vivo repression and overexpression of PLGF, we investigated the contribution of placenta on fetal brain angiogenesis. In human, we performed a comparative molecular and morphological analysis of brain/placenta angiogenesis in alcohol-exposed fetuses. Results showed that prenatal alcohol exposure impairs placental angiogenesis, reduces PLGF levels and consequently alters fetal brain vasculature. Placental repression of PLGF altered brain VEGF-R1 expression and mimicked alcohol-induced vascular defects in the cortex. Over-expression of placental PGF rescued alcohol effects on fetal brain vessels. In human, alcohol exposure disrupted both placental and brain angiogenesis. PLGF expression was strongly decreased and angiogenesis defects observed in the fetal brain markedly correlated with placental vascular impairments. Placental PGF disruption impairs brain angiogenesis and likely predicts brain disabilities after in utero alcohol exposure. PLGF assay at birth could contribute to the early diagnosis of FASD.
| S-EPMC5461764 | biostudies-literature
Project description:Neuroimaging studies have indicated that prenatal alcohol exposure is associated with alterations in the structure of specific brain regions. However, the temporal specificity of such changes and their behavioral consequences are less known. Here we explore the brain structure of infants with in utero exposure to alcohol shortly after birth. T2 structural MRI images were acquired from 28 alcohol-exposed infants and 45 demographically matched healthy controls at 2-4 weeks of age on a 3T Siemens Allegra system as part of large birth cohort study, the Drakenstein Child Health Study (DCHS). Neonatal neurobehavior was assessed at this visit; early developmental outcome assessed on the Bayley Scales of Infant Development III at 6 months of age. Volumes of gray matter regions were estimated based on the segmentations of the University of North Carolina neonatal atlas. Significantly decreased total gray matter volume was demonstrated for the alcohol-exposed cohort compared to healthy control infants (p < 0.001). Subcortical gray matter regions that were significantly different between groups after correcting for overall gray matter volume included left hippocampus, bilateral amygdala and left thalamus (p < 0.01). These findings persisted even when correcting for infant age, gender, ethnicity and maternal smoking status. Both early neurobehavioral and developmental adverse outcomes at 6 months across multiple domains were significantly associated with regional volumes primarily in the temporal and frontal lobes in infants with prenatal alcohol exposure. Alcohol exposure during the prenatal period has potentially enduring neurobiological consequences for exposed children. These findings suggest the effects of prenatal alcohol exposure on brain growth is present very early in the first year of life, a period during which the most rapid growth and maturation occurs.
| S-EPMC6556617 | biostudies-literature
Project description:Antiepileptic drugs may cause congenital malformations. Less is known about the effect on development in infancy and childhood. The aim of this study was to examine whether exposure to antiepileptic drugs during pregnancy has an effect on early child development.From mid-1999 through December 2008, children of mothers recruited at 13-17 weeks of pregnancy were studied in the ongoing prospective Norwegian Mother and Child Cohort Study. Information on birth outcomes were obtained from the Medical Birth Registry (108,264 children), and mothers reported on their child's motor development, language, social skills, and autistic traits using items from standardized screening tools at 18 months (61,351 children) and 36 months (44,147 children) of age. The relative risk of adverse outcomes in children according to maternal or paternal epilepsy with and without prenatal exposure to antiepileptic drugs was estimated as odds ratios (ORs), using logistic regression with adjustment for maternal age, parity, education, smoking, depression/anxiety, folate supplementation, and child congenital malformation or low birth weight.A total of 333 children were exposed to antiepileptic drugs in utero. At 18 months, the exposed children had increased risk of abnormal scores for gross motor skills (7.1% vs. 2.9%; OR 2.0, 95% confidence interval [CI] 1.1-3.7) and autistic traits (3.5% vs. 0.9%; OR 2.7, CI 1.1-6.7) compared to children of parents without epilepsy. At 36 months, the exposed children had increased risk of abnormal score for gross motor skills (7.5% vs. 3.3%; OR 2.2, CI 1.1-4.2), sentence skills (11.2% vs. 4.8%; OR 2.1, CI 1.2-3.6), and autistic traits (6.0% vs. 1.5%; OR 3.4, CI 1.6-7.0). The drug-exposed children also had increased risk of congenital malformations (6.1% vs. 2.9%; OR 2.1, CI 1.4-3.4), but exclusion of congenital malformations did not affect the risk of adverse development. Children born to women with epilepsy who did not use antiepileptic drugs had no increased risks. Children of fathers with epilepsy generally scored within the normal range.Exposure to antiepileptic drugs during pregnancy is associated with adverse development at 18 and 36 months of age, measured as low scores within key developmental domains rated by mothers. Exposures to valproate, lamotrigine, carbamazepine, or multiple antiepileptic drugs were associated with adverse outcome within different developmental domains.
| S-EPMC3766256 | biostudies-literature