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:ImportanceChildren 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.ObjectiveTo determine whether atypical patterns of structural brain development mediate the relationship between household poverty and impaired academic performance.Design, setting, and participantsLongitudinal 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.ExposureHousehold poverty measured by family income and adjusted for family size as a percentage of the federal poverty level.Main outcomes and measuresChildren's scores on cognitive and academic achievement assessments and brain tissue, including gray matter of the total brain, frontal lobe, temporal lobe, and hippocampus.ResultsPoverty 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 relevanceThe 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:ObjectiveTo describe the distribution of pediatricians and family physicians (child physicians) across school districts and examine the association between physician supply and third-grade test scores.Data sources and study settingData come from the January 2020 American Medical Association Physician Masterfile, the 2009-2013 and 2014-2018 waves of American Community Survey 5-Year Data, and the Stanford Education Data Archive (SEDA), which uses test scores from all U.S. public schools. We use covariate data provided by SEDA to describe student populations.Study designThis descriptive analysis constructs a physician-to-child-population ratio for every school district in the country and describes the child population served by the current distribution of physicians. We fit a set of multivariable regression models to estimate the associations between district test score outcomes and district physician supply. Our model includes state fixed effects to control for unobservable state-level factors, as well as a covariate vector of sociodemographic characteristics.Data collectionPublic data from three sources were matched by district ID.Principal findingsPhysicians are highly unequally distributed across districts: nearly 3640 (29.6%) of 12,297 districts have no child physician, which includes 49% of rural districts. Rural children of color in particular have very little access to pediatric care, and this inequality is more extreme when looking exclusively at pediatricians. Districts that have higher child physician supplies tend to have higher academic test scores in early education, independent of community socioeconomic status and racial/ethnic composition. While the national data show this positive relationship (0.012 SD, 95% CI, 0.0103-0.0127), it is most pronounced for districts in the bottom tertile of physician supply (0.163 SD, 95% CI, 0.108-0.219).ConclusionsOur study demonstrates a highly unequal distribution of child physicians in the U.S., and that children with less access to physicians have lower academic performance in early education.
| S-EPMC10339172 | 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:BackgroundPrenatal air pollution exposure is associated with reductions in self-regulation and academic achievement. Self-regulation has been separately linked with academic achievement. Understudied, however, are the contributions of pollution exposure to inhibitory control, a facet of self-regulation, and whether pollution-related inhibitory control deficits are associated with impairment in academic achievement.MethodsParticipants were recruited from a prospective birth cohort. Measures of prenatal airborne polycyclic aromatic hydrocarbons (PAH) during the third trimester of pregnancy, inhibitory control (NEPSY Inhibition) at mean age = 10.4 years, and Woodcock-Johnson Tests of Achievement-III at mean age = 13.7 were available for N = 200 participants. Multiple linear regression examined sex-dependent and sex independent associations among prenatal PAH, childhood inhibitory control, and academic achievement during adolescence, and whether childhood inhibitory control mediated associations between prenatal PAH and academic achievement during adolescence, controlling for ethnicity, maternal country of birth, language of prenatal interview, maternal marital status, maternal years of education, material hardship, quality of home caregiving environment, and early life stress.ResultsAcross all participants, higher prenatal PAH was significantly associated with worse spelling skills (WJ-III Spelling, β = -0.16, 95%Confidence Interval [CI]: 0.30, -0.02, p = .02). Trend level associations between higher prenatal PAH and worse reading comprehension (WJ-III Passage Comprehension, β = -0.13, 95%CI: 0.28, 0.01, p = .07) and math skills (WJ-III Broad Math, β = -0.11, 95%CI: 0.25, 0.03, p = .11) were detected. Across all participants, higher PAH was significantly associated with worse inhibitory control (β = -0.15, 95%CI: 0.29,-0.01 p = .03). Better inhibitory control was significantly associated with better reading comprehension (WJ-III Passage Comprehension, β = 0.22, 95%CI: 0.09, 0.36, p < .002) and math skills (WJ-III Broad Math Index, β = 0.32, 95%CI: 0.19, 0.45, p < .001), and trend level associations with better spelling skills (WJ-III Spelling, β = 0.12, 95%CI: 0.02, 0.26, p = .10). Inhibitory control significantly mediated PAH-related achievement effects for Passage Comprehension (β = -0.61, 95%CI: 1.49, -0.01) and Broad Math Index (β = -1.09, 95%CI: 2.36, -0.03).ConclusionsHigher prenatal PAH exposure and lower childhood inhibitory control were associated with worse spelling, passage comprehension, and math in adolescence. Notably, childhood inhibitory control mediated PAH exposure-related effects on achievement in adolescents. Identifying these potential exposure-related phenotypes of learning problems may promote interventions that target inhibitory control deficits rather than content specific deficits.
| S-EPMC8578437 | 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