Where you live matters: visualizing environmental effects on reading attainment.

BACKGROUND: The way in which socioeconomic status (SES) moderates the etiology of reading attainment has been explored many times, with past work often finding that genetic influences are suppressed under conditions of socioeconomic deprivation and more fully realized under conditions of socioeconomic advantage: a gene-SES interaction. Additionally, past work has pointed toward the presence of gene-location interactions, with the relative influence of genes and environment varying across geographic regions of the same country/state. METHOD: This study investigates the extent to which SES and geographical location interact to moderate the genetic and environmental components of reading attainment. Utilizing data from 2,135 twin pairs in Florida (mean age 13.82 years, range 10.71-17.77), the study operationalized reading attainment as reading comprehension scores from a statewide test and SES as household income. We applied a spatial twin analysis procedure to investigate how twin genetic and environmental estimates vary by geographic location. We then expanded this analysis to explore how the moderating role of SES on said genetic and environmental influences also varied by geographic location. RESULTS: A gene-SES interaction was found, with heritability of reading being suppressed in lower- (23%) versus higher-SES homes (78%). The magnitude of the moderating parameters were not consistent by location, however, and ranged from -0.10 to 0.10 for the moderating effect on genetic influences, and from -0.30 to 0.05 for the moderating effect on environmental influences. For smaller areas and those with less socioeconomic variability, the magnitude of the genetic moderating parameter was high, giving rise to more fully realized genetic influences on reading there. CONCLUSIONS: SES significantly influences reading variability. However, a child's home location matters in both the overall etiology and how strongly SES moderates said etiologies. These results point toward the presence of multiple significant environmental factors that simultaneously, and inseparably, influence the underlying etiology of reading attainment.

Developmental behavioral genetics research on school achievement is missing vulnerable children, to our detriment.

Gene-environment processes tell us how genetic predispositions and environments work together to influence children in schools. One type of gene-environment process that has been extensively studied using behavioral genetics methods is a gene-by-environment interaction. A gene-by-environment interaction shows us when the effect of your context on a phenotype differs depending on your genetic predispositions, or vice versa, when the effect of your genetic predispositions on a phenotype differs depending on your context. Developmental behavioral geneticists interested in children's school achievement have examined many different contexts within the gene-by-environment interaction model, including contexts measured from within children's home and school environments. However, this work has been overwhelmingly focused on WEIRD samples children, leaving us with non-inclusive scientific evidence. This can lead to detrimental outcomes when we overgeneralize this non-inclusive scientific evidence to racialized groups. We conclude with a call to include racialized children in more research samples.

A Meta-Analytical Review of the Genetic and Environmental Correlations between Reading and Attention-Deficit Hyperactivity Disorder Symptoms and Reading and Math.

According to the Multiple Deficit Model, comorbidity results when the genetic and environmental risk factors that increase the liability for a disorder are domain-general. In order to explore the role of domain-general etiological risk factors in the co-occurrence of learning-related difficulties, the current meta-analysis compiled 38 studies of third through ninth-grade children to estimate the average genetic, shared environmental, and nonshared environmental correlations between reading and attention-deficit/hyperactivity disorder (ADHD) symptoms, and reading and math, as well as their potential moderators. Results revealed average genetic, shared and nonshared environmental correlations between reading and ADHD symptoms of .42, .64, and .20, and reading and math of .71, .90, and .56, suggesting that reading and math may have more domain-general risk factors than reading and ADHD symptoms. A number of significant sources of heterogeneity were also found and discussed. These results have important implications for both intervention and classification of learning disabilities.

Cross-Study Differences in the Etiology of Reading Comprehension: a Meta-Analytical Review of Twin Studies.

Numerous twin studies have examined the genetic and environmental etiology of reading comprehension, though it is likely that etiological estimates are influenced by unidentified sample conditions (e.g. Tucker-Drob and Bates, Psychol Sci:0956797615612727, 2015). The purpose of this meta-analysis was to average the etiological influences of reading comprehension and to explore the potential moderators influencing these estimates. Results revealed an average heritability estimate of h2 = 0.59, with significant variation in estimates across studies, suggesting potential moderation. Moderation results indicated publication year, grade level, project, zygosity methods, and response type moderated heritability estimates. The average shared environmental estimate was c2 = 0.16, with publication year, grade and zygosity methods acting as significant moderators. These findings support the role of genetics on reading comprehension, and a small significant role of shared environmental influences. The results suggest that our interpretation of how genes and environments influence reading comprehension should reflect aspects of study and sample.

Genetic and environmental influences on early literacy skills across school grade contexts.

Recent research suggests that the etiology of reading achievement can differ across environmental contexts. In the US, schools are commonly assigned grades (e.g. 'A', 'B') often interpreted to indicate school quality. This study explored differences in the etiology of early literacy skills for students based on these school grades. Participants included twins drawn from the Florida Twin Project on Reading (n = 1313 pairs) aged 4 to 10 years during the 2006-07 school year. Early literacy skills were assessed with DIBELS subtests: Oral Reading Fluency (ORF), Nonsense Word Fluency (NWF), Initial Sound Fluency (ISF), Letter Naming Fluency (LNF), and Phoneme Segmentation Fluency (PSF). School grade data were retrieved from the Florida Department of Education. Multi-group analyses were conducted separately for subsamples defined by 'A' or 'non-A' schools, controlling for school-level socioeconomic status. Results indicated significant etiological differences on pre-reading skills (ISF, LNF, and PSF), but not word-level reading skills (ORF and NWF). There was a consistent trend of greater environmental influences on pre-reading skills in non-A schools, arguably representing 'poorer' environmental contexts than the A schools. Importantly, this is the case outside of resources linked with school-level SES, indicating that something about the direct environment on pre-reading skills in the non-A school context is more variable than for A schools.

The association of parent-reported executive functioning, reading, and math is explained by nature, not nurture.

According to the hybrid model (van Bergen, van der Leij, & de Jong, 2014), the significant association among executive functioning (EF), reading, and math may be partially explained by parent-reported EF's role as a common risk and/or protective factor in reading and math (dis)abilities. The current study used a sample of 434 twin pairs (Mage = 12.12) from Florida to conduct genetically sensitive modeling on children's parent-reported EF, reading, and math skills to determine the common and unique etiological influences among the three domains. EF was measured through parent report and reading and math were measured with standardized test scores drawn from Florida's Progress Monitoring and Reporting Network as well as standardized parent-administered assessments collected by mail. Our trivariate Cholesky modeling showed that no matter which parent-reported EF component was modeled, the overlap of parent-reported EF with reading and math was explained by common genetic influences. Supplemental analysis suggested that this might in part be due to general parent report of problem behaviors. Additionally, significant environmental influences, with higher shared environmental overlap than previous work, were also found for reading and math. Findings indicate that poor parent-reported EF is a common cognitive risk factor for reading and math disabilities, which is driven by a shared genetic basis among all three domains. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

N-acetyl cysteine mitigates the acute effects of cocaine-induced toxicity in astroglia-like cells.

Cocaine has a short half-life of only about an hour but its effects, predominantly on the central nervous system (CNS), are fairly long-lasting. Of all cells within the CNS, astrocytes may be the first to display cocaine toxicity owing to their relative abundance in the brain. Cocaine entry could trigger several early response changes that adversely affect their survival, and inhibiting these changes could conversely increase their rate of survival. In order to identify these changes and the minimal concentrations of cocaine that can elicit them in vitro, rat C6 astroglia-like cells were treated with cocaine (2-4 mM for 1h) and assayed for alterations in gross cell morphology, cytoplasmic vacuolation, viability, reactive oxygen species (ROS) generation, glutathione (GSH) levels, cell membrane integrity, F-actin cytoskeleton, and histone methylation. We report here that all of the above identified features are significantly altered by cocaine, and may collectively represent the key pathology underlying acute toxicity-mediated death of astroglia-like cells. Pretreatment of the cells with the clinically available antioxidant N-acetyl cysteine (NAC, 5 mM for 30 min) inhibited these changes during subsequent application of cocaine and mitigated cocaine-induced toxicity. Despite repeated cocaine exposure, NAC pretreated cells remained highly viable and post NAC treatment also increased viability of cocaine treated cells to a smaller yet significant level. We show further that this alleviation by NAC is mediated through an increase in GSH levels in the cells. These findings, coupled with the fact that astrocytes maintain neuronal integrity, suggest that compounds which target and mitigate these early toxic changes in astrocytes could have a potentially broad therapeutic role in cocaine-induced CNS damage.