Shared Environmental Influences Research Articles

Higher Anxiety Is Associated with Lower Cardiovascular Autonomic Function in Female Twins.

Anxiety symptoms co-occur with cardiovascular health problems, with increasing evidence suggesting the role of autonomic dysfunction. Yet, there is limited behavior genetic research on underlying mechanisms. In this twin study, we investigated the phenotypic, genetic and environmental associations between a latent anxiety factor and three cardiovascular autonomic function factors: interbeat interval (IBI, time between heart beats), heart rate variability (HRV, overall fluctuation of heart-beat intervals) and baroreflex sensitivity (BRS, efficiency in regulating blood pressure [BP]). Multivariate twin models were fit using data of female twins (N = 250) of the Twin Interdisciplinary Neuroticism Study (TWINS). A significant negative association was identified between latent anxiety and BRS factors (r = -.24, 95% CI [-.40, -.07]). Findings suggest that this relationship was mostly explained by correlated shared environmental influences, and there was no evidence for pleiotropic genetic or unique environmental effects. We also identified negative relationships between anxiety symptoms and HRV (r = -.17, 95% CI [-.34, .00]) and IBI factors (r = -.13, 95% CI [-.29, .04]), though these associations did not reach statistical significance. Findings implicate that higher anxiety scores are associated with decreased efficiency in short-term BP regulation, providing support for autonomic dysfunction with anxiety symptomatology. The baroreflex system may be a key mechanism underlying the anxiety-cardiovascular health relationship.

The role of genetic and environmental factors in covariation between anxiety and anger in childhood.

Higher levels of anger expression, as well as lower levels of anger control, have been reported for adults with anxiety disorders compared to individuals without anxiety disorders. Different to the research on adults, very few studies examined the relationship between anxiety and anger in childhood. In our study, we investigated 398 Italian twin pairs (74 MZ male, 70 MZ female, 134 same-sex dizygotic-53 male, 81 female-, and 120 unlike-sex dizygotic twin pairs), aged 8-17 (mean 13.06 ± 2.59): (i) the heritability of a childhood anger phenotype; (ii) the association between five anxiety domains and anger; (iii) the role of possible common etiological factors in explaining the observed comorbidity and overlap in the risk between anxiety phenotypes and anger. The study demonstrated that anger, assessed by CBCL items, is heritable in children at a similar rate to prior studies (40%). Our research found low to moderate rate of correlation between anger and anxiety (from 0.10 to 0.19). Finally, the present study found that the majority of etiological influences on anxiety and anger are independent of each other. Data showed that shared environmental influences have some small effects on the phenotypic covariation between the anxiety phenotypes and anger (12%); whereas unique environmental influences have an almost negligible effect (1%). Our analyses did not reveal the effect of genetic effects in explaining the covariation between these phenotypes.

Genetic and environmental influences on structure of the social brain in childhood

Prosocial behavior and empathy are important aspects of developing social relations in childhood. Prior studies showed protracted structural development of social brain regions associated with prosocial behavior. However, it remains unknown how structure of the social brain is influenced by genetic or environmental factors, and whether overlapping heritability factors explain covariance in structure of the social brain and behavior. The current study examined this hypothesis in a twin sample (aged 7–9-year; N = 512). Bilateral measures of surface area and cortical thickness of the medial prefrontal cortex (mPFC), temporo-parietal junction (TPJ), posterior superior temporal sulcus (pSTS), and precuneus were analyzed. Results showed genetic contributions to surface area and cortical thickness for all brain regions. We found additional shared environmental influences for TPJ, suggesting that this region might be relatively more sensitive to social experiences. Genetic factors also influenced parent-reported prosocial behavior (A = 45%) and empathy (A = 59%). We provided initial evidence that the precuneus shares genetically determined variance with empathy, suggesting a possible small genetic overlap (9%) in brain structure and empathy. These findings show that structure of the social brain and empathy are driven by a combination of genetic and environmental factors, with some factors overlapping for brain structure and behavior.

Neighborhood Deprivation Moderates Shared and Unique Environmental Influences on Hazardous Drinking: Findings from a Cross-Sectional Co-Twin Study

Background: There has been increased interest in the interplay of genetic and environmental factors in the development of problematic alcohol use, including socioeconomic conditions of the neighborhood. Using a co-twin design, we examined the extent to which contributions of genetic, shared environmental, and unique environmental influences on hazardous drinking differed according to levels of neighborhood socioeconomic deprivation. Method: Data came from 1,521 monozygotic (MZ) and 609 dizygotic (DZ) twin pairs surveyed in Washington State. A measure of neighborhood deprivation was created based on census-tract-level variables and the Alcohol Use Disorders Identification Test 3-item instrument was used to assess level of hazardous drinking. We tested a series of nested structural equation models to examine associations among hazardous drinking, neighborhood deprivation, and the variance components (genetic [A], shared [C] and unique environmental [E] influences) of these two constructs, testing for both main effects and moderation by neighborhood deprivation. Results: Neighborhood deprivation was significantly associated with increased hazardous drinking, after accounting for A and C variance common to both phenotypes. Adjusting for within-pair differences in income and education, neighborhood deprivation moderated the magnitude of variance components of hazardous drinking, with the variance attributable to shared environment and non-shared environment increasing in more deprived neighborhoods. Conclusions: Findings point to amplification of early childhood as well as unique adulthood environmental risk on hazardous drinking in areas of greater deprivation.

Adolescent Sexual Development and Peer Groups: Reciprocal Associations and Shared Genetic and Environmental Influences.

Peer groups influence the emergence of sexual behaviors in adolescence, but many details regarding the mechanisms underlying these effects have yet to be described. We examined the phenotypic, genetic, and environmental links between both antisocial and prosocial peer characteristics, and several sexual behaviors from middle childhood to late adolescence (ages 11, 14, and 17years) using a longitudinal twin sample (N = 3762). Antisocial peers predicted greater engagement in both normative (e.g., dating) and non-normative (e.g., early sexual intercourse) sexual behaviors, while prosocial peers were associated with a lower likelihood of engaging in non-normative sexual behaviors. Reciprocal effects were also observed such that early sexual experiences were associated with a more antisocial and less prosocial peer groups later in adolescence. Behavioral genetic models indicated that most of the overlap between peer group characteristics and sexual behavior was due to shared environmental influences. That is, some features of the adolescent environment exert a press toward (or against) antisocial peers and sexual behaviors. Together, the results extend the existing literature by highlighting the ways through which peer affiliations are related to sexual development in adolescence.

On the etiology of internalizing and externalizing problem behavior: A twin-family study.

Internalizing and externalizing behavior problems are established risk factors for many unpleasant outcomes and psychopathology in adulthood, and understanding the interplay between genes and environment is important for deducing implications for therapeutic interventions. Among genetic studies on internalizing and externalizing problem behavior, the heritability estimates differ widely. Most research only uses twin data and other-reports, and therefore certain limitations are inevitable. Our study is the first to investigate genetic and environmental influences on problem behavior using a Nuclear Twin Family Design and self-reports, in order to address these limitations. Internalizing and externalizing problem behavior of 3,087 twin pairs (age 11–23), a sibling, and their parents were analyzed with structural equation modeling to estimate heritability separately for each of three twin birth cohorts. Genetic influences account for about one-third of the variance for both internalizing and externalizing. Shared environmental influences were only found for internalizing, and through the advantages of considering data from the whole twin family, firstly could be identified as solely twin-specific. Our findings could contribute to a better understanding of the gap between heritability based on twin studies and DNA-based heritability (‘missing heritability problem’): Results indicate that heritability estimates gained via classic twin design and other-reports are slightly overestimated and therefore environmental influences, in general, are more important than previous research suggests. Simultaneously, we showed that family-specific environment either contributes to behavior problems only on an individual level, or that it has a lesser influence than originally thought.

Shared liability to pain, common mental disorders, and long-term work disability differs among women and men

Knowledge of factors involved in the associations between pain, common mental disorders, and future work incapacity is still scarce. The aim of this study was to examine the overlap between genetic and environmental factors contributing to depression/anxiety, pain, and future long-term sickness absence (SA) and disability pension (DP) among women and men. The study sample included 47,995 twins born in Sweden 1935 to 1985. Information on self-reported depression/anxiety and back, neck, and shoulder pain was obtained from surveys conducted 1998 to 2002 and 2004 to 2005. Data on long-term SA (>365 days) and DP due to mental and/or musculoskeletal disorders until 2013 were obtained from the National Social Insurance Agency. Shared genetic and environmental influences on depression/anxiety, pain, and SA/DP were estimated by applying structural equation modeling. The prevalence of depression/anxiety was 27% and 14% among women and men, for pain 24% and 19%, and for SA/DP due to mental and musculoskeletal diagnoses 7% and 4%, respectively. Multivariate biometric analyses revealed different patterns of covariation between the 3 phenotypes among women and men. For women, a latent-shared liability to all 3 phenotypes could be identified, mainly attributable to genetic factors (66%). For men, no shared underlying liability was observed. The variation in SA/DP was explained by genetic factors in common with depression/anxiety by 27% and in common with pain by 9%. Common mental disorders, pain, and SA/DP tend to covariate in different ways among women and men. The results may have clinical implications as strategies preventing SA/DP may be different among women and men.

Genetic and Environmental Influence on the Human Functional Connectome.

Detailed mapping of genetic and environmental influences on the functional connectome is a crucial step toward developing intermediate phenotypes between genes and clinical diagnoses or cognitive abilities. We analyzed resting-state functional magnetic resonance imaging data from two adult twin samples (Nos = 446 and 371) to quantify genetic and environmental influence on all pairwise functional connections between 264 brain regions (~35 000 functional connections). Nonshared environmental influence was high across the whole connectome. Approximately 14-22% of connections had nominally significant genetic influence in each sample, 4.6% were significant in both samples, and 1-2% had heritability estimates greater than 30%. Evidence of shared environmental influence was weak. Genetic influences on connections were distinct from genetic influences on a global summary measure of the connectome, network-based estimates of connectivity, and movement during the resting-state scan, as revealed by a novel connectome-wide bivariate genetic modeling procedure. The brain's genetic organization is diverse and not as one would expect based solely on structure evident in nongenetically informative data or lower resolution data. As follow-up, we make novel classifications of functional connections and examine highly localized connections with particularly strong genetic influence. This high-resolution genetic taxonomy of brain connectivity will be useful in understanding genetic influences on brain disorders.

Marital Strain, Support, and Alcohol Use: Results from a Twin Design Statistically Controlling for Genetic Confounding

Background: Marriage is one of the most frequently examined sources of social support and has been shown to protect against alcohol use and abuse. This study examines the relationship between perceived marital strain and support, and alcohol use controlling for additive genetic influence. Methods: Data from monozygotic (MZ) (n = 320) and dizygotic (DZ) (n = 464) twin pairs from the second wave of the National Survey of Midlife Development in the United States (MIDUS II) were used to test whether past year marital strain and support were associated with recent alcohol use. Generalized linear mixed models (GLMM) were estimated, allowing us to control for additive genetic and shared environmental influences as variance components. Results: Marital strain and support had positive, statistically significant associations with alcohol use. However, only the relationship between marital strain and alcohol use remained after controlling for variance in alcohol use attributed to genetics. Conclusions: After accounting for genetics, midlife adults still appear to cope with marital strain via alcohol use. However, this coping is unlikely to result in heavy episodic drinking or alcohol use disorder without other compounding factors.

A longitudinal genetically informed analysis of parental negativity and children's negative emotionality in middle childhood.

Children's negative emotionality (NE) is frequently associated with parental negativity, but causal understanding of this relationship is limited. In addition, little is known about how genetic and environmental factors affect this relationship during middle childhood. We addressed these gaps by applying a quantitative genetic analysis to cross-lagged associations between mothers' and fathers' parental negativity and children's NE during middle childhood. The sample comprised of 456 families when the children were 6.5 years old, and 401 families when the children were 8/9 years old. Mothers' and fathers' negativity and children's NE were assessed using questionnaires. Results showed that variation in parental negativity was mainly accounted for by the environment shared by children, with some indication of an evocative effect of the children's genes on mothers, but not fathers. Children's NE was accounted for by both genetic and shared environmental influences. Parental negativity and children's NE had moderate continuity over the course of two years. Mothers' (but not fathers') negativity when the children were 6.5 years old predicted change in children's NE (rated by the same or the other parent) toward age 8/9 years, but not the other way around. Shared environmental influences were the main contributor to the association between earlier mothers' negativity and later children's NE. Thus, although children's NE was partially heritable, and parenting too was partially accounted for by children's genes, the association between parental negativity and children's NE, at this age, reflects environmental effects and is compatible with mothers' influence on children. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Child Antisocial Behavior Is more Environmental in Origin in Disadvantaged Neighborhoods: Evidence Across Residents' Perceptions and Geographic Scales in Two Samples.

Prior research has suggested that disadvantaged neighborhood contexts alter the etiology of youth antisocial behavior (ASB). Unfortunately, these studies have relied exclusively on governmental data collected in administratively-defined neighborhoods (e.g., Census tracts or block groups, zip codes), a less than optimal approach for studying neighborhood effects. It would thus be important to extend prior findings of GxE using neighborhood sampling techniques, in which disadvantage is assessed via resident informant-reports of the neighborhood. The current study sought to do just this, examining two independent twin samples from the Michigan State University Twin Registry. Neighborhood disadvantage was assessed via maternal and neighbor informant-reports, the latter of which were analyzed multiple ways (i.e., all neighbors within 1km, nearest neighbor, and all neighbors within the County). Analyses revealed clear and consistent evidence of moderation by neighborhood disadvantage, regardless of informant or the specific operationalization of neighborhood. Shared environmental influences on ASB were observed to be several-fold larger in disadvantaged contexts, while genetic influences were proportionally more influential in advantaged neighborhoods. Such findings indicate that neighborhood disadvantage exerts rather profound effects on the origins of youth ASB. Efforts should now be made to identify the active ingredients of neighborhood disadvantage.

Early classroom reading gains moderate shared environmental influences on reading comprehension in adolescence.

Reading is important for children's success in school and beyond, yet many adolescents fail to reach expected levels of proficiency. This highlights the need to better understand the factors that influence reading effectiveness over time, including genes and environment. Greater expression of genetic influence on first- and second-grade reading fluency has been observed in higher quality classroom reading environments. To what degree this early environment continues to influence genetic and other environmental influences on later reading is unknown and was tested in this study. The quality of the early classroom reading environment was approximated by gains in oral reading fluency (ORF) across the school year among first- or second-grade classmates of 546 MZ and 1,016 DZ twin children (mean age=7.13years; SD=0.45) who had reading comprehension scores from a state-wide mandatory test in school year 2013-2014 when most twin pairs were in seventh to tenth grade (mean age=14.41; SD=1.13) in a variable called Class ORF Gain. Biometrical models were fit to the data to assess whether Class ORF Gain moderated the genetic, shared environmental and/or nonshared environmental variance associated with adolescent reading comprehension. Class ORF Gain moderated shared environmental influences on reading comprehension 6-9years later. When early classroom reading gains were poor, variability in reading comprehension in adolescence was high and was associated largely with shared environmental influences. When early classroom reading gains were good, overall and shared environmentally influenced variability in adolescent reading comprehension was lower so that genetic influences were most relevant in explaining that variability. Our findings suggested that classroom reading environment experienced when children were learning to read had a lasting influence on the factors underlying variability in later reading effectiveness.

Elucidating factors underlying parent-offspring similarity in eating pathology in pre- and early puberty: Exploring the possibility of passive gene-environment correlation.

Familial resemblance in eating pathology is typically attributed to parents providing an environment that leads to the development of eating pathology. However, offspring raised by biological parents receive both their environment and genes from their parents, raising the possibility that genetic influences, environmental influences, and/or gene-environment interplay may account for familial resemblance. Past studies have not explored the possibility of parents' genes influencing the environment they provide (i.e., passive gene-environment correlations or "passive rGE"). If present, passive rGE is most likely to "hide" in estimates of shared environmental influence in classical twin models. The current study used a nuclear twin family design to explore the possibility of passive rGE during pre- and early puberty when past studies have demonstrated the importance of shared environmental influence. Additionally, the present study explored whether sibling-specific (i.e., influences specific to the twin generation) or family-specific (i.e., "cultural" influences within the home) environmental influences account for shared environmental influences found in past studies. Participants included preearly pubertal same-sex female twins and their biological parents (N = 547 families) from the Minnesota Twin Family Study and the Michigan State University Twin Registry. Disordered eating was assessed with self-report measures in the twins and parents. Pubertal status was determined using an established cut-off on a self-report measure. Passive rGE was not indicated in this study of pre- and early pubertal twins. Instead, sibling-specific shared environmental and nonshared environmental influences were most influential. Future research should work to identify the sibling-specific environmental influences that contribute to sibling similarity in disordered eating. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Genetic and Environmental Influences on Cognitive Abilities in Extreme Poverty.

To improve global human capital, an understanding of the interplay of endowment across the full range of socioeconomic status (SES) is needed. Relevant data, however, are absent in the nations with the most abject poverty (Tucker-Drob & Bates, 2016), where the lowest heritability and strong effects of SES are predicted. Here we report the first study of biopsychosocial gene-environment interaction in extreme poverty. In a sub-Saharan sample of early teenage twins (N = 3192), we observed substantial (~30-40%) genetic influence on cognitive abilities. Surprisingly, shared environmental influences were similar to those found in adolescents growing in Western affluent countries (25-28%). G × SES moderation was estimated at a` = .06 (p = .355). Family chaos did not moderate genetic effects but did moderate shared environment influence. Heritability of cognitive abilities in extreme poverty appears comparable to Western data. Reduced family chaos may be a modifiable factor promoting cognitive development.

Different Characteristics and Heritabilities of Alcohol Use Disorder Classes: A Population-Based Swedish Study.

The aims of the present study are to identify alcohol use disorder (AUD) classes among a population-based Swedish sample, determine if these classes differ by variables known to be associated with AUD and determine whether some AUD classes have stronger genetic influences than others. A latent class analysis (LCA), based on types of registrations, was conducted on Swedish individuals with an AUD registration born between 1960 and 1990 (N=184,770). These classes were then validated using demographics; patterns of comorbidity with drug abuse, psychiatric disorders and criminal behavior; and neighborhood-level factors, i.e. peer AUD and neighborhood deprivation. The degree of genetic and environmental influence was also investigated. The best-fit LCA had four classes: (a) outpatient/prescription, characterized by a mix of outpatient medical and prescription registrations, (b) low-frequency inpatient, characterized entirely by inpatient medical registrations, with the majority of individuals having one AUD registration, (c) high-frequency mixed, characterized by a mix of all four registration types, with the majority having four or more registrations and (d) crime, characterized almost entirely by criminal registrations. The highest heritability for both males and females was found for Class 3 (61% and 65%, respectively) and the lowest for Class 1 (20% for both), with shared environmental influences accounting for 10% or less of the variance in all Classes. Using comprehensive, nationwide registry data, we showed evidence for four distinct, meaningful classes of AUD with varying degrees of heritability.

Genetic and Environmental Influences on Different Forms of Bullying Perpetration, Bullying Victimization, and Their Co-occurrence

Bullying comes in different forms, yet most previous genetically-sensitive studies have not distinguished between them. Given the serious consequences and the high prevalence of bullying, it is remarkable that the aetiology of bullying and its different forms has been under-researched. We present the first study to investigate the genetic architecture of bullying perpetration, bullying victimization, and their co-occurrence for verbal, physical and relational bullying. Primary-school teachers rated 8215 twin children on bullying perpetration and bullying victimization. For each form of bullying, we investigated, through genetic structural equation modelling, the genetic and environmental influences on being a bully, a victim or both. 34% of the children were involved as bully, victim, or both. The correlation between being a bully and being a victim varied from 0.59 (relational) to 0.85 (physical). Heritability was ~ 70% for perpetration and ~ 65% for victimization, similar in girls and boys, yet both were somewhat lower for the relational form. Shared environmental influences were modest and more pronounced among girls. The correlation between being a bully and being a victim was explained mostly by genetic factors for verbal (~ 71%) and especially physical (~ 77%) and mostly by environmental factors for relational perpetration and victimization (~ 60%). Genes play a large role in explaining which children are at high risk of being a victim, bully, or both. For victimization this suggests an evocative gene-environment correlation: some children are at risk of being exposed to bullying, partly due to genetically influenced traits. So, genetic influences make some children more vulnerable to become a bully, victim or both.

Common genetic architecture and environmental risk factors underpin the anxiety-disordered eating relationship: Findings from an adolescent twin cohort.

Despite established comorbidity between anxiety and disordered eating (DE), and a plethora of research using various methodologies to examine this overlap, use of twin modeling to expose whether a shared genetic liability underpins these conditions remains rare. Data from a longitudinal sample of female twins were selected: measures of risk for DE from Wave 1 (N = 699, 351 pairs, aged 12-15 years), and the Eating Disorder Examination (EDE) and Children's Anxiety Sensitivity Index (CASI) from Wave 2 (N = 669, 338 pairs, aged 16-19 years). At this time, they also completed Children's Anxiety Sensitivity Index (CASI). Bivariate Cholesky decomposition models adjusting for age and body mass index centile investigated the covariance structure between the CASI and EDE. Modeling both genetic and nonshared environmental influences parsimoniously fit these data. All paths were significant. Additive genetic influences were notable for CASI and EDE phenotypes; 14% of the heritable variance was contributed by CASI to the expression of EDE. There was also a smaller but significant contribution of nonshared environmental influences. A multinomial logistic regression indicated body dissatisfaction (RRR = 1.53; 95% CI = 1.07-2.18) differentiated groups with highest EDE scores from the highest CASI scores. Shared genetic and environmental influences appear to underpin the relationship, and potentially the observed comorbidity, between anxiety sensitivity and DE. The age of onset is typically earlier for anxiety than DE, suggesting a significant opportunity for early intervention work to reduce the likelihood of subsequent development of DE.

OLIG2 gene polymorphisms are associated with nasty, unpleasant and uncontrollable thoughts in obsessive-compulsive disorder

Obsessive-compulsive disorder (OCD) is one of 10 major debilitating neuropsychiatric disorders, according to the World Health Organization (WHO), affecting around 2.3% of people worldwide. Obsessive-compulsive symptoms are caused by shared or distinct genetic or environmental influences. Several imaging studies have detected white-matter alterations in OCD, and recent studies have demonstrated thatOCD is associated with variations in the OLIG2 gene. The aim of this study was to investigate whether OLIG2 gene is associated with OCD and its clinical features in a Brazilian sample. We genotyped three variants in OLIG2 gene, rs762178, rs1059004, and rs9653711 in 205 OCD patients and 202 healthy controls by Taqman® methodology. Genotypes and alleles distributions were analyzed by χ2 or Fisher exact tests. The rs762178 and rs9653711 polymorphisms were significantly associated with OCD (P = 0.048 and 0.029, respectively). We also observed an association of rs1059004 and rs9653711 with the presence of Obsessive-Compulsive Inventory-Revised (OCI-R) obsessing (unacceptable thoughts) subscore (P = 0.031 and 0.034, respectively). Moreover, the pair of loci consisting of rs762178 and rs9653711 A-G haplotype was associated with OCD (P < 0.0001). The OLIG2 gene may be involved in OCD, particularly in patients showing nasty, unpleasant and uncontrollable thoughts. However, more studies in larger samples are needed to replicate these findings.

Using discordant twin methods to investigate an environmentally mediated pathway between social support and the reduced likelihood of adolescent psychotic experiences.

Social support has been shown to be associated with a reduced likelihood of developing psychotic experiences in the general population and even amongst those at high risk due to exposure to multiple forms of victimisation (poly-victimised). However, it is unclear whether this association is merely due to the confounding effects of shared environmental and genetic influences, or reverse causality. Therefore, we investigated whether social support has a unique environmentally mediated effect on adolescent psychotic experiences after accounting for familial factors, including genetic factors, and also prior psychopathology. Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 UK-born twins. Adolescents were interviewed at age 18 about psychotic experiences and victimisation exposure since age 12, and their perceptions of social support. Prior childhood mental health problems and psychotic symptoms were assessed at age 12. The discordant twin method was used to disentangle the relative family-wide and unique-environmental effects of social support on psychotic experiences in the general population and among poly-victimised adolescents. Perceived social support, particularly from friends, was found to have a unique environmentally mediated buffering effect on adolescent psychotic experiences in the whole sample and in the high-risk poly-victimised group. The protective effects of social support on adolescent psychotic experiences cannot be accounted for by shared environmental or genetic factors, nor by earlier psychopathology. Our findings suggest that early intervention programmes focused on increasing perceptions of social support have the potential to prevent the emergence of psychotic experiences amongst adolescents.

Differential Influences of Genes and Environment Across the Distribution of Reading Ability.

We partitioned early childhood reading into genetic and environmental sources of variance and examined the full distribution of ability levels from low through normal to high as computed by quantile regression. The full sample comprised twin pairs measured at preschool (n = 977), kindergarten (n = 1028), grade 1 (n = 999), and grade 2 (n = 1000). Quantile regression analyses of the full distribution of literacy ability showed genetic influence in all grades from preschool to grade 2. At preschool, the low end of the distribution had higher genetic influence than the high end of the distribution and the shared environment influence was the opposite. These shared environment influences of preschool became insignificant with formal schooling. This suggests that higher scores in pre-literacy skills (preschool) are more influenced by shared environment factors, though these are short-lived. This study discusses the factors that may be influencing the results.