Shared Environmental Influences Research Articles

The genetic and environmental etiologies of individual differences in early reading growth in Australia, the United States, and Scandinavia

This first cross-country twin study of individual differences in reading growth from post-kindergarten to post-second grade analyzed data from 487 twin pairs from the United States, 267 twin pairs from Australia, and 280 twin pairs from Scandinavia. Data from two reading measures were fit to biometric latent growth models. Individual differences for the reading measures at post-kindergarten in the United States and Australia were due primarily to genetic influences and to both genetic and shared environmental influences in Scandinavia. In contrast, individual differences in growth generally had large genetic influences in all countries. These results suggest that genetic influences are largely responsible for individual differences in early reading development. In addition, the timing of the start of formal literacy instruction may affect the etiology of individual differences in early reading development but have only limited influence on the etiology of individual differences in growth.

Genetic and Environmental Sources of Individual Religiousness: The Roles of Individual Personality Traits and Perceived Environmental Religiousness

In the current study, we examined the genetic and environmental sources of the links between individual religiousness and individual personality traits, perceived parental religiousness, and perceived peer religiousness. Data from 870 individuals (incl. 394 twin pairs) were analyzed. Variance in individual religiousness was significantly influenced by genetic effects, environmental influences shared by twins reared together, and individual-specific environmental influences. Individual religiousness showed significant associations with age, sex, specific personality traits (e.g., agreeableness, openness to values), and perceived religiousness of important social interaction partners, such as parents, best friends, and spouses. The links to personality traits were relatively small and primarily genetically mediated. The associations between individual religiousness and parental religiousness were substantial and mediated by shared environmental effects. These links significantly decreased across age accompanying a significant decrease of shared environmental influences on individual religiousness. The correlations between individual religiousness and perceived religiousness of spouses and best friends were relatively moderate but increased with age. These associations were mediated by genetic as well as nonshared environmental sources accompanying an increase of nonshared environmental influences on individual religiousness with age. The results suggest that inter-individual differences in religiousness are due to multiple sources.

Genetic and Shared Environmental Influences on Interferon-γ Production in Response to Mycobacterium tuberculosis Antigens in a Ugandan Population

Interferon-γ (IFN-γ) is a key cytokine in the immune response to Mycobacterium tuberculosis (Mtb). Many studies established IFN-γ responses are influenced by host genetics, however differed widely by the study design and heritability estimation method. We estimated heritability of IFN-γ responses to Mtb culture filtrate (CF), ESAT-6, and Antigen 85B (Ag85B) in 1,104 Ugandans from a household contact study. Our method separately evaluates shared environmental and genetic variance, therefore heritability estimates were not upwardly biased, ranging from 11.6% for Ag85B to 22.9% for CF. Subset analyses of individuals with latent Mtb infection or without human immunodeficiency virus infection yielded higher heritability estimates, suggesting 10-30% of variation in IFN-γ is caused by a shared environment. Immunosuppression does not negate the role of genetics on IFN-γ response. These estimates are remarkably close to those reported for components of the innate immune response. These findings have implications for the interpretation of IFN-γ response assays and vaccine studies.

The Genetic and Environmental Influence on Adolescent Depressive Symptoms: A Genetic Sensitive Study

Epidemiological and developmental studies showed that one of the obvious phenomena during adolescence is a marked increase in depressive symptoms.Behavioral genetic studies found that shared environmental influences account for the majority of the variance for children's symptoms while genetic factors are substantial for adolescent depressive symptoms.However,whether the results of behavioral genetic studies from Western countries can be generalized to adolescents in China with a collectivism culture remains unexplored.First,prevalence of depression varies dramatically across cultures with a lower rate in China than in other countries.Second,factors that are associated with depressive symptoms and the extent to which these factors are consequential for adolescents' mood are also different across cultures.Existing evidences showed that the quality of family relationships and grades in school had significantly stronger associations with depressive symptoms among Chinese youths than among U.S.youths.Third,genes that contribute to depressive symptoms have different frequencies in different races.Moreover,culture may moderate the expression of genes.Therefore,the first objective of the study was to examine the heritability of adolescent depressive symptoms for boys and girls in China,respectively.Results from the family study,the adoption study and the twin study suggest that adolescent depressive symptoms are heritable(range 15-80%).Moreover,empirical work showed that the relative contributions of genetic and environmental influences to depressive symptoms vary as a function of age.The second objective of the study was to extend previous ones by examining whether the heritability of depressive symptoms in early-adolescence was different from that in mid-adolescence.We hypothesized that the heritability of depressive symptoms in early adolescence was higher than that in middle adolescence according to the theory and empirical work.Depressive symptoms tend to persist over time and the stability is evident in general population samples.The third objective of the study was to examine the contributions of genetic and environmental factors to the stability of adolescent depressive symptoms in early and middle adolescence,respectively.We hypothesized that genetic factors accounted for the stability of depressive symptoms in early adolescence whereas shared environmental influence contributed to the stability of depressive symptoms in middle adolescence.Data for the current study were from the Beijing Twin Study(BeTwiSt).Given obtaining written informed consents from twins and their parents,arrangements were made for the twins to stay in their classrooms after school time.Research staffs were there to answer any questions that students might ask about the questionnaires.After the twins completed the questionnaires,they were asked to provide their saliva samples using the Oragene? DNA self-collection kit(Genotek Inc.).Zygosity was determined by DNA analyses(89.5%) and questionnaire(10.5%).In DNA analyses,nine short tandem repeat(STR) loci which are highly heterogeneous in Chinese population were used.Same-sex twins with at least one different genetic marker were classified as dizygotic twins,otherwise classified as monozygotic twins.508 MZ,176 DZ twins participated in the longitudinal study with the interval of 1.37 years(SD=0.44),and the percentage of male was 46.2%.CDI(Children's Depression Inventory) was used to measure adolescent depressive symptoms and Mx software was used to conduct the unique genetic analyses and bivariate genetic analyses.No gender difference was found in the present study.Genetic factors accounted for more variance of adolescent depressive symptoms in early adolescence than in middle adolescence,and the magnitude of nonshared environmental influence increased with time.Genetic factors contributed to the stability of depressive symptoms in early adolescence whereas environmental influence contributed to the stability of depressive symptoms in middle adolescence.

Supplemental Material for Shared and Unique Genetic and Environmental Influences on Aging-Related Changes in Multiple Cognitive Abilities

Supplemental Material for Shared and Unique Genetic and Environmental Influences on Aging-Related Changes in Multiple Cognitive Abilities

Reading Development in Young Children: Genetic and Environmental Influences

The development of reading skills in typical students is commonly described as a rapid growth across early grades of active reading education, with a slowing down of growth as active instruction tapers. This study examined the extent to which genetics and environments influence these growth rates. Participants were 371 twin pairs, aged approximately 6 through 12, from the Western Reserve Reading Project. Development of word-level reading, reading comprehension, and rapid naming was examined using genetically sensitive latent quadratic growth curve modeling. Results confirmed the developmental trajectory described in the phenotypic literature. Furthermore, the same shared environmental influences were related to early reading skills and subsequent growth, but genetic influences on these factors were unique.

Overlap and specificity of genetic and environmental influences on excessive acquisition and difficulties discarding possessions: Implications for hoarding disorder

A reluctance to discard items, leading to severely cluttered living spaces, is the landmark feature of hoarding disorder (HD). Many, but not all, individuals with HD also excessively acquire, buy or even steal items that they do not need and for which no space is available. In DSM-5, "excessive acquisition" can be coded as a specifier of HD. Despite their consistent co-occurrence, the question of whether excessive acquisition and difficulties discarding possessions share a common etiology remains unanswered. The current study sought to flesh out this relationship by examining the extent of shared genetic and environmental influences on the association between excessive acquisition and difficulties discarding in a community sample of adult, female twins. A total of 5,022 female twins (2,529 pairs; mean age = 55.5 years) completed a self-report measure of hoarding symptoms, including items assessing excessive acquisition and difficulties discarding. The data were analyzed using bivariate twin modeling methods in the statistical program Mx. As expected, we found a strong phenotypic correlation (0.63) between excessive acquisition and difficulty discarding items. Both traits were moderately heritable. The genetic correlation between the traits was estimated to be 0.77 (95% CI: 0.69-0.85), indicating a substantial but imperfect genetic overlap. The non-shared environmental correlation (0.50 [95% CI: 0.42-0.57]), though lower, was also significant. The findings demonstrate a substantial genetic, and more modest environmental, etiological overlap between the excessive acquisition of possessions and difficulties discarding them, providing a possible explanation for their frequent co-occurrence in HD. However, given that the etiological overlap is not perfect, unique etiological influences, particularly environmental, on each phenotype seem plausible.

Genetic and Environmental Influences on Longitudinal Changes in Leisure-Time Physical Activity From Adolescence to Young Adulthood

The aim of this study was to estimate genetic and environmental influences on the longitudinal evolution of leisure-time physical activity habits from adolescence to young adulthood. Data were gathered at four time points, at mean ages 16.2, 17.1, 18.6, and 24.5 years. At baseline, the sample comprised 5,216 monozygotic and dizygotic twins, born 1975-1979, and, at the last follow-up point, of 4,531 monozygotic and dizygotic twins. Physical activity volume was assessed as frequency of leisure-time physical activity and participants were categorized into three groups: inactive, moderately active, and active. Genetic and environmental influences were estimated using a multivariate, longitudinal Cholesky decomposition with a 'multifactorial liability threshold' approach. The results suggest that, in both sexes the heritability of leisure-time physical activity remained moderate (~43-52%) during adolescence, declining to ~30% in young adulthood. Shared environmental influences increased from adolescence (~18-26%) to young adulthood (43% in men and 49% in women). Specific environmental influences remained relatively stable during the total follow-up (~20-30%). New genetic, shared, and specific environmental influences at every follow-up point were suggested by the low correlations across occasions. In conclusion, the study demonstrated gender differences in genetic influences in the evolution of leisure-time physical activity habits from adolescence to young adulthood. However, shared environmental influences, especially in women, were crucial in explaining longitudinal changes in leisure-time physical activity. These outcomes emphasize the need of gender-specific measures to promote physical activity habits during young adulthood.

A Behavioral Genetic Investigation of Weekend Drinking Among an Adult Sample

This study examined common and unique genetic and environmental influences on weekend drinking and weekday drinking reported by US male and female adult participants (mean age = 43.9). Data from 96 monozygotic and 82 dizygotic twin pairs were used to estimate bivariate biometric models of daily levels of weekend and weekday drinking volume. Weekend and weekday drinking volume scores were calculated from end-of-day reports of drinking across eight days. As expected, more drinking occurred during weekends. Biometric models provided evidence of significant additive genetic and nonshared environmental influences on both weekend and weekday drinking. Shared environmental influences were nonsignificant. Genetic influences accounted for a greater proportion of drinking variance during weekdays than weekends (0.36 compared to 0.17). However, these apparent differences in heritability—proportion of total variance accounted for by genetic variance—were due to increased nonshared environmental influences on weekend days, rather than greater genetic influences. The study's limitations are noted. Funded by National Institutes of Health/National Institute of Aging and John D. and Catherine T. MacArthur Foundation.

Genetic and environmental influences on negative life events from late childhood to adolescence.

This multiwave longitudinal study tested two quantitative genetic developmental models to examine genetic and environmental influences on exposure to negative dependent and independent life events. Participants (N=457 twin pairs) completed measures of life events annually from ages 9 to 16. The same genetic factors influenced exposure to dependent events across time and increased in magnitude during the transition to adolescence. Independent events were less genetically influenced than dependent events in boys, but not girls. Shared environmental influences decreased in magnitude as youth transitioned into adolescence. Nonshared environmental influences were mostly age specific and contributed significantly to both types of events at all ages. Results provide theoretical implications for developmental risk pathways to stress exposure and stress-related psychopathology.

Genetic Innovation and Stability in Externalizing Problem Behavior Across Development: A Multi-Informant Twin Study

The use of cross-informant ratings in previous longitudinal studies on externalizing behavior may have obscured the presence of continuity of genetic risk. The current study included latent factors representing the latent estimates of externalizing behavior based on both parent and self-report which eliminated rater-specific effects from these latent estimates. Symptoms of externalizing behavior of 1,480 Swedish twin pairs were obtained at ages 8-9, 13-14, 16-17 and 19-20 both by parent and self-report. Mx modeling was used to estimate additive genetic, shared and specific environmental influences. Genetic continuity was found over the entire developmental period as well as additional sources of genetic influence emerging around early and late adolescence. New unique environmental effects (E) on externalizing behavior arose early in adolescence. The results support both the presence of genetic continuity and change in externalizing behavior during adolescence due to newly emerging genetic and environmental risk factors.

Gene–environment correlation in the development of adolescent substance abuse: Selection effects of child personality and mediation via contextual risk factors

We used a longitudinal twin design to examine selection effects of personality traits at age 11 on high-risk environmental contexts at age 14 and the extent to which these contexts mediated risk for substance abuse at age 17. Socialization at age 11 (willingness to follow rules and endorse conventional values) predicted exposure to contextual risk at age 14. Contextual risk partially mediated the effect of socialization on substance abuse, though socialization also had a direct effect. In contrast, boldness at age 11 (social engagement and assurance, thrill seeking, and stress resilience) also predicted substance abuse directly but was unrelated to contextual risk. There was substantial overlap in the genetic and shared environmental influences on socialization and contextual risk, and genetic risk in socialization contributed to substance abuse indirectly via increased exposure to contextual risk. This suggests that active gene-environment correlations related to individual differences in socialization contributed to an early, high-risk developmental trajectory for adolescent substance abuse. In contrast, boldness appeared to index an independent and direct genetic risk factor for adolescent substance abuse.

A study of changes in genetic and environmental influences on weight and shape concern across adolescence.

The goal of the current study was to examine whether genetic and environmental influences on an important risk factor for disordered eating, weight and shape concern, remained stable over adolescence. This stability was assessed in 2 ways: whether new sources of latent variance were introduced over development and whether the magnitude of variance contributing to the risk factor changed. We examined an 8-item WSC subscale derived from the Eating Disorder Examination (EDE) using telephone interviews with female adolescents. From 3 waves of data collected from female-female same-sex twin pairs from the Australian Twin Registry, a subset of the data (which included 351 pairs at Wave 1) was used to examine 3 age cohorts: 12 to 13, 13 to 15, and 14 to 16 years. The best-fitting model contained genetic and environmental influences, both shared and nonshared. Biometric model fitting indicated that nonshared environmental influences were largely specific to each age cohort, and results suggested that latent shared environmental and genetic influences that were influential at 12 to 13 years continued to contribute to subsequent age cohorts, with independent sources of both emerging at ages 13 to 15. The magnitude of all 3 latent influences could be constrained to be the same across adolescence. Ages 13 to 15 were indicated as a time of risk for the development of high levels of WSC, given that most specific environmental risk factors were significant at this time (e.g., peer teasing about weight, adverse life events), and indications of the emergence of new sources of latent genetic and environmental variance over this period.

A multivariate twin study of early literacy in Japanese kana

This first Japanese twin study of early literacy development investigated the extent to which genetic and environmental factors influence individual differences in prereading skills in 238 pairs of twins at 42months of age. Twin pairs were individually tested on measures of phonological awareness, kana letter name/sound knowledge, receptive vocabulary, visual perception, nonword repetition, and digit span. Results obtained from univariate behavioral-genetic analyses yielded little evidence for genetic influences, but substantial shared-environmental influences, for all measures. Phenotypic confirmatory factor analysis suggested three correlated factors: phonological awareness, letter name/sound knowledge, and general prereading skills. Multivariate behavioral genetic analyses confirmed relatively small genetic and substantial shared environmental influences on the factors. The correlations among the three factors were mostly attributable to shared environment. Thus, shared environmental influences play an important role in the early reading development of Japanese children.

Genetic and environmental influences on eating behaviors in 2.5- and 9-year-old children: a longitudinal twin study.

BackgroundEating behaviors during childhood are related both to children’s diet quality and to their weight status. A better understanding of the determinants of eating behavior during childhood is essential for carrying out effective dietary interventions.MethodsWe assessed the contribution of genetic and environmental factors to variations in selected eating behaviors in early and late childhood. Information on eating behaviors came from questionnaires administered to parents of children participating in the Quebec Newborn Twin Study when the twins were 2.5 and 9 years old (n = 692 children). Dichotomous variables were derived and analyzed using structural equation modeling, as part of a classic twin study design. We performed univariate and bivariate longitudinal analyses to quantify sources of variation and covariation across ages, for several eating behavior traits.ResultsWe found moderate to strong heritability for traits related to appetite such as eating too much, not eating enough and eating too fast. Univariate analysis estimates varied from 0.71 (95% CI: 0.49, 0.87) to 0.89 (0.75, 0.96) in younger children and from 0.44 (0.18, 0.66) to 0.56 (0.28, 0.78) in older children. Bivariate longitudinal analyses indicated modest to moderate genetic correlations across ages (rA varying from 0.34 to 0.58). Common genetic influences explained 17% to 43% of the phenotypic correlation between 2.5 and 9 years for these appetite-related behaviors. In 9-year-old children, food acceptance traits, such as refusing to eat and being fussy about food, had high heritability estimates, 0.84 (0.63, 0.94) and 0.85 (0.59, 0.96) respectively, while in younger children, the shared environment (i.e., common to both twins) contributed most to phenotypic variance. Variances in meal-pattern-related behaviors were mostly explained by shared environmental influences.ConclusionsGenetic predispositions explain a large part of the variations in traits related to appetite during childhood, though our results suggest that as children get older, appetite-related behaviors become more sensitive to environmental influences outside the home. Still, for several traits environmental influences shared by twins appear to have the largest relative importance. This finding supports the notion that familial context has considerable potential to influence the development of healthy eating habits throughout childhood.

Twin Study of Impulsive Buying and its Overlap with Personality

This study explores the origins of individual differences in impulsive buying from a behavioral genetics perspective. It also assesses whether phenotypic associations between personality and impulsive buying tendency can be attributed to overlapping genetic factors. Data were collected via mail for 339 twin pairs. Personality traits according to a five-factor model and impulsive buying were measured. The results indicate that additive genetic, shared environmental, and nonshared environmental influences may be important for individual differences in impulsive buying. Phenotypic correlations with Impulsivity (r = .32), Neuroticism (r = .23), and Extraversion (r = .20) are largely driven by the overlapping genetic influences. Together with age and sex personality traits explain 25% of individual differences in impulsive buying tendency. These results add to our understanding of individual differences in impulsive buying and the nature of its relationship with personality.

Observed Personality in Childhood: Psychometric and Behavioral Genetic Evidence of Two Broad Personality Factors.

We examined broad dimensions of children's personalities (total n = 1056; age = 3.5 to 12 years) based on observers' perceptions following a few hours of structured interaction. Siblings' behaviors during a two-hour cognitive assessment in the home were rated separately by two different observers. Exploratory and confirmatory factor analyses clearly revealed a two-factor solution in three different samples. There was correspondence between parent-rated temperament and the observer-rated factors. Cross-sectional analyses indicated lower Plasticity among older children and higher Stability among older children. Sex differences were negligible. Plasticity and Stability were correlated in the .2 to .3 range. Most of the sibling similarity in the Plasticity was due to additive genetic influences, whereas most sibling similarity in Stability was attributable to shared environmental influences. The findings implicate a biometric factor structure to childhood personality that fits well with emerging bio-social theories of personality development.

Modeling the Etiology of Individual Differences in Early Reading Development: Evidence for Strong Genetic Influences

We explored the etiology of individual differences in reading development from post-kindergarten to post–4th grade by analyzing data from 487 twin pairs tested in Colorado. Data from three reading measures and one spelling measure were fit to biometric latent growth curve models, allowing us to extend previous behavioral genetic studies of the etiology of early reading development at specific time points. We found primarily genetic influences on individual differences at post–1st grade for all measures. Genetic influences on variance in growth rates were also found, with evidence of small, nonsignificant, shared environmental influences for two measures. We discuss our results, including their implications for educational policy.

Attentional threat avoidance and familial risk are independently associated with childhood anxiety disorders

Twin studies in children reveal that familial aggregation of anxiety disorders is due to both genetic and environmental factors. Cognitive biases for threat information are considered a robust characteristic of childhood anxiety. However, little is known regarding the underlying aetiology of such biases and their role in anxiety disorders. A face version of the dot-probe task measuring attentional biases for negative (anger, fear, sad, disgust) and positive (happy) facial expressions was completed by 600, 8-year-old twins; the largest study of its kind. Twin correlations for attentional bias scores were compared to estimate genetic and environmental effects. Parent-report diagnostic interviews identified children with an anxiety disorder. Indices of inferred genetic and familial risk for anxiety disorders were created for each child. Data were analysed using a series of logistic regressions. Anxious children showed greater attentional avoidance of negative faces than nonanxious children; t (548) = 2.55, p < .05. Attentional avoidance was not under genetic or shared environmental influence. Risk for anxiety disorders was predicted by familial factors. Both attentional avoidance and inferred familial risk were significant but independent predictors of anxiety disorders (ORs = .65 and 3.64, respectively). Anxiety-related attentional biases and familial risk play important but independent roles in childhood anxiety disorders. If replicated, these findings indicate that links between genetic risk and anxiety disorders lie outside the domain of attentional processes.

The Colorado Adoption Project.

This paper describes the Colorado Adoption Project (CAP), an ongoing genetically informative longitudinal study of behavioral development. We describe the features of the adoption design used in CAP, and discuss how this type of design uses data from both parent-offspring and related- versus unrelated-sibling comparisons to estimate the importance of genetic and shared environmental influences for resemblance among family members. The paper provides an overview of CAP's history, how subjects were ascertained, recruited, and retained, and the domains of assessment that have been explored since the CAP's initiation in 1975. Findings from some representative papers that make use of data from CAP participants illustrate the study's multifaceted nature as a parent-offspring and sibling behavioral genetic study, a study that parallels a complimentary twin study, a longitudinal study of development, a source of subjects for molecular genetic investigation, and a study of the outcomes of the adoption process itself. As subjects assessed first at age 1 approach age 40, we hope the CAP will establish itself as the first prospective adoption study of lifespan development.