Shared Environmental Influences Research Articles

Added Value Measures in Education Show Genetic as Well as Environmental Influence

Does achievement independent of ability or previous attainment provide a purer measure of the added value of school? In a study of 4000 pairs of 12-year-old twins in the UK, we measured achievement with year-long teacher assessments as well as tests. Raw achievement shows moderate heritability (about 50%) and modest shared environmental influences (25%). Unexpectedly, we show that for indices of the added value of school, genetic influences remain moderate (around 50%), and the shared (school) environment is less important (about 12%). The pervasiveness of genetic influence in how and how much children learn is compatible with an active view of learning in which children create their own educational experiences in part on the basis of their genetic propensities.

Genetic and Environmental Contributions to the Overlap Between Psychological, Fatigue and Somatic Symptoms: A Twin Study in Sri Lanka

Somatic symptoms often co-occur with psychological symptoms but this overlap is poorly understood. Some aspects of this overlap differ in the South Asian context, but it is not clear whether this is a reporting effect or an underlying difference in experienced illness. Home interviews were administered to 4,024 twins randomly selected from a population-based twin register in the Colombo district of Sri Lanka (the CoTASS study). These included assessments of psychological, somatic and fatigue symptoms. The data were analyzed using factor analytic and quantitative genetic approaches. Confirmatory factor analysis showed that the symptoms from the three scales represented three separate dimensions, rather than all tapping into a single dimension. However, familial correlations among the data were most consistent with a common pathway model. This implies that a portion of the underlying vulnerability is common across psychological, fatigue and somatic symptoms. There were sex differences in the etiology of this model, with shared environmental and genetic influences playing different roles in men and women. There is a complex etiological relationship between psychological, fatigue and somatic symptoms. This is similar in Sri Lanka to Western countries, but there may be a greater influence from the family environment, suggesting that care needs to be taken when generalizing research findings between countries. People who complain of certain fatigue or somatic symptoms may well also have psychological symptoms, or may have genetic or environmental vulnerabilities to such problems.

Child and adolescent conduct disorder substantially shares genetic influences with three socioemotional dispositions.

In a representative sample of twin children and adolescents, we tested the hypothesis that a substantial proportion of the genetic and environmental influences underlying conduct disorder (CD) are shared with three socioemotional dispositions: Prosociality, Negative Emotionality, and Daring. Caretaker ratings of each dispositional dimension were uniquely associated with a latent CD dimension that included both caretaker- and youth-reports of CD as indicators. Behavior genetic analyses indicated that moderate-to-high additive genetic and moderate nonshared environmental influences underlie all three dispositions and CD, with modest shared environmental influences on Prosociality. Forty percent of the additive genetic influences and all of the nonshared environmental influences on the latent CD dimension were shared in common with the three socioemotional dispositions. The finding that CD shares a substantial proportion of its genetic influences with three distinct socioemotional dispositions suggests new perspectives on the heterogeneous etiology of CD and new approaches to exploring its specific etiological mechanisms.

DeFries–Fulker Analysis of Longitudinal Reading Performance Data from Twin Pairs Ascertained for Reading Difficulties and from Their Nontwin Siblings

Reading difficulties are both heritable and stable; however, little is known about the etiology of this stability. Results from a preliminary analysis of data from 56 twin pairs who participated in the Colorado Longitudinal Twin Study of Reading Disability (Astrom et al., Twin Res Hum Genet 10:434-439, 2007) suggested that about two-thirds of the proband deficit at follow-up was due to genetic factors that also influenced deficits at their initial assessment. Although our proband sample is now nearly twice as large, it is still relatively small; thus, to increase power, we subjected data from probands, co-twins and their nontwin siblings to a novel extension of DeFries-Fulker analysis (DeFries and Fulker, Behav Genet 15:467-473, 1985; DeFries and Fulker, Acta Genet Med Gemellol, 37, 205-216, 1988). In addition to providing estimates of univariate and bivariate heritability, this analysis facilitates a test of the difference between shared environmental influences for twins versus siblings. Longitudinal composite reading performance scores at 10.6 and 15.5years of age, on average, were analyzed from 33 MZ and 64 DZ twin pairs in which at least one member of each pair had reading difficulties, and from 44 siblings of the probands. Scores were highly stable (.86±.03, across probands, co-twins and siblings) and heritability of the group deficit at initial assessment was .67±.22. Longitudinal bivariate heritability was .59±.21, suggesting that nearly 60% of the proband reading deficit at follow-up is due to genetic factors that influenced reading difficulties at the initial assessment. However, tests for special twin environmental influences were nonsignificant.

Heritability of Response Inhibition in Children

We report the heritability of response inhibition, latency, and variability, which are potential markers of genetic risk in neuropsychiatric conditions. Genetic and environmental influences on cancellation and restraint, response latency, and variability measured in a novel variant of the stop signal task were studied in 139 eight-year-old twin pairs from a birth cohort. Cancellation (50%), restraint (27%), and response latency (41%) showed significant heritability, the balance being non-shared environmental influences and/or error. Response variability was not heritable, with 23% of the variance attributable to shared environmental influences and 77% to non-shared environmental risk or error. The phenotypic correlation between response cancellation and restraint was -.44 and between response latency and restraint was .21. These phenotypic correlations were entirely genetic in origin. The phenotypic correlation between response variability and % successful inhibition was .27, but was not genetic. Cancellation and restraint were heritable and shared genetic influences, indicating that they may be influenced by a common gene or genes. Response latency was moderately heritable and shared genetic influences with restraint, but was not correlated with cancellation. Response variability was not heritable. These results support the potential of response inhibition and latency as endophenotypes in genetic research.

A Systematic Evaluation and Validation of Subtypes of Adolescent Alcohol Use Motives: Genetic and Environmental Contributions

Alcohol use motives are closely associated with specific profiles of alcohol use and reflect a subjectively derived decisional framework based on a motivational style of responding. Adult twin studies typically estimate the heritability of alcohol use motives to be between 7 and 42%, although relatively little is known about genetic and environmental influences upon alcohol use motives in adolescence. Latent class analysis (LCA) models containing 1 through 5 classes were fitted to the data derived from 1,422 adolescent twin and siblings self-reported alcohol use motives. Using twin models, we estimated the genetic, shared, and nonshared environmental influences to the class membership data derived from the LCA. Four drinking motives classes were identified (family-oriented, social, enhancement/social, and coping/social). The coping/social and enhancement/social classes were differentiated from the social class on measures of depression, delinquency, and aggressive behavior. Analyses indicated that nonadditive genetic factors accounted for 76% of the variance in the coping/social motives class and additive genetic influences accounted for 66% of the variance in the social motives class. There was a moderate contribution of genetic factors and shared environmental factors influencing class membership of enhancement/social motivated drinkers (28 and 20% explained variance, respectively). Substantial shared environmental influences were revealed for membership of the family-oriented class (75%). Heritable influences may predispose individuals to drink to cope with negative affect, for social reasons, and to a lesser extent for enhancement. Familial environmental influences shape family-oriented motives for drinking in adolescents.

Exercise Participation in Adolescents and Their Parents: Evidence for Genetic and Generation Specific Environmental Effects

Individual differences in adolescent exercise behavior are to a large extent explained by shared environmental factors. The aim of this study was to explore to what extent this shared environment represents effects of cultural transmission of parents to their offspring, generation specific environmental effects or assortative mating. Survey data on leisure-time exercise behavior were available from 3,525 adolescent twins and their siblings (13-18years) and 3,138 parents from 1,736 families registered at the Netherlands Twin Registry. Data were also available from 5,471 adult twins, their siblings and spouses similar in age to the parents. Exercise participation (No/Yes, using a cut-off criterion of 4 metabolic equivalents and 60min weekly) was based on questions on type, frequency and duration of exercise. A model to analyze dichotomous data from twins, siblings and parents including differences in variance decomposition across sex and generation was developed. Data from adult twins and their spouses were used to investigate the causes of assortative mating (correlation between spouses=0.41, due to phenotypic assortment). The heritability of exercise in the adult generation was estimated at 42%. The shared environment for exercise behavior in adolescents mainly represents generation specific shared environmental influences that seem somewhat more important in explaining familial clustering in girls than in boys (52 versus 41%). A small effect of vertical cultural transmission was found for boys only (3%). The remaining familial clustering for exercise behavior was explained by additive genetic factors (42% in boys and 36% in girls). Future studies on adolescent exercise behavior should focus on identification of the generation specific environmental factors.

Common genetic and environmental contributions to post-traumatic stress disorder and alcohol dependence in young women

The few genetically informative studies to examine post-traumatic stress disorder (PTSD) and alcohol dependence (AD), all of which are based on a male veteran sample, suggest that the co-morbidity between PTSD and AD may be attributable in part to overlapping genetic influences, but this issue has yet to be addressed in females.MethodData were derived from an all-female twin sample (n=3768) ranging in age from 18 to 29 years. A trivariate genetic model that included trauma exposure as a separate phenotype was fitted to estimate genetic and environmental contributions to PTSD and the degree to which they overlap with those that contribute to AD, after accounting for potential confounding effects of heritable influences on trauma exposure. Additive genetic influences (A) accounted for 72% of the variance in PTSD; individual-specific environmental (E) factors accounted for the remainder. An AE model also provided the best fit for AD, for which heritability was estimated to be 71%. The genetic correlation between PTSD and AD was 0.54. The heritability estimate for PTSD in our sample is higher than estimates reported in earlier studies based almost exclusively on an all-male sample in which combat exposure was the precipitating traumatic event. However, our findings are consistent with the absence of evidence for shared environmental influences on PTSD and, most importantly, the substantial overlap in genetic influences on PTSD and AD reported in these investigations. Additional research addressing potential distinctions by gender in the relative contributions of genetic and environmental influences on PTSD is merited.

Does Education Confer a Culture of Healthy Behavior? Smoking and Drinking Patterns in Danish Twins

More education is associated with healthier smoking and drinking behaviors. Most analyses of effects of education focus on mean levels. Few studies have compared variance in health-related behaviors at different levels of education or analyzed how education impacts underlying genetic and environmental sources of health-related behaviors. This study explored these influences. In a 2002 postal questionnaire, 21,522 members of the Danish Twin Registry, born during 1931-1982, reported smoking and drinking habits. The authors used quantitative genetic models to examine how these behaviors' genetic and environmental variances differed with level of education, adjusting for birth-year effects. As expected, more education was associated with less smoking, and average drinking levels were highest among the most educated. At 2 standard deviations above the mean educational level, variance in smoking and drinking was about one-third that among those at 2 standard deviations below, because fewer highly educated people reported high levels of smoking or drinking. Because shared environmental variance was particularly restricted, one explanation is that education created a culture that discouraged smoking and heavy drinking. Correlations between shared environmental influences on education and the health behaviors were substantial among the well-educated for smoking in both sexes and drinking in males, reinforcing this notion.

Confirming the etiology of adolescent acting-out behaviors: an examination of observer-ratings in a sample of adoptive and biological siblings.

A recent meta-analysis revealed moderate shared environmental influences (C) on most forms of child and adolescent psychopathology (Burt, 2009), including antisocial behavior. Critically, however, the research analyzed in this meta-analysis relied largely on specific informant-reports (and particularly parent and child reports), each of which is subject to various sources of rater bias. Observer-ratings of children's behaviors avoid many of these biases, and are thus well suited to verify the presence of C. Given this, we sought to buttress the evidence supporting C in two key ways. First, we sought to confirm that C contributes to observer-ratings in a sample of adoptive siblings, as similarity between adoptive siblings constitutes a 'direct' estimate of C. Second, we sought to confirm that these shared environmental influences persist across informants (i.e., the effects are not specific to the rater or the context in question). The current study examined the etiology of observer-ratings of acting-out behaviors, as well as sources of etiological overlap across observer-ratings, adolescent self-report and maternal-report in sample of over 600 biological and adoptive sibling pairs from the Sibling Interaction and Behavior Study (SIBS). Results revealed moderate and significant shared environmental influences on observer-ratings (31%), as well as on the other informant-reports (20-23%). Moreover, a portion of these effects overlapped across measures (C correlations ranged from .32 to .34). Such findings argue against passive gene-environment correlations (rGE) and rater bias as primary explanations for earlier findings of C on antisocial behavior, and in this way, offer a critical extension of prior work indicating that the role of shared environmental influences on child and adolescent antisocial behavior was dismissed too soon.

Depressive Symptoms and Alcohol Use are Genetically and Environmentally Correlated Across Adolescence

Depressive symptoms and alcohol use are frequently positively associated during adolescence. This study aimed to assess the heritability of each phenotype across adolescence; to assess potential shared liabilities; to examine changes in the nature of shared liabilities across adolescence; and to investigate potential causal relationships between depressive symptoms and alcohol use. We studied a longitudinally assessed sample of adolescent Finnish twins (N=1,282) to test hypotheses about genetic and environmental influences on these phenotypes within and across ages, using data from assessments at ages 12, 14, and 17.5years. The heritability of depressive symptoms is consistent across adolescence (~40-50%), with contributions from common and unique environmental factors. The heritability of alcohol use varies across time (a(2)=.25-.44), and age 14 alcohol use is heavily influenced by shared environmental factors. Genetic attenuation and innovation were observed across waves. Modest to moderate genetic (r(A)=.26-.59) and environmental (r(C)=.30-.63) correlations between phenotypes exist at all ages, but decrease over time. Tests for causal relationships between traits differed across ages and sexes. Intrapair MZ difference tests provided evidence for reciprocal causation in girls at ages 14 and 17.5. Formal causal models suggested significant causal relationships between the variables in both boys and girls. The association between depressive symptoms and alcohol use during adolescence is likely due to a combination of shared genetic and environmental influences and causal influences. These influences are also temporally dynamic, complicating efforts to understand factors contributing to the relationship between these outcomes.

Changes in genetic and environmental influences on the development of nicotine dependence and major depressive disorder from middle adolescence to early adulthood

This longitudinal study used a representative community sample of same-sex twins (485 monozygotic pairs, 271 dizygotic pairs) to study longitudinal changes in genetic and environmental influences on nicotine dependence (NicD) symptoms and major depressive disorder (MDD) symptoms and the longitudinal relationships between NicD and MDD symptoms at three relatively discrete ages spanning middle adolescence to early adulthood (ages 15, 18, and 21). Clinical interviews were used to assess NicD and MDD symptoms lifetime at age 15 and during the previous 3 years at the two subsequent assessments. Biometric models revealed similar patterns of findings for NicD and MDD. Heritability increased with age, particularly between ages 15 and 18. Shared environmental influences were small, and the proportion of variance attributed to shared environmental influences decreased with age. Nonshared environmental influences were moderate to large in magnitude and were entirely age specific. Both NicD and MDD symptoms showed considerable stability from age 15 to 21, and at each age those with one disorder showed elevated rates of the other. However, a cross-lagged model revealed no longitudinal predictive relationships between MDD symptoms and NicD symptoms after accounting for stability of symptoms within disorders. In summary, the transition between middle and late adolescence is a critical period for developmental shifts in the magnitudes of genetic and environmental influences on both MDD and NicD symptoms. Despite similarities in the development of genetic and environmental influences for the two phenotypes, the association between NicD and MDD reflects concurrent covariation rather than one phenotype being an antecedent influence on the subsequent development of the other.

Predicting individual differences in reading comprehension: a twin study

We examined the Simple View of reading from a behavioral genetic perspective. Two aspects of word decoding (phonological decoding and word recognition), two aspects of oral language skill (listening comprehension and vocabulary), and reading comprehension were assessed in a twin sample at age 9. Using latent factor models, we found that overlap among phonological decoding, word recognition, listening comprehension, vocabulary, and reading comprehension was primarily due to genetic influences. Shared environmental influences accounted for associations among word recognition, listening comprehension, vocabulary, and reading comprehension. Independent of phonological decoding and word recognition, there was a separate genetic link between listening comprehension, vocabulary, and reading comprehension and a specific shared environmental link between vocabulary and reading comprehension. There were no residual genetic or environmental influences on reading comprehension. The findings provide evidence for a genetic basis to the "Simple View" of reading.

Effects of Heritability, Shared Environment, and Nonshared Intrauterine Conditions on Child and Adolescent BMI

Heritability studies of BMI, based upon twin samples, have identified genetic and shared environmental components of BMI, but have been largely silent about the nonshared environmental factors. Intrauterine factors have been identified as having significant long-term effects on BMI and may be a critical source of nonshared environmental influence. Extant studies based on samples of either unrelated individuals or twins cannot separate the effects of genetics, shared environments, and nonshared intrauterine conditions because the one lacks variation in the degree of relatedness and the other has insufficient variation in intrauterine conditions. This study improves upon these prior studies by using a large, sibling-based sample to examine heritability, shared environmental, and nonshared intrauterine influences on BMI during two age periods in childhood (6-8 years; 12-14 years). The primary interest was in determining the effects of the intrauterine environment on BMI as a component of the nonshared environment and in determining whether there were sex-specific differences in heritability and/or in the intrauterine factors. These were estimated using regression-based techniques introduced by DeFries and Fulker. Heritability of BMI was estimated to be 0.20-0.28 at 6-8 years and 0.46-0.61 at 12-14 years. Differences in heritability were found at 12-14 years between same-sex as compared to mixed-sex pairs. The shared environmental effect was significant at 6-8 years but insignificant at 12-14 years. Differences in birth weight were significant in all groups at 6-8 years suggesting long-term effects of the nonshared intrauterine environment; at 12-14 years, birth weight was no longer significant for girls.

The Etiology of Stability and Change in Religious Values and Religious Attendance

Studies have demonstrated little to no heritability for adolescent religiosity but moderate genetic, shared environmental, and nonshared environmental influences on adult religiosity. Only one longitudinal study of religiosity in female twins has been conducted (Koenig et al., Dev Psychol 44:532-543, 2008), and reported that persistence from mid to late adolescence is due to shared environmental factors, but persistence from late adolescence to early adulthood was due to genetic and shared environmental factors. We examined the etiology of stability and change in religious values and religious attendance in males and females during adolescence and early adulthood. The heritability of both religious values and religious attendance increased from adolescence to early adulthood, although the increase was greater for religious attendance. Both genetic and shared environmental influences contributed to the stability of religious values and religious attendance across adolescence and young adulthood. Change in religious values was due to both genetic and nonshared environmental influences specific to early adulthood, whereas change in religious attendance was due in similar proportions to genetic, shared environmental, and non-shared environmental influences.

Family Background Buys an Education in Minnesota but Not in Sweden

Educational attainment, the highest degree or level of schooling obtained, is associated with important life outcomes, at both the individual level and the group level. Because of this, and because education is expensive, the allocation of education across society is an important social issue. A dynamic quantitative environmental-genetic model can help document the effects of social allocation patterns. We used this model to compare the moderating effect of general intelligence on the environmental and genetic factors that influence educational attainment in Sweden and the U.S. state of Minnesota. Patterns of genetic influence on educational outcomes were similar in these two regions, but patterns of shared environmental influence differed markedly. In Sweden, shared environmental influence on educational attainment was particularly important for people of high intelligence, whereas in Minnesota, shared environmental influences on educational attainment were particularly important for people of low intelligence. This difference may be the result of differing access to education: state-supported access (on the basis of ability) to a uniform higher-education system in Sweden versus family-supported access to a more diverse higher-education system in the United States.

Commentary: Smoking during pregnancy--genes and environment weigh in

Commentary: Smoking during pregnancy--genes and environment weigh in

The Etiology of Diverse Receptive Language Skills at 12 Years

In the 2nd decade of life, language skills expand in both quantitative and qualitative ways. The etiology of these new skills and the relationships among them have been little explored. Taking advantage of widespread access to inexpensive and fast Internet connections in the United Kingdom, we administered four Web-based measures of receptive language development--Vocabulary, Listening Grammar, Figurative Language, and Making Inferences--to a sample of 12-year-old twin pairs (N=4,892) participating in the Twins Early Development Study (TEDS; Oliver & Plomin, 2007). The 4 measures showed moderate phenotypic intercorrelation. All 4 showed moderate genetic influence (a2 between .25 and .36) and low shared environmental influence (c2 between .13 and .19). The median genetic correlation among the 4 measures was .87, indicating strong genetic overlap among them. A latent factor score for Language, based on the common variance among the measures, showed substantial genetic influence (a2=.59) and moderate shared environmental influence (c2=.28). A small but significant sex difference favored females on the Listening Grammar and Making Inferences tests, but there was no evidence for sex differences in the etiology of any of the measures. Despite the emergence of new skills at this developmental period, from the etiological perspective, language skills remain relatively undifferentiated at an etiological level.

Genetic Influence on Literacy Constructs in Kindergarten and First Grade: Evidence from a Diverse Twin Sample

Historically, twin research on reading has been conducted on older children and the generalizability of results across racial/ethnic/socioeconomic groups is unclear. To address these gaps, early literacy skills were examined among 1,401 twin pairs in kindergarten and 1,285 twin pairs in first grade (ages 5-7). A multi-group analysis was conducted separately for subsamples defined by neighborhood income while controlling for race/ethnicity within each grade. Substantial additive genetic and shared environmental effects were found for early literacy skills measured in kindergarten. In first grade, variance in early reading was associated with large additive genetic effects for middle and high neighborhood income twins, but shared environmental influence was substantial for low neighborhood income twins. Results suggest that the etiological architecture of some early literacy skills may differ across economic contexts.

Genetic and Environmental Influences on Disordered Gambling in Men and Women

Women now represent nearly half of all individuals in treatment for pathological gambling (PG), but relatively little is known about the causes of PG among women or potential sex differences in the causes of PG. To (1) investigate the role of genetic and environmental risk factors in the development of disordered gambling (DG) among women and (2) determine the extent to which the genetic and environmental risk of DG among women differs quantitatively or qualitatively from the risk of DG among men. (Disordered gambling refers to the full continuum of gambling-related problems that includes PG disorder.) Twin study. The national community-based Australian Twin Registry. Four thousand seven hundred sixty-four individuals from 2889 twin pairs; twins were aged 32 to 43 years and 57% were women. Main Outcome Measure Disordered gambling was defined based on lifetime DSM-IV PG symptom counts. The estimate of the proportion of variation in liability for DG due to genetic influences was 49.2% (95% confidence interval, 26.7-60.9). There was no evidence for shared environmental influences contributing to variation in DG liability. There was no evidence for quantitative or qualitative sex differences in the causes of variation in DG liability. This study establishes for the first time that genes are as important in the etiology of DG in women as they are in men and that the susceptibility genes contributing to variation in liability for DG are likely to overlap considerably in men and women.