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Drinking alcohol is a normal behavior in many societies, and prior studies have demonstrated it has both genetic and environmental sources of variation. Using two very large samples of twins and their first-degree relatives (Australia ≈ 20,000 individuals from 8,019 families; Virginia ≈ 23,000 from 6,042 families), we examine whether there are differences: (1) in the genetic and environmental factors that influence four interrelated drinking behaviors (quantity, frequency, age of initiation, and number of drinks in the last week), (2) between the twin-only design and the extended twin design, and (3) the Australian and Virginia samples. We find that while drinking behaviors are interrelated, there are substantial differences in the genetic and environmental architectures across phenotypes. Specifically, drinking quantity, frequency, and number of drinks in the past week have large broad genetic variance components, and smaller but significant environmental variance components, while age of onset is driven exclusively by environmental factors. Further, the twin-only design and the extended twin design come to similar conclusions regarding broad-sense heritability and environmental transmission, but the extended twin models provide a more nuanced perspective. Finally, we find a high level of similarity between the Australian and Virginian samples, especially for the genetic factors. The observed differences, when present, tend to be at the environmental level. Implications for the extended twin model and future directions are discussed.

Introduction: Previous studies in adolescents were not adequately powered to accurately disentangle genetic and environmental influences on smoking initiation (SI) across adolescence., Methods: Mega-analysis of pooled genetically informative data on SI was performed, with structural equation modeling, to test equality of prevalence and correlations across cultural backgrounds, and to estimate the significance and effect size of genetic and environmental effects according to the classical twin study, in adolescent male and female twins from same-sex and opposite-sex twin pairs (N = 19 313 pairs) between ages 10 and 19, with 76 358 longitudinal assessments between 1983 and 2007, from 11 population-based twin samples from the United States, Europe, and Australia., Results: Although prevalences differed between samples, twin correlations did not, suggesting similar etiology of SI across developed countries. The estimate of additive genetic contributions to liability of SI increased from approximately 15% to 45% from ages 13 to 19. Correspondingly, shared environmental factors accounted for a substantial proportion of variance in liability to SI at age 13 (70%) and gradually less by age 19 (40%)., Conclusions: Both additive genetic and shared environmental factors significantly contribute to variance in SI throughout adolescence. The present study, the largest genetic epidemiological study on SI to date, found consistent results across 11 studies for the etiology of SI. Environmental factors, especially those shared by siblings in a family, primarily influence SI variance in early adolescence, while an increasing role of genetic factors is seen at later ages, which has important implications for prevention strategies., Implications: This is the first study to find evidence of genetic factors in liability to SI at ages as young as 12. It also shows the strongest evidence to date for decay of effects of the shared environment from early adolescence to young adulthood. We found remarkable consistency of twin correlations across studies reflecting similar etiology of liability to initiate smoking across different cultures and time periods. Thus familial factors strongly contribute to individual differences in who starts to smoke with a gradual increase in the impact of genetic factors and a corresponding decrease in that of the shared environment., (© The Author 2017. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

For over 100 years, the genetics of human anthropometric traits has attracted scientific interest. In particular, height and body mass index (BMI, calculated as kg/m2) have been under intensive genetic research. However, it is still largely unknown whether and how heritability estimates vary between human populations. Opportunities to address this question have increased recently because of the establishment of many new twin cohorts and the increasing accumulation of data in established twin cohorts. We started a new research project to analyze systematically (1) the variation of heritability estimates of height, BMI and their trajectories over the life course between birth cohorts, ethnicities and countries, and (2) to study the effects of birth-related factors, education and smoking on these anthropometric traits and whether these effects vary between twin cohorts. We identified 67 twin projects, including both monozygotic (MZ) and dizygotic (DZ) twins, using various sources. We asked for individual level data on height and weight including repeated measurements, birth related traits, background variables, education and smoking. By the end of 2014, 48 projects participated. Together, we have 893,458 height and weight measures (52% females) from 434,723 twin individuals, including 201,192 complete twin pairs (40% monozygotic, 40% same-sex dizygotic and 20% opposite-sex dizygotic) representing 22 countries. This project demonstrates that large-scale international twin studies are feasible and can promote the use of existing data for novel research purposes.

Objective: Despite an increasing recognition that psychiatric disorders can be diagnosed as early as preschool, little is known how early genetic and environmental risk factors contribute to the development of psychiatric disorders during this very early period of development., Method: We assessed infant temperament at age 1, and attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and separation anxiety disorder (SAD) at ages 3 through 5 years in a sample of Hispanic twins. Genetic, shared, and non-shared environmental effects were estimated for each temperamental construct and psychiatric disorder using the statistical program MX. Multivariate genetic models were fitted to determine whether the same or different sets of genes and environments account for the co-occurrence between early temperament and preschool psychiatric disorders., Results: Additive genetic factors accounted for 61% of the variance in ADHD, 21% in ODD, and 28% in SAD. Shared environmental factors accounted for 34% of the variance in ODD and 15% of SAD. The genetic influence on difficult temperament was significantly associated with preschool ADHD, SAD, and ODD. The association between ODD and SAD was due to both genetic and family environmental factors. The temperamental trait of resistance to control was entirely accounted for by the shared family environment., Conclusions: There are different genetic and family environmental pathways between infant temperament and psychiatric diagnoses in this sample of Puerto Rican preschool age children.

Although there is increasing evidence that genetic factors influence gestational age, it is unclear to what extent this is due to fetal and/or maternal genes. In this study, we apply a novel analytical model to estimate genetic and environmental contributions to pregnancy history records obtained from 165,952 Swedish families consisting of offspring of twins, full siblings, and half-siblings (1987-2008). Results indicated that fetal genetic factors explained 13.1% (95% confidence interval (CI): 6.8, 19.4) of the variation in gestational age at delivery, while maternal genetic factors accounted for 20.6% (95% CI: 18.1, 23.2). The largest contribution to differences in the timing of birth were environmental factors, of which 10.1% (95% CI: 7.0, 13.2) was due to factors shared by births of the same mother, and 56.2% (95% CI: 53.0, 59.4) was pregnancy specific. Similar models fit to the same data dichotomized at clinically meaningful thresholds (e.g., preterm birth) resulted in less stable parameter estimates, but the collective results supported a model of homogeneous genetic and environmental effects across the range of gestational age. Since environmental factors explained most differences in the timing of birth, genetic studies may benefit from understanding the specific effect of fetal and maternal genes in the context of these yet-unidentified factors.

The hippocampus expresses a large number of androgen receptors; therefore, in men it is potentially vulnerable to the gradual age-related decline of testosterone levels. In the present study we sought to elucidate the nature of the relationship between testosterone and hippocampal volume in a sample of middle-aged male twins (average age 55.8 years). We found no evidence for a correlation between testosterone level and hippocampal volume, as well as no indication of shared genetic influences. However, a significant moderating effect of testosterone on the genetic and environmental determinants of hippocampal volume was observed. Genetic influences on hippocampal volume increased substantially as a function of increasing testosterone level, while environmental influences either decreased or remained stable. These findings provide evidence for an apparent gene-by-hormone interaction on hippocampal volume. To the best of our knowledge, this is the first study to demonstrate that the heritability of a brain structure in adults may be modified by an endogenous biological factor., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Previous research has demonstrated stability of cognitive ability and marked heritability during adulthood, but questions remain about the extent to which genetic factors account for this stability. We conducted a 35-year longitudinal assessment of general cognitive ability using the Armed Forces Qualification Test administered to 7,232 male twins in early adulthood and readministered to a subset of 1,237 twins during late middle age. The proportion of variance in cognitive functioning explained by genetic factors was .49 in young adulthood and .57 in late middle age. The correlation between the two administrations was .74 with a genetic correlation of 1.0, indicating that the same genetic influences operated at both times. Genetic factors were primarily responsible for stability, and nonshared environmental factors were primarily responsible for change. The genetic factors influencing cognition may change across other eras, but the same genetic influences are operating from early adulthood to late middle age.

Following the publication of Purcell's approach to the modeling of gene by environment interaction in 2002, the interest in G x E modeling in twin and family data increased dramatically. The analytic techniques described by Purcell were designed for use with continuous data. Here we explore the re-parameterization of these models for use with ordinal and binary outcome data. Analysis of binary and ordinal data within the context of a liability threshold model traditionally requires constraining the total variance to unity to ensure identification. Here, we demonstrate an alternative approach for use with ordinal data, in which the values of the first two thresholds are fixed, thus allowing the total variance to change as function of the moderator. We also demonstrate that when using binary data, constraining the total variance to unity for a given value of the moderator is sufficient to ensure identification. Simulation results indicate that analyses of ordinal and binary data can recover both the raw and standardized patterns of results. However, the scale of the results is dependent on the specification of (threshold or variance) constraints rather than the underlying distribution of liability. Example Mx scripts are provided.

The extended twin kinship design allows the simultaneous testing of additive and nonadditive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission (Eaves et al., 1999). It also handles the contribution of these sources of variance to the (co)variation of multiple phenotypes. Keller et al. (2008) extended this comprehensive model for family resemblance to allow or a flexible specification of assortment and vertical transmission. As such, it provides a general framework which can easily be reduced to fit subsets of data such as twin-parent data, children-of-twins data, etc. A flexible Mx specification of this model that allows handling of these various designs is presented in detail and applied to data from the Virginia 30,000. Data on height, body mass index, smoking status, church attendance, and political affiliation were obtained from twins and their families. Results indicate that biases in the estimation of variance components depend both on the types of relative available for analysis, and on the underlying genetic and environmental architecture of the phenotype of interest.

Background: If the adaptive significance of specific fears changes with age, the genetic contribution to individual differences may be lowest at the age of greatest salience. The roles of genes and environment in the developmental-genetic trajectory of five common childhood fears are explored in 1094 like-sex pairs of male and female monozygotic and dizygotic twins assessed on up to three occasions during adolescence (ages 8-18 years)., Methods: Dichotomous self-ratings of a cluster of five correlated fears from Ollendick's schedule of fears (FSSC-R) were extracted for subjects at each occasion of assessment. The effects of genes and environment on overall level of fears and rates of adolescent decline were explored by fitting an item-response theory ('IRT') model that allowed for individual genetic and environmental differences in initial fear level ('intercept') and rates of adolescent change ('slope') across the repeated waves of measurement. Different forms of the model were explored using Markov Chain Monte Carlo (MCMC) methods to derive the posterior distribution of subject and item parameters from the raw responses., Results: Additive genetic differences affect the common factor underlying the five fear-items. The same genes also affect rates of change with age, especially in boys. Male adolescents with higher overall genetic predisposition to childhood fears tended to show slower recovery with age than subjects with relatively low initial values. Thus, the genetic variance apparently increases with age., Conclusions: This finding is consistent with a prediction that the regulation of genetic differences will be strongest, and thus the additive genetic variance will be smallest, at the age when the particular stimulus is most salient. Items differed in the extent to which they were sensitive to underlying random differences in the rate of developmental change. Individual differences in rates of change with age were more marked in boys than girls.

Context: While the nature of common fears changes over development, we do not know whether genetic effects on fear-proneness are developmentally stable or developmentally dynamic., Objective: To determine the temporal pattern of genetic and environmental effects on the level of intensity of common fears., Design: Prospective, 4-wave longitudinal twin study. Structural modeling was performed with Mx., Setting: General community., Participants: Two thousand four hundred ninety twins and their parents from the Swedish Twin Study of Child and Adolescent Development., Main Outcome Measure: The level of parent- and/or self-reported fears obtained at ages 8 to 9, 13 to 14, 16 to 17, and 19 to 20 years., Results: Thirteen questionnaire items formed 3 distinct fear factors: situational, animal, and blood/injury. For all 3 fears, the best-fit model revealed developmentally dynamic effects and, in particular, evidence for both genetic attenuation and innovation. That is, genetic factors influencing fear intensity at age 8 to 9 years decline substantially in importance over time. Furthermore, new sets of genetic risk factors impacting fear intensity "come on line" in early adolescence, late adolescence, and early adulthood. As the twins aged, the influence of the shared environment declined and unique environment increased. No sex effects were found for situational fears while for animal and blood/injury fears, genetic factors in males and females were correlated but not identical. Shared environmental factors were both more important and more stable for animal fears than for situational or blood/injury fears., Conclusions: Genetic effects on fear are developmentally dynamic from middle childhood to young adulthood. As children age, familial-environmental influences on fears decline in importance.

Genetic and environmental influences on cognitive components of reading span in 345 middle-aged male twin pairs were examined. Shared variance among word recognition (reading only), digits forward (short-term memory only), and reading span (concurrent reading plus memory) was almost entirely mediated by common genetic influences. Overall heritability was .52 for word recognition, .27 for digits forward, and .51 for reading span. All of the genetic influences on word recognition and digits forward, but only about one-half of the genetic influences on reading span, came from a common latent phenotype. The genetic influences that were specific to reading span were concluded to most likely reflect an executive function component. Implications for genetic studies of aging and prefrontal brain function are discussed., ((PsycINFO Database Record (c) 2007 APA, all rights reserved).)

Background: Although parental divorce is associated with increased substance use and internalizing problems, experiencing the separation of one's parents may not cause these outcomes. The relations may be due to genetic or environmental selection factors, characteristics that lead to both marital separation and offspring functioning., Method: We used the Children of Twins (CoT) Design to explore whether unmeasured genetic or environmental factors related to the twin parent, and measured characteristics of both parents, account for the association between parental divorce and offspring substance use and internalizing problems., Results: The association between parental divorce and offspring substance use problems remained robust when controlling for genetic and environmental risk from the twin parent associated with parental divorce, and measured characteristics of both parents. The results do not prove, but are consistent with, a causal connection. In contrast, the analyses suggest that shared genetic liability in parents and their offspring accounts for the increased risk of internalizing problems in adult offspring from divorced families., Conclusions: The study illustrates that unmeasured genetic and environmental selection factors must be considered when studying parental divorce. In explaining associations between parental divorce and young-adult adjustment, our evidence suggests that selection versus causal mechanisms may operate differently for substance abuse (a causal relation) and internalizing problems (an artifact of selection). The CoT design only controls for the genetic and environmental characteristics of one parent; thus, additional genetically informed analyses are needed.

Three dimensions of temperament -- difficult temperament, unadaptablility and unsociability -- were assessed in the first year of life by maternal interview in twins born in Puerto Rico during 2001 and 2002. Eight hundred and sixty-five eligible mothers (80%) were traced and interviewed. Model-fitting results showed that additive genetic factors and the individual specific environment contributed to variation in all three dimensions. In addition, the pattern of variances and correlations suggested that sibling contrast effects influence ratings of difficult temperament. Moderate effects of the shared environment contributed to ratings of adaptability and sociability. There was a significant genetic correlation between difficult temperament and unadaptability. Genetic and environmental effects do not differ significantly between boys and girls. The study is the first population-based study of Puerto Rican twins and one of few to attempt the assessment of behavior in the first year. Preliminary results for difficult temperament and sociability were consistent with those in other populations and ages. In contrast, a significant effect of the shared environment on the temperamental trait of unadaptability has not been reported previously.

The children of twins (COT) design has been proposed as an alternative to the adoption study to resolve the direct effects of parental treatment from secondary parent-child association due to genetic factors. The basic analytical approach compares the parent-offspring correlation with the correlation between children and the monozygotic (MZ) twins of their parents. We show that a significant difference between these correlations does not imply direct environmental causality when the measured parental treatment in question is dyadic, that is, influenced by both parents even when mating is random. Nongenetic causal effects yield very similar patterns of correlation to secondary genetic effects on dyadic treatment variables. The fact that many candidate environments, such as parental divorce, are dyadic gives reason to question the interpretation of their correlations with behavior in the children of twins.

Objective: Both genetic and common environmental influences contribute to twin associations for substance use; however, twin concordance rates may vary by environmental setting, indicating the presence of genetic-environmental interactions. The present study examined whether measures of family adaptability and cohesion may moderate the genetic influence on risk for alcohol use among female adolescents., Method: We examined such interactions through the application of log-linear models using data from the Virginia Twin Study of Adolescent Behavioral Development, a longitudinal study with extensive home interviews of adolescent (8-17 year old) female twins (386 monozygotic [MZ] pairs, 185 dizygotic [DZ] pairs) and their parents., Results: Twin concordance for alcohol use varied by average twin/parent reports of parental closeness. Differences between MZ-DZ correlations for alcohol use in families with low parental closeness, for example, were 0.97 and 0.67 (p < .001), respectively, compared with 0.79 and 0.73 (p = .24) for high parental closeness families. In addition, differences in twin concordance regardless of zygosity were found with greater twin similarities for alcohol use in strict families compared with leniently disciplined families, suggesting that the twin association interacts with common environmental influences on alcohol use., Conclusions: These results indicate that the genetic effects on adolescent alcohol use interact with the measured family environment and that the heritability of alcohol use may vary according to quality of the parental relationship. If confirmed, prevention programs may benefit from this knowledge, tailoring their intervention to quality of parental relationship.

Akiake's Information Criterion (AIC) is commonly used in univariate twin modeling of a discrete trait to prune a full model into a more parsimonious submodel. It is possible that this practice could introduce bias and inaccuracy, and we could identify no prior systematic study of these issues. Thus, we used simulation to investigate the performance of AIC-guided modeling across a broad range of parameters. Our simulations indicated that the use of the AIC to determine the "best" univariate model for a discrete trait tended to yield the incorrect model rather frequently. Moreover the parameter estimates of the "best" model by AIC were biased sharply upward as were the associated 95% confidence intervals. These results suggest that the use of AIC to guide twin modeling for univariate discrete traits should either be abandoned or used with great caution.

Background: A critical issue in devising effective interventions for the treatment of children's behavioral and emotional problems identifying genuine family environmental factors that place children at risk. In most twin and family studies, environmental factors are confounded with both direct genetic risk from parents and the indirect effect of genes influencing parents' ability to provide an optimal rearing environment. The present study was undertaken to determine whether parental psychopathology, specifically parental antisocial behavior (ASP), is a genuine environmental risk factor for juvenile conduct disturbance, depression and hyperactivity, or whether the association between parental ASP and children's behavioral and emotional problems can be explained as a secondary consequence of the intergenerational transmission of genetic factors. Methods: An extended children of twins design comprised of data collected on 2,674 adult female and male twins, their spouses, and 2,454 of their children was used to test whether genetic and/or family environmental factors best accounted for the association between parental antisocial behavior and children's behavioral problems. An age-matched sample of 2,826 juvenile twin pairs from the Virginia Twin Study of Adolescent Behavioral Development was also included to examine developmental differences in gene expression by partitioning child-specific transmissible effects from those effects that persist into adulthood. The fit of alternative models was evaluated using the statistical program Mx. Results: We found distinct patterns of transmission between parental antisocial behavior and juvenile conduct, depression and hyperactivity. Genetic and family environmental factors accounted for the resemblance between parents' ASP and children's conduct disturbance. Family environmental factors alone explained the association between child depression and parental ASP, and the impact of parental ASP on hyperactivity was entirely genetic. Conclusions: These findings underscore differences in the contribution of genetic and environmental factors on the patterns of association between parental antisocial behavior and juvenile psychopathology, having important clinical implications for the prevention and amelioration of child behavioral and emotional problems.

Background: Despite the increased risk of depression and conduct problems in children of depressed parents, the mechanism by which parental depression affects their children's behavioral and emotional functioning is not well understood. The present study was undertaken to determine whether parental depression represents a genuine environmental risk factor in children's psychopathology, or whether children's depression/conduct can be explained as a secondary consequence of the genetic liability transmitted from parents to their offspring. Methods: Children of Twins (COT) data collected on 2,674 adult female and male twins, their spouses, and 2,940 of their children were used to address whether genetic and/or family environmental factors best account for the association between depression in parents and depression and conduct problems in their children. Data collected on juvenile twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were also included to estimate child-specific genetic and environmental influences apart from those effects arising from the transmission of the parental depression itself. The fit of alternative Children of Twin models were evaluated using the statistical program "Mx." Results: The most compelling model for the association between parental and juvenile depression was a model of direct environmental risk. Both family environmental and genetic factors accounted for the association between parental depression and child conduct disturbance. Conclusions: These findings illustrate how a genetically mediated behavior such as parental depression can have both an environmental and genetic impact on children's behavior. We find developmentally specific genetic factors underlying risk to juvenile and adult depression. A shared genetic liability influences both parental depression and juvenile conduct disturbance, implicating child conduct disturbance (CD) as an early indicator of genetic risk for depression in adulthood. In summary, our analyses demonstrate differences in the impact of parental depression on different forms of child psychopathology, and at various stages of development.

Background: If the adaptive significance of specific fears changes with age, the genetic contribution to individual differences may be lowest at the age of greatest salience. The roles of genes and environment in the developmental-genetic trajectory of five common childhood fears are explored in 1094 like-sex pairs of male and female monozygotic and dizygotic twins assessed on up to three occasions during adolescence (ages 8-18 years). Methods: Dichotomous self-ratings of a cluster of five correlated fears from Ollendick's schedule of fears (FSSC-R) were extracted for subjects at each occasion of assessment. The effects of genes and environment on overall level of fears and rates of adolescent decline were explored by fitting an item-response theory ("IRT") model that allowed for individual genetic and environmental differences in initial fear level ("intercept") and rates of adolescent change ("slope") across the repeated waves of measurement. Different forms of the model were explored using Markov Chain Monte Carlo (MCMC) methods to derive the posterior distribution of subject and item parameters from the raw responses. Results: Additive genetic differences affect the common factor underlying the five fear-items. The same genes also affect rates of change with age, especially in boys. Male adolescents with higher overall genetic predisposition to childhood fears tended to show slower recovery with age than subjects with relatively low initial values. Thus, the genetic variance apparently increases with age. Conclusions: This finding is consistent with a prediction that the regulation of genetic differences will be strongest, and thus the additive genetic variance will be smallest, at the age when the particular stimulus is most salient. Items differed in the extent to which they were sensitive to underlying random differences in the rate of developmental change. Individual differences in rates of change with age were more marked in boys than girls.

The authors explore the contributions of social and genetic influences to religious attitudes and practices in a population-based sample of 11-18 year olds and their mothers who responded to a Religious Attitudes and Practices Inventory and Religious Rearing Practices Inventory respectively. Contrary to genetic studies examining adult religious behavior, genetic influences were small, accounting for only 10 percent of the variance. Rather, the effects of the social environment were much larger, greater than 50 percent, and a majority of offspring similarity was explained by familial rearing. In light of the divergent finding between adults and adolescents, one supporting a socialization model and the other a genetic model, the importance of integrating genetic and social science methodology for complex social behaviors is discussed. (Contains 8 tables and 1 note.)

Although glucocorticoid receptors are highly expressed in the prefrontal cortex, the hippocampus remains the predominant focus in the literature examining relationships between cortisol and brain. We examined phenotypic and genetic associations of cortisol levels with the thickness of prefrontal and anterior cingulate cortex regions, and with hippocampal volume in a sample of 388 middle-aged male twins who were 51-59 years old. Small but significant negative phenotypic associations were found between cortisol levels and the thickness of left dorsolateral (superior frontal gyrus, left rostral middle frontal gyrus) and ventrolateral (pars opercularis, pars triangularis, pars orbitalis) prefrontal regions, and right dorsolateral (superior frontal gyrus) and medial orbital frontal cortex. Most of the associations remained significant after adjusting for general cognitive ability, cardiovascular risk factors, and depression. Bivariate genetic analyses suggested that some of the associations were primarily accounted for by shared genetic influences; that is, some of the genes that tend to result in increased cortisol levels also tend to result in reduced prefrontal cortical thickness. Aging has been associated with reduced efficiency of hypothalamic-pituitary-adrenal function, frontal lobe shrinkage, and increases in health problems, but our present data do not allow us to determine the direction of effects. Moreover, the degree or the direction of the observed associations and the extent of their shared genetic underpinnings may well change as these individuals age. Longitudinal assessments are underway to elucidate the direction of the associations and the genetic underpinnings of longitudinal phenotypes for changes in cortisol and brain morphology.

Cortisol is an indicator of hypothalamic–pituitary–adrenal axis responsivity to stress, but few twin studies have examined the heritability of cortisol concentrations in adults across the diurnal cycle and in different contexts. Saliva samples were provided by 783 middle-aged male twins on one laboratory and two home days as part of the Vietnam Era Twin Study of Aging. Significant cortisol heritability estimates were found for laboratory measures only: awakening (.56); 30 min after awakening (.48); 1000 h (.42); mean output across the day (.43); and mean cortisol awakening response (.64). Twin correlations at home were low. In the laboratory, they were unchanged for fraternal twins, but increased for identical twins. Greater measurement error at home did not appear to account for home-laboratory differences. The results suggest that genetic factors influence cortisol responses to specific environmental stressors. Thus, cortisol levels are correlated in identical twins only when they undergo similar experiences.

Prior research has documented a strong and positive correlation between completed education and adults’ mental health. Researchers often describe this relationship using causal language: higher levels of education are thought to enhance people’s skills, afford important structural advantages, and empower better coping mechanisms, all of which lead to better mental health. An alternative explanation—the social selection hypothesis—suggests that schooling is a proxy for unobserved endowments and/or preexisting conditions that confound the relationship between the two variables. In this article, we seek to adjudicate between these hypotheses using a relatively large, US-based sample of identical adult twins. By relating within-twin-pair differences in education to within-twin-pair differences in mental health, we are able to control for the influence of genetic traits and shared family characteristics that may otherwise bias the estimates associated with educational attainment. Results from our analyses suggest that the observed association between education and mental health is attributable to confounding on unobserved variables. This finding holds across mental health conditions, is robust to several sensitivity checks, and survives a falsification test. Theoretical implications for the study of educational gradients in mental health are discussed. [ABSTRACT FROM AUTHOR]