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Subjective health ratings are associated with dementia risk such that those who rate their health more poorly have increased risk for dementia. The genetic and environmental mechanisms underlying this association are unclear, as prior research cannot rule out whether the association is due to genetic confounds. The current study addresses this gap in two samples of twins, one from Sweden (N = 548) and one from Denmark (N = 4,373). Using genetically-informed, bivariate regression models, we assessed whether additive genetic effects explained the association between subjective health and dementia risk as indexed by a latent variable proxy measure. Age at intake, sex, education, depressive symptomatology, and follow-up time between subjective health and dementia risk assessments were included as covariates. Results indicate that genetic variance and other sources of confounding accounted for the majority of the effect of subjective health ratings on dementia risk. After adjusting for genetic confounding and other covariates, a small correlation was observed between subjective health and latent dementia risk in the Danish sample (rE = −.09, p <.05). The results provide further support for the genetic association between subjective health and dementia risk, and also suggest that subjective ratings of health measures may be useful for predicting dementia risk. [ABSTRACT FROM AUTHOR]

Nutrition and diet are key modifiable risk factors for the rising burden of non-communicable diseases like cardio-vascular diseases and diabetes in low- and middle- income countries (LMICs). The nutritional transition in dietary behaviours in LMICs has most likely contributed to this problem. Although traditionally assumed to be environmental, dietary choices are also genetically influenced. Twin study designs can be used to investigate the relative influence of genes and environment on nutrition intake, eating behaviours and associated psychological health. The overall aim of this project is to: provide proof-of-concept for the feasibility of using dietary (biomarker) data within the Children-of-Twin design in nutrition studies, develop laboratory skills and statistical genetic skills and establish a Sri Lankan-specific food composition database. Currently, a pilot study is being conducted with 304 individuals (38 Monozygotic twin pairs, 38 Dizygotic twin pairs and their male or female adult offspring). Questionnaire data on nutritional intake, eating behaviours, psychological well-being, physical health, and bio-specimens are being collected. A Sri Lankan-specific food composition database was developed, training sessions on macro and micro element analysis in biological samples and statistical genetics skills development were conducted and Community Engagement and Involvement programs were carried out in two districts of Sri Lanka. [ABSTRACT FROM AUTHOR]

Low- and middle-income countries (LMICs) globally have undergone rapid urbanisation, and changes in demography and health behaviours. In Sri Lanka, cardio-vascular disease and diabetes are now leading causes of mortality. High prevalence of their risk factors, including hypertension, dysglycaemia and obesity have also been observed. Diet is a key modifiable risk factor for both cardio-vascular disease and diabetes as well as their risk factors. Although typically thought of as an environmental risk factor, dietary choice has been shown to be genetically influenced, and genes associated with this behaviour correlate with metabolic risk indicators. We used Structural Equation Model fitting to investigate the aetiology of dietary choices and cardio-metabolic phenotypes in COTASS, a population-based twin and singleton sample in Colombo, Sri Lanka. Participants completed a Food Frequency Questionnaire (N = 3934) which assessed frequency of intake of 14 food groups including meat, vegetables and dessert or sweet snacks. Anthropometric (N = 3675) and cardio-metabolic (N = 3477) phenotypes were also collected including weight, blood pressure, cholesterol, fasting plasma glucose and triglycerides. Frequency of consumption of most food items was found to be largely environmental in origin with both the shared and non-shared environmental influences indicated. Modest genetic influences were observed for some food groups (e.g. fruits and leafy greens). Cardio-metabolic phenotypes showed moderate genetic influences with some shared environmental influence for Body Mass Index, blood pressure and triglycerides. Overall, it seemed that shared environmental effects were more important for both dietary choices and cardio-metabolic phenotypes compared to populations in the Global North. [ABSTRACT FROM AUTHOR]

Despite the relevance of semantic fluency measures to risk for dementia and psychiatric disorders, little is known about their genetic and environmental architecture in mid-to-late life. Participants represent 21,684 middle-aged and older adult twins (M = 60.84 years, SD = 11.21; Range 40-89) from six studies from three countries participating in the Interplay of Genes and Environment across Multiple Studies (IGEMS) consortium. All completed the same measure of semantic fluency (naming animals in 60 seconds). Results revealed small-to-moderate phenotypic associations with age and education, with education more strongly and positively associated with fluency performance in females than males. Heritability and environmental influences did not vary by age. Environmental variance was smaller with higher levels of education, but this effect was observed only in males. This is the largest study to examine the genetic and environmental architecture of semantic fluency, and the first to demonstrate that environmental influences vary based on levels of education.

Using baseline (ages 9–10) and two-year follow-up (ages 11–12) data from monozygotic and dizygotic twins enrolled in the longitudinal Adolescent Brain Cognitive DevelopmentSM Study, we investigated the genetic and environmental contributions to microstructure and volume of nine subcortical gray matter regions. Microstructure was assessed using diffusion MRI data analyzed using restriction spectrum imaging (RSI) and diffusion tensor imaging (DTI) models. The highest heritability estimates (estimate [95% confidence interval]) for microstructure were found using the RSI model in the pallidum (baseline: 0.859 [0.818, 0.889], follow-up: 0.835 [0.787, 0.871]), putamen (baseline: 0.859 [0.819, 0.889], follow-up: 0.874 [0.838, 0.902]), and thalamus (baseline: 0.855 [0.814, 0.887], follow-up: 0.819 [0.769, 0.857]). For volumes the corresponding regions were the caudate (baseline: 0.831 [0.688, 0.992], follow-up: 0.848 [0.701, 1.011]) and putamen (baseline: 0.906 [0.875, 0.914], follow-up: 0.906 [0.885, 0.923]). The subcortical regions displayed high genetic stability (rA = 0.743–1.000) across time and exhibited unique environmental correlations (rE = 0.194–0.610). Individual differences in both gray matter microstructure and volumes can be largely explained by additive genetic effects in this sample. [ABSTRACT FROM AUTHOR]

This study tested whether multiple domains of social adversity, including neighborhood opportunity/deprivation and life stress, moderate genetic (A), common environmental (C), and unique environmental (E) influences on externalizing behaviors in 760 same-sex twin pairs (332 monozygotic; 428 dizygotic) ages 10–11 from the ABCD Study. Proportion of C influences on externalizing behavior increased at higher neighborhood adversity (lower overall opportunity). A decreased and C and E increased at lower levels of educational opportunity. A increased at lower health-environment and social-economic opportunity levels. For life stress, A decreased and E increased with number of experienced events. Results for educational opportunity and stressful life experiences suggest a bioecological gene-environment interaction pattern such that environmental influences predominate at higher levels of adversity, whereas limited access to healthcare, housing, and employment stability may potentiate genetic liability for externalizing behavior via a diathesis-stress mechanism. More detailed operationalization of social adversity in gene-environment interaction studies is needed. [ABSTRACT FROM AUTHOR]

Although there is evidence for non-shared environmental links between parenting and problem behavior, so far, age-, informant-, and parent-specific patterns for both internalizing and externalizing problem behaviors have not been examined within one study yet. Using the twin differences design, the present study aimed to test how maternal and paternal parenting systematically act as a source of non-shared environment for problem behavior across different age groups and informants. We examined 1327 monozygotic twin pairs and their parents drawn from three birth cohorts of the German TwinLife study. Our results revealed that particularly child-reported less positive and more negative parenting by both parents contribute significantly to the unique environmental variance of problem behavior, although we did not find a clear pattern across age groups. Our study underlines the necessity of controlling for genetic confounding to uncover the truly environmentally mediated (and thus environmentally influenceable) pathways between parenting and problem behavior. A practical implication could be that it may be useful to primarily consider the child's perspective and focus on maternal as well as paternal parenting in interventions that address parenting to reduce problem behavior. [ABSTRACT FROM AUTHOR]

Social relationships play a critical role in health and well-being throughout life. We analyzed the genetic and environmental variance co-variance structure for social support and strain across four sets of relationships including with one's co-twin, spouse/partner, family and friends. The sample included 5288 Norwegian twins aged 40-80. Older people reported less support from their co-twin and friends and less strain from their family and friends. Genetic influences contribute importantly to variation across all the measures, with estimates ranging from 0 to 58%; variance due to shared environmental influences was most important for the twin-relationship, ranging from 0.11 to 0.42%. Social support was negatively correlated with social strain across all sets of relationships. With the exception of the co-twin relationship, these associations were primarily mediated by genetic and non-shared environmental effects.

The genetic and environmental underpinnings of sleep quality have been widely investigated. However, less is known about the etiology of the different sleep quality components and their associations. Subjective sleep quality has been studied most commonly using the Pittsburgh Sleep Quality Index (PSQI). Therefore, this work aimed to study the structure of sleep quality dimensions in a population-based twin sample by examining the etiology of the associations among the PSQI components themselves and between them. The sample comprised 2129 participants from the Murcia Twin Registry. In order to study the phenotypic, genetic and environmental structure of the PSQI we used three alternative multivariate twin models including all seven sub-scales of the PSQI (subjective sleep quality, latency, duration, efficiency, disturbances, use of sleeping medication and daytime dysfunction): a multivariate model (with seven separate correlated factors), a common pathway model and an independent pathway model. The multivariate correlated factors model showed the best fit to the data. All twin models indicated significant genetic overlap among most of the PSQI components, except daytime dysfunction and use of sleep medication. Bivariate heritability explained between 25 and 50% of the covariance for most associations between dimensions. Furthermore, the common pathway model showed that around one third of the variance (0.32; CI 95% 0.18.0.43) of a latent factor common to all questionnaire dimensions is explained by genetic factors. Genetic influences on a latent factor common to all questionnaire dimensions produced the same heritability estimates as the PSQI global score. However, sleep quality dimensions showed considerable specificity regarding its genetic-environmental structure. [ABSTRACT FROM AUTHOR]

We analyzed the contribution of genetic factors on the association between puberty timing and body mass index (BMI) using longitudinal data and two approaches: (i) genetic twin design and (ii) polygenic scores (PGS) of obesity indices. Our data were derived from Finnish cohorts: 9080 twins had information on puberty timing and BMI and 2468 twins also had genetic data. Early puberty timing was moderately associated with higher BMI in childhood in both boys and girls; in adulthood these correlations were weaker and largely disappeared after adjusting for childhood BMI. The largest proportion of these correlations was attributable to genetic factors. The higher PGSs of BMI and waist circumference were associated with earlier timing of puberty in girls, whereas weaker associations were found in boys. Early puberty is not an independent risk factor for adult obesity but rather reflects the association between puberty timing and childhood BMI contributed by genetic predisposition. [ABSTRACT FROM AUTHOR]

Multivariate twin and family studies are one of the most important tools to assess diseases inheritance as well as to study their genetic and environment interrelationship. The multivariate analysis of twin and family data is in general based on structural equation modelling or linear mixed models that essentially decomposes sources of covariation as originally suggested by Fisher. In this paper, we propose a flexible and unified statistical modelling framework for analysing multivariate Gaussian and non-Gaussian twin and family data. The non-normality is taken into account by actually modelling the mean and variance relationship, while the covariance structure is modelled by means of a linear covariance model including the option to model the dispersion components as functions of known covariates in a regression model fashion. The marginal specification of our models allows us to extend classic models and biometric indices such as the bivariate heritability, genetic, environmental and phenotypic correlations to non-Gaussian data. We illustrate the proposed models through simulation studies and six data analyses and provide computational implementation in R through the package mglm4twin. [ABSTRACT FROM AUTHOR]

Anxiety symptoms are common in later life and are associated with diverse adverse health outcomes. Little is known about how genetic and environmental influences on anxiety symptoms might vary across older adulthood. The purpose of this study was to explore change and stability of contributions to anxiety symptoms across older adulthood. We examined data from the Swedish Adoption/Twin Study of Aging (SATSA). Between the years 1984 and 2010, 2021 participants (including 753 complete twin pairs) completed up to seven assessments containing two measures of anxiety symptoms. Longitudinal genetic simplex models were fit to examine the stability and change in genetic and environmental influences. Amplification of genetic factors at ages 75-80 suggests tentative new genetic contributions to anxiety symptoms. These findings suggest that the heritability of anxiety symptoms may increase later in life. Physiological factors associated with aging are discussed as potential factors explaining this increase.

Despite emerging interest in gene-environment interaction (GxE) effects, there is a dearth of studies evaluating its potential relevance apart from specific hypothesized environments and biometrical variance trends. Using a monozygotic within-pair approach, we evaluated evidence of G×E for body mass index (BMI), depressive symptoms, and cognition (verbal, spatial, attention, working memory, perceptual speed) in twin studies from four countries. We also evaluated whether APOE is a 'variability gene' across these measures and whether it partly represents the 'G' in G×E effects. In all three domains, G×E effects were pervasive across country and gender, with small-to-moderate effects. Age-cohort trends were generally stable for BMI and depressive symptoms; however, they were variable-with both increasing and decreasing age-cohort trends-for different cognitive measures. Results also suggested that APOE may represent a 'variability gene' for depressive symptoms and spatial reasoning, but not for BMI or other cognitive measures. Hence, additional genes are salient beyond APOE.

Variability in psychiatric response following stressful/traumatic life events is frequently observed. There is also variability in propensity for alcohol use disorder (AUD) such that some can consume substantial amounts and not develop AUD symptoms whereas others develop an AUD. Our group has applied discrepancy-based approaches to capture psychiatric resilience (PR) and alcohol resistance (AR), both moderately heritable. This study sought to (1) examine the genetic and environmental correlation of these constructs and (2) model qualitative and quantitative sex effects. Data came from a large twin sample (N = 4501 twin pairs) with self-report measures and interviews assessing distress symptoms, stressful life events, alcohol use, and AUD. Correlated liability model results suggested a moderate degree of genetic correlation between PR and AR (0.54) due to the same genetic factors in males and females. Findings highlight the shared genetic predisposition of these resilience/resistance constructs while emphasizing the impact of unique environmental experiences. [ABSTRACT FROM AUTHOR]

Externalizing behavior is substantially affected by genetic effects, which are moderated by environmental exposures. However, little is known about whether these moderation effects differ depending on individual characteristics, and whether moderation of environmental effects generalizes across different environmental domains. With a large sample (N = 1,441 individuals) of early adolescent twins (ages 11 and 13), using a longitudinal multi-informant design, we tested interaction effects between negative emotionality and both positive and negative aspects of three key social domains: parents, peers, and schools, on the phenotypic variance as well as the etiology of externalizing. Negative emotionality moderated some of the environmental effects on the phenotypic, genetic, and environmental variance in externalizing, with adolescents at both ends of the negative emotionality distribution showing different patterns of sensitivity to the tested environmental influences. This is the first use of gene-environment interaction twin models to test individual differences in environmental sensitivity, offering a new approach to study such effects. [ABSTRACT FROM AUTHOR]

Chronic cigarette use has been consistently associated with differences in the neuroanatomy of smokers relative to nonsmokers in case-control studies. However, the etiology underlying the relationships between brain structure and cigarette use is unclear. A community-based sample of male twin pairs ages 51-59 (110 monozygotic pairs, 92 dizygotic pairs) was used to determine the extent to which there are common genetic and environmental influences between brain structure and average lifetime cigarette use. Brain structure was measured by high-resolution structural magnetic resonance imaging, from which subcortical volume and cortical volume, thickness and surface area were derived. Bivariate genetic models were fitted between these measures and average lifetime cigarette use measured as cigarette pack-years. Widespread, negative phenotypic correlations were detected between cigarette pack-years and several cortical as well as subcortical structures. Shared genetic and unique environmental factors contributed to the phenotypic correlations shared between cigarette pack-years and subcortical volume as well as cortical volume and surface area. Brain structures involved in many of the correlations were previously reported to play a role in specific aspects of networks of smoking-related behaviors. These results provide evidence for conducting future research on the etiology of smoking-related behaviors using measures of brain morphology.

The Classical Twin Method (CTM) compares the similarity of monozygotic (MZ) twins with that of dizygotic (DZ) twins to make inferences about the relative importance of genes and environment in the etiology of individual differences. The design has been applied to thousands of traits across the biomedical, behavioral and social sciences and is arguably the most widely used natural experiment known to science. The fundamental assumption of the CTM is that trait relevant environmental covariation within MZ pairs is the same as that found within DZ pairs, so that zygosity differences in within-pair variance must be due to genetic factors uncontaminated by the environment. This equal environments assumption (EEA) has been, and still is hotly contested, and has been mentioned as a possible contributing factor to the missing heritability conundrum. In this manuscript, we introduce a new model for testing the EEA, which we call the Augmented Classical Twin Design which uses identity by descent (IBD) sharing between DZ twin pairs to estimate separate environmental variance components for MZ and DZ twin pairs, and provides a test of whether these are equal. We show through simulation that given large samples of DZ twin pairs, the model provides unbiased estimates of variance components and valid tests of the EEA under strong assumptions (e.g. no epistatic variance, IBD sharing in DZ twins estimated accurately etc.) which may not hold in reality. Sample sizes in excess of 50,000 DZ twin pairs with genome-wide genetic data are likely to be required in order to detect substantial violations of the EEA with moderate power. Consequently, we recommend that the Augmented Classical Twin Design only be applied to datasets with very large numbers of DZ twin pairs (> 50,000 DZ twin pairs), and given the strong assumptions relating to the absence of epistatic variance, appropriate caution be exercised regarding interpretation of the results. [ABSTRACT FROM AUTHOR]

Since 1987, a group of behavior geneticists have been teaching an annual methodology workshop on how to use state-of-the-art methods to analyze genetically informative data. In the early years, the focus was on analyzing twin and family data, using information of their known genetic relatedness to infer the role of genetic and environmental factors on phenotypic variation. With the rapid evolution of genotyping and sequencing technology and availability of measured genetic data, new methods to detect genetic variants associated with human traits were developed and became the focus of workshop teaching in alternate years. Over the years, many of the methodological advances in the field of statistical genetics have been direct outgrowths of the workshop, as evidence by the software and methodological publications authored by workshop faculty. We provide data and demographics of workshop attendees and evaluate the impact of the methodology workshops on scientific output in the field by evaluating the number of papers applying specific statistical genetic methodologies authored by individuals who have attended workshops. [ABSTRACT FROM AUTHOR]

The distinction between genetic influences on the covariance (or bivariate heritability) and genetic correlations in bivariate twin models is often not well-understood or only one is reported while the results show distinctive information about the relation between traits. We applied bivariate twin models in a large sample of adolescent twins, to disentangle the association between well-being (WB) and four complex traits (optimism, anxious-depressed symptoms (AD), aggressive behaviour (AGG), and educational achievement (EA)). Optimism and AD showed respectively a strong positive and negative phenotypic correlation with WB, the negative correlation of WB and AGG is lower and the correlation with EA is nearly zero. All four traits showed a large genetic contribution to the covariance with well-being. The genetic correlations of well-being with optimism and AD are strong and smaller for AGG and EA. We used the results of the models to explain what information is retrieved based on the bivariate heritability versus the genetic correlations and the (clinical) implications. [ABSTRACT FROM AUTHOR]

The assumption in the twin model that genotypic and environmental variables are uncorrelated is primarily made to ensure parameter identification, not because researchers necessarily think that these variables are uncorrelated. Although the biasing effects of such correlations are well understood, a method to estimate these parameters in the twin model would be useful. Here we explore the possibility of relaxing this assumption by adding polygenic scores to the (univariate) twin model. We demonstrate that this extension renders the additive genetic (A)—common environmental (C) covariance (σAC) identified. We study the statistical power to reject σAC = 0 in the ACE model and present the results of simulations. [ABSTRACT FROM AUTHOR]

We present a procedure to simultaneously fit a genetic covariance structure model and a regression model to multivariate data from mono- and dizygotic twin pairs to test for the prediction of a dependent trait by multiple correlated predictors. We applied the model to aggressive behavior as an outcome trait and investigated the prediction of aggression from inattention (InA) and hyperactivity (HA) in two age groups. Predictions were examined in twins with an average age of 10 years (11,345 pairs), and in adult twins with an average age of 30 years (7433 pairs). All phenotypes were assessed by the same, but age-appropriate, instruments in children and adults. Because of the different genetic architecture of aggression, InA and HA, a model was fitted to these data that specified additive and non-additive genetic factors (A and D) plus common and unique environmental (C and E) influences. Given appropriate identifying constraints, this ADCE model is identified in trivariate data. We obtained different results for the prediction of aggression in children, where HA was the more important predictor, and in adults, where InA was the more important predictor. In children, about 36% of the total aggression variance was explained by the genetic and environmental components of HA and InA. Most of this was explained by the genetic components of HA and InA, i.e., 29.7%, with 22.6% due to the genetic component of HA. In adults, about 21% of the aggression variance was explained. Most was this was again explained by the genetic components of InA and HA (16.2%), with 8.6% due to the genetic component of InA. [ABSTRACT FROM AUTHOR]

We investigated how the COVID-19 crisis and the extraordinary experience of lockdown affected young adults in England and Wales psychologically. One month after lockdown commenced (T2), we assessed 30 psychological and behavioural traits in more than 4000 twins in their mid-twenties and compared their responses to the same traits assessed in 2018 (T1). Mean changes from T1 to T2 were modest and inconsistent. Contrary to the hypothesis that major environmental changes related to COVID-19 would result in increased variance in psychological and behavioural traits, we found that the magnitude of individual differences did not change from T1 to T2. Twin analyses revealed that while genetic factors accounted for about half of the reliable variance at T1 and T2, they only accounted for ~ 15% of individual differences in change from T1 to T2, and that nonshared environmental factors played a major role in psychological and behavioural changes. Shared environmental influences had negligible impact on T1, T2 or T2 change. Genetic factors correlated on average.86 between T1 and T2 and accounted for over half of the phenotypic stability, as would be expected for a 2-year interval even without the major disruption of lockdown. We conclude that the first month of lockdown has not resulted in major psychological or attitudinal shifts in young adults, nor in major changes in the genetic and environmental origins of these traits. Genetic influences on the modest psychological and behavioural changes are likely to be the result of gene–environment correlation not interaction. [ABSTRACT FROM AUTHOR]

Study Objectives: Twin studies have provided data about the relative weight of genetic and environmental factors on sleep variables over the last few decades. However, heritability is a non-intuitive concept and it is often misunderstood even amongst the scientific community. This study aimed to analyze: (1) understanding of the meaning of heritability of insomnia; (2) the accuracy of estimations of heritability in the general population regarding three sleep traits (sleep duration, sleep quality and insomnia); (3) perceptions of the effectiveness of different treatments for insomnia depending on how the disorder is presented (i.e. having an environmental or genetic etiology) and whether the subject's estimate of genetic influence on sleep traits impacted beliefs about the effectiveness of different treatments. Methods: Participants (N = 3658) completed a survey which included: questions about general genetic knowledge; a specific question about the meaning of heritability; estimates of heritability of three different sleep traits; and the effectiveness of different treatments for insomnia depending on how the etiology of this condition was presented. Results: Fewer than 25% of the participants selected the correct description of the heritability of insomnia. Almost half of the sample incorrectly believed that heritability refers to the chance of passing a disorder onto their children. We also found that participants provided different estimates for the effectiveness of different treatments depending on the presumed etiology of the disorder. Conclusion: Most people do not have accurate knowledge about the concept of heritability. People's assumptions about the etiology of a disorder may influence which treatments they consider most effective. [ABSTRACT FROM AUTHOR]

Heteropaternal superfecundation (HP) occurs when two or more ova are fertilized by sperm from separate males. The resulting siblings are genetically equivalent to half-siblings and share, on average, 25% of their inherited genetic material. In the absence of genetic testing HP siblings could be treated as dizygotic (DZ) twins in behavioral genetic analyses and bias heritability estimates in phenotypic decomposition models. However, the extent to which such misclassification could affect calculated estimates of heritability is currently unknown. Employing simulation analyses, the current study assessed the potential biasing impact across a variety of conditions varying by proportions of DZ twins, sample sizes, and low, moderate, and high levels of genetic and environmental contribution to phenotypic variance. Overall, the results indicated that misclassified HP siblings had minimal impact on estimates of heritability. Nonetheless, greater attention should be paid to the identification of HP siblings within existing and future twin datasets. [ABSTRACT FROM AUTHOR]

Self-esteem is an attitude about the self that predicts psychopathology and general well-being. Parenting practices have been shown to be related to self-esteem, but these estimates are confounded because parents and children share genes. The aim of the present study was to use the monozygotic (MZ) twin difference design to isolate the non-shared environmental impact of remembered parenting on self-esteem. In a sample of 1328 adults (345 MZ twin pairs, 319 DZ twin pairs), retrospective reports of maternal and paternal affection were related to self-esteem, all of which were significantly heritable. Using MZ difference scores, paternal affection differences, but not maternal affection differences, were significantly related to self-esteem differences. These results suggest that parenting provided by the father directly impacts self-esteem through non-shared environmental mechanisms. Maternal affection, on the other hand, impacts self-esteem through shared genes (not shared environment, as shared environment was not a significant aspect of self-esteem). This has implications for parenting intervention programs. [ABSTRACT FROM AUTHOR]

Objective: To explore and apply multimodel inference to test the relative contributions of latent genetic, environmental and direct causal factors to the covariation between two variables with data from the classical twin design by estimating model-averaged parameters. Methods: Behavior genetics is concerned with understanding the causes of variation in phenotypes and the causes of covariation between two or more phenotypes. Two variables may correlate as a result of genetic, shared environmental or unique environmental factors contributing to variation in both variables. Two variables may also correlate because one or both directly cause variation in the other. Furthermore, covariation may result from any combination of these sources, leading to 25 different identified structural equation models. OpenMx was used to fit all these models to account for covariation between two variables collected in twins. Multimodel inference and model averaging were used to summarize the key sources of covariation, and estimate the magnitude of these causes of covariance. Extensions of these models to test heterogeneity by sex are discussed. Results: We illustrate the application of multimodel inference by fitting a comprehensive set of bivariate models to twin data from the Virginia Twin Study of Psychiatric and Substance Use Disorders. Analyses of body mass index and tobacco consumption data show sufficient power to reject distinct models, and to estimate the contribution of each of the five potential sources of covariation, irrespective of selecting the best fitting model. Discrimination between models on sample size, type of variable (continuous versus binary or ordinal measures) and the effect size of sources of variance and covariance. Conclusions: We introduce multimodel inference and model averaging approaches to the behavior genetics community, in the context of testing models for the causes of covariation between traits in term of genetic, environmental and causal explanations. [ABSTRACT FROM AUTHOR]

Type D (Distressed) personality combines negative affectivity (NA) and social inhibition (SI) and is associated with an increased risk of cardiovascular disease. We aimed to (1) validate a new proxy based on the Achenbach System of Empirically Based Assessment (ASEBA) for Type D personality and its NA and SI subcomponents and (2) estimate the heritability of the Type D proxy in an extended twin-pedigree design in the Netherlands Twin Register (NTR). Proxies for the dichotomous Type D classification, and continuous NA, SI, and NAxSI (the continuous measure of Type D) scales were created based on 12 ASEBA items for 30,433 NTR participants (16,449 twins and 13,984 relatives from 11,106 pedigrees) and sources of variation were analyzed in the 'Mendel' software package. We estimated additive and non-additive genetic variance components, shared household and unique environmental variance components and ran bivariate models to estimate the genetic and non-genetic covariance between NA and SI. The Type D proxy showed good reliability and construct validity. The best fitting genetic model included additive and non-additive genetic effects with broad-sense heritabilities for NA, SI and NAxSI estimated at 49%, 50% and 49%, respectively. Household effects showed small contributions (4–9%) to the total phenotypic variation. The genetic correlation between NA and SI was.66 (reflecting both additive and non-additive genetic components). Thus, Type D personality and its NA and SI subcomponents are heritable, with a shared genetic basis for the two subcomponents. [ABSTRACT FROM AUTHOR]

Drug and alcohol use is associated with risky sexual behavior (RSB). It is unclear whether this association is due to correlated liabilities (e.g., third variables influencing both traits), or whether use of drugs and alcohol during sexual decision making increases RSB. This study addresses this question by fitting a series of biometrical models using over 800 twin pairs assessed in early adulthood (m = 25.21 years). Measures included an index of sex under the influence (e.g., frequency that drugs or alcohol affect sexual decision making), number of lifetime sexual partners, and a general measure of substance use. Analyses suggest the covariance among these measures is explained by both genetic and environmental correlated liabilities. The overlap was not specific to sex under the influence, but was shared with a measure of general substance use. Models testing necessary but not sufficient parameters for direction of causation suggest that sex under the influence is unlikely to cause an increase in RSB; more evidence for reverse causation was found. [ABSTRACT FROM AUTHOR]

Although stress is frequently considered an environmental factor, dependent stressful life events (SLEs)––stressors that result from one's actions or behaviors––may in fact be evoked by a genetic liability. It has been suggested that dependent SLEs may be partially caused by poor executive function (EFs), higher-level cognitive abilities that enable individuals to implement goal-directed behavior. We investigated the possibility of genetic and environmental overlap between SLEs and EFs in a longitudinal twin study. We found high genetic stability in the number of dependent SLEs from age 23 to age 29, suggesting that the number of dependent stressors show persistence across time due to their genetic etiology. In addition, there was a nominally significant negative genetic correlation between a Common EF latent factor and dependent SLEs at age 23. The genetic stability of dependent SLEs and association with Common EF provides insight into how some behaviors may lead to persistent stress. [ABSTRACT FROM AUTHOR]

The adult self report (ASR) is a well-validated instrument with multiple scales relating to adult psychopathology. Recently, an 18-item version has been introduced, the brief problem monitor (BPM) to measure Internalizing behavior (INT), Externalizing behavior (EXT), and attention problems (ATT). The present study compared the BPM and ASR and investigated how well the BPM can serve as a supplement or an alternative for the ASR for specific clinical and scientific purposes. In a large sample of adult twins (N = 9.835) from the Netherlands Twin Register (NTR), we compared the internal consistency, clinical classification concordance, means, and variances of the ASR and BPM. Using the classical twin design, we investigated the genetic covariance structure. For external validation, the associations between subjective well-being and different subscales of the ASR and BPM were compared. The internal consistency of the BPM scales (around α = 0.75) was somewhat lower than the ASR (α ~ 0.85). The BPM Externalizing scale showed the lowest internal consistency (α = 0.63). ASR and BPM scores showed good clinical classification concordance (0.61–0.80) and high correlations (r > 0.88). A small reversed sex difference in the BPM Externalizing scale appeared (women > men). Genetic (0.34–0.54) and environmental components (0.46–0.66) explained the variance to a similar extent for the ASR and BPM. The phenotypic and genetic associations with well-being were comparable. In situations where sum scores are sufficient, the BPM performs as well as the longer ASR. Depending on the situation and goal, it is worth considering the BPM as an alternative for the ASR to reduce the participant burden. [ABSTRACT FROM AUTHOR]

Low levels of childhood inhibitory control (IC) are phenotypically and genetically associated with externalizing behavior problems and attention deficit hyperactivity disorder (ADHD). Unfortunately, there is little research on this topic in early childhood, when IC first emerges. This investigation extends the previous findings of contemporaneous genetic covariance between parent-rated and laboratory-assessed IC and ADHD at age 2 by examining longitudinal links between IC at age two and ADHD behavior problems at age three in a sample of 314 same-sex twin pairs (145 monozygotic or MZ, 169 dizygotic or DZ). There were significant phenotypic associations between both parent and laboratory IC assessments at age two and later ADHD behavioral problems (correlations ranged from −.15 to −.44). In our model-fitting strategy, we included measures of ADHD and IC at age 2 as predictors of ADHD at age 3. Longitudinal genetic analyses showed that phenotypic covariance between age two IC and ADHD behavior problems one year later were explained by overlapping genetic variance (genetic correlations ranged from −.28 to −.60). However, these effects were not unique to IC and reflect variance shared with ADHD at age 2. Parent-rated IC at age two showed higher phenotypic and genetic covariance with ADHD at age three than lab ratings of IC at age two. This is the first investigation examining genetic covariance between parent and lab-based IC at age two and ADHD behavior problems at age three. Findings show that after accounting for co-occurring ADHD, early temperamental IC is not a unique genetic risk factor for later ADHD. [ABSTRACT FROM AUTHOR]

We estimated the genetic covariance matrix among four inattention (INATT) and four hyperactivity (HYP) measures in the classical twin design. Data on INATT and HYP symptom counts were obtained in mono- and dizygotic twin pairs (N = 1593) with an average age of 12.2 years (sd =.51). We analyzed maternal ratings of INATT and HYP based on the Conners' Parent Rating Scale (CPRS), the Strengths and Weaknesses of ADHD-symptoms and Normal-behavior (SWAN), and teacher ratings based on the Conners' Teacher rating scale (CTRS) and the ASEBA Teacher Rating Form (TRF). Broad-sense heritabilities, corrected for the main effects of sex and for random teacher rater effects, were large (ranging from.658 to.912). The results reveal pervasive and strong broad-sense genetic effects on INATT and HYP phenotypes with the phenotypic covariance among the phenotypes largely due to correlated genetic effects. Specifically between 79.9 and 99.9% of the phenotypic covariance among the HYP measures, and between 81.0 and 93.5% of the INATT measures are attributable to broad-sense genetic effects. Overall, the present results, pertaining to the broad-sense heritabilities and shared genetic effects, support the current genome-wide association meta-analytic approach to identifying pleiotropic genetic variants. [ABSTRACT FROM AUTHOR]

The characterizing features of autism spectrum disorder (ASD) are continuously distributed in nature; however, prior twin studies have not systematically incorporated this knowledge into estimations of concordance and discordance. We conducted a quantitative analysis of twin–twin similarity for autistic trait severity in three existing data sets involving 366 pairs of uniformly-phenotyped monozygotic (MZ) twins with and without ASD. Probandwise concordance for ASD was 96%; however, MZ trait correlations differed markedly for pairs with ASD trait burden below versus above the threshold for clinical diagnosis, with R2s on the order of 0.6 versus 0.1, respectively. Categorical MZ twin discordance for ASD diagnosis is rare and more appropriately operationalized by standardized quantification of twin–twin differences. Here we provide new evidence that although ASD itself is highly heritable, variation-in-severity of symptomatology above the diagnostic threshold is substantially influenced, in contrast, by non-shared environmental factors which may identify novel targets of early ASD amelioration. [ABSTRACT FROM AUTHOR]

This study used a twin cohort to investigate the association of autism spectrum disorder (ASD) and autistic traits with somatic health. A total of 344 twins (172 pairs; mean age 15.56 ± 5.62 years) enriched for ASD and other neurodevelopmental conditions were examined. Medical history and current physical problems were collected with a validated questionnaire to determine twin's somatic health. The Social Responsiveness Scale (SRS-2) was used to measure the participant's severity of autistic traits. Identified somatic health issues with significant within-twin pair differences were tested in relation to both ASD diagnosis and autistic traits in a co-twin control model. Twins with ASD exhibited more neurological and immunological health problems compared to those without ASD (p = 0.005 and p = 0.004, respectively). The intra-pair differences of neurological conditions and SRS-2 score were significantly correlated in monozygotic twins differing for autism traits (r = 0.40, p = 0.001), while the correlation was not found for immunological problems. In addition, a conditional model for analysis of within-twin pair effects revealed an association between neurological problems and clinical ASD diagnosis (Odds ratio per neurological problem 3.15, p = 0.02), as well as autistic traits (β = 10.44, p = 0.006), after adjusting for possible effects of co-existing attention deficit hyperactivity disorder and general intellectual abilities. Our findings suggest that neurological problems are associated with autism, and that non-shared environmental factors contribute to the overlap for both clinical ASD and autistic traits. Further population-based twin studies are warranted to validate our results and examine in detailed the shared genetic and environmental contributions of neurological problems and ASD. [ABSTRACT FROM AUTHOR]

We investigated the familial clustering of different classes of voluntary regular exercise behavior in extended twin-family pedigrees. In contrast to the earlier work based on twin data only, this allowed us to estimate the contributions of shared household effects (C), additive (A), and non-additive (D) genetic effects on voluntary exercise behavior. To test whether shared household effects were inflated by assortative mating we examined the causes of spousal resemblance. For adolescent and adult participants (aged 16 to 65) in the Netherlands Twin Register we constructed 19,543 pedigrees which specified all relations among nuclear family members and larger families in the register (N = 50,690 individuals). Data were available on total weekly MET minutes spent on leisure time exercise, and on total weekly MET minutes spent on exercise activities in team-based, solitary, competitive, non-competitive, externally paced and internally paced exercise. We analyzed the data in the Mendel software package (Lange et al. in Bioinformatics 29(12):1568–1570, 2013) under multiple definitions of household sharing and used data from spouses of twins to test phenotypic assortment, social homogamy, and marital interaction as potential sources of spousal resemblance. Results confirmed the influence of genetic factors on the total volume of weekly exercise behavior throughout the life span. Broad sense heritability ranged from 34 to 41% (19–26% A, 12–21% D), and did not depend on the definition for household sharing. Engaging in team-based, competitive, externally paced activities (e.g., soccer) was ~ 13% more heritable than engaging in non-competitive, solitary activities (e.g., jogging). Having shared a household as siblings explained 4–8% of the variance in adult exercise behavior, whereas sharing a household by spouses yielded higher C estimates (20–24%), as it incorporates spousal resemblance. Spousal resemblance was explained by both social homogamy and marital interaction, with little evidence for phenotypic assortment. We conclude that both the amount of voluntary exercise behavior and the preference for specific classes of exercise activities in adults is explained by additive and non-additive genetic factors and unique environmental influences that include correlated exercise behavior of spouses. [ABSTRACT FROM AUTHOR]

The Louisville Twin Study (LTS) began in 1958 and became a premier longitudinal twin study of cognitive development. The LTS continuously collected data from twins through 2000 after which the study closed indefinitely due to lack of funding. Now that the majority of the sample is age 40 or older (61.36%, N = 1770), the LTS childhood data can be linked to midlife cognitive functioning, among other physical, biological, social, and psychiatric outcomes. We report results from two pilot studies in anticipation of beginning the midlife phase of the LTS. The first pilot study was a participant tracking study, in which we showed that approximately 90% of the Louisville families randomly sampled (N = 203) for the study could be found. The second pilot study consisted of 40 in-person interviews in which twins completed cognitive, memory, biometric, and functional ability measures. The main purpose of the second study was to correlate midlife measures of cognitive functioning to a measure of biological age, which is an alternative index to chronological age that quantifies age as a function of the breakdown of structural and functional physiological systems, and then to relate both of these measures to twins' cognitive developmental trajectories. Midlife IQ was uncorrelated with biological age (−.01) while better scores on episodic memory more strongly correlated with lower biological age (−.19 to −.31). As expected, midlife IQ positively correlated with IQ measures collected throughout childhood and adolescence. Additionally, positive linear rates of change in FSIQ scores in childhood significantly correlated with biological age (−.68), physical functioning (.71), and functional ability (−.55), suggesting that cognitive development predicts lower biological age, better physical functioning, and better functional ability. In sum, the Louisville twins can be relocated to investigate whether and how early and midlife cognitive and physical health factors contribute to cognitive aging. [ABSTRACT FROM AUTHOR]

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

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

We analyzed how the effects of genetic and environmental factors on the perceptions of family interaction change from early to late adolescence. The data were collected by postal surveys on Finnish twins (N = 4808) at 12, 14 and 17 years of age and analyzed using genetic twin modeling. Additive genetic factors explained a modest share of the variation in perceived relational support (a2 = 0.30 in boys and 0.18 in girls) and relational tensions (a2 = 0.13 and 0.14, respectively) at 12 years of age, with the proportions becoming larger through 17 years of age (a2 = 0.53 in boys and 0.49 in girls for relational support; a2 = 0.35 in boys and 0.33 in girls for relational tensions). Simultaneously, the role of environment shared by co-twins decreased. These findings suggest that the associations between perceived family interaction and other factors in adulthood should be interpreted with caution, because they partly reflect genetic background, whereas in childhood, they may provide more reliable information on parental characteristics. [ABSTRACT FROM AUTHOR]

The objective of this study was to examine the genetic and environmental contributions to shyness throughout the school-age period. Participants were 553 twin pairs from the ongoing prospective longitudinal Quebec Newborn Twin Study. Teacher-rated measures of shyness were collected at five time-points from age 6–12 years. On average, shyness was moderately stable over time (r = 0.23–0.33) and this stability was almost entirely accounted for by genetic factors. Genetic factors at age 6 accounted for 44% of individual differences and these early genetic factors also explained individual differences at all subsequent ages (6–22%). Non-shared environmental factors explained most of individual differences at single time-points (51–63%), and did not account for stability in shyness. Contributions of shared environment were not significant. Our results suggest that the stability in shyness is mostly accounted for by early and persistent genetic contributions. [ABSTRACT FROM AUTHOR]

While a standard part of twin modeling, the magnitude of shared environment (c2) is rarely examined by comparing estimates obtained using other methods. To clarify these effects on familial resemblance, we estimated c2 for 20 diverse phenotypes in: (i) monozygotic and dizygotic twins, (ii) all step-siblings, and (iii) reared together and apart half-siblings, ascertained from the Swedish general population. The mean c2 estimates (± 95% CIs) differed across methods and were higher from twins (0.18; 0.13-0.23) than from the step (0.12; 0.09-0.14) and half-sibs (0.09; 0.06-0.13). c2 estimates correlated moderately across these three methods (ICC = + 0.28). When step-siblings from blended (each sib biologically related to one parent) and adoption-like families (one sib offspring of both parents and one of neither), were examined separately, resemblance was much lower in the latter. We need to clarify the range of environmental processes now considered together under the term "shared environment." [ABSTRACT FROM AUTHOR]

Datasets comprising twins and their children can be a useful tool for understanding the nature of intergenerational associations between parent and offspring phenotypes. In the present article we explore structural equation models previously used to analyse Children-of-Twins data, highlighting some limitations and considerations. We then present new variants of these models, showing that extending the models to include multiple offspring per parent addresses several of the limitations discussed. Accompanying the updated models, we provide power calculations and demonstrate with application to simulated data. We then apply to intergenerational analyses of height and weight, using a sub-study of the Norwegian Mother and Child Cohort (MoBa); the Intergenerational Transmission of Risk (IToR) project, wherein all kinships in the MoBa data have been identified (a children-of-twins-and-siblings study). Finally, we consider how to interpret the findings of these models and discuss future directions. [ABSTRACT FROM AUTHOR]

Decades of research into the etiology of conduct disorder (CD) has yet to yield a consensus on the existence of sex differences in underlying genetic and environmental influences. This may be partly due to the failure of many previous studies to make a distinction between non-aggressive and aggressive CD symptoms or test for potential developmental changes in sex differences in the etiology of conduct problems. To address these gaps, we fit a series of univariate and bivariate biometric sex-difference models to self-reported non-aggressive and aggressive CD symptoms in a community-based sample of twins (N = 1548, ages 9-17 year), grouped into ages 9-13 and 14-17 years. Relative model fit was evaluated using the Bayesian Information Criterion (BIC), which favors parsimony, and by Chi square difference tests. The univariate sex-scalar model provided the best fit to the data for both non-aggressive and aggressive CD symptoms at ages 9-13 and 14-17 years. Thus, the same genetic and environmental factors influenced CD symptoms in both sexes, but the total variability was lower in females than males. At both ages, the heritability of non-aggressive CD symptoms was lower than heritability of aggressive CD symptoms, and shared environmental effects were only observed for non-aggressive CD symptoms. However, estimates for genetic and environmental factors could be not be constrained to be equal across age groups for either CD subtype, suggesting substantive developmental changes in the relative influence of genetic and environmental factors on individual differences in CD symptoms. For both subtypes, the heritability was larger, and shared environmental effect smaller, in the older age group than the younger age group. A bivariate quantitative sex differences model provided the best fit to the data at ages 9-13 years. Covariation between non-aggressive and aggressive CD symptoms was due to overlapping shared and non-shared environmental factors in males and females but the overall covariation was greater in males than females. In contrast, at ages 14-17 years, the sex-scalar bivariate model provided the best fit to the data, and covariation between non-aggressive and aggressive CD symptoms was due to overlapping genetic and non-shared environmental factors. Thus, the etiology of self-reported conduct disorder varied substantially by symptom type and age. However, quantitative sex differences were only apparent when the covariation between the two subtypes was considered. [ABSTRACT FROM AUTHOR]

Internalizing and externalizing behaviors are heritable, and show genetic stability during childhood and adolescence. Less work has explored how genes influence individual differences in developmental trajectories. We estimated ACE biometrical latent growth curve models for the Teacher Report Form (TRF) and parent Child Behavior Checklist (CBCL) internalizing and externalizing scales from ages 7 to 16 years in 408 twin pairs from the Colorado Longitudinal Twin Study. We found that Intercept factors were highly heritable for both internalizing and externalizing behaviors (a2 = .61-.92), with small and nonsignificant environmental influences for teacher-rated data but significant nonshared environmental influences for parent-rated data. There was some evidence of heritability of decline in internalizing behavior (Slopes for teacher and parent ratings), but the Slope genetic variance was almost entirely shared with that for the Intercept when different than zero. These results suggest that genetic effects on these developmental trajectories operate primarily on initial levels and stability, with no significant unique genetic influences for change. Finally, cross-rater analyses of the growth factor scores revealed moderate to large genetic and environmental associations between growth factors derived from parents' and teachers' ratings, particularly the Intercepts. [ABSTRACT FROM AUTHOR]

We used a sub-sample from the Older Australian Twins Study to estimate the heritability of performance on three tests of language ability: Boston Naming Test (BNT), Letter/Phonemic Fluency (FAS) and Category/Semantic Fluency (CFT) Tests. After adjusting for age, sex, education, mood, and global cognition (GC), heritability estimates obtained for the three tests were 0.35, 0.59, and 0.20, respectively. Multivariate analyses showed that the genetic correlation were high for BNT and CFT (0.61), but low for BNT and FAS (0.17), and for FAS and CFT (0.28). Genetic modelling with Cholesky decomposition indicated that the covariation between the three measures could be explained by a common genetic factor. Environmental correlations between the language ability measures were low, and there were considerable specific environmental influences for each measure. Future longitudinal studies with language performance and neuroimaging data can further our understanding of genetic and environmental factors involved in the process of cognitive aging. [ABSTRACT FROM AUTHOR]

We investigated the etiological role of genetic and environmental influences for two milestones of tobacco and alcohol use: age of initiation, and speed of progression to dependence (latency). Study participants included 1352 monozygotic and 1422 dizygotic twins (mean age at assessment = 24.31). Earlier ages of initiation significantly increased the likelihood of developing dependence, but were associated with longer dependence latencies for tobacco and alcohol. Latencies to dependence were heritable traits for tobacco (a² = 0.63) and alcohol (a² = 0.64). Genetic influences contributing to early age of initiation were associated with faster latencies to dependence but sometimes were counteracted by environmental factors, the extent to which depended on substance and, sometimes, sex. Our findings may have important implications for public policy and add to the literature by characterizing the genetic and environmental contributions to the speed of progression to tobacco and alcohol dependence. [ABSTRACT FROM AUTHOR]

A previous meta-analysis (Van der Linden et al., Psychol Bull 143:36-52, 2017) showed that the General Factor of Personality (GFP) overlaps with ability as well as trait emotional intelligence (EI). The correlation between trait EI and the GFP was so high (ρ = 0.88) in that meta-analysis that these two may be considered virtually identical constructs. The present study builds on these findings by examining whether the strong phenotypic correlation between the GFP and trait EI has a genetic component. In a sample of monozygotic and dizygotic twins, the heritability estimates for the GFP and trait EI were 53 and 45%, respectively. Moreover, there was a strong genetic correlation of r = .90 between the GFP and trait EI. Additional analyses suggested that a substantial proportion of the genetic correlations reflects non-additive genetic effects (e.g., dominance and epistasis). These findings are discussed in light of evolutionary accounts of the GFP. [ABSTRACT FROM AUTHOR]

By taking advantage of the natural variation in genetic relatedness among identical (monozygotic: MZ) and fraternal (dizygotic: DZ) twins, twin studies are able to estimate genetic and environmental contributions to complex human behaviors. Recently concerns have been raised about the accuracy of twin studies in light of findings of genetic and epigenetic changes in twins. One of the concerns raised is that MZ twins are not 100% genetically and epigenetically similar because they show variations in their genomes and epigenomes leading to inaccurate estimates of heritability. This article presents findings from a simulation study that examined the degree of bias in estimates of heritability and environmentality when the genetic and epigenetic similarity of MZ twins differs from 1.00 and when the genetic and epigenetic similarity of DZ twins differs from 0.50. The findings suggest that in the standard biometric model when MZ or DZ twin similarity differs from 1.00 or 0.50, respectively, the variance that should be attributed to genetic influences is instead attributed to nonshared environmental influences, thus deflating the estimates of genetic influences and inflating the estimates of nonshared environmental influences. Although estimates of genetic and nonshared environmental influences from the standard biometric model were found to deviate from 'true' values, the bias was usually smaller than 10% points indicating that the interpretations of findings from previous twin studies are mostly correct. [ABSTRACT FROM AUTHOR]

The present twin study combined self- and peer assessments of twins' general homophobia targeting gay men in order to replicate previous behavior genetic findings across different rater perspectives and to disentangle self-rater-specific variance from common variance in self- and peer-reported homophobia (i.e., rater-consistent variance). We hypothesized rater-consistent variance in homophobia to be attributable to genetic and nonshared environmental effects, and self-rater-specific variance to be partially accounted for by genetic influences. A sample of 869 twins and 1329 peer raters completed a seven item scale containing cognitive, affective, and discriminatory homophobic tendencies. After correction for age and sex differences, we found most of the genetic contributions (62%) and significant nonshared environmental contributions (16%) to individual differences in self-reports on homophobia to be also reflected in peer-reported homophobia. A significant genetic component, however, was self-report-specific (38%), suggesting that self-assessments alone produce inflated heritability estimates to some degree. Different explanations are discussed. [ABSTRACT FROM AUTHOR]

For the participants in the Netherlands Twin Register (NTR) we constructed the extended pedigrees which specify all relations among nuclear and larger twin families in the register. A total of 253,015 subjects from 58,645 families were linked to each other, to the degree that we had information on the relations among participants. We describe the algorithm that was applied to construct the pedigrees. For > 30,000 adolescent and adult NTR participants data were available on harmonized neuroticism scores. We analyzed these data in the Mendel software package (Lange et al., Bioinformatics 29(12):1568-1570, 2013) to estimate the contributions of additive and non-additive genetic factors. In contrast to much of the earlier work based on twin data rather than on extended pedigrees, we could also estimate the contribution of shared household effects in the presence of non-additive genetic factors. The estimated broad-sense heritability of neuroticism was 47%, with almost equal contributions of additive and non-additive (dominance) genetic factors. A shared household effect explained 13% and unique environmental factors explained the remaining 40% of the variance in neuroticism. [ABSTRACT FROM AUTHOR]