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The magnitude of genetic and environmental factors and the influence of contrast effects on attention-deficit hyperactivity disorder (ADHD) symptomatology were examined on a sample of 900 twin pairs, aged 7–13, participating in the Virginia Twin Study of Adolescent Behavioral Development (VTSABD). In addition, the genetic and environmental correlations between ADHD and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatology were estimated. A series of structural models was applied to maternal ratings from a telephone survey, designed to screen for the three dimensions of ADHD symptomatology (hyperactivity, impulsivity, and inattention) and ODD/CD symptomatology. Model-fitting results suggested that ADHD symptomatology is highly heritable and influenced mostly by additive genetic, specific environmental, and contrast effects. However, this analysis could not exclude with statistical significance additional effects from dominance. The results of the best-fitting bivariate model suggested that the genetic correlation between the two traits is 50% and replicated previous findings of a common genetic factor influencing the comorbidity of ADHD and ODD/CD symptomatologies. [ABSTRACT FROM AUTHOR]

Genetically informative longitudinal data about menstrual disorders allow us to address the extent to which the same genetic risk mechanisms are operating throughout the reproductive life cycle. We investigate the relative contributions of genes and environment to individual differences in menstrual symptomatology reported at two waves, 8 years apart, of a longitudinal Australian twin study. Twins were questioned in 1980–1982 and 1988–1990 about levels of menstrual pain, flow, and perceived limitation by menses. Longitudinal genetic analysis was based on 728 pairs (466 MZ and 262 DZ) who were regularly menstruating at both survey waves. A bivariate Cholesky model was fitted to the two-wave data separately for flow, pain, and limitation variables. The baseline model comprised common genetic and environmental factors influencing responses at both waves and specific effects influencing only the second-wave response. We also included age as a covariate in the model. Proportions of the longitudinally stable variance in menstrual flow, pain, and limitation attributable to genetic and individual environmental effects were calculated for the best-fitting models. Genetic factors accounted for 39% of the longitudinally stable variation in menstrual flow, 55% for pain, and 77% for limitation. The remaining stable variance was due to individual environmental factors (61, 45, and 23%, respectively). Therefore the stable variance over the 8-year interval was largely environmentally influenced for menstrual flow, was approximately equally determined by genetic and by nonshared environmental influences in the case of pain, and was due almost entirely to genetic influences for limitation by periods. We demonstrate for the first time that the same genetic influences are operative throughout the reproductive life span. [ABSTRACT FROM AUTHOR]

Two pilot studies were conducted. First, the validity of a measure of infant–caregiver attachment for twins was assessed. Sixteen twin pairs from the Louisville Twin Study (LTS) were assessed in the Strange Situation (SS) at ages 19 or 25 months. Concordance between the LTS procedure and the SS procedure for assessing attachment was 78.1%, significantly greater than chance. Second, twin similarity for attachment as measured by the LTS procedure was assessed. Videotapes of 34 MZ pairs and 26 DZ pairs at ages 18 and 24 months were rated in terms of attachment behavior. MZ concordance for attachment was 67.6%, significantly greater than the DZ concordance rate of 38.5%. Results are discussed in the context of current debate in attachment theory. [ABSTRACT FROM AUTHOR]

Electroencephalographic (EEG) coherence has been suggested to be an index of the connectivity of the brain. It represents the coupling between two EEG signals from different brain areas and is mathematically analogous to a cross-correlation in the frequency domain. We obtained data from 167 pairs of 5-year-old twins to study genetic and environmental influences on individual differences in intrahemispheric coherences. Coherence was computed in the theta band (4.0 to 7.5 cycles/s) between prefrontal, frontal, central, parietal, and occipital regions during quiet rest. Univariate genetic analyses of the data showed moderate to strong genetic influences for all coherences. Broad heritabilities ranged from 30 to 71%, with a mean heritability of 49%. With one exception, no sex differences were found. Split-half reliabilities varied with interelectrode distances, ranging from .91 for the shortest distance to .62 for the longest distance. When split-half reliabilities are compared with heritabilities, the data suggest that for corticocortical connections between adjacent brain areas, a large part of the variance is explained by “true” environmental influences, whereas for longer connections, that is, sensory to frontal areas, the variance is mostly genetic in origin. [ABSTRACT FROM AUTHOR]

In several litter-bearing species, prenatal exposure of a female fetus to hormones from adjacent male fetuses can lead to later effects on various anatomical and behavioral characteristics of the female, including a number related to reproduction. To see if such traits are also affected in humans, adult female twins from a large Australian sample who had male cotwins were compared to females with female cotwins on 90 questionnaire items related to reproductive functions. No substantial effects could be clearly demonstrated, although some weak effects remained a possibility. Some variables, such as age at first menstruation, age at first pregnancy, and height, were consistent in direction with results from the animal literature, although the effect sizes were small and not statistically significant. [ABSTRACT FROM AUTHOR]

A number of studies have demonstrated associations between sensation seeking traits and measures of impulsivity. This study examined genetic contributions to the observed correlations between imupulsivity and sensation seeking traits. Fifty-seven pairs of identical and 49 pairs of fraternal twins who were reared apart and 90 individuals who also participated in the Minnesota Study of Twins Reared Apart completed the Control scale of the Multidimensional Personality Questionnaire (MPQ; Tellegen, 1982) and the four subscales of the Sensation Seeking Scale (SSS; Zuckerman, 1979), Consistent with previous studies, the Control scale was significantly correlated with the SSS. A Cholesky decomposition of the data indicated that the phenotypic correlations between the Control scale and the four subscales of the SSS were mediated almost entirely by genetic factors. In the final reduced model the proportion of the genetic variance of the Control scale in common with the SSS was estimated as 55%, and the rest of the genetic variance (45%) was attributed to the genetic variance specific to the Control scale. The results emphasize the importance of common biological mechanisms underlying associations between impulsivity and sensation seeking traits. [ABSTRACT FROM AUTHOR]

In order to assess the genetic etiology of the comorbidity of reading and mathematics difficulties, data were ascertained from two samples: (1) 102 identical and 77 same-sex fraternal twin pairs in which at least one member of each pair is reading disabled and (2) 42 identical and 23 same-sex fraternal twin pairs in which at least one member is math disabled. Composite reading and mathematics performance data from each sample were fitted to the basic multiple regression model for the analysis of selected twin data and its bivariate extension. Resulting estimates of bivariate heritability and the genetic correlation between the reading and the mathematics performance measures suggest that the comorbidity between mathematics and reading difficulties is due in part to genetic influences. [ABSTRACT FROM AUTHOR]

Age-related changes are analyzed in the correlation of 3416 monozygotic and 3780 dizygotic U.S. twin pairs aged between 9 and 75+ years for conservatism scores derived from a 28-item social attitude inventory. The effects of the shared environment are overwhelming in twins aged 20 years or younger. In older twins, genetic effects appear to play a larger role. A more dynamic conception of the interaction between genes and environment in the development of complex human differences is needed. [ABSTRACT FROM AUTHOR]

Two thousand five hundred seventy pairs of Norwegian MZ and like-sexed and unlike-sexed DZ twins aged 18–25 years completed questionnaires with information about symptoms of anxiety and depression and alcohol consumption. The aim of the study was to estimate sex-specific genetic and environmental effects unique to symptoms of anxiety/depression and to alcohol consumption and effects common to the two phenotypes. Five models fitted the data almost equally well. The heritability estimate from these models ranged from .23 to .57 for male alcohol consumption, from .39 to .59 for female alcohol consumption, from .25 to .48 for male anxiety/depression, and from .45 to .56 for female anxiety/depression. The phenotypic correlation between alcohol and anxiety/depression in males (r = .23) could be fully explained by common genetic effects. The correlation in females (r = .18) was caused by individual environmental factors together with either genetic effects or family environment. [ABSTRACT FROM AUTHOR]

Many twin registers hold information on flat file systems such as those provided by statistical packages or spreadsheets. Demographic details may be maintained separately from data collected in multiple different studies, leading to considerable problems with data consistency, redundancy, and integration. Ad hoc requests may be difficult. Implementation of a relational database system permits storage and maintenance of all records, simple data entry and validation procedures, linking of information from different projects with security of access, and the flexibility to provide rapid answers to ad hoc enquiries using standard Structured Query Language (SQL). Twin data provide a challenge for relational database design which rests on the technique of normalization and the use of unique identifiers to access associated groups of variables; for twins, “uniqueness” must preserve identification of both the pair and the individual twin subjects in the data structure to enable flexible access to and analysts of the data. An application on the Institute of Psychiatry Volunteer Twin Register (IOPVTR) database is described, through reference to one study of a sample of the twins, with simulated data. We show how a balance of adherence to database design principles and attention to ongoing clerical and research procedures has been used to produce an integrated, flexible, and open-ended system. [ABSTRACT FROM AUTHOR]

Variation in peripheral nerve conduction velocity (PNCV) and intelligence was studied in 18-year-old Dutch twins. It has been suggested that both brain nerve conduction velocity and PNCV are positively correlated with intelligence (Reed, 1984) and that heritable differences in nerve conduction velocity may explain part of the well-established heritability of intelligence. The relationship among IQ, obtained with the Wechsler Adult Intelligence Scale, and median nerve PNCV was examined in 159 twin pairs. Genetic analyses showed a heritability of 81% for IQ and 66% for onset PNCV. The small but significant phenotypic correlation between IQ and onset PNCV (.15) was entirely mediated by common genetic factors. Analyses of difference scores for PNCV of this study and PNCV from the same subjects collected at age 16 suggest that there might still be development in PNCV in this age interval. This maturation is highly controlled by genetic factors. It is suggested that variation in IQ that is associated with nerve conduction velocity becomes apparent only after the developmental processes in peripheral nerves are completed. This is in line with the suggestion of increasing heritability of IQ in adulthood. [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., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

We examined interactions among genetic, biological, and ecological variables predicting externalizing behaviors in preschool and middle childhood. Specifically, we examined prediction of externalizing behaviors from birth complications and negative emotionality, each moderated by genetic risk for aggression and ecological risk factors of insensitive parenting and low family income. At ages 4 and 5 years, 170 twin pairs and 5 triplet sets (N = 355 children) were tested; 166 of those children were tested again at middle childhood (M = 7.9 years). Multilevel linear modeling results showed generally that children at high genetic risk for aggression or from low-income families were likely to have high scores on externalizing, but for children not at high risk, those with increased birth complications or more negative emotionality had high scores on externalizing. This study underscores the importance of considering biological variables as moderated by both genetic and ecological variables as they predict externalizing behaviors across early childhood., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Trajectories of youth antisocial behavior (ASB) are characterized by both continuity and change. Twin studies have further indicated that genetic factors underlie continuity, while environmental exposures unique to each child in a given family underlie change. However, most behavioral genetic studies have examined continuity and change during relatively brief windows of development (e.g., during childhood but not into adolescence). It is unclear whether these findings would persist when ASB trajectories are examined across multiple stages of early development (i.e., from early childhood into emerging adulthood). Our study sought to fill this gap by examining participants assessed up to five times between the ages of 3 and 22 years using an accelerated longitudinal design in the Michigan State University Twin Registry (MSUTR). We specifically examined the etiologies of stability and change via growth curve modeling and a series of univariate and bivariate twin analyses. While participants exhibited moderate-to-high rank-order stability, mean levels of ASB decreased linearly with age. Genetic and nonshared environmental influences that were present in early childhood also contributed to both stability and change across development, while shared environmental contributions were negligible. In addition, genetic and nonshared environmental influences that were not yet present at the initial assessment contributed to change over time. Although ASB tended to decrease in frequency with age, participants who engaged in high levels of ASB during childhood generally continued to do so throughout development. Moreover, the genetic and nonshared environmental contributions to ASB early in development also shaped the magnitude of the decrease with age., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Anxiety not only concerns mental wellbeing but also negatively impacts other areas of health. Yet, there is limited research on (a) the genetic and environmental aetiology of such relationships; (b) sex differences in aetiology and (c) non-European samples. In this study, we investigated the genetic and environmental variation and covariation of anxiety symptoms and eight components of health-related quality of life (QoL), as measured by the short form health survey (SF-36), using genetic twin model fitting analysis. Data was drawn from the Colombo Twin and Singleton Study (COTASS), a population-based sample in Sri Lanka with data on twins (N = 2921) and singletons (N = 1027). Individual differences in anxiety and QoL traits showed more shared environmental (family) effects in women. Men did not show familial effects. Anxiety negatively correlated with all eight components of QoL, mostly driven by overlapping unique (individual-specific) environmental effects in both sexes and overlapping shared environmental effects in women. This is the first study in a South Asian population supporting the association between poor mental health and reduced QoL, highlighting the value of integrated healthcare services. Associations were largely environmental, on both individual and family levels, which could be informative for therapy and intervention.

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.

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.

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.

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.

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.

It remains a challenge to determine whether children resemble their parents due to nature, nurture, or a mixture of both. Here we used a design that exploits the distinction between transmitted and non-transmitted alleles in genetic transmission from parent to offspring. Two separate polygenic scores (PGS) were calculated on the basis of the transmitted and non-transmitted alleles. The effect of the non-transmitted PGS is necessarily mediated by parental phenotypes, insofar as they contribute to the rearing environment of the offspring (genetic nurturing). We calculated transmitted and non-transmitted PGSs associated with adult educational attainment (EA) and PGSs associated with childhood ADHD in a general population sample of trios, i.e. child or adult offspring and their parents (N = 1120-2518). We tested if the EA and ADHD (non-)transmitted PGSs were associated with childhood academic achievement and ADHD in offspring. Based on the earlier findings for shared environment, we hypothesized to find genetic nurturing for academic achievement, but not for ADHD. In adults, both transmitted (R 2  = 7.6%) and non-transmitted (R 2  = 1.7%) EA PGSs were associated with offspring EA, evidencing genetic nurturing. In children around age 12, academic achievement was associated with the transmitted EA PGSs (R 2  = 5.7%), but we found no support for genetic nurturing (R 2  ~ 0.1%). The ADHD PGSs were not significantly associated with academic achievement (R 2  ~ 0.6%). ADHD symptoms in children were only associated with transmitted EA PGSs and ADHD PGSs (R 2  = 1-2%). Based on these results, we conclude that the associations between parent characteristics and offspring outcomes in childhood are mainly to be attributable to the effects of genes that are shared by parents and children.

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.

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.

Externalizing psychopathology in early adolescence is a highly heritable risk factor for drug use, yet how it relates to marijuana use development is not well-characterized. We evaluate this issue in independent twin samples from Colorado (N = 2608) and Minnesota (N = 3630), assessed from adolescence to early adulthood. We used a biometric latent growth model of marijuana use frequency with data from up to five waves of assessment from ages 14 to 30, to examine change in marijuana use and its relationship with a factor model of adolescent externalizing psychopathology. The factor structure of adolescent externalizing psychopathology was similar across samples, as was the association between that common factor and early marijuana use (Minnesota r = 0.67 [0.60, 0.75]; Colorado r = 0.69 [0.59, 0.78]), and increase in use (Minnesota r = 0.18 [0.10, 0.26]; Colorado r = 0.20 [0.07, 0.34]). Early use was moderately heritable in both samples (Minnesota h 2 = 0.57 [0.37, 0.79]; Colorado h 2 = 0.42 [0.14, 0.73]). Increase in use was highly heritable in Minnesota (h 2 = 0.82 [0.72, 0.88]), less so in Colorado (h 2 = 0.22 [0.01, 0.66]), and shared environmental effects were larger in Colorado (c 2 = 0.55 [0.14, 0.83]) than Minnesota (c 2 = 0 [0, 0.06]). We found moderate genetic correlations between externalizing psychopathology and early use in both samples. Finally, additional analyses in the Minnesota sample indicated that marijuana use decreased during the late 20s. This decline is strongly heritable (h 2 = 0.73 [0.49, 0.91]) and moderately negatively correlated with adolescent externalizing psychopathology (r = - 0.41 [- 0.54, - 0.28]). Adolescent externalizing psychopathology is genetically correlated with change in late adolescent marijuana use (late teens, early 20s), as well as maintenance of use in early adulthood (late 20 s) even after controlling for the effects of early use.

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.

Genome-wide studies often exclude family members, even though they are a valuable source of information. We identified parent-offspring pairs, siblings and couples in the UK Biobank and implemented a family-based DNA-derived heritability method to capture additional genetic effects and multiple sources of environmental influence on neuroticism and years of education. Compared to estimates from unrelated individuals, total heritability increased from 10 to 27% and from 17 to 56% for neuroticism and education respectively by including family-based genetic effects. We detected no family environmental influences on neuroticism. The couple similarity variance component explained 35% of the variation in years of education, probably reflecting assortative mating. Overall, our genetic and environmental estimates closely replicate previous findings from an independent sample. However, more research is required to dissect contributions to the additional heritability by rare and structural genetic effects, assortative mating, and residual environmental confounding. The latter is especially relevant for years of education, a highly socially contingent variable, for which our heritability estimate is at the upper end of twin estimates in the literature. Family-based genetic effects could be harnessed to improve polygenic prediction.

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.

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.

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.

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 (a 2  = 0.30 in boys and 0.18 in girls) and relational tensions (a 2  = 0.13 and 0.14, respectively) at 12 years of age, with the proportions becoming larger through 17 years of age (a 2  = 0.53 in boys and 0.49 in girls for relational support; a 2  = 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.

In GWAS of imaging phenotypes (e.g., by the ENIGMA and CHARGE consortia), the growing number of phenotypes considered presents a statistical challenge that other fields are not experiencing (e.g. psychiatry and the Psychiatric Genetics Consortium). However, the multivariate nature of MRI measurements may also be an advantage as many of the MRI phenotypes are correlated and multivariate methods could be considered. Here, we compared the statistical power of a multivariate GWAS versus the current univariate approach, which consists of multiple univariate analyses. To do so, we used results from twin models to estimate pertinent vectors of SNP effect sizes on brain imaging phenotypes, as well as the residual correlation matrices, necessary to estimate analytically the statistical power. We showed that for subcortical structure volumes and hippocampal subfields, a multivariate GWAS yields similar statistical power to the current univariate approach. Our analytical approach is as accurate but ~ 1000 times faster than simulations and we have released the code to facilitate the investigation of other scenarios, may they be outside the field of imaging genetics.

While a standard part of twin modeling, the magnitude of shared environment (c 2 ) is rarely examined by comparing estimates obtained using other methods. To clarify these effects on familial resemblance, we estimated c 2 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 c 2 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). c 2 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."