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Parenting behaviors have long been recognized as crucial to children's healthy development. However, examinations of the etiology of these behaviors are less prevalent. The current study investigated the driving forces behind parental warmth and discipline, particularly whether they are related more to traits within the parent or reactions to characteristics of the child. To explore this question, three robust factors of child temperament--effortful control, negative affectivity, and surgency/extraversion--and five parent personality traits were examined in association with parent behaviors through differential parenting within 185 four-year-old twin pairs (370 children; 56% girls; 90% White; predominantly middle class). Genetic analyses showed that parents tend to treat both children similarly in terms of parental warmth, but they treat children less similarly in terms of discipline, regardless of child zygosity. Multilevel linear regressions showed that within twin pairs, the child with higher effortful control received less discipline from parents than their cotwin. Analyses also showed that parent agreeableness was significantly related to parent warmth above and beyond other personality traits and child temperament. This study clarified the direction of effects and genetic contributions to parenting behaviors, supporting previous literature that discipline acts in reaction to the child, whereas warmth is more driven by parent personality. This research suggests the importance of focusing on child temperament and parent personality as they relate to parenting behaviors, allowing clinicians and parents to more effectively correct maladaptive parenting behaviors and encourage healthy and adaptive parenting behaviors, thus promoting positive outcomes for children.

Prior theoretical and empirical research has highlighted links between positive parenting and the socioeconomic characteristics of the family's neighborhood, but has yet to illuminate the etiologic origins of this association. One possibility is that the various predictors of parenting outlined by Belsky (1984; e.g., characteristics of the child, characteristics of the parent, and contextual influences) may matter more in some neighborhood contexts than in others. To examine this possibility, we conducted etiologic moderation analyses in a sample of 1,030 families of twins (average age 8 years; 51% male, 49% female; racial composition: 82% White, 10% Black, 1% Asian, 1% Indigenous, and 6% multiracial) from the Twin Study of Behavioral and Emotional Development in Children in the Michigan State University Twin Registry. Neighborhood and parenting were assessed using multiple informants and assessment strategies (neighborhood and family informants, administrative data, and videotaped parent-child interactions). Results pointed to strong evidence of etiologic moderation, such that child effects on positive mothering were prominent in neighborhoods with little opportunity and near zero in neighborhoods with ample opportunity. Such findings not only reframe the magnitude of child effects on the parenting they receive as context-dependent, but also indicate that mothers in impoverished neighborhoods may be more responsive to their children's characteristics than mothers in neighborhoods with ample opportunity.

Purpose: The aim of this study is to establish which specific cognitive abilities are phenotypically related to reading skill in adolescence and determine whether this phenotypic correlation is explained by polygenetic overlap. Method: In an Australian population sample of twins and non-twin siblings of European ancestry (734 [less than or equal to] N [less than or equal to] 1542 [50.7% < F < 66%], mean age = 16.7, range = 11-28 years) from the Brisbane Adolescent Twin Study, mixed-effects models were used to test the association between a dyslexia polygenic score (based on genome-wide association results from a study of 51,800 dyslexics versus >1 million controls) and quantitative cognitive measures. The variance in the cognitive measure explained by the polygenic score was compared to that explained by a reading difficulties phenotype (scores that were lower than 1.5 SD below the mean reading skill) to derive the proportion of the association due to genetic influences. Results: The strongest phenotypic correlations were between poor reading and verbal tests R[superscript 2] up to 6.2%); visuo-spatial working memory was the only measure that did not show association with poor reading. Dyslexia polygenic scores could completely explain the phenotypic covariance between poor reading and most working memory tasks and were most predictive of performance on a test of arithmetic (R[superscript 2] = 2.9%). Conclusion: Shared genetic pathways are thus highlighted for the commonly found association between reading and mathematics abilities, and for the verbal short-term/working memory deficits often observed in dyslexia.

We compared dyad-focused maternal speech (protoconversations and maternal speech describing the dyad) in interactions of mothers with their twin and singleton infants. Nine twins and nine singletons, coming from urban areas of Crete (Greece), were video-recorded at home in spontaneous face-to-face interactions with their mothers, from the 2nd to the 6th month at 30-day intervals. Continuous micro-analysis revealed that the following: (a) variations in proto-conversations favoured singleton compared to twin infants; (b) twin and singleton mothers addressed different, but possibly of equivalent communicative significance, verbal comments to their infants within protoconversations; (c) both twin and singleton mothers showed age-variant efforts for conversation with their young infants. Though we showed quantitative variations of maternal dyad-focused speech between mother-singleton infant and mother-twin infant dyads, both singleton and twin mothers used devices of equivalent communicative significance and age-variant attempts to respond sensitively to their infants' expressive behaviours according to the latter's age-related motives for communication.

In this report, we look at the challenges posed by the outbreak of COVID-19 and how the Executive Board of these two congresses succeeded in overcoming those challenges and holding two congresses. The approach for a large festival with different virtual setting components provided a suitable solution that led to exemplary achievements and created an appropriate model for future virtual or combined virtual and face-to-face events. These events proved that pandemic problems could not limit the organizers, pushing them to make better use of the facilities and turning this threat into an opportunity., (© 2021 Wiley Periodicals LLC.)

Behavior genetic methods are useful for examining mechanisms underlying the interaction between genetic and family environmental factors of internalizing problem behavior (INT). Previous twin studies, however, have shown little consistency in interaction patterns, depending on type and operationalization of measured environments. The aim of the current study was to explore different gene-by-environment interaction patterns among different family-level environmental risk factors and resources known to correlate with INT. Using an empirical-based approach, we combined various indicators of the family environment to derive four dimensions: "positive parenting," "negative parenting," "lack of parental resources," and "socioeconomic status." We then used a genetically informed design of twins raised in the same family to test whether interaction patterns followed a diathesis stress or vantage sensitivity model formulation. The sample consisted of 2,089 twin pairs and their families from two twin birth cohorts (ages 11 and 17) participating in Wave 1 of the German TwinLife study of social inequalities. In line with a vantage sensitivity pattern of interaction and with the bioecological model of development (Bronfenbrenner & Ceci, 1994), evidence for a general mechanism of gene-environment interaction with increasing nonshared environmental variance for more adverse and less propitious family conditions was found. In preadolescence, parenting behavior had a greater moderating influence on INT compared to general family conditions like socioeconomic status. Interventions for INT that directly involve parents, thus, may be more important in preadolescent populations whereas individual interventions for adolescents may be more successful if they are adapted to different levels of socioeconomic status.

The ability to perceive approximate numerosity is present in many animal species, and emerges early in human infants. Later in life, it is moderately heritable and associated with mathematical abilities, but the etiology of the Approximate Number System (ANS) and its degree of independence from other cognitive abilities in infancy is unknown. Here, we assessed the phenotypic specificity as well as the influence of genetic and environmental factors on the ANS in a sample of 5-month-old twins (N = 514). We found a small-to-moderate but statistically significant effect of genetic factors on ANS acuity (heritability = 0.18, 95% CI: 0.02, 0.33), but only when differences in numerosity were relatively large (1:4 ratio). Non-verbal ability assessed with the Mullen Scales of Early Learning (MSEL) was found to be heritable (0.47; 95% CI: 0.34, 0.57) and the phenotypic association between ANS acuity and non-verbal ability performance was close to zero. Similarly, we found no association between ANS acuity and general attention during the task. An unexpected weak but statistically significant negative association between ANS acuity and scores on the receptive language scale of the MSEL was found. These results suggest that early ANS function may be largely independent from other aspects of non-verbal development. Further, variability in ANS in infancy seems to, to some extent, reflect genotypic differences in the population.

Background: Children's academic achievement is considerably influenced by genetic factors, which rarely operate independently of environmental influences such as teachers' behaviour. Praise and punitive discipline are commonly used management strategies by teachers. However, their effects on the genetic expression of children's academic achievement are still unclear. Aims: This study examined potential gene-environment interactions in the associations between children's estimated genetic disposition for academic achievement and teachers' use of praise and punitive discipline in predicting academic achievement. Sample: The participants were 165 twin pairs in sixth grade (M = 12.1 years). Methods: Teachers reported on children's academic achievement, as well as on their own behaviour. Results: Multilevel regression analyses showed significant interactions between children's estimated genetic disposition for academic achievement and teachers' use of praise and punitive discipline, respectively, in predicting academic achievement. These interactions indicated an enhancement process, suggesting that genetically advantaged children are those most likely to benefit from regular praise and infrequent punishments from their teacher. Moreover, genetically advantaged children were not more (nor less) likely to receive praise or punishments than other students. However, students from underprivileged backgrounds were less likely to receive praise from their teachers. Conclusions: The results emphasize the importance of teachers' regular use of praise and infrequent punitive discipline to help genetically advantaged children reach their full potential. Future studies should investigate other protective factors of the school environment that might reduce the role of genetic influences that undermine disadvantaged youth's academic achievement.

Transposable elements (TEs) have been implicated in autism spectrum disorder (ASD). However, our understanding of their roles is far from complete. Herein, we explored de novo TE insertions (dnTEIs) and de novo variants (DNVs) across the genomes of dizygotic twins with ASD and their parents. The neuronal regulatory elements had a tendency to harbor dnTEIs that were shared between twins, but ASD-risk genes had dnTEIs that were unique to each twin. The dnTEIs were 4.6-fold enriched in enhancers that are active in embryonic stem cell (ESC)-neurons (p < 0.001), but DNVs were 1.5-fold enriched in active enhancers of astrocytes (p = 0.0051). Our findings suggest that dnTEIs and DNVs play a role in ASD etiology by disrupting enhancers of neurons and astrocytes.

Empathy and executive functions (EFs) are multimodal constructs that enable individuals to cope with their environment. Both abilities develop throughout childhood and are known to contribute to social behavior and academic performance in young adolescents. Notably, mentalizing and EF activate shared frontotemporal brain areas, which in previous studies of adults led researchers to suggest that at least some aspects of empathy depend on intact EF mechanisms. Despite the substantial development that empathy and EF undergo during adolescence, no study to date has systematically examined the associations between components of empathy and EF in this age group. Here, we explore these associations using data from an online battery of tasks, collected as part of a longitudinal twin study (N = 593; M[subscript age] 11.09 ± 0.2; 53.46% female, Israeli adolescents from Jewish decent). Using a confirmatory factor analysis, we quantified the associations between the main components of empathy (mentalizing and interpersonal concern) and of EF (working memory [WM], inhibition and shifting [IaS]). We found that WM was related to both mentalizing and interpersonal concern, whereas IaS were related to mentalizing but not to interpersonal concern. We also discuss the genetic and environmental contributions to individual differences in each factor. Our findings show both similarities and differences from previous findings in adults, suggesting that the ongoing brain maturation processes and environmental age-dependent experiences in adolescence may affect the developing relation between cognitive and emotional development. These results have implications for better understanding and treating clinical populations demonstrating executive or emotional deficits, specifically during adolescence.

Estimates of shared environmental influence on educational attainment (EA) using the Classical Twin Design (CTD) have been enlisted as genetically sensitive measures of unequal opportunity. However, key assumptions of the CTD appear violated for EA. In this study we compared CTD estimates of shared environmental influence on EA with estimates from a Nuclear Twin and Family Design (NTFD) in the same 982 German families. Our CTD model estimated shared environmental influence at 43%. After accounting for assortative mating, our best fitting NTFD model estimated shared environmental influence at 26%, disaggregating this into twin-specific shared environments (16%) and environmental influences shared by all siblings (10%). Only the sibling shared environment captures environmental influences that reliably differ between families, suggesting the CTD substantially overestimates between-family differences in educational opportunity. Moreover, parental education was found to have no environmental effect on offspring education once genetic influences were accounted for.

The non-cognitive skills self-control and grit are often considered predictors of school performance, but whether this relationship is causal remains unclear. We investigated the causality of this association using a twin design. Specifically, we evaluated the direct impact of self-control and grit on school performance, while controlling for genetic or environmental influences common to all three traits (i.e., confounding). Teachers of 4891 Dutch 12-year-old twin pairs (of which 3837 were complete pairs) completed a survey about school performance (school grades), self-control (ASEBA self-control scale), and the perseverance aspect of grit. Our analysis aimed to determine the direct impact of self-control and grit on school performance, while simultaneously controlling for genetic or environmental confounding. Establishing the regression relationship corrected for confounding supports the interpretation of the regression relationship as causal. In all analyses, we corrected for sex, rater bias of the teachers, and parental socioeconomic status. Initially, in the standard regression, self-control, and grit explained 28.4% of the school performance variance. However, allowing for genetic confounding (due to genetic pleiotropy) revealed that most of this association could be attributed to genetic influences that the three traits share. In the presence of genetic pleiotropy, the phenotypic regression of school performance on self-control and grit accounted for only 4.4% (i.e., the effect size association with the causal hypothesis). In conclusion, self-control and grit predict school performance primarily due to genetic pleiotropy, with a much smaller causal effect (R[superscript 2] = 4.4%). This suggests that interventions targeting self-control and grit alone may yield limited improvements in school performance.

Dysregulation of biological stress response, as measured by cortisol output, has been a primary candidate mechanism for how social experiences become biologically embedded. Cortisol is the primary output of the hypothalamic pituitary adrenal (HPA) axis. Cortisol levels vary systematically across the day and change in response to both sudden, acute stress experiences as well as prolonged exposure to environmental stress. Using data from 8- to 15-year-old twins in the Texas Twin Project, we investigate the extent to which genetic influences are shared across different measures of cortisol output: chronic cortisol accumulations in hair (n = 1,104), diurnal variation in salivary output (n = 488), and salivary response to a standardized, acute in-laboratory stressor (n = 537). Multivariate twin models indicate that genetic factors regulating cortisol response to the in-laboratory stressor are separable from those regulating baseline cortisol levels, naturally occurring diurnal variation in cortisol, and hair cortisol levels. These findings illustrate that novel environments can reveal unique genetic variation, reordering people in terms of their observed phenotype rather than only magnifying or mitigating preexisting differences.

Background: Educational attainment is connected to many important life outcomes, and the previous research has already focused on identifying its genetic and environmental components. However, most of these studies used twin data only and did not incorporate information from other family members. Twin studies typically decompose the phenotypic variance into genetic, shared, and unique environment components. In this study design, the shared environment component encompasses the influence of parents and the shared environments of twins and siblings independent of parents (e.g., teachers, schools, and peers). The classical twin design (CTD) conflates these influences as part of the shared environment. This shortcoming can be overcome using the nuclear twin family design (NTFD), which enables separation of the parental and shared twin/sibling environmental components. Aims: The aim of this study was to broaden the understanding of the aetiology of educational attainment using the nuclear twin family design to provide a detailed account of the genetic and environmental effects on the type of school leaving certificate. Sample: The data of 1,048 monozygotic and 916 dizygotic same-sex twins, their biological parents, and non-twin full biological siblings of the German project TwinLife were used in the nuclear twin family design. Methods: Structural equation modelling (SEM) techniques were used to analyse the variance-covariance patterns of the ordinal outcome variable. Results: Genetic influences were found to make up around 60% of variance, whilst environmental influences shared by all siblings, educational influences shared by the twins only, and non-shared environmental influences explained the remaining variance in equal amounts. Environmental transmission from parent to offspring was found to be negligible. Conclusion: Through its advanced design, our study extends the previous work enabling more detailed and robust estimations of sources of variance and contributes to a better understanding of the complex aetiology of educational attainment.

Feeling inhibited and socially not at ease is reflected in the trait social inhibition (SI). SI is associated with psychopathology that arises in young adulthood, such as anxiety. We aim for a better insight into the genetic and environmental contributions to SI across the life span, and as such examine their contributions to SI stability and change across adolescent and adult life span. We analyzed cohort-sequential longitudinal data from the Netherlands Twin Register (NTR), spanning a period of 25 years (Men (N, %): 17855, 37.4%; Age (Median, IQR): 19 years, 16-26 years; 7474 complete MZ twins and 8799 complete DZ twins). The data were organized into 7 age groups: <14 (preadolescence), 15-16 (early adolescence), 17-18 (mid adolescence), 19-20 (late adolescence), 21-30 (young adulthood), 31-40 (adulthood), 41+ (middle-age-older adulthood). SI was assessed with the ASEBA-based proxy questionnaire. Phenotypic stability was established across the entire age range. Next, a longitudinal genetic simplex model was fitted to estimate the genetic and environmental contributions to the observed phenotypic stability. Results showed SI correlated well across follow-up of a single decade (0.44 [greater than or equal to] r [greater than or equal to] 0.59) and moderately across the 25 years (0.23 - 0.32) from adolescence to middle-age and older. Broad-sense heritability (h2) was between 40 and 48% across the 7 age groups. Additive and nonadditive genetic effects together explained most of the stability of SI across the life span (about 60-90% of the phenotypic correlation between ages), whereas environmental effects played a lesser role (about 10-40%). Concluding, SI, known to increase the risk of internalizing psychopathology, is phenotypically stable across the life span, which is largely attributable to genetic contributions to individual differences in SI.

Given the importance of writing for academic achievement, this study aimed to understand how early oral language contributes to later writing skills. The first objective was to determine if preschool language skills were associated with high school writing, and if so, whether they contributed directly or indirectly through school age language. The second aim was to explore the extent to which genetic and environmental factors explained these potential associations. The sample was drawn from the Quebec Newborn Twin Study, a longitudinal follow-up of twins born in the greater Montreal area, Quebec, Canada. Language skills were assessed when children were 1.5, 2.5, 6, 7, 10, and 12 years old. Writing skills were measured at 15 years old. Participants who completed the writing task in French were included in the study (n = 316 twin pairs: 46% males). Mothers of these participants self-identified mostly as White. About 74% of them had a postsecondary diploma or certificate, and 27% further had a university degree. Most families had an income higher than 30,000 CND. Results indicate that preschool language was modestly associated with high school writing (r = 0.25) and that school age language fully mediated this association. Genes explained 53% of the association between preschool language and school age language and 64% of the association between school age language and high school writing. These results highlight the developmental continuity from oral to written language from preschool to high school and show that genetic factors largely account for this continuity.

This study investigated the association between autism and self-reported eating problems and the influence of gender on the association, in a sample of adolescent and adult twins (N = 192). Autistic traits and autism diagnosis were associated with both total and specific eating problems, including selective eating and sensory sensitivity during mealtimes. Interaction effects indicated a stronger association between autistic traits and total eating problems in females, as well as more difficulties with eating in social contexts among autistic females. In within-pair analyses, where unmeasured confounders including genes and shared environment are implicitly controlled for, the association was lost within monozygotic pairs, which might further indicate a genetic influence on the relationship between autism and eating problems.

Twins regularly score nearly a standard deviation below the population mean on standardized measures of cognitive development in infancy but recover to the population mean by early childhood, making rapid gains through the toddler years. To date, only polynomial growth models have been fit to model cognitive recovery across childhood, limiting the applicability of the growth parameters to later developmental periods. We fit a nonlinear asymptotic Gompertz growth model to prospective cognitive scores from 1,153 individual twins from 578 families (47.9% male, 91.5% White, 61.6% monozygotic) measured at 16 time points between 3 months and 15 years. Twins displayed a lower asymptote of 86.47 (0.90 SD below the population mean) and gained on average 17.01 points, achieving an upper asymptote of 103.48. Growth was observed to be most rapid at 3.26 years, highlighting the importance of the toddler years in cognitive development. Biometric analyses revealed that shared environmental factors accounted for the majority of the variance in initial cognitive ability as well as asymptotic growth in cognitive ability. Gestational age and family socioeconomic status (SES) were robust predictors of cognitive growth. Results from the present study provide insight into the growth processes underlying the recovery of cognitive ability to the population mean for children evincing slight delays in their initial cognitive ability. In particular, findings highlight prenatal factors and family economic resources as important aspects of the environment in the recovery of cognitive ability.

Future orientation tends to prevent engagement in risk behaviours and results in good academic performance among adolescents. Our study aimed to establish whether genetic factors contributed to future orientation among Chinese adolescents. We recruited 988 pairs of twins from Beijing. By constructing a high-order A (additive genetic variance) C (common environmental variance) E (unique environmental variance) model, we found that heritability and a common environment contributed significantly to the development of future orientation among adolescents. Moreover, this study did not detect significant heritability differences in future orientation between girls and boys. In addition, there was a negative relationship between age and heritability of future orientation but a positive relationship between age and non-shared environmental effect on the development of future orientation. Our findings provide empirical evidence for the heritability of future orientation, suggesting that both genetics and common environment influence its development.

Executive functions (EFs) and intelligence (IQ) are phenotypically correlated. In twin studies, latent variables for EFs and IQ display moderate to high heritability estimates; however, they show variable genetic correlations in twin studies spanning childhood to middle age. We analyzed data from over 11,000 children (9- to 10-year-olds, including 749 twin pairs) in the Adolescent Brain Cognitive Development (ABCD) Study to examine the phenotypic and genetic relations between EFs and IQ in childhood. We identified two EF factors--Common EF and Updating-Specific--which were both related to IQ (rs = 0.64-0.81). Common EF and IQ were heritable (53%-67%), and their genetic correlation (rG = 0.86) was not significantly different than 1. These results suggest that EFs and IQ are phenotypically but not genetically separable in middle childhood, meaning that this phenotypic separability may be influenced by environmental factors.

There is considerable variability in the extent to which young people with developmental language disorder (DLD) experience mental health difficulties. What drives these individual differences remains unclear. In the current article, data from the Twin Early Development Study were used to investigate the genetic and environmental influences on psychopathology in children and adolescents with DLD (n = 325) and those without DLD (n = 865). Trivariate models were fitted to investigate etiological influences on DLD and psychopathology, and bivariate heterogeneity and homogeneity models were fitted and compared to investigate quantitative differences in etiological influences on psychopathology between those with and without DLD. The genetic correlation between DLD and internalizing problems in childhood was significant, suggesting that their co-occurrence is due to common genetic influences. Similar, but nonsignificant effects were observed for externalizing problems. In addition, genetic influences on internalizing problems, but not externalizing problems, appeared to be higher in young people with DLD than those without DLD, suggesting that the presence of DLD may exacerbate genetic risk for internalizing problems. These findings indicate that genetic influences on internalizing problems may also confer susceptibility to DLD (or vice versa) and that DLD serves as an additional risk factor for those with a genetic predisposition for internalizing problems.

The current analysis investigates genetic and environmental influences on the bidirectional relationships between temperament and general cognitive ability (GCA). Measures of GCA and three temperament factors (persistence, approach, and reactivity) were collected from 486 children ages 4-9 years (80% white, 50% female) from the Louisville Twin Study from 1976 to 1998. The results indicated a bidirectional dynamic model of temperament influencing subsequent GCA and GCA influencing subsequent temperament. The dynamic relationship between temperament and GCA arose primarily from shared genetic variance, particularly in families with higher socioeconomic status, where input from temperament contributed on average 20% to genetic variance in GCA versus 0% in lower SES families.

In this article, it is argued that it makes sense to define and distinguish three levels of human intelligence: intelligence as genotypical potential, intelligence as actualised in environmental interaction, and intelligence as measured by tests (IQ). This raises the questions of what is meant by the term "intelligence as potential", and how and in what sense does a child's cognitive potential express the parents' potential and genetics? The larger the number of genes involved in a certain trait, the more possibilities emerge for the formation of new combinations for that trait. The degree of similarity between a child and their parents depends on the "unique" combination of innate genes in each newborn child. The more genes are connected with a human trait or ability, the more refined or intricate the structure of the distribution for that trait in a population will be. The question of how a parents' genes relate to their children's genes has been studied, among other things, in 'twin studies'. Another relevant, but complicated question concerns the relation between genetics (nature) and environment (nurture). Nature appears to be at work in nurture, while nurture influences processes of nature. In psychological research, some DNA differences can be used to predict psychological differences, called polygenic scores. In this context, it is argued that individual cognitive growth comes about by all kinds of influences; psychologists call such influences 'bidirectional' influences. It is also argued that, ultimately, it is the individual human explorative "activity" that is responsible and a strong catalyst for the development and mastery of human traits and for the cognitive qualifications of all newborn children.

The goal of the present study was to replicate Burt et al. (2009) and Hou et al. (2013) findings by determining the contribution of peers' deviance to changes in participants' (monozygotic [MZ] twins') self-reported delinquency from mid- to late adolescence while controlling for possible gene-environment correlations (rGE) through the use of the cotwin method in the context of a cross-lagged design. Two separate samples were used to this purpose. The first sample included 289 MZ-twin pairs (48.42% female; 65.5% of European descent, 21.7% of African descent, 12.8% other; average age at first assessment = 16.20 years) and relied on perceived measures of peer deviance, as in the two original studies. The second sample comprised 181 MZ-twin pairs (50.67% female; 84% of European descent, 3% of African descent, 2% of Asian descent, 2% Native North Americans, and 9% unspecified; average age at first assessment = 13.05 years) and used direct measures to assess peers' deviance. Participants in the first sample were part of a large representative sample of American adolescents, whereas the second sample included families with twins born in a large Canadian city. Results showed that within-pair differences in self-reported delinquency were stable from midadolescence to late adolescence in both samples. As in Burt et al. (2009) and Hou et al. (2013) within-pair differences in peer deviance did not predict changes in within-pair differences in self-reported delinquency in both samples (i.e., no socialization effect). In contrast to Burt et al. (2009) and Hou et al. (2013), however, we found no predictive link from twins' self-reported delinquency to peers' deviance (i.e., no selection effect). Finally, as in Burt et al. (2009) we found that peers' deviance was stable from middle to late adolescence and that peers' deviance and participants' delinquency were cross-sectionally correlated in the first sample, but not in the second sample. These results are interpreted in the context of the ongoing debate in regard to peers' socialization vs selection effects.

One of the most consistent findings to emerge from domestic/intimate partner violence (IPV) research is that IPV tends to "run in the family." Social learning theories appear to be consistent with empirical data, but almost no attention has been given to alternative explanations, including that genetic factors explain intergenerational transmission of IPV. Data for this study were drawn from wave 4 of the National Longitudinal Study of Adolescent Health (Add Health). Three indicators of IPV were measured and genetic factors accounted for 24% of the variance in hitting one's partner, 54% of the variance in injuring one's partner, and 51% of the variance in forcing sexual activity on one's partner. The shared environment explained none of the variance across all three indicators and the nonshared environment explained the remainder of the variance. These findings point to the importance of genetic factors in the etiology of IPV., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

We used a classical twin design and measures of neighborhood walkability and social deprivation, using each twin's street address, to examine genetic and environmental influences on the residential location of 1389 same-sex pairs from a US community-based twin registry. Within-pair correlations and structural equation models estimated these influences on walkability among younger (ages 18-24.9) and older (ages 25+) twins. Adjusting for social deprivation, walkability of residential location was primarily influenced by common environment with lesser contributions of unique environment and genetic factors among younger twins, while unique environment most strongly influenced walkability, with small genetic and common environment effects, among older twins. Thus, minimal variance in walkability was explained by shared genetic effects in younger and older twins, and confirms the importance of environmental factors in walkability of residential locations., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Children with attention deficit hyperactivity disorder (ADHD) often experience co-occurring emotional problems. ADHD with this comorbidity is associated with poorer outcomes than ADHD without comorbidity. Better understanding of the etiology of comorbidity could improve prevention of negative outcomes for children with ADHD. The sample consisted of 567 twin pairs, 3,632 sibling pairs, and 2,340 cousin pairs from the Norwegian Mother, Father and Child Cohort Study. Mothers rated offspring symptoms of ADHD, anxiety, and depression at 8 years of age. Biometric modeling was performed to examine genetic and environmental contributions to co-occurring symptoms of ADHD and emotional problems in the children. We fitted four variable (inattention, hyperactivity/impulsivity, anxiety, and depression) covariance matrices of additive genetic, common environmental, twin- and individual-specific environmental effects. Genetic, shared environmental, and individual-specific environmental factors contributed to the correlation between ADHD and depression. The pattern was similar for both inattention and hyperactivity/impulsivity. Familial risk factors (genetic and shared environment), but not individual-specific environmental factors contributed to the positive correlations between each of the two ADHD subdomains and anxiety. The genetic contributions to ADHD-depression comorbidity only partly overlapped with genetic contributions to ADHD-anxiety comorbidity. Our findings indicate that shared risk factors for ADHD and comorbid depression were familial as well as individual-specific, while shared risk factors for ADHD and comorbid anxiety were primarily familial.

Autism spectrum disorder is associated with sensory processing alterations, such as sensory hyper- and hypo-responsiveness. Twin studies are scarce in this field, but they are necessary in order to disentangle the genetic and environmental contributions to this association. Furthermore, it is unclear how different neurodevelopmental/psychiatric conditions contribute to altering sensory processing. We investigated the association between autistic traits/autism spectrum disorder diagnosis and sensory processing alterations in twins (N = 269), using the adult/adolescent sensory profile, which differentiates four sub-domains: Low Registration, Sensation Seeking, Sensory Sensitivity, and Sensation Avoiding. While the associations between autistic traits and "Low Registration" and "Sensation Avoiding" persisted within monozygotic (genetically identical) twins, "Sensory Sensitivity" was only associated with autistic traits within dizygotic twins. In multivariate analyses with different neurodevelopmental/psychiatric diagnoses as predictor variables, autism spectrum disorder and attention deficit hyperactivity disorder were the strongest predictors for two adult/adolescent sensory profile sub-domains each. The results suggest that the association between autistic traits and "Sensory Sensitivity" is influenced by genetics while non-shared environmental factors influence the associations between autistic traits and "Low Registration" and "Sensation Avoiding." They further indicate that altered sensory processing is not specific to autism spectrum disorder, while autism spectrum disorder is a strong predictor of certain sensory processing alterations, even when controlling for other (comorbid) neurodevelopmental/psychiatric conditions.

White matter microstructure is under strong genetic control, yet it is largely unknown how genetic influences change from childhood into adulthood. In one of the largest brain mapping studies ever performed, we determined whether the genetic control over white matter architecture depends on age, sex, socioeconomic status (SES), and intelligence quotient (IQ). We assessed white matter integrity voxelwise using diffusion tensor imaging at high magnetic field (4-Tesla), in 705 twins and their siblings (age range 12-29; 290 M/415 F). White matter integrity was quantified using a widely accepted measure, fractional anisotropy (FA). We fitted gene-environment interaction models pointwise, to visualize brain regions where age, sex, SES and IQ modulate heritability of fiber integrity. We hypothesized that environmental factors would start to outweigh genetic factors during late childhood and adolescence. Genetic influences were greater in adolescence versus adulthood, and greater in males than in females. Socioeconomic status significantly interacted with genes that affect fiber integrity: heritability was higher in those with higher SES. In people with above-average IQ, genetic factors explained over 80% of the observed FA variability in the thalamus, genu, posterior internal capsule, and superior corona radiata. In those with below-average IQ, however, only around 40% FA variability in the same regions was attributable to genetic factors. Genes affect fiber integrity, but their effects vary with age, sex, SES and IQ. Gene-environment interactions are vital to consider in the search for specific genetic polymorphisms that affect brain integrity and connectivity., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Parent-child similarity is a function of genetic and environmental transmission. In addition, genetic effects not transmitted to offspring may drive parental behavior, thereby affecting the rearing environment of the child. Measuring genetic proclivity directly, through polygenic risk scores (PRSs), provides a way to test for the effect of nontransmitted parental genotype, on offspring outcome, termed a "genetic nurture" effect--in other words, if and how parental genomes might affect their children through the environment. The current study used polygenic risk scores for smoking initiation, cigarettes per day, and drinks per week to predict substance use in a sample of 3,008 twins, assessed prospectively from age 17-29, and their parents, from the Minnesota Center for Twin and Family Research. Mixed-effects models were used to test for a genetic nurture effect whereby parental PRSs predict offspring tobacco and alcohol use after statistically adjusting for offspring's own PRS. Parental smoking initiation PRS predicted offspring cigarettes per day at age 24 ([beta] = 0.103, 95% CI [0.03, 0.17]) and alcohol use at age 17 ([beta] = 0.091, 95% CI [0.04, 0.14]) independent of shared genetics. There was also a suggestive independent association between the parent PRS and offspring smoking at age 17 ([beta] = 0.096; 95% CI [0.02, 0.17]). Mediation analyses provided some evidence for environmental effects of parental smoking, alcohol use, and family socioeconomic status. These findings, and more broadly the molecular genetic method used, have implications on the identification of environmental effects on developmental outcomes such as substance use. [The article was co-written with the GWAS & Sequencing Consortium of Alcohol and Nicotine Use (GSCAN).]

The authors investigated genetic and environmental contributions to the relationships between children's (N=9,319 twin pairs) prosocial behavior and parental positivity and negativity toward them. Children's prosocial behavior was rated by parents at ages 3, 4, and 7 and by teachers at age 7. At each age, parents described their feelings and discipline toward each twin. Parental positivity was indexed by positive feelings and positive, non-coercive discipline, and parental negativity was indexed by negative feelings and coercive, punitive discipline. Genetics and the environment both contributed to individual differences in prosocial behavior and in parenting. At all ages, parental positivity correlated positively, and parental negativity correlated negatively with prosocial behavior. Genetic factors largely mediated the negative correlation between prosocial behavior and parental negativity. Shared environmental effects contributed mainly to the positive relationship between prosocial behavior and parental positivity. This pattern was found both cross-sectionally and longitudinally. The findings point to the importance of children's characteristics and of the parent-child relationship in family processes., (((c) 2006 APA, all rights reserved).)

Researchers have identified sources of individual differences in writing across beginning and developing writers. The aim of the present study was to further clarify the sources of this variability by investigating the extent to which there are differences in genetic and environmental factors underlying the associations between lexical diversity, syntactic knowledge, and semantic cohesion knowledge in relation to writing. Differences were examined across two developmental phases of writing: beginning (i.e., elementary school) and developing (i.e., middle school). Participants included 262 twin pairs (M[subscript age]= 10.88 years) in elementary school and 247 twin pairs (M[subscript age] =13.21 years) in middle school. Twins were drawn from the Florida Twin Project on Reading, Behavior, and Environment. Biometric models were conducted separately for subgroups defined by phase of writing development. Results indicated significant etiological differences in writing components across the two phases, such that effects associated with genes and non-shared environment were greater while effects associated with shared environment were lower in developing writers as compared to beginning writers. Furthermore, results showed that child-specific environment was the largest contributor to individual differences in writing components and their covariation for both beginning and developing writers. These results imply that even direct instruction about writing in schools may be having different effects on children based on their unique experiences.

Nonresponse occurs when individuals either have no chance of being included in a study (noncoverage), refuse to take part (unit nonresponse), or fail to give complete information (item nonresponse). The purpose of this article is to test the possible biasing effects of nonresponse on the results of behavioral-genetic studies. Simulations and a real data 'natural' experiment were used to determine the impact of nonresponse on estimates of additive genetic and environmental effects. The simulations used realistic twin-pair correlations and models of nonresponse derived from prior research. The real data 'natural experiment' used data from a nationally representative birth-cohort twin study (E-Risk Study) and compared model results from families who had responded to a mail survey to those from all study cases. Results showed that the primary influence of nonresponse was to attenuate the effect of the shared environment and to inflate estimates of nonshared environment and additive genetic effects. At high levels of nonresponse a spurious nonadditive genetic effect (suggesting genetic dominance) was also found. Study nonresponse was shown to have the potential to bias the findings of behavioral-genetic research. Design and analysis methods that can be used to alleviate this potentially important biasing effect in behavioral-genetic studies are discussed in light of these findings.

The present study examined, within a longitudinal family-informed design and across middle childhood, the predictive associations between preference for solitude and social wariness, two forms of social withdrawal, and peer difficulties. Specifically, preference for solitude, rather than social wariness, was expected to predict peer victimization and rejection, two aspects of peer difficulties. A total of 1,014 children from the Quebec Newborn Twin Study were assessed by teachers and peers at ages 6, 7, and 10 years. Multilevel analyses conducted across three levels, between family, within family, and within person, revealed that preference for solitude, rather than social wariness, increased the risk for peer difficulties in terms of both peer victimization and peer rejection. Specifically, preference for solitude was systematically associated with peer rejection starting at age 6 years and became progressively associated with peer victimization over time. This pattern was found both between and within families. In addition, the predictive association with peer rejection was found within genetically identical, monozygotic twin pairs, suggesting that this predictive association existed after taking into account genetic vulnerabilities. Social wariness was systematically unrelated to peer difficulties. These findings suggest that preference for solitude, rather than social wariness, is a risk factor for peer difficulties. They underscore the relevance of distinguishing these dimensions of social withdrawal and illustrate the usefulness of a family-informed design to document the processes underlying childhood social adjustment.

This study investigates the factors driving football players with identical training experience and genetics to have dramatically different career paths. We studied two paired cases from a pool of 32 talented U-20 players who were twice World Champions. The first paired case is a set of monozygotic twins that played football for exactly the same period of time yet only one of them was selected for the national team. The second paired case refers to an outstanding player who got injured and withdrew from his football career and the player who replaced him in the national team. Semi-structured interviews were conducted and then analyzed inductively. The results provide a description of opportunities (affordances) that could only be taken by those who were ready to act skillfully when such rare event occurred. To act on such affordances (or not) may dramatically change the outcome of a player's career. These results suggest that expert performance and high achievement emerge from circumstances resulting from the self-organization of several performer-environmental factors. Acting on such opportunities (affordances) implies being perceptually attuned to and ready for unpredictable events. This research builds on the ecological dynamics approach and provides a basis for further understanding of expertise and expert performance.

CRISPR-cas technology is being incorporated into undergraduate biology curriculum through lab experiences to immerse students in modern technology that is rapidly changing the landscape of science, medicine and agriculture. We developed and implemented an educational module that introduces students to CRISPR-cas technology in a Genetic course and an Advanced Genetics course. Our primary teaching objective was to immerse students in the design, strategy, conceptual modeling, and application of CRISPR-cas technology using the current research claim of the modification of the CCR5 gene in twin girls. This also allowed us to engage students in an open conversation about the bioethical implications of heritable germline and non-heritable somatic genomic editing. We assessed student-learning outcomes and conclude that this learning module is an effective strategy for teaching undergraduates the fundamentals and application of CRISPR-cas gene editing technology and can be adapted to other genes and diseases that are currently being treated with CRISPR-cas technology.

The Danish Twin Registry was initiated at the Copenhagen University Institute for Human Genetics in 1954 by professor Tage Kemp and his assistants, Bent Harvald and Mogens Hauge. The project was until 1960 primarily financed by US National Cancer Institutes. Twin pairs both of same and different sex, born 1870-1910 were drawn from the birth registers and followed-up through the national registers until death or present place of living. Later on same sex pairs born 1911-30 were added. Besided cancer a multitude of other disorders were registered. Intensive studies on identical twins grown up apart were undertaken by Niels Juel-Nielsen, on criminal behaviour by Karl O. Christiansen, on smoking habits by Elisabeth Raaschou-Nielsen, on peptic ulcer by Kaj Gotlieb Jensen, on schizophrenia by Margit Fischer. Among early remarkable results should be mentioned the modest influence of genetic versus environmental factors in most cases of cancer, the strong genetic impact in mental and moral qualities, the approximate genetic/environmental ratio of 50/50 for the orgin of criminal behaviour and a corresponding ratio of 25/75 for life expectancy. In 1971 the Danish Twin Registry was moved to Odense Universty.

According to the hybrid model (van Bergen, van der Leij, & de Jong, 2014), the significant association among executive functioning (EF), reading, and math may be partially explained by parent-reported EF's role as a common risk and/or protective factor in reading and math (dis)abilities. The current study used a sample of 434 twin pairs (M[subscript age] = 12.12) from Florida to conduct genetically sensitive modeling on children's parent-reported EF, reading, and math skills to determine the common and unique etiological influences among the three domains. EF was measured through parent report and reading and math were measured with standardized test scores drawn from Florida's Progress Monitoring and Reporting Network as well as standardized parent-administered assessments collected by mail. Our trivariate Cholesky modeling showed that no matter which parent-reported EF component was modeled, the overlap of parent-reported EF with reading and math was explained by common genetic influences. Supplemental analysis suggested that this might in part be due to general parent report of problem behaviors. Additionally, significant environmental influences, with higher shared environmental overlap than previous work, were also found for reading and math. Findings indicate that poor parent-reported EF is a common cognitive risk factor for reading and math disabilities, which is driven by a shared genetic basis among all three domains.

The association between physical fitness and age-related differences in cognition and brain structure has been studied fairly extensively during development and aging, yet comparatively less in young adulthood. The current study examined 1,195 young adults aged 22 to 36 (54% female; 67% Caucasian) to better understand associations between physical fitness--grip strength and submaximal cardiovascular endurance--and age-related differences in executive function (EF), memory, and average cortical thickness. EF, memory, and cortical thickness were negatively associated with age, and higher endurance was positively associated with EF and memory. Neither physical fitness measure associated with cortical thinning. To follow-up on these analyses, data from monozygotic (n = 149 pairs) and dizygotic (n = 93 pairs) twins were used to estimate the degree to which heritability versus environment might contribute to the observed associations between cognition and endurance. Environmental effects shared by monozygotic and dizygotic twins alike were estimated to account for roughly 50% of the correlation between endurance and cognition (EF and memory). Heritability and nonshared environmental effects were inconsistent across EF and memory. Overall, these findings suggest an association between cardiovascular endurance and age-related differences in cognition in young adulthood and that these associations may be independent of cortical thinning. Whereas there was consistent evidence for a moderate contribution of the shared environment, there was limited and inconsistent evidence for a role of heritability.

Purpose: This review article summarizes a program of longitudinal investigation of twins' language acquisition with a focus on causal pathways for specific language impairment (SLI) and nonspecific language impairment in children at 4 and 6 years with known history at 2 years. Method: The context of the overview is established by legacy scientific papers in genetics, language, and SLI. Five recent studies of twins are summarized, from 2 to 16 years of age, with a longitudinal perspective of heritability over multiple speech, language, and cognitive phenotypes. Results: Replicated moderate-to-high heritability is reported across ages, phenotypes, full population estimates, and estimates for clinical groups. Key outcomes are documentation of a twinning effect of risk for late language acquisition in twins that persists through 6 years of age, greater for monozygotic than dizygotic twins (although zygosity effects disappear at 6 years); heritability is greater for grammar and morphosyntax than other linguistic dimensions, from age 2 years through age 16 years, replicated within twin samples at subsequent age levels and across twin samples at age 16 years. Conclusion: There is consistent support for legacy models of genetic influences on language acquisition, updated with a more precise growth signaling disruption model supported by twin data, as well as singleton data of children with SLI and nonspecific language impairment.

Objective: To assess, by use of a population based twin register, if there are sex and age differences in genetic and environmental influences on inter-individual variation in BMI among middle-aged and elderly subjects., Design: Twin study., Subjects: 1233 like-sex Danish twin pairs (213 MZ male, 322 DZ male, 280 MZ female, 418 DZ female pairs, age: 46-76 years, BMI: 15-45 kg/m2)., Measurements: Self-reported height and weight., Methods: Proportions of variance due to genetic and environmental factors were estimated from variance-covariance matrices using the structural equation model approach., Results: The most parsimonious explanation of the data was provided by a model that included additive genetic and non-shared environmental factors with the latter fixed to be equal across sex and age. The heritability of BMI was estimated to be 0.46 for males aged 46-59 years, 0.61 for males aged 60-76 years, 0.77 for females aged 46-59 years and 0.75 for females aged 60-76 years., Conclusion: As in earlier studies, the present one showed a high heritability of BMI throughout adult life, with genetic influences being mainly additive and environmental influences being non-shared, without evidence for major impact of genetic dominance or shared environment. Most twin, family and adoption studies do not suggest important sex or age differences in magnitude of genetic effects, but we found that females had greater heritability than males, and that heritability in males increased by age.

School genetics is changing. Nowadays, students are more likely to be introduced to the idea that many characteristics of organisms, including those of humans, are not determined by the actions of just one or two genes but result from interactions between the products of many genes and the environments of each organism. This article asks whether there is a place in school science for teaching about the genetics of inheritance. There are arguments in favour of such teaching but also risks.

Classroom-level influences on literacy skills in kindergarten through Grade 2, and on literacy and numeracy skills in Grades 3, 5, 7, and 9, were examined by comparing the similarity of twins who shared or did not share classrooms with each other. We analyzed two samples using structural equation modeling adapted for twin data. The first, Study 1, was of Australia-wide tests of literacy and numeracy, with 1,098; 1,080; 790, and 812 complete twin pairs contributing data for Grades 3, 5, 7, and 9, respectively. The second, Study 2, was of literacy tests from 753 twin pairs from kindergarten through Grade 2, which included a sample of United States and Australian students and was a reanalysis and extension of Byrne et al. (2010). Classroom effects were mostly nonsignificant; they accounted for only 2-3% of variance in achievement when averaged over tests and grades. Although the averaged effects may represent a lower-bound figure for classroom effects, and the design cannot detect classroom influences limited to individual students, the results are at odds with claims in public discourse of substantial classroom-level influences, which are mostly portrayed as teacher effects.

This study examined the mediating role of emotional availability in the relation between parent positive personality and toddler problem behavior. The sample comprised 654 twins at 12 and 32 months. Primary caregivers (>95% mothers) completed six measures indexing parent positive personality assessed at 12 months, and emotional availability and toddler problem behaviors assessed at both times. Parent positive personality was positively associated with emotional availability and negatively associated with problem behavior. The indirect path from parent positive personality to problem behavior through emotional availability was significant, and parent positive personality was no longer significantly related to problem behavior, suggesting full mediation. Although problem behaviors were heritable, over half of the variance was due to the shared environment, pointing to early childhood as a time when parent characteristics and behaviors may have maximum influence. Parental emotional responsiveness could serve to reduce problem behaviors in young children.

Visual disengagement has been hypothesized as an endophenotype for autism. In this study we used twin modelling to assess the role of genetics in basic measures of visual disengagement, and tested their putative association to autistic traits in the general population. We used the Gap Overlap task in a sample of 492 twins. Results showed that most of the covariance among eye movement latencies across conditions was shared and primarily genetic. Further, there were unique genetic contributions to the Gap condition, but not to the Overlap condition--i.e. the one theorized to capture visual disengagement. We found no phenotypic association between autistic traits and disengagement, thus not supporting the hypothesis of visual disengagement as an endophenotype for autistic traits.