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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.

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.

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.

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.

Background: The number line task assesses the ability to estimate numerical magnitudes. People vary greatly in this ability, and this variability has been previously associated with mathematical skills. However, the sources of individual differences in number line estimation and its association with mathematics are not fully understood. Aims: This large-scale genetically sensitive study uses a twin design to estimate the magnitude of the effects of genes and environments on: (1) individual variation in number line estimation and (2) the covariation of number line estimation with mathematics. Samples: We used over 3,000 8- to 16-year-old twins from the United States, Canada, the United Kingdom, and Russia, and a sample of 1,456 8- to 18-year-old singleton Russian students. Methods: Twins were assessed on: (1) estimation of numerical magnitudes using a number line task and (2) two mathematics components: fluency and problem-solving. Results: Results suggest that environments largely drive individual differences in number line estimation. Both genes and environments contribute to different extents to the number line estimation and mathematics correlation, depending on the sample and mathematics component. Conclusions: Taken together, the results suggest that in more heterogeneous school settings, environments may be more important in driving variation in number line estimation and its association with mathematics, whereas in more homogeneous school settings, genetic effects drive the covariation between number line estimation and mathematics. These results are discussed in the light of development and educational settings.

The present study used a genetically informed design of twins raised in the same family (375 monozygotic and 290 dizygotic twins; 50.2% girls) to examine the association between adolescents' genetic risk for depressive symptoms and the course of the parent-child relationship quality throughout adolescence. Depressive symptoms and the quality of the parent-adolescent relationships were measured through adolescents' self-reports from ages 13 to 17. Group-based trajectory modeling revealed that most adolescents experienced high-quality relationships with both of their parents, characterized by high levels of warmth and low levels of conflict, and marked by gradual changes over adolescence. However, 3% of adolescents showed a trajectory of high and increasing conflict with their mothers and 16% of adolescents showed a trajectory of low warmth with their fathers, which decreased until mid-adolescence before increasing thereafter. Moreover, in line with an evocative gene-environment correlation process, a higher genetic vulnerability to depressive symptoms increased the likelihood of following a more problematic relationship trajectory with parents. This rGE was mediated by adolescents' actual depressive behavior symptoms. Results also suggest that adolescents' depression symptoms may affect girls' and boys' relationship with their parents in a similar way, with specific sex-patterns revolving more around the sex of the parent.

This twin study examined the genetic and environmental etiology of vocabulary, syntax, and their association in first graders. French-speaking same-sex twins (n = 555) completed two vocabulary tests, and two scores of syntax were calculated from their spontaneous speech at 7 years of age. Multivariate latent factor genetic analyses showed that lexical skills were influenced mainly by the environment shared between the twins, whereas syntactic skills were influenced exclusively by genes and unique environment. Moreover, the moderate association between vocabulary and syntax was mostly due to common genetic factors. These novel findings may be attributable to the use of latent factors and the population studied. More research is needed to determine the specific factors involved in lexical and syntactic skills at this developmental period.

This investigation examines the spread of problem behaviors (substance use and delinquency) between twin siblings. A sample of 628 twins (151 male twin pairs and 163 female twin pairs) drawn from the Quebec Newborn Twin Study completed inventories describing delinquency and substance use at ages 13, 14, and 15. A 3-wave longitudinal actor-partner interdependence model (APIM) identified avenues whereby problem behaviors spread from one twin to another. Problems did not spread directly between twins across domains. Instead, 2 indirect pathways were identified: (a) Problems first spread interindividually (between twins) within a behavioral domain, then spread intraindividually (within twins) across behavioral domains (e.g., Twin A delinquency ? Twin B delinquency ? Twin B substance use); and (b) problems first spread intraindividually (within twins) across behavioral domains, then spread interindividually (between twins) within a behavioral domain (e.g., Twin A delinquency ? Twin A substance use ? Twin B substance use). Controls for genetic effects, gene--environment correlations, friend substance use and delinquency, and parenting behaviors increase confidence in the conclusion that twin siblings uniquely contribute to the spread of problem behaviors during adolescence. Twin sibling influence is a risk factor for illicit substance use, both because substance use by one twin predicts substance use by the other twin, but also because delinquency in one twin predicts delinquency in the other twin, which then gives rise to greater substance use.

Exposure to deviant friends has been found to be a powerful source of influence on children's and adolescents' aggressive behavior. However, the contribution of deviant friends may have been overestimated because of a possible non-accounted gene-environment correlation (rGE). In this study, we used a cross-lagged design to test whether friends' physical aggression at age 10 predicts an increase in participants' physical aggression from age 10 to age 13 years. Participants were 201 pairs of monozygotic twins who are part of the Quebec Longitudinal Twin Study. We performed two sets of analyses. In the first set of analyses, using twins as singletons, we found that teacher-rated friends' physical aggression predicted an increase in each twin's self-reported physical aggression from age 10 to age 13, above and beyond auto-regressive and concurrent links. Second, we used within-pair differences in regard to friends' physical aggression to predict an increase in within-pair differences in physical aggression, thus accounting for family-wide influences, including a likely rGE at age 10. No significant association was found, however. These results suggest that part of the influence attributed to friends in past studies may have been due to common underlying genetic effects on both physical aggression and association with physically aggressive friends.

This study used a genetically controlled design to examine the direction and the magnitude of effects in the over-time associations between perceived relationship quality with mothers and adolescent maladjustment (i.e., depressive symptoms and delinquency). A total of 163 monozygotic (MZ) twins pairs (85 female pairs, 78 male pairs) completed questionnaires at ages 13 and 14. Non-genetically controlled path analyses models (in which one member of each twin dyad was randomly selected for analyses) were compared with genetically controlled path analyses models (in which MZ-twin difference scores were included in analyses). Results from the non-genetically controlled models revealed a) child-driven effects in the longitudinal associations between adolescent perceived maternal support and depressive symptoms, and b) parent-driven and child-driven effects in the longitudinal association between perceived maternal negativity and adolescent delinquent behaviors. However, results from the genetically controlled models revealed only child-driven effect, suggesting that, purported parent-driven effects were a product of error arising from potential gene-environment correlations (rGE).

Background: The phenotypic and genetic associations between decoding skills and ADHD dimensions have been documented but less is known about the association with reading comprehension. The aim of the study is to document the phenotypic and genetic associations between reading comprehension and ADHD dimensions of inattention and hyperactivity/impulsivity in early schooling and compare them to those with decoding skills. Methods: Data were collected in two population-based samples of twins (Quebec Newborn Twin Study-QNTS) and singletons (Quebec Longitudinal Study of Child Development-QLSCD) totaling ˜ 2300 children. Reading was assessed with normed measures in second or third grade. Teachers assessed ADHD dimensions in kindergarten and first grade. Results: Both decoding and reading comprehension were correlated with ADHD dimensions in a similar way: associations with inattention remained after controlling for the other ADHD dimension, behavior disorder symptoms and nonverbal abilities, whereas associations with hyperactivity/impulsivity did not. Genetic modeling showed that decoding and comprehension largely shared the same genetic etiology at this age and that their associations with inattention were mostly explained by shared genetic influences. Conclusion: Both reading comprehension and decoding are uniquely associated with inattention through a shared genetic etiology.

This study tested 2 related hypotheses. The first holds that high co-rumination anticipates heightened internalizing problems. The second holds that positive relationships with friends exacerbate the risk for internalizing problems arising from co-rumination. A sample of MZ twins followed from birth (194 girls and 170 boys) completed (a) self-reports of friendship support, friendship negativity, and co-rumination with friends at age 12 and (b) measures of anxiety and depression at ages 12 and 13. Using a monozygotic twins-difference design, within-pair differences in co-rumination predicted increased within-pair differences in anxiety (but not depression), after removing the covariance between co-rumination and perceptions of friendship. In other words, the difference in co-rumination within each monozygotic twin pair predicted an increase in the difference in their anxiety levels, but not the difference in their depression levels. The discussion focuses on nonshared environmental influences, because the monozygotic twin-difference design eliminates the possibility that associations were driven by heritability or by shared environmental factors that underlie friendship experiences and internalizing problems.

Several authors consider high and frequent conflicts between friends during childhood as a serious risk for subsequent conduct problems such as generalized physical aggression toward others (e.g., Kupersmidt, Burchinal, & Patterson, 1995; Sebanc, 2003). Although it seems logical to assume that friendship conflict could have some negative consequences on children's behaviors, some scholars have suggested that a certain amount of conflict between friends may actually promote social adjustment (e.g., Laursen & Pursell, 2009). The aim of this study was to investigate the role of friendship conflict in regard to the development of generalized physical aggression toward others in the early school years (i.e., from kindergarten to Grade 1), as well as the moderating role of relational (i.e., shared positive affect and dyadic conflict resolution skills) and personal (i.e., children's sex and genetic liability for aggression) characteristics in this context. The sample included 745 twins assessed through teacher, peer, child, and friend ratings in kindergarten and Grade 1. Friendship conflict in kindergarten was linearly related to an increase in boys' but not girls' generalized physical aggression. However, shared positive affect and conflict resolution skills mitigated the prospective associations between friendship conflict and generalized physical aggression. These results were independent of children's sex, genetic risk for physical aggression, and initial levels of generalized physical aggression in kindergarten. Fostering a positive relationship between friends at school entry may buffer against the risk associated with experiencing friendship conflict.

Enriched environments may moderate the effect of genetic factors on prosocial leadership (gene-environment interaction, G × E). However, positive environmental experiences may also themselves be influenced by a genetic disposition for prosocial leadership (gene-environment correlation, rGE). Relating these processes to friendships, the present study examined (a) whether children with a genetic disposition for prosocial leadership possess a greater number of reciprocal friends (rGE) and (b) whether the number of reciprocal friends interacts with the effect of genetic factors on children's prosocial leadership (G × E). The sample comprised 275 twin pairs assessed in Grade 1 (mean age 84.7 months). Reciprocal friendship and prosocial leadership behavior were measured via peer nominations. Consistent with rGE, a genetic disposition for prosocial leadership was related to an increased likelihood of friendship. Moreover, consistent with a compensation process, environmental influences played a stronger role than genetic influences in prosocial leadership when children had many friends.

This study used a genetically informed design to assess the effects of friends' and nonfriends' reticent and dominant behaviors on children's observed social reticence in a competitive situation. Potential gene-environment correlations (rGE) and gene-environment interactions (GxE) in the link between (a) friends' and nonfriends' behaviors and (b) children's social reticence were examined. The sample comprised 466 twin children (i.e., the target children), each of whom was assessed in kindergarten together with a same-sex friend and two nonfriend classmates of either sex. Multilevel regression analyses revealed that children with a genetic disposition for social reticence showed more reticent behavior in the competitive situation and were more likely to affiliate with reticent friends (i.e., rGE). Moreover, a higher level of children's reticent behavior was predicted by their friends' higher social reticence (particularly for girls) and their friends' higher social dominance, independently of children's genetic disposition. Children's social reticence was also predicted by their nonfriends' behaviors. Specifically, children were less reticent when male nonfriends showed high levels of social reticence in the competitive situation, and this was particularly true for children with a genetic disposition for social reticence (i.e., GxE). Moreover, children genetically vulnerable for social reticence seemed to foster dominant behavior in their female nonfriend peers (i.e., rGE). In turn, male nonfriends seemed to be more dominant as soon as the target children were reticent, even if the target children did not have a stable genetic disposition for this behavior.

Using a genetically informed design, this study examined the additive and interactive effects of genetic risk, personal peer victimization experiences, and peer victimization experienced by others on children's aggression and depression symptoms. Of major interest was whether these effects varied depending on whether or not the victimized others were children's close friends. The sample comprised 197 monozygotic and same-sex dizygotic twin pairs reared together (95 female pairs) assessed in Grade 4. Each twin's victimization experiences and victimization experienced by his or her friends and other classmates were measured using individuals' reports about their own levels of peer victimization. Aggression was assessed using peer nominations, and depression was measured using self-reports. Indicative of a possible social-learning mechanism or the emotional contagion of anger, multilevel regressions showed that personal victimization experiences were related to especially high levels of aggression when close friends where also highly victimized, albeit only in boys. Moreover, in line with social comparison theory, the effect of frequent personal victimization experiences on depressive feelings was much weaker when close friends were also highly victimized than when close friends were not or were only rarely victimized. Finally, a high level of peer victimization experienced by other classmates was related to a lower level of aggression in girls and boys, possibly because of a heightened sense of threat in classrooms where many suffer attacks from bullies. All of these results were independent of children's genetic risk for aggression or depression. Theoretical and practical implications are discussed. (Contains 3 tables and 2 figures.)

This study assessed the genetic and environmental contributions to peer difficulties in the early school years. Twins' peer difficulties were assessed longitudinally in kindergarten (796 twins, "M"[subscript age] = 6.1 years), Grade 1 (948 twins, "M"[subscript age] = 7.1 years), and Grade 4 (868 twins, "M"[subscript age] = 10 years) through multiple informants. The multivariate results revealed that genetic factors accounted for a strong part of both yearly and stable peer difficulties. At the univariate level, the genetic contributions emerged progressively, as did a growing consensus among informants with respect to those who experienced peer difficulties. These results underline the need to intervene early and persistently, and to target the child and the peer context to prevent peer difficulties and their consequences. (Contains 3 tables and 3 figures.)

The goal of this study was to examine how different types of social experiences in kindergarten relate to Grade 1 academic achievement, while controlling for possible genetic and shared environmental influences through the use of the monozygotic (MZ) twin difference method. Social experiences in kindergarten included relationship quality with the larger peer group (i.e., rejection and victimization), relationship quality with one's best friend, and relationship quality with the teacher. Control variables included parental hostility-coercion, child cognitive skills and externalizing problems, and equivalent social experiences in Grade 1. Participants consisted of 223 MZ twin pairs ages 6 years at Time 1 (T1) and 7 years at Time 2 (T2). Results showed that within-pair differences in peer rejection and in poor teacher-child relationship quality at T1 uniquely predicted differences in MZ twins' academic achievement at T2. Mechanisms that could account for the possible causal role of these social experiences in regard to children's school achievement are discussed. (Contains 2 figures and 6 tables.)

Background: Genetic risk for depressive behavior may increase the likelihood of exposure to environmental stressors (gene-environment correlation, rGE). By the same token, exposure to environmental stressors may moderate the effect of genes on depressive behavior (gene-environment interaction, GxE). Relating these processes to a peer-related stressor in childhood, the present study examined (1) whether genetic risk for depressive behavior in children is related to higher levels of rejection by the peer group (rGE) and (2) whether peer rejection moderates the effect of genetic factors on children's depressive behavior (GxE). Methods: The sample comprised 336 twin pairs (MZ pairs = 196, same-sex DZ pairs = 140) assessed in kindergarten (mean age 72.7 months). Peer acceptance/rejection was measured via peer nominations. Depressive behavior was measured through teacher ratings. Results: Consistent with rGE, a moderate overlap of genetic effects was found between peer acceptance/rejection and depressive behavior. In line with GxE, genetic effects on depressive behavior varied across levels of peer acceptance/rejection. Conclusions: An increased genetic disposition for depressive behavior is related to a higher risk of peer rejection (rGE). However, genes play a lesser role in explaining individual differences in depressive behavior in rejected children than in accepted children (GxE).

Based on a sample of 406 seven-year-old twins, this study examined whether exposure to friends' social or physical aggression, respectively, moderates the effect of heritability on children's own social and physical aggression. Univariate analyses showed that children's own social and physical aggression were significantly explained by genetic factors, whereas friends' social and physical aggression represented "true" environmental factors that were unrelated to children's genetic dispositions. Multivariate analyses further suggested a possible gene-environment interaction in the link between friends' and children's physical aggression but not in the link between friends' and children's social aggression. Instead, friends' social aggression was directly related to children's social aggression, in addition to genetic effects on this behavior. Theoretical and practical implications of these results are discussed.

Using a genetic design of 840 60-month-old twins, this study investigated the genetic and environmental contributions to (a) individual differences in four components of cognitive school readiness, (b) the general ability underlying these four components, and (c) the predictive association between school readiness and school achievement. Results revealed that the contribution of the shared environment for cognitive school readiness was substantial. Genetic effects were more important for the core abilities underlying school readiness than for each specific skill, although shared environment remained the largest factor overall. Genetic, shared, and non-shared environmental factors all accounted for the predictive association between school readiness and early school achievement. These results contribute to a better understanding of the early determinants of school readiness. [This research was partially supported by the Canadian Institutes of Health Research, the Canada Research Chair Program, the Fonds qurbecois de la recherche sur la societe et la culture (FQRSC), the Quebec Ministry of Health and Social Services, and the Fonds de la recherche en sante du Quebec.]

This study compared the contribution of genes and environment to teacher-rated reactive and proactive aggression in 6-year-old twin pairs (172 pairs: 55 monozygotic girls, 48 monozygotic boys, 33 dizygotic girls, 36 dizygotic boys). Genetic effects accounted for 39% of the variance of reactive aggression and for 41% of the variance of proactive aggression. The remainder of the variance was explained by unique environmental effects. Genetic as well as unique environmental effects were significantly correlated across reactive and proactive aggression (genetic correlation = 0.87, environmental correlation = 0.34), but this overlap was largely due to a common underlying form of aggression (i.e., teacher-rated physical aggression). Once common etiological factors due to physical aggression were accounted for, reactive and proactive aggression shared no other genes and only a few environmental influences, although additional specific genetic and environmental effects were observed for both reactive and proactive aggression. These specific effects indicate that both reactive and proactive aggression may be influenced mostly by socialization experiences that are specific to each type of aggression and only to a very small degree by specific genes.

Background: Children who consistently withdraw from social situations face increased risk for later socioemotional difficulties. Twin studies indicate that genetic factors substantially account for the persistence of social withdrawal over time. However, the molecular genetic etiology of chronic courses of social wariness and preference for solitude, two dimensions of social withdrawal, remains undocumented. The objectives of the present study were (a) to identify high‐risk trajectories for social wariness and preference for solitude in childhood and (b) to examine whether falling on these high‐risk trajectories can be predicted by specific polygenic scores for mental health traits and disorders and by a general polygenic predisposition to these traits. Methods: Teachers evaluated 971 genotyped children at five occasions (age 6 to 12 years) from two prospective longitudinal studies, the Quebec Newborn Twin Study and the Quebec Longitudinal Study of Child Development. Developmental trajectories for social wariness and preference for solitude were identified. We tested whether polygenic scores for attention deficit hyperactivity disorder, autism spectrum disorder, depression, loneliness, and subjective well‐being, as well as a general mental health genetic risk score derived across these traits, were associated with the developmental trajectories. Results: Polygenic scores differentially predicted social wariness and preference for solitude. Only the loneliness polygenic score significantly predicted the high trajectory for social wariness. By contrast, the general mental health genetic risk score factor was associated with the trajectory depicting high‐chronic preference for solitude. Conclusions: Distinct associations were uncovered between the polygenic scores, social wariness, and preference for solitude. [ABSTRACT FROM AUTHOR]

Adolescent alcohol use demonstrates distinct developmental trajectories with different times of onset, levels, and rates of growth. Twin research on adolescent alcohol use has shown that genetic influences are consistent with a gradual growth of risks, whereas non-shared environmental influences are more consistent with an accumulation of risks over time. The current study investigated the relative contributions of genetic and environmental influences on shaping different developmental trajectories of alcohol use through adolescence. Self-reported past year alcohol use was collected from 877 Canadian twins (47.1% males) at age 13, 14, 15, and 17 years. Growth mixture models were fit to examine different developmental trajectories of alcohol use, and biometric liability threshold models were fit to investigate genetic and environmental influences on the liability of belonging to identified trajectories. Three trajectories were identified: low (15.1%), early onset (8.2%), and normative increasing (76.7%). Memberships in the low and early-onset group were under genetic (27.6% and 34.7%), shared (42.4% and 21.5%), and non-shared environment influences (30.0% and 43.8%). Membership in the normative increasing group was under genetic (37.7%) and non-shared environment influences (62.3%). Non-shared environmental influences were significantly larger for the normative increasing trajectory than for the low trajectory. These findings provide a more refined picture of genetic and environmental influences in the development of alcohol use in subgroups of adolescents. Genetic and environmental influences both matter, but to different degrees in different trajectories. Future research should identify specific shared and non-shared environmental experiences that distinguish different trajectories. [ABSTRACT FROM AUTHOR]

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

Background: Heritability of antisocial behaviour is estimated at approximately 50% and involves multiple genes.AimsTo investigate the cumulative genetic effects of 116 single nucleotide polymorphisms mapping to 11 candidate serotonergic genes and antisocial behaviours, in adolescence and in early adulthood.Method: Participants were 410 male members of the Quebec Longitudinal Study of Kindergarten Children, a population-based cohort followed up prospectively from age 6 to age 23. The serotonergic genes were selected based on known physiological processes and prior associations with antisocial behaviours. Antisocial behaviours were self-reported and assessed by using semi-structured interviews in adolescence and in adulthood.Results: Cumulative, haplotype-based contributions of serotonergic genes conferring risk and protection for antisocial behaviours were detected by using multilocus genetic profile risk scores (MGPRSs) and multilocus genetic profile protection scores (MGPPSs). Cumulatively, haplotype-based MGPRSs and MGPPSs contributed to 9.6, 8.5 and 15.2% of the variance in general delinquency in adolescence, property/violent crimes in early adulthood and physical partner violence in early adulthood, respectively.Conclusions: This study extends previous research by showing a cumulative effect of multiple haplotypes conferring risk and protection to antisocial behaviours in adolescence and early adulthood. The findings further support the relevance of concomitantly considering multiple serotonergic polymorphisms to better understand the genetic aetiology of antisocial behaviours. Future studies should investigate the interplay between risk and protective haplotype-based multilocus genetic profile scores with the environment.Declaration Of Interest: I.O.-M. holds a Canada Research Chair in the developmental origins of vulnerability and resilience. [ABSTRACT FROM AUTHOR]

Background: Using a longitudinal twin design and a latent growth curve/autoregressive approach, this study examined the genetic–environmental architecture of substance use across adolescence. Methods: Self-reports of substance use (i.e. alcohol, marijuana) were collected at ages 13, 14, 15, and 17 years from 476 twin pairs (475 boys, 477 girls) living in the Province of Quebec, Canada. Substance use increased linearly across the adolescent years. Results: ACE modeling revealed that genetic, as well as shared and non-shared environmental factors explained the overall level of substance use and that these same factors also partly accounted for growth in substance use from age 13 to 17. Additional genetic factors predicted the growth in substance use. Finally, autoregressive effects revealed age-specific non-shared environmental influences and, to a lesser degree, age-specific genetic influences, which together accounted for the stability of substance use across adolescence. Conclusions: The results support and expand the notion that genetic and environmental influences on substance use during adolescence are both developmentally stable and developmentally dynamic. [ABSTRACT FROM AUTHOR]

This review describes a bio-psycho-social approach to understanding and preventing the development of chronic physical aggression. The debate on the developmental origins of aggression has historically opposed genetic and environmental mechanisms. Recent studies have shown that the frequency of physical aggression peaks in early childhood and then decreases until old age. Molecular genetic studies and twin studies have confirmed important genetic influences. However, recent epigenetic studies have highlighted the important role of environments in gene expression and brain development. These studies suggest that interrelated bio-psycho-social channels involved in the development of chronic physical aggression are generally the product of an intergenerational transmission process occurring through assortative mating, genetic inheritance, and the inheritance of physical and social environmental conditions that handicap brain functioning and support the use of physical aggression to solve problems. Given these intergenerational mechanisms and physical aggression onset in infancy, it appears clear that preventive interventions should start early in pregnancy, at the latest. [ABSTRACT FROM AUTHOR]

Background: Few studies are grounded in a developmental framework to study proactive and reactive aggression. Furthermore, although distinctive correlates, predictors and outcomes have been highlighted, proactive and reactive aggression are substantially correlated. To our knowledge, no empirical study has examined the communality of genetic and environmental underpinning of the development of both subtypes of aggression. The current study investigated the communality and specificity of genetic-environmental factors related to heterogeneity in proactive and reactive aggression’s development throughout childhood. Methods: Participants were 223 monozygotic and 332 dizygotic pairs. Teacher reports of aggression were obtained at 6, 7, 9, 10 and 12 years of age. Joint development of both phenotypes were analyzed through a multivariate latent growth curve model. Set point, differentiation, and genetic maturation/environmental modulation hypotheses were tested using a biometric decomposition of intercepts and slopes. Results: Common genetic factors accounted for 64% of the total variation of proactive and reactive aggression’s intercepts. Two other sets of uncorrelated genetic factors accounted for reactive aggression’s intercept (17%) on the one hand, and for proactive (43%) and reactive (13%) aggression’s slopes on the other. Common shared environmental factors were associated with proactive aggression’s intercept (21%) and slope (26%) and uncorrelated shared environmental factors were also associated with reactive aggression’s slope (14%). Common nonshared environmental factors explained most of the remaining variability of proactive and reactive aggression slopes. Conclusions: A genetic differentiation hypothesis common to both phenotypes was supported by common genetic factors associated with the developmental heterogeneity of proactive and reactive aggression in childhood. A genetic maturation hypothesis common to both phenotypes, albeit stronger for proactive aggression, was supported by common genetic factors associated with proactive and reactive aggression slopes. A shared environment set point hypothesis for proactive aggression was supported by shared environmental factors associated with proactive aggression baseline and slope. Although there are many common features to proactive and reactive aggression, the current research underscores the advantages of differentiating them when studying aggression. [ABSTRACT FROM AUTHOR]

Background: Difficult temperament in infancy is a risk factor for forms of later internalizing and externalizing psychopathology, including depression and anxiety. A better understanding of the roots of difficult temperament requires assessment of its early development with a genetically informative design. The goal of this study was to estimate genetic and environmental contributions to individual differences in infant negative emotionality, their persistence over time and their influences on stability between 5 and 18 months of age. Method: Participants were 244 monozygotic and 394 dizygotic twin pairs (49.7% male) recruited from birth. Mothers rated their twins for negative emotionality at 5 and 18 months. Longitudinal analysis of stability and innovation between the two time points was performed in Mplus. Results: There were substantial and similar heritability (approximately 31%) and shared environmental (57.3%) contributions to negative emotionality at both 5 and 18 months. The trait’s interindividual stability across time was both genetically- and environmentally- mediated. Evidence of innovative effects (i.e., variance at 18 months independent from variance at 5 months) indicated that negative emotionality is developmentally dynamic and affected by persistent and new genetic and environmental factors at 18 months. Conclusions: In the first two years of life, ongoing genetic and environmental influences support temperamental negative emotionality but new genetic and environmental factors also indicate dynamic change of those factors across time. A better understanding of the source and timing of factors on temperament in early development, and role of sex, could improve efforts to prevent related psychopathology. [ABSTRACT FROM AUTHOR]

Background: Developmental dyslexia (DD) and attention deficit/hyperactivity disorder (ADHD) are among the most common neurodevelopmental disorders, whose etiology involves multiple risk factors. DD and ADHD co-occur in the same individuals much more often than would be expected by chance. Several studies have found significant bivariate heritability, and specific genes associated with either DD or ADHD have been investigated for association in the other disorder. Moreover, there are likely to be gene-by-gene and gene-by-environment interaction effects (G × G and G × E, respectively) underlying the comorbidity between DD and ADHD. We investigated the pleiotropic effects of 19 SNPs spanning five DD genes (DYX1C1, DCDC2, KIAA0319, ROBO1, and GRIN2B) and seven DD environmental factors (smoke, miscarriage, birth weight, breastfeeding, parental age, socioeconomic status, and parental education) for main, either (a) genetic or (b) environmental, (c) G × G, and (d) G × E upon inattention and hyperactivity/ impulsivity. We then attempted replication of these findings in an independent twin cohort. Methods: Marker-trait association was analyzed by implementing the Quantitative Transmission Disequilibrium Test (QTDT). Environmental associations were tested by partial correlations. G × G were investigated by a general linear model equation and a family-based association test. G × E were analyzed through a general test for G × E in sib pair-based association analysis of quantitative traits. Results: DCDC2-rs793862 was associated with hyperactivity/impulsivity via G × G (KIAA0319) and G × E (miscarriage). Smoke was significantly correlated with hyperactivity/impulsivity. We replicated the DCDC2 × KIAA0319 interaction upon hyperactivity/impulsivity in the twin cohort. Conclusions: DD genetic (DCDC2) and environmental factors (smoke and miscarriage) underlie ADHD traits supporting a potential pleiotropic effect. [ABSTRACT FROM AUTHOR]

De novo mutations (DNM) are an important source of rare variants and are increasingly being linked to the development of many diseases. Recently, the paternal age effect has been the focus of a number of studies that attempt to explain the observation that increasing paternal age increases the risk for a number of diseases. Using disease-free familial quartets we show that there is a strong positive correlation between paternal age and germline DNM in healthy subjects. We also observed that germline CNVs do not follow the same trend, suggesting a different mechanism. Finally, we observed that DNM were not evenly distributed across the genome, which adds support to the existence of DNM hotspots. [ABSTRACT FROM AUTHOR]

This study examined the genetic and environmental architecture of early gambling involvement and substance use to determine whether genetic or environmental factors that contribute to substance use also put young adolescents at risk for early involvement in gambling. Self-reports of substance use and gambling involvement were collected at age 13 years from 279 Monozygotic and Dizygotic twin pairs. Univariate ACE modeling revealed that genetic and nonshared environmental factors almost equally accounted for gambling involvement, with no contribution from shared environmental factors. In contrast, both shared and nonshared environmental factors played important roles in substance use; the contribution of genetic factors was also substantial. Bivariate analyses identified a significant, albeit modest, overlap between the genetic influence on gambling involvement and the genetic influence on substance use. The results shed light on the etiology of early gambling involvement and substance use, suggesting that preventive interventions targeting common risk factors may also need to be complemented by modules that are specific to each behavior. [ABSTRACT FROM AUTHOR]

Background: Chronic physical aggression (CPA) is characterized by frequent use of physical aggression from early childhood to adolescence. Observed in approximately 5% of males, CPA is associated with early childhood adverse environments and long-term negative consequences. Alterations in DNA methylation, a covalent modification of DNA that regulates genome function, have been associated with early childhood adversity. Aims: To test the hypothesis that a trajectory of chronic physical aggression during childhood is associated with a distinct DNA methylation profile during adulthood. Methods: We analyzed genome-wide promoter DNA methylation profiles of T cells from two groups of adult males assessed annually for frequency of physical aggression between 6 and 15 years of age: a group with CPA and a control group. Methylation profiles covering the promoter regions of 20 000 genes and 400 microRNAs were generated using MeDIP followed by hybridization to microarrays. Results: In total, 448 distinct gene promoters were differentially methylated in CPA. Functionally, many of these genes have previously been shown to play a role in aggression and were enriched in biological pathways affected by behavior. Their locations in the genome tended to form clusters spanning millions of bases in the genome. Conclusions: This study provides evidence of clustered and genome-wide variation in promoter DNA methylation in young adults that associates with a history of chronic physical aggression from 6 to 15 years of age. However, longitudinal studies of methylation during early childhood will be necessary to determine if and how this methylation variation in T cells DNA plays a role in early development of chronic physical aggression. [ABSTRACT FROM AUTHOR]

Background: High frequency of physical aggression is the central feature of severe conduct disorder and is associated with a wide range of social, mental and physical health problems. We have previously tested the hypothesis that differential DNA methylation signatures in peripheral T cells are associated with a chronic aggression trajectory in males. Despite the fact that sex differences appear to play a pivotal role in determining the development, magnitude and frequency of aggression, most of previous studies focused on males, so little is known about female chronic physical aggression. We therefore tested here whether or not there is a signature of physical aggression in female DNA methylation and, if there is, how it relates to the signature observed in males. Methodology/Principal Findings: Methylation profiles were created using the method of methylated DNA immunoprecipitation (MeDIP) followed by microarray hybridization and statistical and bioinformatic analyses on T cell DNA obtained from adult women who were found to be on a chronic physical aggression trajectory (CPA) between 6 and 12 years of age compared to women who followed a normal physical aggression trajectory. We confirmed the existence of a well-defined, genome-wide signature of DNA methylation associated with chronic physical aggression in the peripheral T cells of adult females that includes many of the genes similarly associated with physical aggression in the same cell types of adult males. Conclusions: This study in a small number of women presents preliminary evidence for a genome-wide variation in promoter DNA methylation that associates with CPA in women that warrant larger studies for further verification. A significant proportion of these associations were previously observed in men with CPA supporting the hypothesis that the epigenetic signature of early life aggression in females is composed of a component specific to females and another common to both males and females. [ABSTRACT FROM AUTHOR]

Objective This study examined whether (a) a genetic disposition for physical health problems increases the risk of peer victimization and (b) peer victimization interacts with genetic vulnerability in explaining physical health problems. Methods Participants were 167 monozygotic and 119 dizyogtic twin pairs. Physical symptoms were assessed in early childhood and early adolescence. Peer victimization was assessed in middle childhood. Results Genetic vulnerability for physical health problems in early childhood was unrelated to later peer victimization, but genetic vulnerability for physical health problems during early adolescence increased the risk of victimization. Victimization did not interact with genetic factors in predicting physical symptoms. Environmental, not genetic, factors had the greatest influence on the development of physical symptoms in victims. Conclusion Genetic vulnerability for physical health problems in early adolescence increases the risk of peer victimization. Whether victims suffer a further increase in physical symptoms depends on the presence of protective environmental factors. [ABSTRACT FROM AUTHOR]

Background: Animal and human studies suggest that inflammation is associated with behavioral disorders including aggression. We have recently shown that physical aggression of boys during childhood is strongly associated with reduced plasma levels of cytokines IL-1α, IL-4, IL-6, IL-8 and IL-10, later in early adulthood. This study tests the hypothesis that there is an association between differential DNA methylation regions in cytokine genes in T cells and monocytes DNA in adult subjects and a trajectory of physical aggression from childhood to adolescence. Methodology/Principal Findings: We compared the methylation profiles of the entire genomic loci encompassing the IL-1α, IL-6, IL-4, IL-10 and IL-8 and three of their regulatory transcription factors (TF) NFkB1, NFAT5 and STAT6 genes in adult males on a chronic physical aggression trajectory (CPA) and males with the same background who followed a normal physical aggression trajectory (control group) from childhood to adolescence. We used the method of methylated DNA immunoprecipitation with comprehensive cytokine gene loci and TF loci microarray hybridization, statistical analysis and false discovery rate correction. We found differentially methylated regions to associate with CPA in both the cytokine loci as well as in their transcription factors loci analyzed. Some of these differentially methylated regions were located in known regulatory regions whereas others, to our knowledge, were previously unknown as regulatory areas. However, using the ENCODE database, we were able to identify key regulatory elements in many of these regions that indicate that they might be involved in the regulation of cytokine expression. Conclusions: We provide here the first evidence for an association between differential DNA methylation in cytokines and their regulators in T cells and monocytes and male physical aggression. [ABSTRACT FROM AUTHOR]

The study examined whether reciprocal friendship quantity or quality can mitigate genetic vulnerability for depression symptoms in children. The sample comprised 168 monozygotic twin pairs and 126 same-sex dizygotic twin pairs assessed in Grade 4 (mean age = 10.04 years). Friendship participation was measured via reciprocal nominations of close friendships within the classroom. Friendship quality was measured through self-reports. Depression symptoms were measured through teacher and peer reports. Genetic vulnerability for depression symptoms was unrelated to friendship participation or the number of reciprocal friends, but it was negatively related to positive friendship quality. In line with gene–environment interaction, genetic risk effects on depression symptoms were mitigated in girls who had at least one close reciprocal friend. In boys, only moderate main effects of genetic vulnerability and friendship participation were found but no interaction between them. However, among boys with at least one reciprocal friend, a greater number of friends was related to fewer depression symptoms whereas no cumulative effect of friendship was found for girls. Finally, positive friendship quality was related to fewer depression symptoms in girls and boys even when controlling for genetic risk. The findings emphasize the importance of teaching social interactional skills that promote high-quality friendship relations to help prevent the development of depression symptoms in children. [ABSTRACT FROM AUTHOR]

Background: The polyamine system has been implicated in a number of psychiatric conditions, which display both alterations in polyamine levels and altered expression of genes related to polyamine metabolism. Studies have identified associations between genetic variants in spermidine/spermine N1-acetyltransferase (SAT1) and both anxiety and suicide, and several polymorphisms appear to play important roles in determining gene expression. Methodology/Principal Findings: We genotyped 63 polymorphisms, spread across four polyaminergic genes (SAT1, spermine synthase (SMS), spermine oxidase (SMOX), and ornithine aminotransferase like-1 (OATL1)), in 1255 French-Canadian individuals who have been followed longitudinally for 22 years. We assessed univariate associations with anxiety, mood disorders, and attempted suicide, as assessed during early adulthood. We also investigated the involvement of gene-environment interactions in terms of childhood abuse, and assessed internalizing and externalizing symptoms as endophenotypes mediating these interactions. Overall, each gene was associated with at least one main outcome: anxiety (SAT1, SMS), mood disorders (SAT1, SMOX), and suicide attempts (SAT1, OATL1). Several SAT1 polymorphisms displayed disease-specific risk alleles, and polymorphisms in this gene were involved in gene-gene interactions with SMS to confer risk for anxiety disorders, as well as gene-environment interactions between childhood physical abuse and mood disorders. Externalizing behaviors demonstrated significant mediation with regards to the association between OATL1 and attempted suicide, however there was no evidence that externalizing or internalizing behaviors were appropriate endophenotypes to explain the associations with mood or anxiety disorders. Finally, childhood sexual abuse did not demonstrate mediating influences on any of our outcomes. Conclusions/Significance: These results demonstrate that genetic variants in polyaminergic genes are associated with psychiatric conditions, each of which involves a set of separate and distinct risk alleles. As several of these polymorphisms are associated with gene expression, these findings may provide mechanisms to explain the alterations in polyamine metabolism which have been observed in psychiatric disorders. [ABSTRACT FROM AUTHOR]

Although peer victimization places children at serious risk for aggressive behavior, not all victimized children are aggressive. The diathesis–stress hypothesis of disease proposes that an environmental stressor such as peer victimization should to lead to maladjustment mostly in those individuals with preexisting genetic vulnerabilities. Accordingly, this study examined whether the link between peer victimization and child aggression is moderated by children's genetic risk for such behavior. Using a sample of 506 6-year-old twins, peer victimization was assessed through peer nominations and aggressive behavior was assessed through peer and teacher reports. Children's genetic risk for aggression was estimated as a function of their co-twin's aggression and the pair's zygosity. Genetic modeling showed that peer victimization is an environmentally driven variable that is unrelated to children's genetic disposition. Results also provided support for the notion of a gene–environment interaction between peer victimization and child's genetic risk for aggressive behavior, albeit only in girls. For boys, peer victimization was related to aggression regardless of the child's genetic risk for such behavior. Different socialization experiences in girls' compared to boys' peer groups may explain the different pattern of results for girls and boys. [ABSTRACT FROM PUBLISHER]

Using a genetic design of 234 six-year-old twins, this study examined (a) the contribution of genes and environment to social versus physical aggression, and (b) whether the correlation between social and physical aggression can be explained by similar genetic or environmental factors or by a directional link between the phenotypes. For social aggression, substantial (shared and unique) environmental effects but only weak genetic effects were found. For physical aggression, significant effects of genes and unique environment were found. Bivariate modeling suggests that social and physical aggression share most of their underlying genes but only very few overlapping environmental factors. The correlation between the two phenotypes can also be explained by a directional effect from physical to social aggression. [ABSTRACT FROM AUTHOR]

Many youths who are victimized by peers suffer from depression symptoms. However, not all bullying victims show depression symptoms and individuals’ biological sensitivity may play an important moderating role in this regard. In line with this notion, peer victimization has been associated with increased depressive symptoms in youth with higher basal cortisol secretion. It is unclear, however, whether this moderating effect of cortisol really concerns the environmental effect of peer victimization on depression. Indeed, genetic factors can also influence individuals’ environmental experiences, including peer victimization, and part of these genetic factors may be those associated with depression. Using a genetically informed design based on 159 monozygotic and 120 dizygotic twin pairs (52% girls) assessed at age 14 years, this study examined whether cortisol secretion moderates the environmental or the genetic association between peer victimization and depression symptoms. Salivary cortisol at awakening was obtained with buccal swabs during four school week days. Peer victimization and depression were assessed via self-reports. Cholesky modeling revealed that peer victimization was associated with depression symptoms via both genetic and environmental pathways. Moreover, the environmental association between peer victimization and depression symptoms steadily increased with increasing levels of morning cortisol. The genetic association between peer victimization and depression symptoms also varied, albeit less, as a function of individuals’ cortisol secretion. These findings support the hypothesis that peer victimization increases internalizing psychopathology mainly in youth with heightened biological reactivity to environmental conditions. [ABSTRACT FROM AUTHOR]

Background: The tropomyosin-related kinase B (TrkB)/brain-derived neurotrophic factor system has been associated with psychiatric disorders, and animal models of defects in this system suggest that it might have a particular role in anxiety. Methods: DNA sequencing and cloning were used to identify a mutation in TrkB, and four different cell lines were used to assess functionality. Clinical samples were from a 22-year longitudinal cohort representative of the Quebec general population (n = 640 subjects), randomly selected when they were in kindergarten. Anxiety-related traits were measured with the Social Behaviour Questionnaire, the Diagnostic Assessment of Personality Pathology-Brief Questionnaire, and the Diagnostic Interview Schedule for DSM-IIIR. Results: An 11 base pair deletion in TrkB is significantly associated with increases in anxiety traits during childhood and the development of anxiety disorders in adulthood. We found that this deletion impaired transcription in some human cell lines. Conclusions: The identification of this deletion provides additional support for the role of TrkB in modulating anxiety-related traits in human. [ABSTRACT FROM AUTHOR]

Objective: To examine whether kindergarten children's genetic liability to physically aggress moderates the contribution of friends' aggression to their aggressive behaviors.Method: Teacher and peer reports of aggression were available for 359 6-year-old twin pairs (145 MZ, 212 DZ) as well as teacher and peer reports of aggression of the two best friends of each twin. Children's genetic risk for aggression was based on their cotwin's aggression status and the pair's zygosity.Results: Children's aggression was highly heritable. Unique environment accounted for most of the variance in friends' aggression, although there was also a small genetic contribution (15%). Both genetic liability to aggression and having aggressive friends predicted twins' aggression. However, the contribution of aggressive friends to children's aggression was strongest among genetically vulnerable children. This result was similar for boys and girls, despite sex differences in both aggression and the level of aggression of friends.Conclusions: Affiliation with aggressive friends at school entry is a significant environmental risk factor for aggression, especially for children genetically at risk for aggressive behaviors. Developmental models of aggression need to take into account both genetic liability and environmental factors in multiple settings, such as the peer context, to more precisely describe and understand the various developmental pathways to aggression. The implications for early prevention programs are discussed. [ABSTRACT FROM AUTHOR]