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This study aimed to identify joint trajectories of peer cyber and traditional victimization from ages 13 to 17 and individual, family, peer, and school risk factors associated with group membership. The sample was composed of 1,194 adolescents (54.2% girls). Cyber and traditional victimization were assessed at ages 13, 15, and 17. The results first revealed a low/increasing and a high/decreasing trajectories for cybervictimization and a low/decreasing and a moderate/chronic for traditional victimization. Conditional probabilities suggested that cybervictims had a high probability of being victims on school grounds, whereas traditional victims were not necessarily the target of cybervictimization. Four joint trajectory groups were also identified. With the low victimization group as the reference category, the results revealed that different sets of predictors were associated with membership in the three other joint trajectory groups. The results are discussed in relation to intervention and prevention strategies.

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.

This study aimed to identify joint trajectories of peer cyber and traditional victimization from ages 13 to 17 and individual, family, peer, and school risk factors associated with group membership. The sample was composed of 1,194 adolescents (54.2% girls). Cyber and traditional victimization were assessed at ages 13, 15, and 17. The results first revealed a low/increasing and a high/decreasing trajectories for cybervictimization and a low/decreasing and a moderate/chronic for traditional victimization. Conditional probabilities suggested that cybervictims had a high probability of being victims on school grounds, whereas traditional victims were not necessarily the target of cybervictimization. Four joint trajectory groups were also identified. With the low victimization group as the reference category, the results revealed that different sets of predictors were associated with membership in the three other joint trajectory groups. The results are discussed in relation to intervention and prevention strategies.

Purpose - The goal of this study was to test a new approach to deviancy training, that is, the shaping and reinforcing of disruptive behaviors in social interaction, which considers not only reinforcement, but also the modeling processes involved, as well as children’s roles as either providers or receivers of the training. Design/Methodology/Approach - Using teacher reports and observations from a semi naturalistic experimental setting with young children, we examined the prevalence of provided and received modeling and positive reinforcement, as well as the concurrent contribution of behavior problems on these processes in friendship dyads using a convenience sample of six year old twins (N = 783; 386 boys). Frequency analyses and linear and logistic regressions were conducted. Findings - Results indicated that modeling and positive reinforcement – provided and received – were prevalent in this low-risk sample, that behavior problems were associated mainly with provided dimensions, and that deviancy training processes were also displayed between disruptive and non-disruptive children. Practical implications – Findings are relevant to peer oriented programs designed to prevent antisocial behaviors. Prevention should target these mixed friendships where deviant behavior likely begins. Originality/value - This study provides preliminary support for a new measure of deviancy training, underscores the importance of the roles taken by children, and shows that deviancy training takes place between disruptive and non-disruptive young children.

Background: Proactive aggression (PA) describes an instrumental behavior that is goal-oriented, whereas reactive aggression (RA) refers to an angry or frustrated aggressive response to a real or perceived threat. Little is known about the respective roles of genetic (G) and environmental (E) factors associated with PA and RA during childhood. The objectives of this study were to investigate a) the G-E etiology of the commonality between PA and RA and b) the presence of G or E components specific to PA or RA throughout childhood (i.e., from 6 to 12 years of age). Methods: Participants were 254 monozygotic and 413 dizygotic pairs. Teacher reports of PA and RA were obtained at 6, 7, 9, 10 and 12 years of age. Results: Throughout childhood, genetic factors accounted for most of the common variance between PA and RA, as well as their specificity. Shared environment played no role. Specifically, genetic factors common to PA and RA explained between 39% and 45% of the variance in PA, and between 27% and 42% of the variance in RA. Genetic factor also uniquely accounted for only but a small percentage (9% at 6 years and 3% at 9 years old) of the variation in PA. As for RA, three distinctive genetic factors contributed to phenotypic variation throughout childhood and explained between 12% and 22% of variance. Conclusions: Dynamic genetic factors accounted for the commonality in PA and RA, and for the specificity of RA. Few genetic factors were unique to PA; in contrast, for RA, an early, specific and persistent genetic factor was found alongside new genetic factors that appeared at later ages. These results challenge theoretical models that focus primarily on the effects of environmental factors in the etiology of reactive and proactive aggression.

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.

BACKGROUND : Previous gene-environment interaction studies of CU traits have relied on the candidate gene approach, which does not account for the entire genetic load of complex phenotypes. Moreover, these studies have not examined the role of positive environmental factors such as warm/rewarding parenting. The aim of the present study was to determine whether early warm/rewarding parenting moderates the genetic contributions (i.e., heritability) to callous-unemotional (CU) traits at school age. METHODS : Data were collected in a population sample of 662 twin pairs (Quebec Newborn Twin Study - QNTS). Mothers reported on their warm/rewarding parenting. Teachers assessed children's CU traits. These reports were subjected to twin modeling. RESULTS : Callous-unemotional traits were highly heritable, with the remaining variance accounted for by nonshared environmental factors. Warm/rewarding parenting significantly moderated the role of genes in CU traits; heritability was lower when children received high warm/rewarding parenting than when they were exposed to low warm/rewarding parenting. CONCLUSIONS : High warm/rewarding parenting may partly impede the genetic expression of CU traits. Developmental models of CU traits need to account for such gene-environment processes.

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.

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.

Background: Several studies have shown that the in utero environment, which can be indexed by birth weight (BW), is associated with cortical morphology in adolescence and adulthood. Work in monozygotic (MZ) twins suggests that this association is driven by non‐shared environmental factors. This correlation could be the result of in utero impacts on DNA methylation. The aim of the present study with MZ twins is to replicate the association between discordance in BW and brain morphology and test whether discordance in DNA methylation mediates this relationship. Methods: One hundred and four adolescent MZ twins (52 pairs, of which 42% were male pairs) who have been followed regularly since birth underwent T1 weighted structural MRI, and epigenome‐wide assessment of DNA methylation from saliva at age 15. Results: Co‐twins had very similar measures of DNA methylation and cortical morphology. Higher BW members of a twin pair had increased total cortical surface area, and decreased cortical thickness compared to their lower BW sibling. BW Discordance was positively associated with both cortical surface area and cortical volume discordance. Genes involved in neurodevelopment were tentatively identified as mediators of both the BW ‐ cortical volume, and BW‐ cortical surface area relationships. Conclusions: The association between BW and cortical morphology in adolescence appears to be attributable to in utero environmental effects, and DNA methylation may play a role in mediating this relationship

Prenatal and early postnatal adversities have been shown to be associated with brain development. However, we do not know how much of this association is confounded by genetics, nor whether the postnatal environment can moderate the impact of in utero adversity. This study used a monozygotic (MZ) twin design to assess (1) the association between birth weight (BW) and brain volume in adolescence, (2) the association between within-twin-pair BW discordance and brain volume discordance in adolescence, and (3) whether the association between BW and brain volume in adolescence is mediated or moderated by early negative maternal parenting behaviours. These associations were assessed in a sample of 108 MZ twins followed longitudinally since birth and scanned at age 15. The total grey matter (GM) and white matter (WM) volumes were obtained using the Diffeomorphic Anatomical Registration Through Exponentiated Lie Algebra (DARTEL) toolbox in the Statistical Parametric Mapping version 8 (SPM8). We found that the BW was significantly associated with the total GM and WM volumes, particularly in the superior frontal gyrus and thalamus. Within-twin-pair discordance in BW was also significantly associated with within-pair discordance in both the GM and the WM volumes, supporting the hypothesis that the specific in utero environment is associated with brain development independently of genetics. Early maternal hostile parenting behaviours and depressive symptoms were associated with total GM volume but not WM volume. Finally, greater early maternal hostility may moderate the association between the BW and GM volume in adolescence, since the positive association between the BW and total GM volume appeared stronger at higher levels of maternal hostility (trend). Together, these findings support the importance of the in utero and early environments for brain development.

Objective: Exposure to maternal depression during early childhood is a well-documented risk factor for offspring’s internalizing problems, but the long-term risk and the psychosocial mechanisms underlying the association remain largely unknown. We examined whether maternal depression during early childhood was associated with offspring internalizing problems in adolescence, and the extent to which negative parenting, peer victimization, and poor friendship quality during middle childhood mediated this association. Method: We report on a population-based sample of children (n = 1,443) followed-up from 5 months to 15 years. We use yearly assessments of the exposure variable, that is, maternal depression (5 months to 5 years); the putative mediators, that is, peer victimization, friendship quality, and parenting practices (6−12 years); and assessment of the outcome variables at 15 years: self-reported major depressive (MD), generalized anxiety (GA), and social phobia (SP) symptoms. Structural equation modeling was used to test mediation by peer and family relationships. Results: Exposure to maternal depression during early childhood was associated with higher levels of adolescent MD, GA, and SP. Peer victimization was the only significant mediator and explained 35.9% of the association with adolescent MD, 22.1% of that with GA, and 22.1% of that with SP. Conclusion: Exposure to maternal depression prior to age 5 years was associated with depression, anxiety, and social phobia extending to adolescence via its impact on peer victimization during middle childhood. Particular attention should be paid to victimization as one potential psychosocial factor via which maternal depression is associated with adolescent internalizing problems.

BACKGROUND : Previous gene-environment interaction studies of CU traits have relied on the candidate gene approach, which does not account for the entire genetic load of complex phenotypes. Moreover, these studies have not examined the role of positive environmental factors such as warm/rewarding parenting. The aim of the present study was to determine whether early warm/rewarding parenting moderates the genetic contributions (i.e., heritability) to callous-unemotional (CU) traits at school age. METHODS : Data were collected in a population sample of 662 twin pairs (Quebec Newborn Twin Study - QNTS). Mothers reported on their warm/rewarding parenting. Teachers assessed children's CU traits. These reports were subjected to twin modeling. RESULTS : Callous-unemotional traits were highly heritable, with the remaining variance accounted for by nonshared environmental factors. Warm/rewarding parenting significantly moderated the role of genes in CU traits; heritability was lower when children received high warm/rewarding parenting than when they were exposed to low warm/rewarding parenting. CONCLUSIONS : High warm/rewarding parenting may partly impede the genetic expression of CU traits. Developmental models of CU traits need to account for such gene-environment processes.

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.

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.

Gambling participation and low academic performance are related during adolescence, but the causal mechanisms underlying this link are unclear. It is possible that gambling participation impairs academic performance. Alternatively, the link between gambling participation and low academic performance could be explained by common underlying risk factors such as impulsivity and socio-family adversity. It could also be explained by other current correlated problem behaviors such as substance use. The goal of the present study was to examine whether concurrent and longitudinal links between gambling participation and low academic performance exist from age 14 to age 17 years, net of common antecedent factors and current substance use. A convenience sample of 766 adolescents (50.6% males) from a longitudinal twin sample participated in the study. Analyses revealed significant, albeit modest, concurrent links at both ages between gambling participation and academic performance. There was also a longitudinal link between gambling participation at age 14 and academic performance at age 17, which persisted after controlling for age 12 impulsivity and socio-family adversity as well as current substance use. Gambling participation predicts a decrease in academic performance during adolescence, net of concurrent and antecedent personal and familial risk factors.

Objective Exposure to maternal depression during early childhood is a well-documented risk factor for offspring’s internalizing problems, but the long-term risk and the psychosocial mechanisms underlying the association remain largely unknown. We examined whether maternal depression during early childhood was associated with offspring internalizing problems in adolescence, and the extent to which negative parenting, peer victimization, and poor friendship quality during middle childhood mediated this association. Method We report on a population-based sample of children (n = 1,443) followed-up from 5 months to 15 years. We use yearly assessments of the exposure variable, that is, maternal depression (5 months to 5 years); the putative mediators, that is, peer victimization, friendship quality, and parenting practices (6−12 years); and assessment of the outcome variables at 15 years: self-reported major depressive (MD), generalized anxiety (GA), and social phobia (SP) symptoms. Structural equation modeling was used to test mediation by peer and family relationships. Results Exposure to maternal depression during early childhood was associated with higher levels of adolescent MD, GA, and SP. Peer victimization was the only significant mediator and explained 35.9% of the association with adolescent MD, 22.1% of that with GA, and 22.1% of that with SP. Conclusion Exposure to maternal depression prior to age 5 years was associated with depression, anxiety, and social phobia extending to adolescence via its impact on peer victimization during middle childhood. Particular attention should be paid to victimization as one potential psychosocial factor via which maternal depression is associated with adolescent internalizing problems.

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, G×E). 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 (G×E). 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 G×E, 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 (G×E).

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.

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.

Gambling participation and low academic performance are related during adolescence, but the causal mechanisms underlying this link are unclear. It is possible that gambling participation impairs academic performance. Alternatively, the link between gambling participation and low academic performance could be explained by common underlying risk factors such as impulsivity and socio-family adversity. It could also be explained by other current correlated problem behaviors such as substance use. The goal of the present study was to examine whether concurrent and longitudinal links between gambling participation and low academic performance exist from age 14 to age 17 years, net of common antecedent factors and current substance use. A convenience sample of 766 adolescents (50.6% males) from a longitudinal twin sample participated in the study. Analyses revealed significant, albeit modest, concurrent links at both ages between gambling participation and academic performance. There was also a longitudinal link between gambling participation at age 14 and academic performance at age 17, which persisted after controlling for age 12 impulsivity and socio-family adversity as well as current substance use. Gambling participation predicts a decrease in academic performance during adolescence, net of concurrent and antecedent personal and familial risk factors.

Multiple studies have shown that reading abilities and attention-deficit/hyperactivity disorder symptoms, mainly inattention symptoms, are phenotypically and genetically associated during childhood. However, few studies have looked at these associations during adolescence to investigate possible developmental changes. The aim of the study is to examine the genetic and environmental etiology of the associations between inattention and hyperactivity reported by parents, and reading accuracy, reading speed, and word reading in a population-based twin sample (Quebec Newborn Twin Study). Participants were between 14 and 15 years of age at the time of testing (N = 668-837). Phenotypic results showed that when nonverbal and verbal abilities were controlled, inattention, but not hyperactivity/impulsivity, was a modest and significant predictor of reading accuracy, reading speed, and word reading. The associations between inattention and all reading abilities were partly explained by genetic and unique environmental factors. However, the genetic correlations were no longer significant after controlling for verbal abilities. In midadolescence, inattention is the attention-deficit/hyperactivity disorder dimension associated with reading abilities, but they could also share genetic factors with general verbal skills.

This study investigated the stable and transient genetic and environmental contributions to individual differences in number knowledge in the transition from preschool (age 5) to Grade 1 (age 7) and to the predictive association between early number knowledge and later math achievement (age 10–12). We conducted genetic simplex modeling across these three time points. Genetic variance was transmitted from preschool number knowledge to late-elementary math achievement; in addition, significant genetic innovation (i.e., new influence) occurred at ages 10 through 12 years. The shared and nonshared environmental contributions decreased during the transition from preschool to school entry, but shared and nonshared environment contributed to the continuity across time from preschool number knowledge to subsequent number knowledge and math achievement. There was no new environmental contribution at time points subsequent to preschool. Results are discussed in light of their practical implications for children who have difficulties with mathematics, as well as for preventive intervention.

Objective – To test the associations between the timing and chronicity of maternal depression symptoms (MDS) and children’s long term verbal abilities. Study Design – Participants were n=1073 mother-child pairs from a population-based birth cohort in Canada. MDS were assessed at ages 5 months, 1½, 3½, and 5 years using the Center for Epidemiologic Studies Depression Scale (CES-D). Verbal abilities were measured at 5, 6, and 10 years using the Peabody Picture Vocabulary Test-Revised (PPVT-R). Multiple linear regression models were used to estimate the association between timing (early: 5 months and/or 1½ years vs late: 3½ and/or 5 years) and chronicity (5 months, 1½, 3½ and 5 years) of exposure to elevated MDS and children’s mean PPVT-R scores. Results – Children exposed to chronic MDS had lower PPVT-R scores than children never exposed (Mean difference=9.04[95%CI=2.28-15.80]), exposed early (10.08[3.33-16.86]) and exposed late (8.69[1.85-15.53]). There were no significant differences between scores of children in the early compared to the late exposure group (1.41[-1.11-3.93]). We controlled for mother-child interactions, family functioning, SES, PPVT-R administration language, child’s birth order, and maternal IQ, psychopathology, education, native language, age at birth of child, and parenting practices. Maternal IQ, (h2 =0.028), native language (h2 =0.009), and MDS (h2 =0.007) had the largest effect sizes. Conclusion – Exposure to chronic MDS in early childhood is associated with lower levels of verbal abilities in middle childhood. Further research is needed in larger community samples to test the association between MDS and children’s long term language skills.

This study investigated the stable and transient genetic and environmental contributions to individual differences in number knowledge in the transition from preschool (age 5) to Grade 1 (age 7) and to the predictive association between early number knowledge and later math achievement (age 10–12). We conducted genetic simplex modeling across these three time points. Genetic variance was transmitted from preschool number knowledge to late-elementary math achievement; in addition, significant genetic innovation (i.e., new influence) occurred at ages 10 through 12 years. The shared and nonshared environmental contributions decreased during the transition from preschool to school entry, but shared and nonshared environment contributed to the continuity across time from preschool number knowledge to subsequent number knowledge and math achievement. There was no new environmental contribution at time points subsequent to preschool. Results are discussed in light of their practical implications for children who have difficulties with mathematics, as well as for preventive intervention.

Introduction By and large, studies have reported moderate contributions of genetic factors to cortisol secreted in the early morning and even smaller estimates later in the day. In contrast, the cortisol awakening response (CAR) has shown much stronger heritability estimates, which prompted the hypothesis that the etiology of cortisol secretion may vary according to the time of day. A direct test of this possibility has, however, not yet been performed. Objective To describe the specific and common etiology of the CAR, awakening level and cortisol change from morning to evening in an age-homogenous sample of twin adolescents. Methods A total of 592 participants of the Québec Newborn Twin Study, a population-based 1995–1998 cohort of families with twins in Canada, have collected saliva at awakening, 30 min later, at the end of afternoon and in the evening over four collection days. Results Multivariate Cholesky models showed both specific and common sources of variance between the CAR, awakening and cortisol diurnal change. The CAR had the strongest heritability estimates, which, for the most part, did not overlap with the other indicators. Conversely, similar magnitudes of genetic and environmental contributions were detected at awakening and for diurnal change, which partially overlapped. Conclusion Our study unraveled differences between the latent etiologies of the CAR and the rest of the diurnal cycle, which may contribute to identify regulatory genes and environments and detangle how these indicators each relate to physical and mental health.

BACKGROUND: Both genetic and environmental factors are known to affect body mass index (BMI), but detailed understanding of how their effects differ during childhood and adolescence is lacking. OBJECTIVES: We analyzed the genetic and environmental contributions to BMI variation from infancy to early adulthood and the ways they differ by sex and geographic regions representing high (North America and Australia), moderate (Europe), and low levels (East Asia) of obesogenic environments. DESIGN: Data were available for 87,782 complete twin pairs from 0.5 to 19.5 y of age from 45 cohorts. Analyses were based on 383,092 BMI measurements. Variation in BMI was decomposed into genetic and environmental components through genetic structural equation modeling. RESULTS: The variance of BMI increased from 5 y of age along with increasing mean BMI. The proportion of BMI variation explained by additive genetic factors was lowest at 4 y of age in boys (a(2) = 0.42) and girls (a(2) = 0.41) and then generally increased to 0.75 in both sexes at 19 y of age. This was because of a stronger influence of environmental factors shared by co-twins in midchildhood. After 15 y of age, the effect of shared environment was not observed. The sex-specific expression of genetic factors was seen in infancy but was most prominent at 13 y of age and older. The variance of BMI was highest in North America and Australia and lowest in East Asia, but the relative proportion of genetic variation to total variation remained roughly similar across different regions. CONCLUSIONS: Environmental factors shared by co-twins affect BMI in childhood, but little evidence for their contribution was found in late adolescence. Our results suggest that genetic factors play a major role in the variation of BMI in adolescence among populations of different ethnicities exposed to different environmental factors related to obesity.

Introduction: In the last decades, cortisol has been extensively studied in association to early exposure to adversity as well as in the etiology of a number of physical and mental problems. While saliva and blood samples allow the measurement of acute changes in cortisol secretion, hair samples are thought to provide a valid retrospective measure of chronic cortisol secretion over an extended period of time. Nevertheless, the existing protocol for hair collection involves considerable financial and logistical challenges when performed in large epidemiological studies. Objective: This study aimed to validate an adapted collection protocol asking participants to sample their hair at home and to send it back to our laboratory by regular mail. Methods: Participants were 34 teenagers between 17 and 18 years of age. They participated in two hair collections: (a) at home, with the help of someone they know, and (b) in our laboratory, with a trained research assistant. Results: We noted a strong correlation between cortisol ascertained from hair collected at home and at the laboratory. No mean difference in cortisol levels could be detected between the two protocols. Moreover, we showed that a wide range of hair-related, sociodemographic, lifestyle factors that may be associated with hair cortisol levels did not affect the association between cortisol measures derived from each protocol. Conclusion: Our study provides initial support that reliable measures of chronic cortisol secretion could be obtained by asking adolescents to collect a sample of their hair at home and send them to the laboratory by regular mail. This adapted protocol has considerable financial and logistical advantages in large epidemiological studies.

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 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.

Introduction: By and large, studies have reported moderate contributions of genetic factors to cortisol secreted in the early morning and even smaller estimates later in the day. In contrast, the cortisol awakening response (CAR) has shown much stronger heritability estimates, which prompted the hypothesis that the etiology of cortisol secretion may vary according to the time of day. A direct test of this possibility has, however, not yet been performed. Objective: To describe the specific and common etiology of the CAR, awakening level and cortisol change from morning to evening in an agehomogenous sample of twin adolescents. Methods: A total of 592 participants of the Québec Newborn Twin Study, a population-based 1995-1998 cohort of families with twins in Canada, have collected saliva at awakening, 30 minutes later, at the end of afternoon and in the evening over four collection days. Results: Multivariate Cholesky model showed both specific and common sources of variance between the CAR, awakening and cortisol diurnal change. The CAR had the strongest heritability estimates, which, for the most part, did not overlap with the other indicators. Conversely, similar magnitudes of genetic and environmental contributions were detected at awakening and for diurnal change, which partially overlapped. Conclusion: Our study unraveled differences between the latent etiologies of the CAR and the rest of the diurnal cycle, which may contribute to identify regulatory genes and environments and detangle how these indicators each relate to physical and mental health.

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.

BACKGROUND: Both genetic and environmental factors are known to affect body mass index (BMI), but detailed understanding of how their effects differ during childhood and adolescence is lacking. OBJECTIVES: We analyzed the genetic and environmental contributions to BMI variation from infancy to early adulthood and the ways they differ by sex and geographic regions representing high (North America and Australia), moderate (Europe), and low levels (East Asia) of obesogenic environments. DESIGN: Data were available for 87,782 complete twin pairs from 0.5 to 19.5 y of age from 45 cohorts. Analyses were based on 383,092 BMI measurements. Variation in BMI was decomposed into genetic and environmental components through genetic structural equation modeling. RESULTS: The variance of BMI increased from 5 y of age along with increasing mean BMI. The proportion of BMI variation explained by additive genetic factors was lowest at 4 y of age in boys (a(2) = 0.42) and girls (a(2) = 0.41) and then generally increased to 0.75 in both sexes at 19 y of age. This was because of a stronger influence of environmental factors shared by co-twins in midchildhood. After 15 y of age, the effect of shared environment was not observed. The sex-specific expression of genetic factors was seen in infancy but was most prominent at 13 y of age and older. The variance of BMI was highest in North America and Australia and lowest in East Asia, but the relative proportion of genetic variation to total variation remained roughly similar across different regions. CONCLUSIONS: Environmental factors shared by co-twins affect BMI in childhood, but little evidence for their contribution was found in late adolescence. Our results suggest that genetic factors play a major role in the variation of BMI in adolescence among populations of different ethnicities exposed to different environmental factors related to obesity.

Introduction: In the last decades, cortisol has been extensively studied in association to early exposure to adversity as well as in the etiology of a number of physical and mental problems. While saliva and blood samples allow the measurement of acute changes in cortisol secretion, hair samples are thought to provide a valid retrospective measure of chronic cortisol secretion over an extended period of time. Nevertheless, the existing protocol for hair collection involves considerable financial and logistical challenges when performed in large epidemiological studies. Objective: This study aimed to validate an adapted collection protocol asking participants to sample their hair at home and to send it back to our laboratory by regular mail. Methods: Participants were 34 teenagers between 17 and 18 years of age. They participated in two hair collections: a) at home, with the help of someone they know, and b) in our laboratory, with a trained research assistant. Results: We noted a strong correlation between cortisol ascertained from hair collected at home and at the laboratory. No mean difference in cortisol levels could be detected between the two protocols. Moreover, we showed that a wide range of hair-related, sociodemographic, lifestyle factors that may be associated with hair cortisol levels did not affect the association between cortisol measures derived from each protocol. Conclusion: Our study provides initial support that reliable measures of chronic cortisol secretion could be obtained by asking adolescents to collect a sample of their hair at home and send them to the laboratory by regular mail. This adapted protocol has considerable financial and logistical advantages in large epidemiological studies.

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 (GxG and GxE, 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 1) genetic or 2) environmental, 3) G×G, and 4) 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. GxG were investigated by a general linear model equation and a family-based association test. GxE were analyzed through a general test for GxE 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.

Background: Several studies have shown that the in utero environment, which can be indexed by birth weight (BW), is associated with cortical morphology in adolescence and adulthood. Work in monozygotic (MZ) twins suggests that this association is driven by non‐shared environmental factors. This correlation could be the result of in utero impacts on DNA methylation. The aim of the present study with MZ twins is to replicate the association between discordance in BW and brain morphology and test whether discordance in DNA methylation mediates this relationship. Methods: One hundred and four adolescent MZ twins (52 pairs, of which 42% were male pairs) who have been followed regularly since birth underwent T1 weighted structural MRI, and epigenome‐wide assessment of DNA methylation from saliva at age 15. Results: Co‐twins had very similar measures of DNA methylation and cortical morphology. Higher BW members of a twin pair had increased total cortical surface area, and decreased cortical thickness compared to their lower BW sibling. BW Discordance was positively associated with both cortical surface area and cortical volume discordance. Genes involved in neurodevelopment were tentatively identified as mediators of both the BW ‐ cortical volume, and BW‐ cortical surface area relationships. Conclusions: The association between BW and cortical morphology in adolescence appears to be attributable to in utero environmental effects, and DNA methylation may play a role in mediating this relationship

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.

Multiple studies have shown that reading abilities and attention-deficit/hyperactivity disorder symptoms, mainly inattention symptoms, are phenotypically and genetically associated during childhood. However, few studies have looked at these associations during adolescence to investigate possible developmental changes. The aim of the study is to examine the genetic and environmental etiology of the associations between inattention and hyperactivity reported by parents, and reading accuracy, reading speed, and word reading in a population-based twin sample (Quebec Newborn Twin Study). Participants were between 14 and 15 years of age at the time of testing (N = 668-837). Phenotypic results showed that when nonverbal and verbal abilities were controlled, inattention, but not hyperactivity/impulsivity, was a modest and significant predictor of reading accuracy, reading speed, and word reading. The associations between inattention and all reading abilities were partly explained by genetic and unique environmental factors. However, the genetic correlations were no longer significant after controlling for verbal abilities. In midadolescence, inattention is the attention-deficit/hyperactivity disorder dimension associated with reading abilities, but they could also share genetic factors with general verbal skills.

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

Comorbidity is frequent among disruptive behaviors (DB) and leads to mental health problems during adolescence and adulthood. However, the early developmental origins of this comorbidity have so far received little attention. This study investigated the developmental comorbidity of three DB categories during early childhood: hyperactivity-impulsivity, non-compliance, and physical aggression. Joint developmental trajectories of DB were identified based on annual mother interviews from age 1½ to 5 years, in a population-representative birth-cohort (N = 2045). A significant proportion of children (13 % to 21 %, depending on the type of DB) consistently displayed high levels of hyperactivity-impulsivity, non-compliance, or physical aggression from age 1½ to 5 years. Developmental comorbidity was frequent, especially for boys: 10 % of boys and 3.7 % of girls were on a stable trajectory with high levels of symptoms for the three categories of DB. Significant associations were observed between preschool joint-trajectories of DB and indicators of DB and school adjustment assessed by teachers in first grade. Preschoolers who maintained high levels of hyperactivity-impulsivity, non-compliance, and physical aggression, displayed the highest number of DB symptoms in first grade for all categories according to their teacher. They were also among the most disadvantaged of their class for school adjustment indicators. Thus, DB manifestations and developmental comorbidity of DB are highly prevalent in infancy. Early childhood appears to be a critical period to prevent persistent and comorbid DB that leads to impairment at the very beginning of school attendance and to long-term serious health and social adjustment problems.

In both adolescents and adults, gambling problems and depressive symptoms co-occur and share some common risk factors (e.g., impulsivity and socio-family risk). However, little is known about (1) the developmental course of the co-morbidity of these problems; (2) variables that may moderate the effect of these common risk factors on gambling problems and depressive symptoms. Of specific interest could be individuals’ social relationships with significant others such as parents and friends, because research shows that they moderate the effect of other risk factors on gambling problems and depressive symptoms. The goals of this study were to: (a) identify developmental pathways for gambling problems and depressive symptoms, with a focus on co-morbidity; (b) assess the moderating effect of relationship quality with parents and friends on the link between common risk factors and the trajectories of gambling problems and depressive symptoms. Study participants were 878 males. Predictors were assessed during childhood and adolescence and gambling problems and depressive symptoms were assessed in late adolescence and young adulthood. Latent class analysis revealed four distinct joint trajectories of gambling problems and depressive symptoms. Subsequent logistic regression revealed that impulsivity predicted membership in all pathogenic trajectories, and quality of the relationship with parents predicted membership in depressogenic trajectories. In addition, we found that the membership in the comorbid trajectory can be predicted by an interaction between friendship quality and socio-family risk

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 (GxG and GxE, 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 1) genetic or 2) environmental, 3) G×G, and 4) 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. GxG were investigated by a general linear model equation and a family-based association test. GxE were analyzed through a general test for GxE 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.

Purpose - The goal of this study was to test a new approach to deviancy training, that is, the shaping and reinforcing of disruptive behaviors in social interaction, which considers not only reinforcement, but also the modeling processes involved, as well as children’s roles as either providers or receivers of the training. Design/Methodology/Approach - Using teacher reports and observations from a semi naturalistic experimental setting with young children, we examined the prevalence of provided and received modeling and positive reinforcement, as well as the concurrent contribution of behavior problems on these processes in friendship dyads using a convenience sample of six year old twins (N = 783; 386 boys). Frequency analyses and linear and logistic regressions were conducted. Findings - Results indicated that modeling and positive reinforcement – provided and received – were prevalent in this low-risk sample, that behavior problems were associated mainly with provided dimensions, and that deviancy training processes were also displayed between disruptive and non-disruptive children. Practical implications – Findings are relevant to peer oriented programs designed to prevent antisocial behaviors. Prevention should target these mixed friendships where deviant behavior likely begins. Originality/value - This study provides preliminary support for a new measure of deviancy training, underscores the importance of the roles taken by children, and shows that deviancy training takes place between disruptive and non-disruptive young children.

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

Comorbidity is frequent among disruptive behaviors (DB) and leads to mental health problems during adolescence and adulthood. However, the early developmental origins of this comorbidity have so far received little attention. This study investigated the developmental comorbidity of three DB categories during early childhood: hyperactivity-impulsivity, non-compliance, and physical aggression. Joint developmental trajectories of DB were identified based on annual mother interviews from age 1½ to 5 years, in a population-representative birth-cohort (N = 2045). A significant proportion of children (13 % to 21 %, depending on the type of DB) consistently displayed high levels of hyperactivity-impulsivity, non-compliance, or physical aggression from age 1½ to 5 years. Developmental comorbidity was frequent, especially for boys: 10 % of boys and 3.7 % of girls were on a stable trajectory with high levels of symptoms for the three categories of DB. Significant associations were observed between preschool joint-trajectories of DB and indicators of DB and school adjustment assessed by teachers in first grade. Preschoolers who maintained high levels of hyperactivity-impulsivity, non-compliance, and physical aggression, displayed the highest number of DB symptoms in first grade for all categories according to their teacher. They were also among the most disadvantaged of their class for school adjustment indicators. Thus, DB manifestations and developmental comorbidity of DB are highly prevalent in infancy. Early childhood appears to be a critical period to prevent persistent and comorbid DB that leads to impairment at the very beginning of school attendance and to long-term serious health and social adjustment problems.

In both adolescents and adults, gambling problems and depressive symptoms co-occur and share some common risk factors (e.g., impulsivity and socio-family risk). However, little is known about (1) the developmental course of the co-morbidity of these problems; (2) variables that may moderate the effect of these common risk factors on gambling problems and depressive symptoms. Of specific interest could be individuals’ social relationships with significant others such as parents and friends, because research shows that they moderate the effect of other risk factors on gambling problems and depressive symptoms. The goals of this study were to: (a) identify developmental pathways for gambling problems and depressive symptoms, with a focus on co-morbidity; (b) assess the moderating effect of relationship quality with parents and friends on the link between common risk factors and the trajectories of gambling problems and depressive symptoms. Study participants were 878 males. Predictors were assessed during childhood and adolescence and gambling problems and depressive symptoms were assessed in late adolescence and young adulthood. Latent class analysis revealed four distinct joint trajectories of gambling problems and depressive symptoms. Subsequent logistic regression revealed that impulsivity predicted membership in all pathogenic trajectories, and quality of the relationship with parents predicted membership in depressogenic trajectories. In addition, we found that the membership in the comorbid trajectory can be predicted by an interaction between friendship quality and socio-family risk

Prenatal and early postnatal adversities have been shown to be associated with brain development. However, we do not know how much of this association is confounded by genetics, nor whether the postnatal environment can moderate the impact of in utero adversity. This study used a monozygotic (MZ) twin design to assess (1) the association between birth weight (BW) and brain volume in adolescence, (2) the association between within-twin-pair BW discordance and brain volume discordance in adolescence, and (3) whether the association between BW and brain volume in adolescence is mediated or moderated by early negative maternal parenting behaviours. These associations were assessed in a sample of 108 MZ twins followed longitudinally since birth and scanned at age 15. The total grey matter (GM) and white matter (WM) volumes were obtained using the Diffeomorphic Anatomical Registration Through Exponentiated Lie Algebra (DARTEL) toolbox in the Statistical Parametric Mapping version 8 (SPM8). We found that the BW was significantly associated with the total GM and WM volumes, particularly in the superior frontal gyrus and thalamus. Within-twin-pair discordance in BW was also significantly associated with within-pair discordance in both the GM and the WM volumes, supporting the hypothesis that the specific in utero environment is associated with brain development independently of genetics. Early maternal hostile parenting behaviours and depressive symptoms were associated with total GM volume but not WM volume. Finally, greater early maternal hostility may moderate the association between the BW and GM volume in adolescence, since the positive association between the BW and total GM volume appeared stronger at higher levels of maternal hostility (trend). Together, these findings support the importance of the in utero and early environments for brain development.

Background: Proactive aggression (PA) describes an instrumental behavior that is goal-oriented, whereas reactive aggression (RA) refers to an angry or frustrated aggressive response to a real or perceived threat. Little is known about the respective roles of genetic (G) and environmental (E) factors associated with PA and RA during childhood. The objectives of this study were to investigate a) the G-E etiology of the commonality between PA and RA and b) the presence of G or E components specific to PA or RA throughout childhood (i.e., from 6 to 12 years of age). Methods: Participants were 254 monozygotic and 413 dizygotic pairs. Teacher reports of PA and RA were obtained at 6, 7, 9, 10 and 12 years of age. Results: Throughout childhood, genetic factors accounted for most of the common variance between PA and RA, as well as their specificity. Shared environment played no role. Specifically, genetic factors common to PA and RA explained between 39% and 45% of the variance in PA, and between 27% and 42% of the variance in RA. Genetic factor also uniquely accounted for only but a small percentage (9% at 6 years and 3% at 9 years old) of the variation in PA. As for RA, three distinctive genetic factors contributed to phenotypic variation throughout childhood and explained between 12% and 22% of variance. Conclusions: Dynamic genetic factors accounted for the commonality in PA and RA, and for the specificity of RA. Few genetic factors were unique to PA; in contrast, for RA, an early, specific and persistent genetic factor was found alongside new genetic factors that appeared at later ages. These results challenge theoretical models that focus primarily on the effects of environmental factors in the etiology of reactive and proactive aggression.

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.

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.