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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, remain undocumented. The objectives of the present study were 1) to identify high-risk trajectories for social wariness and preference for solitude in childhood, and 2) 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. Conclusion. Distinct associations were uncovered between the polygenic scores, social wariness, and preference for solitude.

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, remain undocumented. The objectives of the present study were 1) to identify high-risk trajectories for social wariness and preference for solitude in childhood, and 2) 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. Conclusion. Distinct associations were uncovered between the polygenic scores, social wariness, and preference for solitude.

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.

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.

Background Lead exposure predicts altered neurodevelopment and lower intelligence quotient (IQ) in children, but few studies have examined this association in children who have relatively low blood lead concentrations. Objectives To test the associations between blood lead concentrations and cognitive function in Canadian preschoolers, with a possible moderation by sex. Methods The data were gathered from 609 mother-child pairs from the Maternal–Infant Research on Environmental Chemicals (MIREC) Study. Lead was measured in umbilical and maternal blood, and in children's venous blood at age 3–4 years. Cognitive function was measured with the Wechsler Preschool and Primary Scale of Intelligence (WPPSI-III) at 3–4 years. We tested the relationship between WPPSI-III scores and blood lead concentrations with multiple linear regression, adding child sex as a moderator. Results Median blood lead concentrations for the mother at 1st trimester and 3rd trimester of pregnancy, and for cord and child blood were 0.60 μg/dL, 0.58 μg/dL, 0.79 μg/dL and 0.67 μg/dL, respectively. We found no association between cord blood lead concentrations and WPPSI-III scores in multivariable analyses. However, cord blood lead concentrations showed a negative association with Performance IQ in boys but not in girls (B = 3.44; SE = 1.62; 95% CI: 0.82, 5.98). No associations were found between WPPSI-III scores and prenatal maternal blood or concurrent child blood lead concentrations. Conclusions Prenatal blood lead concentrations below 5 μg/dL were still associated with a decline in cognitive function in this Canadian cohort, but only for boys.

Background: Prenatal exposure to polybrominated diphenyl ethers (PBDEs) has been associated with cognitivedeficits and behavioral problems in children. To date, no study has examined this exposure in association withneurobehavioral development in infants younger than 12 months assessed with observational tasks. Objectives: This study examined the relation between prenatal PBDE concentrations and predisposition tofrustration, assessed by the arm restraint task (ART), in Canadian infants. Methods: In a prospective longitudinal study conducted in Canada, exposure to nine PBDE congeners wasmeasured in maternal plasma during the first trimester of pregnancy. The ART was used to measure predis-position to frustration in infancy (N = 333; mean age = 6.9 months), as assessed by negative vocalizations(crying and screaming) and physical reactivity (discomfort movements). Results: Maternal plasma PBDE-47 concentrations collected during pregnancy were associated with negativevocalizations using the ART (adjusted Relative Risk [aRR] = 1.04, 95% CI: 1.00, 1.09). Prenatal PBDE-99concentrations during pregnancy were also related to a shift to the left in the tail of the distribution of onset ofnegative vocalizations as measured by a decrease of 38 s (95% CI: −78.1, 1.3) in the 75th quantile of thedistribution for infants whose mothers had detectable levels of PBDE-99 compared to infants of mothers withundetectable levels. Similarly, infants whose mothers had detectable levels of PBDE-100 showed an increase of24.1 s (95% CI: 4.1, 44.1) in the 75th quantile of the distribution of proportion of time in negative vocalizationscompared with infants of mothers with undetectable levels. Finally, the association between PBDE-47 and PBDE-153, and physical reactivity was significantly modified by sex (p < 0.1), with opposite patterns in girls andboys. Conclusions: Prenatal exposure to PBDEs was associated with increased incidence of crying and screaming withdelayed onset of discomfort movement, w

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.

Background: Prenatal exposure to polybrominated diphenyl ethers (PBDEs) has been associated with cognitivedeficits and behavioral problems in children. To date, no study has examined this exposure in association withneurobehavioral development in infants younger than 12 months assessed with observational tasks. Objectives: This study examined the relation between prenatal PBDE concentrations and predisposition tofrustration, assessed by the arm restraint task (ART), in Canadian infants. Methods: In a prospective longitudinal study conducted in Canada, exposure to nine PBDE congeners wasmeasured in maternal plasma during the first trimester of pregnancy. The ART was used to measure predis-position to frustration in infancy (N = 333; mean age = 6.9 months), as assessed by negative vocalizations(crying and screaming) and physical reactivity (discomfort movements). Results: Maternal plasma PBDE-47 concentrations collected during pregnancy were associated with negativevocalizations using the ART (adjusted Relative Risk [aRR] = 1.04, 95% CI: 1.00, 1.09). Prenatal PBDE-99concentrations during pregnancy were also related to a shift to the left in the tail of the distribution of onset ofnegative vocalizations as measured by a decrease of 38 s (95% CI: −78.1, 1.3) in the 75th quantile of thedistribution for infants whose mothers had detectable levels of PBDE-99 compared to infants of mothers withundetectable levels. Similarly, infants whose mothers had detectable levels of PBDE-100 showed an increase of24.1 s (95% CI: 4.1, 44.1) in the 75th quantile of the distribution of proportion of time in negative vocalizationscompared with infants of mothers with undetectable levels. Finally, the association between PBDE-47 and PBDE-153, and physical reactivity was significantly modified by sex (p < 0.1), with opposite patterns in girls andboys. Conclusions: Prenatal exposure to PBDEs was associated with increased incidence of crying and screaming withdelayed onset of discomfort movement, w