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Peer victimisation has been associated with depressive symptoms during adolescence, however not all peer victimised adolescents will exhibit such symptoms. This study tested whether having a genetic predisposition to developing depression increased the risk of experiencing depressive symptoms in peer victimised youth. To date, no study has explored such gene-environment interaction using a polygenic risk score for depression (PRS-depression) in the context of peer victimisation and depressive symptoms in adolescence.The sample included 748 participants born in 1997/98 from the Quebec Longitudinal Study of Child Development with genotype data and prospectively collected information on peer victimisation (12-13 years) obtained from both self- and teacher-reports, as well as self-reported depressive symptoms (15-17 years). The PRS-depression was based on the genome-wide association meta-analysis of broad depression by Howard et al. (2019).Self- and teacher-reported peer victimisation in early adolescence were both associated with depressive symptoms in adolescence (β = 0.34, p .001; β = 0.14, p = .001 respectively), and this association remained significant when accounting for PRS-depression (β = 0.33, p .001; β = 0.13, p = .002 respectively). PRS-depression was independently associated with depressive symptoms, but there was no significant PRS-depression by peer victimisation interaction (self-reported and teacher-reported). PRS-depression was correlated with self-reported, but not teacher-reported, peer victimisation.Our findings suggested that a partial measure of an individual's genetic predisposition to depression, as measured by PRS-depression, and being exposed to peer victimisation (self- and teacher-reported) were independently associated with depressive symptoms in adolescence. Furthermore, PRS-depression did not exacerbate the risk of depressive symptoms among adolescents who had been peer victimised. Lastly, we found evidence of a gene-environment correlation between PRS-depression and self-reported peer victimisation. Future studies are needed to replicate this finding and to further understand the role of genetic predispositions in experiencing depressive symptoms following peer victimisation.

BackgroundAnxiety and depressive disorders often co-occur and the order of their emergence may be associated with different clinical outcomes. However, minimal research has been conducted on anxiety-anxiety comorbidity. This study examined factors associated with anxiety comorbidity and anxiety-MDD temporal sequence.MethodsOnline, self-report data were collected from the UK-based GLAD and COPING NBR cohorts (N = 38,775). Logistic regression analyses compared differences in sociodemographic, trauma, and clinical factors between single anxiety, anxiety-anxiety comorbidity, anxiety-MDD (major depressive disorder) comorbidity, and MDD-only. Additionally, anxiety-first and MDD-first anxiety-MDD were compared. Differences in familial risk were assessed in those participants with self-reported family history or genotype data.ResultsAnxiety-anxiety and anxiety-MDD had higher rates of self-reported anxiety or depressive disorder diagnoses, younger age of onset, and higher recurrence than single anxiety. Anxiety-MDD displayed greater clinical severity/complexity than MDD only. Anxiety-anxiety had more severe current anxiety symptoms, less severe current depressive symptoms, and reduced likelihood of self-reporting an anxiety/depressive disorder diagnosis than anxiety-MDD. Anxiety-first anxiety-MDD had a younger age of onset, more severe anxiety symptoms, and less likelihood of self-reporting a diagnosis than MDD-first. Minimal differences in familial risk were found.LimitationsSelf-report, retrospective measures may introduce recall bias. The familial risk analyses were likely underpowered.ConclusionsAnxiety-anxiety comorbidity displayed a similarly severe and complex profile of symptoms as anxiety-MDD but distinct features. For anxiety-MDD, first-onset anxiety had an earlier age of onset and greater severity than MDD-first. Anxiety disorders and comorbidity warrant further investigation and attention in research and practice.

Social wariness and preference for solitude, two dimensions of social withdrawal, show unique associations with various socioemotional difficulties in childhood, including internalizing and peer problems. However, their early childhood predictors remain vastly undocumented. The present study aimed to examine whether early indicators of reactivity in situations of unfamiliarity such as behavioral inhibition, affect, and cortisol independently, or in interaction with emotion regulation as indexed by vagal tone, predict later social wariness and preference for solitude. Participants were 1209 children from the Quebec Newborn Twin Study. Vagal tone was assessed at 5 months, and behavioral inhibition, affect, and cortisol were assessed at 19 months in situations of unfamiliarity. Mothers, teachers, and peers evaluated social wariness and preference for solitude repeatedly from 4 to 10 years old. Findings show that three temperamental dimensions, social inhibition, nonsocial inhibition, and affect accounted for the variability in reactions to unfamiliarity. Behavioral inhibition to social unfamiliarity at 19 months predicted social wariness during the preschool years. Poor vagal regulation at 5 months exacerbated the risk associated with negative affect at 19 months to predict preference for solitude during the preschool years. Overall, results show that social wariness and preference for solitude may follow different developmental pathways.

Objectives were to examine whether 1) temperament and cortisol response in situations of unfamiliarity at 19 months predict social wariness and preference for solitude throughout childhood; 2) these predictive associations vary as a function of vagal regulation. Participants were 1199 children from the Quebec Newborn Twin Study, followed from 5 months to 10 years old (51% girl; 86% White). Findings show that behavioral inhibition to social unfamiliarity independently predicted both dimensions of social withdrawal in preschool. Low vagal suppression exacerbated the risk associated with negative affect manifested in unfamiliar situations to predict preference for solitude in preschool. In contrast, high vagal suppression increased the risk associated with strong cortisol response to unfamiliarity to predict social wariness in grade school.

The present study documented in two distinct population-based samples the contribution of preschool fluid and crystallized cognitive abilities to school achievement in primary school and examined the mediating role of crystallized abilities in this sequence of predictive associations. In both samples, participants were assessed on the same cognitive abilities at 63 months (sample 1, n = 1072), and at 41 and 73 months (sample 2, n = 1583), and then with respect to their school achievement from grade 1 (7 years) to grade 6 (12 years). Preschool crystallized abilities were found to play a key role in predicting school achievement. They contributed substantially to school achievement in the early school years, but more modestly in the later years, due to the strong auto-regression of school achievement. They also mediated the association between fluid abilities and later school achievement in the early grades of school, with the former having modest direct contribution to the latter in the later grades. These findings are discussed regarding their implication for preventive interventions.

Background. Children who consistently withdraw from social situations face increased risk for later socioemotional difficulties. Twin studies indicate that genetic factors account for a substantial share in 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 unexplored. The objectives were 1) to identify high-risk trajectories for social wariness and preference for solitude in the childhood years, and 2) to examine whether the assignment to these high-risk trajectories can be predicted by polygenic scores for mostly adult mental health traits and disorders and by a general polygenic predisposition to these traits. Methods. Teachers evaluated 1133 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 differently predicted social wariness and preference for solitude. Only the loneliness polygenic score significantly predicted the elevated trajectory for social wariness. By contrast, the general mental health genetic risk score factor was associated with the trajectory depicting high and chronic preference for solitude. Conclusion. Distinct associations were uncovered between the polygenic scores, social wariness, and preference for solitude. These results point to multiple genetic processes underlying the development of social withdrawal, as well as the potential value of preference for solitude as an endophenotype for the later onset and persistence of mental health difficulties in adulthood.

Few studies have examined the genetic and environmental pathways through which formal daycare attendance and school readiness are associated. The purpose of this study was to explore if daycare attendance could moderate genetic and environmental contributions to school readiness. A sample of 648 (85% White; 50% Female) pairs of twins was used to compute a GxE, CxE and ExE interaction analyses. Each standard deviation of formal daycare intensity (high number of hours per week), but not age of onset decreased the contribution of shared environment (-0.13) but not genes or unique environment to school readiness. The results support the hypothesis that daycare acts as a normalizing environment, possibly buffering the negative effects from low-quality home environments on cognitive abilities.