Mechanisms and pathways linking kindergarten behavior problems with mid-life employment earnings for males from low-income neighborhoods.

Childhood behavior problems are associated with reduced labor market participation and lower earnings in adulthood, but little is known about the pathways and mechanisms that explain these associations. Drawing on a 33-year prospective birth cohort of White males from low-income backgrounds (n = 1040), we conducted a path analysis linking participants' teacher-rated behavior problems at age 6 years-that is, inattention, hyperactivity, aggression-opposition, and low prosociality-to employment earnings at age 35-39 years obtained from tax records. We examined three psychosocial mediators at age 11-12 years (academic, behavioral, social) and two mediators at age 25 years (non-high school graduation, criminal convictions). Our findings support the notion that multiple psychosocial pathways-especially low education attainment-link kindergarten behavior problems to lower employment earnings decades later.

Association of childhood bullying victimisation with suicide deaths: findings from a 50-year nationwide cohort study.

BACKGROUND: Bullying victimisation has been associated with increased risk of suicide ideation and attempt throughout the lifespan, but no study has yet examined whether it translates to a greater risk of death by suicide. We aimed to determine the association of bullying victimisation with suicide mortality. METHODS: Participants were drawn from the 1958 British birth cohort, a prospective follow-up of all births in 1 week in Britain in 1958. We conducted logistic regressions on 14 946 participants whose mothers reported bullying victimisation at 7 and 11 years with linked information on suicide deaths through the National Health Service Central Register. RESULTS: Fifty-five participants (48 males) had died by suicide between the age 18 and 52 years. Bullying victimisation was associated with suicide mortality; a one standard deviation increases in bullying victimisation linked to an increased odds for suicide mortality [odds ratio (OR) 1.29; 1.02-1.64] during adulthood. The OR attenuated by 11% after adjustment for individual (e.g. behavioural and emotional problems) and familial characteristics (e.g. adverse childhood experiences, 1.18; 0.92-1.51). Analysis of bullying victimisation frequency categories yields similar results: compared with individuals who had not been bullied, those who had been frequently bullied had an increased odds for suicide mortality (OR 1.89; 0.99-3.62). CONCLUSION: Our study suggests that individuals who have been frequently bullied have a small increased risk of dying by suicide, when no other risk factors is considered. Suicide prevention might start in childhood, with bullying included in a range of inter-correlated vulnerabilities encompassing behavioural and emotional difficulties and adverse experiences within the family.

Polygenic risk score and peer victimisation independently predict depressive symptoms in adolescence: results from the Quebec Longitudinal Study of Children Development.

BACKGROUND: 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. METHODS: 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). RESULTS: Self- and teacher-reported peer victimisation in early adolescence were both associated with depressive symptoms in adolescence (ß = 0.34, p < .001; ß = 0.14, p = .001 respectively), and this association remained significant when accounting for PRS-depression (ß = 0.33, p < .001; ß = 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. CONCLUSIONS: 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.

Increased urban greenspace in childhood associated with lower inattention deficit among adolescents.

PURPOSE: There is a growing interest in assessing the benefits of exposure to urban greenspace on mental health due to the increased urbanization of youth and concerns for their mental health. We investigated the prospective associations of residential greenspace in childhood and mental health in adolescence. Use of a well-characterized birth cohort permitted adjustment for a range of potential confounding factors including family and neighborhood characteristics in addition to prior mental health problems, and exploration of moderation effects by sex and family socioeconomic status. METHODS: We analyzed longitudinal data collected from 742 urban-dwelling participants of the Quebec Longitudinal Study of Children Development. The Normalized Difference Vegetation Index (NDVI) within 250, 500, and 1000 m buffer zones surrounding the home residence was used to indicate childhood exposure to greenspace. Six self-reported mental health problems at 15/17 years were examined using the Mental Health and Social Inadaptation questionnaire: inattention, hyperactivity/impulsivity, conduct, depression, anxiety, and suicidal ideation. RESULTS: Childhood urban greenspace was associated with lower inattention problems in both females and males. We observed a 0.14 reduced standard deviation (SD) (ß = - 0.14, SE = 0.05, p < 0.01) in relation to an interquartile range (IQR) increase of NDVI (0.15) at the 250 m buffer zone, and similar results were found in 500 m and 1000 m buffer zones. These associations only slightly attenuated after adjustment for individual (sex, childhood mental health), family (family SES, maternal age at birth, parental mental health, family composition), and neighborhood (material and social deprivation) characteristics (ß = - 0.13, SE = 0.06, p = 0.03). No association was found for other mental health problems, and no moderation associations of sex or family socioeconomic status were observed. CONCLUSION:  These findings suggest that increasing residential greenspace in cities may be associated with modest benefits in attentional capacities in youth, necessitating further research to elucidate the underlying mechanisms.

Maternal depressive symptoms and children's cognitive school readiness: the role of gene-environment interplay.

Maternal depressive symptoms are a robust risk factor for poor cognitive outcomes in children, yet the role of gene-environment interplay in this association is not well understood. The objective of this study was to evaluate gene-environment interaction in the association between maternal depressive symptoms and children's cognitive school readiness. Data come from a population-based birth cohort of 538 twin pairs. Maternal depressive symptoms were self-reported (Centre for Epidemiologic Studies Depression Scale) when children were aged 6 and 18 months (a mean score was used). Children's cognitive school readiness was assessed using the Lollipop Test when children were aged 5 years. Analyses were conducted with structural equation modeling. Maternal depressive symptoms were correlated with children's cognitive school readiness (r = -0.10). Shared environmental factors explained most of the variance in children's cognitive school readiness (52%). The remaining variance was accounted for by genetic (30%) and nonshared environmental factors (18%). As the level of maternal depressive symptoms increased, the relative contribution of nonshared environmental factors to the variance in children's cognitive school readiness increased (0.14 [95% CI: 0.04 to 0.24]), whereas the relative contribution of genetic factors decreased (-0.28 [-0.64 to 0.08]). In contexts of elevated maternal depressive symptoms, environmental - and potentially modifiable - factors may be especially important for shaping children's cognitive outcomes. This suggests that interventions to improve the early childhood environment of children exposed to maternal depressive symptoms may improve their cognitive outcomes.

Trajectories of suicide attempts from early adolescence to emerging adulthood: prospective 11-year follow-up of a Canadian cohort.

BACKGROUND: Suicide is a leading cause of mortality in youth, yet the course of suicide attempts is poorly documented. We explored the vulnerable transition from adolescence to emerging adulthood to identify group trajectories and risk factors. METHODS: The National Longitudinal Survey of Children and Youth is a prospective representative cohort of Canadian children. We followed participants aged 7-11 years in 1994-95 to age 23 (2008-09). We modelled self-reported past-year suicide attempts (ages 12 to 23 years) using growth mixture models. We analysed risk factors from self- and parent-report questionnaires at pre-adolescence (ages 10-11) and early adolescence (ages 12-13) using multinomial logistic regressions. Analyses were adjusted for sample non-response and attrition. RESULTS: In 2233 participants answering questions on teen and adult suicide attempts, we identified three trajectories: never attempted (96.0%), adolescence-limited (2.0%) and persisting into adulthood (2.0%). Adolescent girls aged 12-13 with depression/anxiety symptoms, and with mothers experiencing depression had higher risks of adolescence-limited than never-attempted [relative risk RR 9.27 (95% confidence interval: 1.73-49.82); 2.03 (1.02-3.32), for each standard deviation increase; 1.07 (1.00-1.15); respectively]. Preteen ADHD symptoms increased the risk of attempts persisting into adulthood as compared to never-attempted [RR 2.05 (1.29-3.28) for each standard deviation increase]. Suicide death of schoolmate/acquaintance increased risks of an adulthood trajectory as compared to never-attempted and adolescence-limited [RR 8.41 (3.04-23.27) and 6.63 (1.29-34.06), respectively]. CONCLUSION: In half the participants attempting suicide, attempts continued into adulthood. We stress the need for preventive strategies in early adolescence and differential clinical/educational interventions as identified for each trajectory.

Longitudinal Links Between Gambling Participation and Academic Performance in Youth: A Test of Four Models.

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.

Friendship Experiences and Anxiety Among Children: A Genetically Informed Study.

This study examined (a) whether, in line with a gene-environment correlation (rGE), a genetic disposition for anxiety puts children at risk of having anxious friends or having no reciprocal friends; (b) to what extent these friendship experiences are related to anxiety symptoms, when controlling for sex and genetic disposition for this trait; and (c) the additive and interactive predictive links of the reciprocal best friend's anxiety symptoms and of friendship quality with children's anxiety symptoms. Using a genetically informed design based on 521 monozygotic and ic twins (264 girls; 87% of European descent) assessed in Grade 4 (M age = 10.04 years, SD = .26), anxiety symptoms and perceived friendship quality were measured with self-report questionnaires. Results indicated that, in line with rGE, children with a strong genetic disposition for anxiety were more likely to have anxious friends than nonanxious friends. Moreover, controlling for their genetic risk for anxiety, children with anxious friends showed higher levels of anxiety symptoms than children with nonanxious friends but did not differ from those without reciprocal friends. Additional analyses suggested a possible contagion of anxiety symptoms between reciprocal best friends when perceived negative features of friendship were high. These results underline the importance of teaching strategies such as problem solving that enhance friendship quality to limit the potential social contagion of anxiety symptoms.

The dark side of friends: a genetically informed study of victimization within early adolescents' friendships.

Using a genetically informed twin design, this study examined (a) whether, in line with gene-environment correlation (rGE), a genetic disposition for anxiety puts children at risk of being victimized by a close friend or by other peers, and (b) whether, in line with gene-environment interaction (GxE), victimization by a close friend or by other peers moderates the expression of a genetic disposition for anxiety. Participants were 268 monozygotic and dizygotic twin pairs (MZ males = 71, MZ females = 80, DZ males = 56, DZ females = 61; 87% of European descent) assessed via questionnaires in Grade 8 (M age = 14.06 years, SD = 3.60). Participants reported about their victimization by a close friend and by other peers and their anxiety level. Victimization by a close friend and victimization by other peers were uncorrelated. In line with rGE, genetic factors related to anxiety predicted victimization by other peers, whereas victimization by a close friend was not predicted by heritable characteristics. Moreover, in line with a suppression process of GxE, victimization by other peers reduced the role of genetic factors in explaining interindividual differences in anxiety. In contrast, in line with a diathesis-stress process of GxE, victimization by a close friend fostered the expression of a genetic disposition for anxiety. Victimization by a close friend seems to happen to adolescents regardless of their personal, heritable characteristics. If it does occur, however, it is a source of distress mostly for youth with a genetic vulnerability for anxiety.

The Expression of Genetic Risk for Aggressive and Non-aggressive Antisocial Behavior is Moderated by Peer Group Norms.

Numerous studies have shown that aggressive and non-aggressive antisocial behaviors are important precursors of later adjustment problems. There is also strong empirical evidence that both types of antisocial behavior are partially influenced by genetic factors. However, despite its important theoretical and practical implications, no study has examined the question whether environmental factors differentially moderate the expression of genetic influences on the two types of antisocial behavior. Using a genetically informed design based on 266 monozygotic and dizygotic twin pairs, this study examined whether the expression of genetic risk for aggressive and non-aggressive antisocial behavior varies depending on the peer group's injunctive norms (i.e., the degree of acceptability) of each type of antisocial behavior. Self-reported aggressive and non-aggressive antisocial behavior and classroom-based sociometric nominations were collected when participants were 10 years old. Multivariate genetic analyses revealed some common genetic factors influencing both types of antisocial behavior (i.e., general antisocial behavior) as well as genetic influences specific to non-aggressive antisocial behavior. However, genetic influences on general antisocial behavior, as well as specific genetic influences on non-aggressive antisocial behavior, vary depending on the injunctive classroom norms regarding these behaviors. These findings speak to the power of peer group norms in shaping aggressive and non-aggressive antisocial behavior. They also contribute further to understanding the distinctive development of both types of antisocial behavior. Finally, they may have important implications for prevention purposes.

Gene-environment processes linking peer victimization and physical health problems: a longitudinal twin study.

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

Strong genetic contribution to peer relationship difficulties at school entry: findings from a longitudinal twin study.

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

Gene-environment processes linking aggression, peer victimization, and the teacher-child relationship.

Aggressive behavior in middle childhood is at least partly explained by genetic factors. Nevertheless, estimations of simple effects ignore possible gene-environment interactions (G × E) or gene-environment correlations (rGE) in the etiology of aggression. The present study aimed to simultaneously test for G × E and rGE processes between aggression, on the one hand, and peer victimization and the teacher-child relationship in school, on the other hand. The sample comprised 124 MZ pairs and 93 DZ pairs assessed in Grade 1 (mean age = 84.7 months). Consistent with rGE, children with a presumed genetic disposition for aggression were at an increased risk of peer victimization, whereas in line with G × E, a positive relationship with the teacher mitigated the genetically mediated expression of aggression.

A monozygotic twin difference study of friends' aggression and children's adjustment problems.

This study used the monozygotic (MZ) twin difference method to examine whether differences in friends' aggression increased the differences in MZ twins' aggression and depressive symptoms from kindergarten to Grade 1 and whether perceived victimization by the friend played a mediating role in this context. Participants were 223 MZ twin pairs. Results showed that differences in kindergarten friends' aggression significantly predicted an increased difference in MZ twins' aggression from kindergarten (mean age = 6.7 years) to Grade 1 (mean age = 7.5 years) for both boys and girls. Differences in perceived victimization by the friend mediated this association, albeit only in boys. Differences in perceived victimization by the friend also predicted an increase in MZ twins' differences in depressive symptoms. These results support the importance of friendship experiences during early childhood.

Examining the impact of a social skills training program on preschoolers' social behaviors: a cluster-randomized controlled trial in child care centers.

BACKGROUND: Preschoolers regularly display disruptive behaviors in child care settings because they have not yet developed the social skills necessary to interact prosocially with others. Disruptive behaviors interfere with daily routines and can lead to conflict with peers and educators. We investigated the impact of a social skills training program led by childcare educators on children's social behaviors and tested whether the impact varied according to the child's sex and family socio-economic status. METHODS: Nineteen public Child Care Centers (CCC, n = 361 children) located in low socio-economic neighborhoods of Montreal, Canada, were randomized into one of two conditions: 1) intervention (n = 10 CCC; 185 children) or 2) wait list control (n = 9 CCC; 176 children). Educators rated children's behaviors (i.e., disruptive and prosocial behaviors) before and after the intervention. Hierarchical linear mixed models were used to account for the nested structure of the data. RESULTS: At pre-intervention, no differences in disruptive and prosocial behaviors were observed between the experimental conditions. At post-intervention, we found a significant sex by intervention interaction (ß intervention by sex = - 1.19, p = 0.04) indicating that girls in the intervention condition exhibited lower levels of disruptive behaviors compared to girls in the control condition (f2 effect size = - 0.15). There was no effect of the intervention for boys. CONCLUSIONS: Girls may benefit more than boys from social skills training offered in the child care context. Studies with larger sample sizes and greater intervention intensity are needed to confirm the results. TRIAL REGISTRATION: Current clinical trial number is ISRCTN84339956 (Retrospectively registered in March 2017). No amendment to initial protocol.

Gene-environment interplay between peer rejection and depressive behavior in children.

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

Peer Alcohol Use Differentially Amplifies Genetic and Environmental Effects on Different Developmental Trajectories of Adolescent Alcohol Use.

PURPOSE: The purpose of the study was to investigate how peer alcohol use moderates genetic and environmental influences on three different developmental trajectories of alcohol use during adolescence: low (continuously low levels of use), early-onset fast-escalating (initiated use early, the level of use increased quickly), and normative increasing (started at a low level and increased steadily) using biometric modeling. METHODS: Data were from a longitudinal study on a sample of population-based adolescent twins (N = 842, 52.7% female, 84% European Caucasian). Adolescents self-reported past-year alcohol use at age 13, 14, 15, and 17 years. Adolescents' nominated friends reported their own past-year alcohol use at age 13, 15, and 17 years. RESULTS: Genetic and environmental influences on adolescents' alcohol use trajectories were differentially moderated by friends' alcohol use in different trajectories. Gene-environment interaction was implicated in the low and early-onset trajectories, such that genetic contributions were amplified when friends used more alcohol. Environment-environment interaction was involved in the normative increasing and early-onset trajectories, such that person-specific environmental contributions were amplified when friends' alcohol use increased. CONCLUSIONS: Adolescent alcohol use remains a major public health issue, with peer alcohol use being a major risk factor. These findings suggest that close supervision to reduce deviant peer affiliation as well as preventions targeting peer group norms of alcohol use might be especially beneficial for adolescents following the normative increasing and early-onset trajectories.

Gene-environment interaction between peer victimization and child aggression.

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

Genetic and environmental influences on body size in early childhood: a twin birth-cohort study.

Genetic and environmental contributions to body size from birth to 5 years in a population-based twin cohort were studied. Sex differences in gene-environment etiology were also explored. Analyses used data from the Quebec Newborn Twin Study (QNTS), a population-based birth cohort of 672 twin pairs. The final sample consisted of 177 complete twin pairs. Heritability of weight was moderate at birth while common environmental factors accounted for almost half of the variance. Influence of family environment disappeared by 5 months and genetic effects were high (approximately 90%) for both sexes at 5 months and 5 years. Adjustment of weight for height yielded similar results as for weight alone. Slight but significant sex-limitation of genetic effects was observed at 5 months. Overall, genetic factors accounted for 40% of birthweight variance, with intrauterine environment influences explaining almost half. However, genetic factors accounted for most of the variance in weight. These results do not imply a lack of environmental effects on body weight, but rather a lack of: (1) environmental effects that are independent from genetic liability, and/or (2) a lack of significant environmental variation in the population (e.g., uniform nutritional habits) that leaves genetic differences between children to generate most of the variance in weight.

Personal and familial predictors of peer victimization trajectories from primary to secondary school.

Using a sample of 767 children (403 girls, 364 boys), this study aimed to (a) identify groups with distinct trajectories of peer victimization over a 6-year period from primary school through the transition to secondary school, and (b) examine the associated personal (i.e., aggression or internalizing problems) and familial (family status, socioeconomic status, the parent-child relationship) predictors. Peer victimization was assessed via self-reports from Grades 4 through 9 (ages 10 through 15 years), aggression and internalizing problems were assessed in Grade 4 via peer nominations, and the parent-child relationship was assessed in Grade 7 (i.e., right after the transition to secondary school) via parent-reports. Growth Mixture modeling revealed 1 group (62%) who experienced little victimization in primary school and even less in secondary school, another group (31%) who was victimized in primary but not or much less in secondary school, and a third group (7%) who was chronically victimized in both school contexts. Boys were more likely than girls to follow any elevated victimization trajectory. Chronic victimization across primary and secondary school was predicted by nonintact family status and a combination of both internalizing problems and aggression compared with nonvictimized youth. In contrast, transitory victimization during primary but not in secondary school was predicted by aggression, but not internalizing problems. Support as well as conflict in the parent-child relationship also showed significant, albeit distinct associations with the different peer victimization trajectories. (PsycINFO Database Record