Peer victimization is associated with a wide range of mental health problems in youth, yet few studies described its association with mental health comorbidities.

To test the association between peer victimization timing and intensity and mental health comorbidities, we used data from 1216 participants drawn from the Quebec Longitudinal Study of Child Development, a population-based birth cohort. Peer victimization was self-reported at ages 6–17 years, and modeled as four trajectory groups: low, childhood-limited, moderate adolescence-emerging, and high-chronic. The outcomes were the number and the type of co-occurring self-reported mental health problems at age 20 years. Associations were estimated using negative binomial and multinomial logistic regression models and adjusted for parent, family, and child characteristics using propensity score inverse probability weights.

Youth in all peer victimization groups had higher rates of co-occurring mental health problems and higher likelihood of comorbid internalizing-externalizing problems [odds ratios ranged from 2.06, 95% confidence interval (CI) 1.52–2.79 for childhood-limited to 4.34, 95% CI 3.15–5.98 for high-chronic victimization] compared to those in the low victimization group. The strength of these associations was highest for the high-chronic group, followed by moderate adolescence-emerging and childhood-limited groups. All groups also presented higher likelihood of internalizing-only problems relative to the low peer victimization group.

Irrespective of timing and intensity, self-reported peer victimization was associated with mental health comorbidities in young adulthood, with the strongest associations observed for high-chronic peer victimization. Tackling peer victimization, especially when persistent over time, could play a role in reducing severe and complex mental health problems in youth.

Youth who attempt suicide are more at risk for later mental disorders and suicide. However, little is known about their long-term socioeconomic outcomes.

We investigated associations between youth suicide attempts and adult economic and social outcomes.

Participants were drawn from the Quebec Longitudinal Study of Kindergarten Children (n = 2140) and followed up from ages 6 to 37 years. Lifetime suicide attempt was assessed at 15 and 22 years. Economic (employment earnings, retirement savings, welfare support, bankruptcy) and social (romantic partnership, separation/divorce, number of children) outcomes were assessed through data linkage with government tax return records obtained from age 22 to 37 years (2002–2017). Generalised linear models were used to test the association between youth suicide attempt and outcomes adjusting for background characteristics, parental mental disorders and suicide, and youth concurrent mental disorders.

By age 22, 210 youths (9.8%) had attempted suicide. In fully adjusted models, youth who attempted suicide had lower annual earnings (average last 5 years, US$ −4134, 95% CI −7950 to −317), retirement savings (average last 5 years, US$ −1387, 95% CI −2982 to 209), greater risk of receiving welfare support (risk ratio (RR) = 2.05, 95% CI 1.39 to 3.04) and were less likely to be married/cohabiting (RR = 0.82, 95% CI 0.73 to 0.93), compared with those who did not attempt suicide. Over a 40-year working career, the loss of individual earnings attributable to suicide attempts was estimated at US$98 384.

Youth who attempt suicide are at risk of poor adult socioeconomic outcomes. Findings underscore the importance of psychosocial interventions for young people who have attempted suicide to prevent long-term social and economic disadvantage.

While childhood externalizing, internalizing and comorbid problems have been associated with suicidal risk, little is known about their specific associations with suicidal ideation and attempts. We examined associations between childhood externalizing, internalizing and comorbid problems and suicidal ideation (without attempts) and attempts by early adulthood, in males and females.

Participants were from the Quebec Longitudinal Study of Kindergarten Children, a population-based study of kindergarteners in Quebec from 1986 to 1988 and followed-up until 2005. We captured the co-development of teacher-rated externalizing and internalizing problems at age 6–12 using multitrajectories. Using the Diagnostic Interview Schedule administered at age 15 and 22, we identified individuals (1) who never experienced suicidal ideation/attempts, (2) experienced suicidal ideation but never attempted suicide and (3) attempted suicide.

The identified profiles were no/low problems (45%), externalizing (29%), internalizing (11%) and comorbid problems (13%). After adjusting for socioeconomic and familial characteristics, children with externalizing (OR 2.00, CI 1.39–2.88), internalizing (OR 2.34, CI 1.51–3.64) and comorbid (OR 3.29, CI 2.05–5.29) problems were at higher risk of attempting suicide (v. non-suicidal) by age 22 than those with low/no problems. Females with comorbid problems were at higher risk of attempting suicide than females with one problem. Childhood problems were not associated with suicidal ideation. Externalizing (OR 2.01, CI 1.29–3.12) and comorbid problems (OR 2.28, CI 1.29–4.03) distinguished individuals who attempted suicide from those who thought about suicide without attempting.

Childhood externalizing problems alone or combined with internalizing problems were associated with suicide attempts, but not ideation (without attempts), suggesting that these problems confer a specific risk for suicide attempts.

This study aimed to identify perinatal and early-life factors associated with trajectories of psychopathic traits across childhood.

Participants were 1631 children (51.5% girls) from the Quebec Longitudinal Study of Child Development. A wide range of perinatal and early-life factors were assessed from pregnancy to age 2.5 years using medical files and mothers’ reports. Psychopathic traits were assessed via teachers’ reports at ages 6, 7, 8, 10, and 12 years. Latent class growth analyses and multinomial logistic regressions controlling for child sex were conducted. Two-way interaction effects between perinatal/early-life factors and child sex were explored.

Four trajectories of psychopathic traits were identified: High-stable (4.48%), Increasing (8.77%), Decreasing (11.46%), and Low-stable (75.29%). A few perinatal factors and most child-level and family-level early-life factors significantly increased the odds of following the High-stable v. the Low-stable trajectory. Higher levels of psychotropic exposures during pregnancy, socioeconomic adversity, child's physical aggression, child's opposition, mother's depressive symptoms, and hostile parenting increased the likelihood of following the Increasing instead of the Low-stable trajectory. Higher socioeconomic adversity, mother's depressive symptoms, and inconsistent parenting were associated with membership to the High-stable instead of the Decreasing trajectory. Most associations were not moderated by child sex.

These results shed light on the perinatal and early-life factors that are associated with specific pathways of psychopathic traits during childhood and suggest that different factors could be targeted to prevent the exacerbation (v. low and stable levels) or the stability at high levels (v. attenuation) of these traits.

Childhood disruptive behaviors are highly prevalent and associated with adverse long-term social and economic outcomes. Trajectories of welfare receipt in early adulthood and the association of childhood behaviors with high welfare receipt trajectories have not been examined.

Boys (n = 1000) from low socioeconomic backgrounds were assessed by kindergarten teachers for inattention, hyperactivity, aggression, opposition, and prosociality, and prospectively followed up for 30 years. We used group-base trajectory modeling to estimate trajectories of welfare receipt from age 19–36 years using government tax return records, then examined the association between teacher-rated behaviors and trajectory group membership using mixed effects multinomial regression models.

Three trajectories of welfare receipt were identified: low (70.8%), declining (19.9%), and chronic (9.3%). The mean annual personal employment earnings (US$) for the three groups at age 35/36 years was $36 500 (s.d. = $24 000), $15 600 (s.d. = $16 275), and $1700 (s.d. = $4800), respectively. Relative to the low welfare receipt group, a unit increase in inattention (mean = 2.64; s.d. = 2.32, range = 0–8) at age 6 was associated with an increased risk of being in the chronic group (relative risk ratio; RRR = 1.16, 95% CI 1.03–1.31) and in the declining group (RRR = 1.13, 95% CI 1.03–1.23), after adjustment for child IQ and family adversity, and independent of other behaviors. Family adversity was more strongly associated with trajectories of welfare receipt than any behavior.

Boys from disadvantaged backgrounds exhibiting high inattention in kindergarten are at elevated risk of chronic welfare receipt during adulthood. Screening and support for inattentive behaviors beginning in kindergarten could have long-term social and economic benefits for individuals and society.

Heritability of antisocial behaviour is estimated at approximately 50% and involves multiple genes.

To investigate the cumulative genetic effects of 116 single nucleotide polymorphisms mapping to 11 candidate serotonergic genes and antisocial behaviours, in adolescence and in early adulthood.

Participants were 410 male members of the Quebec Longitudinal Study of Kindergarten Children, a population-based cohort followed up prospectively from age 6 to age 23. The serotonergic genes were selected based on known physiological processes and prior associations with antisocial behaviours. Antisocial behaviours were self-reported and assessed by using semi-structured interviews in adolescence and in adulthood.

Cumulative, haplotype-based contributions of serotonergic genes conferring risk and protection for antisocial behaviours were detected by using multilocus genetic profile risk scores (MGPRSs) and multilocus genetic profile protection scores (MGPPSs). Cumulatively, haplotype-based MGPRSs and MGPPSs contributed to 9.6, 8.5 and 15.2% of the variance in general delinquency in adolescence, property/violent crimes in early adulthood and physical partner violence in early adulthood, respectively.

This study extends previous research by showing a cumulative effect of multiple haplotypes conferring risk and protection to antisocial behaviours in adolescence and early adulthood. The findings further support the relevance of concomitantly considering multiple serotonergic polymorphisms to better understand the genetic aetiology of antisocial behaviours. Future studies should investigate the interplay between risk and protective haplotype-based multilocus genetic profile scores with the environment.

I.O.-M. holds a Canada Research Chair in the developmental origins of vulnerability and resilience.

Using a longitudinal twin design and a latent growth curve/autoregressive approach, this study examined the genetic–environmental architecture of substance use across adolescence.

Self-reports of substance use (i.e. alcohol, marijuana) were collected at ages 13, 14, 15, and 17 years from 476 twin pairs (475 boys, 477 girls) living in the Province of Quebec, Canada. Substance use increased linearly across the adolescent years.

ACE modeling revealed that genetic, as well as shared and non-shared environmental factors explained the overall level of substance use and that these same factors also partly accounted for growth in substance use from age 13 to 17. Additional genetic factors predicted the growth in substance use. Finally, autoregressive effects revealed age-specific non-shared environmental influences and, to a lesser degree, age-specific genetic influences, which together accounted for the stability of substance use across adolescence.

The results support and expand the notion that genetic and environmental influences on substance use during adolescence are both developmentally stable and developmentally dynamic.

The monoamine oxidase A (MAOA) gene has been shown to moderate the impact of maltreatment on antisocial behaviour. Replication efforts have, however, yielded inconsistent results.

To investigate whether the interaction between the MAOA gene and violence is present across the full distribution of violence or emerges at higher levels of exposure.

Participants were 327 male members of the Québec Longitudinal Study of Kindergarten Children. Exposure to violence comprised retrospective reports of mother's and father's maltreatment, sexual and physical abuse. Conduct disorder and antisocial personality symptoms were assessed in semi-structured interviews and partner violence, property-violent crimes and arrest were self-reported.

Non-linear interactions between the MAOA gene and violence were detected, suggesting that the genetic moderation may come about once a certain level of violence is experienced.

Future studies should investigate the mechanisms translating substantial violence exposure, which could, subsequently, trigger the expression of genetically based differences in antisocial behaviour.

Adolescent substance use is associated with both earlier childhood behavioural problems and serious lifetime addiction problems later in life.

To examine whether, and through which mechanisms, targeting risk factors in early childhood prevents substance use across adolescence.

Disruptive kindergarten boys (n = 172) living in Montreal were randomly allocated to a preventive intervention and a control condition. The intervention was delivered over 2 years (7–9 years of age) with two main components: (a) social and problem-solving skills training for the boys; and (b) training for parents on effective child-rearing skills.

Adolescent substance use, up to 8 years post-intervention, was reduced in those who received the intervention (d = 0.48−0.70). Of most interest, the intervention effects were explained partly by reductions in impulsivity, antisocial behaviour and affiliation with less deviant peers during pre-adolescence (11–13 years).

Adolescent substance use may be indirectly prevented by selectively targeting childhood risk factors that disrupt the developmental cascade of adolescent risk factors for substance use.