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Childhood maltreatment is linked with later depressive symptoms, but not every maltreated child will experience symptoms later in life. Therefore, we investigate whether genetic predisposition for depression (i.e., polygenic score for depression, PGSDEP) modifies the association between maltreatment and depressive symptoms, while accounting for different types of maltreatment and whether it was evaluated through prospective and retrospective reports. The sample included 541–617 participants from the Quebec Longitudinal Study of Child Development with information on maltreatment, including threat, deprivation, assessed prospectively (5 months–17 years) and retrospectively (reported at 23 years), PGSDEP and self-reported depressive symptoms (20–23 years). Using hierarchical linear regressions, we found that retrospective, but not prospective indicators of maltreatment (threat/deprivation/cumulative) were associated with later depressive symptoms, above and beyond the PGSDEP. Our findings also show the presence of gene–environment interactions, whereby the association between maltreatment (retrospective cumulative maltreatment/threat, prospective deprivation) and depression was strengthened among youth with higher PGSDEP scores. Consistent with the Diathesis-Stress hypothesis, our findings suggest that a genetic predisposition for depression may exacerbate the putative impact of maltreatment on later depressive symptoms, especially when maltreatment is retrospective. Understanding the gene–environment interplay emerging in the context of maltreatment has the potential to guide prevention efforts.
To determine the validity of parent reports (PRs) of ADHD in preschoolers, we assessed hyperactivity/impulsivity (HI) and inattention (IN) in 1114 twins with PRs at 1.5, 2.5, 4, 5, 14, 15, and 17 years, and teacher-reports at 6, 7, 9, 10, and 12. We examined if preschool PRs (1) predict high HI/IN trajectories, and (2) capture genetic contributions to HI/IN into adolescence. Group-based trajectory analyses identified three 6–17 years trajectories for both HI and IN, including small groups with high HI (N = 88, 10.4%, 77% boys) and IN (N = 158, 17.3%, 75% boys). Controlling for sex, each unit of HI PRs starting at 1.5 years and at 4 years for IN, increased more than 2-fold the risk of belonging to the high trajectory, with incremental contributions (Odds Ratios = 2.5–4.5) at subsequent ages. Quantitative genetic analyses showed that genetic contributions underlying preschool PRs accounted for up to a quarter and a third of the heritability of later HI and IN, respectively. Genes underlying 1.5-year HI and 4-year IN contributed to 6 of 8 later HI and IN time-points and largely explained the corresponding phenotypic correlations. Results provide phenotypic and genetic evidence that preschool parent reports of HI and IN are valid means to predict developmental risk of ADHD.
To examine how food insecurity in childhood up to adolescence relates to eating habits and weight status in young adulthood.
Design:
A longitudinal study design was used to derive trajectories of household food insecurity from age 4·5 to 13 years. Multivariable linear and logistical regression analyses were performed to model associations between being at high risk of food insecurity from age 4·5 to 13 years and both dietary and weight outcomes at age 22 years.
Setting:
A birth cohort study conducted in the Province of Quebec, Canada.
Participants:
In total, 698 young adults participating in the Québec Longitudinal Study of Child Development.
Results:
After adjusting for sex, maternal education and immigrant status, household income and type of family, being at high risk (compared with low risk) of food insecurity in childhood up to adolescence was associated with consuming higher quantities of sugar-sweetened beverages (ßadj: 0·64; 95 % CI (0·27, 1·00)), non-whole-grain cereal products (ßadj: 0·32; 95 % CI (0·07, 0·56)) and processed meat (ßadj: 0·14; 95 % CI (0·02, 0·25)), with skipping breakfast (ORadj: 1·97; 95 % CI (1·08, 3·53)), with eating meals prepared out of home (ORadj: 3·38; 95 % CI (1·52, 9·02)), with experiencing food insecurity (ORadj: 3·03; 95 % CI (1·91, 4·76)) and with being obese (ORadj: 2·01; 95 % CI (1·12, 3·64)), once reaching young adulthood.
Conclusion:
Growing up in families experiencing food insecurity may negatively influence eating habits and weight status later in life. Our findings reinforce the importance of public health policies and programmes tackling poverty and food insecurity, particularly for families with young children.
While converging evidence suggests that both environmental and genetic factors underlie variations in diurnal cortisol, the extent to which these sources of influence vary according to socioeconomic status (SES) has seldom been investigated, particularly in adolescence. To investigate whether a distinct genetic and environmental contribution to youth’s diurnal cortisol secretion emerges according to family SES and whether the timing of these experiences matters. Participants were 592 twin pairs, who mostly came from middle-income and intact families and for whom SES was measured in childhood and adolescence. Diurnal cortisol was assessed at age 14 at awakening, 30 min later, in the afternoon and evening over four nonconsecutive days. SES–cortisol phenotypic associations were specific to the adolescence period. Specifically, higher awakening cortisol levels were detected in wealthier backgrounds, whereas higher cortisol awakening response (CAR) and diurnal changes were present at both ends of the SES continuum. Moreover, smaller genetic contributions emerged for awakening cortisol in youth from poorer compared to wealthier backgrounds. The results suggest that the relative contribution of inherited factors to awakening cortisol secretion may be enhanced or suppressed depending on the socio-family context, which may help to decipher the mechanisms underlying later adjustment.
Peer victimization is associated with a wide range of mental health problems in youth, yet few studies described its association with mental health comorbidities.
Methods
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.
Results
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.
Conclusions
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.
This study aimed to identify perinatal and early-life factors associated with trajectories of psychopathic traits across childhood.
Methods
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.
Results
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.
Conclusions
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 adversity and anxiety have been associated with increased risk for internalizing disorders later in life and with a range of brain structural abnormalities. However, few studies have examined the link between harsh parenting practices and brain anatomy, outside of severe maltreatment or psychopathology. Moreover, to our knowledge, there has been no research on parenting and subclinical anxiety symptoms which remain persistent over time during childhood (i.e., between 2.5 and 9 years old). Here, we examined data in 94 youth, divided into four cells based on their levels of coercive parenting (high / low) and of anxiety (high / low) between 2.5 and 9 years old. Anatomical images were analyzed using voxel-based morphometry (VBM) and FreeSurfer. Smaller gray matter volumes in the prefrontal cortex regions and in the amygdala were observed in youth with high versus low levels of harsh parenting over time. In addition, we observed significant interaction effects between parenting practices and subclinical anxiety symptoms in rostral anterior cingulate cortical thickness and in amygdala volume. These youth should be followed further in time to identify which youth will or will not go on to develop an anxiety disorder, and to understand factors associated with the development of sustained anxiety psychopathology.
We examined whether adolescents’ loneliness and social withdrawal mediated the association between maternal depressive symptoms and adolescent suicidality. Secondary analyses on the Québec Longitudinal Study of Child Development data were conducted (n = 1,623). Each mother completed the Centre for Epidemiologic Studies Depression Scale (at child ages 5 months, 1.5, 3.5, 5, and 7 years). Adolescent's social withdrawal (adolescent, father, and teacher reported at 10, 12, and 13 years) and loneliness (adolescent reported at 10, 12, and 13 years), were assessed using items from the Social Behavior Questionnaire and the Loneliness and Social Satisfaction Questionnaire, respectively. Adolescents completed self-reports to assess suicidal thoughts and attempts at 13, 15, 17, and 20 years. Children of mothers with higher levels of maternal depressive symptoms had an increased risk for suicidality (OR = 1.15, 95% CI: 1.03–1.28). Loneliness explained 16% of the total effect of maternal depressive symptoms on adolescent suicidality (indirect effect OR = 1.02, 95% CI: 1.00–1.04). There was no indirect effect of maternal depressive symptoms on adolescent suicidal outcomes via social withdrawal (indirect effect OR = 1.00, 95% CI: 0.99–1.02). Interventions that target loneliness may be beneficial for decreasing the risk for suicidality among adolescents of mothers with depressive symptoms.
We performed viral culture of respiratory specimens in 118 severe acute respiratory coronavirus virus 2 (SARS-CoV-2)–infected healthcare workers (HCWs), ∼2 weeks after symptom onset. Only 1 HCW (0.8%) had a positive culture. No factors for prolonged viral shedding were identified. Infectivity is resolved in nearly all HCWs ∼2 weeks after symptom onset.
Maternal depressive symptoms (MDSs) are negatively associated with children's academic performance, with stronger effects sometimes reported in boys. However, few studies have tested the mechanisms of this association. We examined the mediating role of school engagement and peer victimization in this association and tested for sex differences.
Methods
Participants were 1173 families from a population-based longitudinal Canadian study. MDSs were self-reported annually using the Centre for Epidemiologic Studies Depression Scale (child's age: 5 months to 5 years). Data on mediators (peer victimization, cognitive, behavioral, and emotional school engagement) were reported annually from ages 6–10 by multiple informants including children, parents, and teachers using items from validated scales. Mathematics, reading, and writing exam scores at age 12 were obtained from standardized exams administered by Québec's Ministry of Education and Teaching. Structural equation modeling was used to test mediation by school experiences in boys and girls.
Results
Exposure to MDSs was negatively associated with mathematics, reading, and writing scores in girls and with mathematics only in boys. Cognitive and behavioral engagement significantly mediated the association between MDSs and mathematics, reading, and writing scores in girls. There were no significant mediators for boys.
Conclusions
Prevention and intervention strategies aiming to improve school engagement might be beneficial for daughters of mothers experiencing depressive symptoms. Further research is needed to replicate these findings and to identify the mechanisms explaining this association in boys.
We aimed to identify groups of children presenting distinct perinatal adversity profiles and test the association between profiles and later risk of suicide attempt.
Methods
Data were from the Québec Longitudinal Study of Child Development (QLSCD, N = 1623), and the Avon Longitudinal Study of Parents and Children (ALSPAC, N = 5734). Exposures to 32 perinatal adversities (e.g. fetal, obstetric, psychosocial, and parental psychopathology) were modeled using latent class analysis, and associations with a self-reported suicide attempt by age 20 were investigated with logistic regression. We investigated to what extent childhood emotional and behavioral problems, victimization, and cognition explained the associations.
Results
In both cohorts, we identified five profiles: No perinatal risk, Poor fetal growth, Socioeconomic adversity, Delivery complications, Parental mental health problems (ALSPAC only). Compared to children with No perinatal risk, children in the Poor fetal growth (pooled estimate QLSCD-ALSPAC, OR 1.89, 95% CI 1.04–3.44), Socioeconomic adversity (pooled-OR 1.42, 95% CI 1.08–1.85), and Parental mental health problems (OR 1.74, 95% CI 1.27–2.40), but not Delivery complications, profiles were more likely to attempt suicide. The proportion of this effect mediated by the putative mediators was larger for the Socioeconomic adversity profile compared to the others.
Conclusions
Perinatal adversities associated with suicide attempt cluster in distinct profiles. Suicide prevention may begin early in life and requires a multidisciplinary approach targeting a constellation of factors from different domains (psychiatric, obstetric, socioeconomic), rather than a single factor, to effectively reduce suicide vulnerability. The way these factors cluster together also determined the pathways leading to a suicide attempt, which can guide decision-making on personalized suicide prevention strategies.
This paper is a revised and updated edition of a previous description of the Quebec Newborn Twin Study (QNTS), an ongoing prospective longitudinal follow-up of a birth cohort of twins born between 1995 and 1998 in the greater Montreal area, Québec, Canada. The goal of QNTS is to document individual differences in the cognitive, behavioral, and social-emotional aspects of developmental health across childhood, their early genetic and environmental determinants, as well as their putative role in later social-emotional adjustment, school, health, and occupational outcomes. A total of 662 families of twins were initially assessed when the twins were aged 6 months. These twins and their family were then followed regularly. QNTS now has 16 waves of data collected or planned, including 5 in preschool. Over the last 24 years, a broad range of physiological, cognitive, behavioral, school, and health phenotypes were documented longitudinally through multi-informant and multimethod measurements. QNTS also entails extended and detailed multilevel assessments of proximal (e.g., parenting behaviors, peer relationships) and distal (e.g., family income) features of the child’s environment. QNTS children and a subset of their parents have been genotyped, allowing for the computation of a variety of polygenic scores. This detailed longitudinal information makes QNTS uniquely suited for the study of the role of the early years and gene–environment transactions in development.
Our aim was to assess whether infants influence the quantity and quality of their mothers’ speech to them and, in turn, whether this maternal speech influences children's later language. As 189 mothers interacted with each of their twins at age 0;5, we calculated the number of utterances, the proportion of sensitive utterances, and the proportion of self-repeated utterances they produced. We later assessed the twins’ language comprehension and production when they were 1;6, 2;6, and 5;2. Quantity of maternal speech predicted child language at 5;2, whereas sensitivity predicted child language at 2;6 and 5;2 and partial self-repetition predicted child language at 1;6. Conversely, sensitivity and partial self-repetition in maternal speech at 0;5 were associated with genetic factors from the child, indicating that infant characteristics influence the quality of maternal speech. Overall, our findings stress the importance of considering both directions in the association between maternal speech and child characteristics.
Among children exposed to elevated maternal depression symptoms (MDS), recent studies have demonstrated reduced internalizing and externalizing problems for those who have attended formal childcare (i.e., center-based, family-based childcare). However, these studies did not consider whether childcare attendance is associated with benefits for the child only or also with reduced MDS. Using a four-wave longitudinal cross-lagged model, we evaluated whether formal childcare attendance was associated with MDS or child behavior problems and whether it moderated longitudinal associations between MDS and child behavior problems and between child behavior problems and MDS. The sample was drawn from a population-based cohort study and consisted of 908 biologically related mother–child dyads, followed from 5 months to 5 years. Attending formal childcare was not associated with MDS or child behavior problems but moderated the association between MDS at 3.5 years and child internalizing and externalizing problems at 5 years as well as between girls’ externalizing problems at 3.5 years and MDS at 5 years. No other moderation of formal childcare was found. Findings suggest that attending formal childcare reduces the risks of behavior problems in the context of MDS but also the risk of MDS in the context of girls’ externalizing problems.
Paludification is the most common process of peatland formation in boreal regions. In this study, we investigated the autogenic (e.g., topography) and allogenic (fire and climate) factors triggering paludification in different geomorphological contexts (glaciolacustrine silty-clayey and fluvioglacial deposits) within the Québec black spruce (Picea mariana)–moss boreal forest. Paleoecological analyses were conducted along three toposequences varying from a forest on mineral soil to forested and semi-open peatlands. Plant macrofossil and charcoal analyses were performed on basal peat sections (≤50 cm) and thick forest humus (<40 cm) to reconstruct local vegetation dynamics and fire history involved in the paludification process. Results show that primary paludification started in small topographic depressions after land emergence ca. 8000 cal yr BP within rich fens. Lateral peatland expansion and secondary paludification into adjacent forests occurred between ca. 5100 and 2300 cal yr BP and resulted from low-severity fires during a climatic deterioration. Fires that reduced or eliminated entirely the organic layer promoted the establishment of Sphagnum in microdepressions. Paludification resulted in the decline of some coniferous species such as Abies balsamea and Pinus banksiana. The paleoecological approach along toposequences allowed us to understand the spatiotemporal dynamics of paludification and its impacts on the vegetation dynamics over the Holocene.
Heritability of antisocial behaviour is estimated at approximately 50% and involves multiple genes.
Aims
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.
Method
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.
Results
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.
Conclusions
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.
Declaration of interest:
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.
Methods
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.
Results
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.
Conclusions
The results support and expand the notion that genetic and environmental influences on substance use during adolescence are both developmentally stable and developmentally dynamic.
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.