Body mass index across development and adolescent hair cortisol: the role of persistence, variability, and timing of exposure.

BACKGROUND: Research suggests a putative role of the glucocorticoid stress hormone cortisol in the accumulation of adiposity. However, obesity and weight fluctuations may also wear and tear physiological systems promoting adaptation, affecting cortisol secretion. This possibility remains scarcely investigated in longitudinal research. This study tests whether trajectories of body mass index (BMI) across the first 15 years of life are associated with hair cortisol concentration (HCC) measured two years later and whether variability in BMI and timing matter. METHODS: BMI (kg/m2) was prospectively measured at twelve occasions between age 5 months and 15 years. Hair was sampled at age 17 in 565 participants. Sex, family socioeconomic status, and BMI measured concurrently to HCC were considered as control variables. RESULTS: Latent class analyses identified three BMI trajectories: "low-stable" (59.2%, n = 946), "moderate" (32.6%, n = 507), and "high-rising" (8.2%, n = 128). BMI variability was computed by dividing the standard deviation of an individual's BMI measurements by the mean of these measurements. Findings revealed linear effects, such that higher HCC was noted for participants with moderate BMI trajectories in comparison to low-stable youth (ß = 0.10, p = 0.03, 95% confidence interval (CI) = [0.02-0.40]); however, this association was not detected in the high-rising BMI youth (ß = -0.02, p = 0.71, 95% CI = [-0.47-0.32]). Higher BMI variability across development predicted higher cortisol (ß = 0.17, p = 0.003, 95% CI = [0.10-4.91]), additively to the contribution of BMI trajectories. BMI variability in childhood was responsible for that finding, possibly suggesting a timing effect. CONCLUSIONS: This study strengthens empirical support for BMI-HCC association and suggests that more attention should be devoted to BMI fluctuations in addition to persistent trajectories of BMI.

Concurrent and prospective associations between family socioeconomic status, social support and salivary diurnal and hair cortisol in adolescence.

BACKGROUND: Exposure to socioeconomic adversity is hypothesized to impact hypothalamic-pituitary-adrenal (HPA) axis activity and cortisol secretion, but existing evidence is inconsistent. Yet, few studies have investigated this association using a developmental approach that considers potential protective contextual factors. This study examined the role of stability and changes in family socioeconomic status (SES) in the prediction of multiple cortisol indicators and tested whether social support moderated these associations. METHODS: Participants were part of a population-based sample of twin pairs recruited at birth. Family SES was assessed in early childhood (ages 0-5) and mid-adolescence (age 14). Social support was assessed at ages 14 and 19. Diurnal cortisol (n = 569) was measured at age 14 at awakening, 30 min later, in the afternoon and evening over four non-consecutive days. Hair cortisol concentration (HCC, n = 704) was measured at age 19. All data were collected before the pandemic and multilevel regression models were conducted to account for the nested data structure. RESULTS: Youth exposed to lower family SES levels in childhood and mid-adolescence had a flatter diurnal slope and higher HCC compared with those who experienced upward socioeconomic mobility in mid-adolescence. Contrastingly, mid-adolescence SES showed no association with the diurnal slope or HCC for youth from higher-SES households in early childhood. Moreover, youth raised in higher-SES families in early childhood had a higher CAR in mid-adolescence if they reported greater social support in mid-adolescence. Social support also moderated the SES-cortisol association in mid-adolescence, with higher-SES youth showing higher awakening cortisol secretion when reporting more social support. CONCLUSIONS: Our findings support the hypothesis that early socioeconomic adversity sensitizes HPA axis activity to later socioeconomic disadvantage, which may bear consequences for socioemotional and behavioral functioning.

Reconsidering the failure model: Using a genetically controlled design to assess the spread of problems from reactive aggression to internalizing symptoms through peer rejection across the primary school years.

According to the failure model (Patterson & Capaldi, 1990), peer rejection is the intermediary link between problem behaviors and internalizing symptoms. The present study tested the model with 464 monozygotic and same-sex dizygotic twin pairs (234 female, 230 male dyads). Teacher-reported reactive aggression and internalizing symptoms, and peer-reported peer rejection were collected at ages 6, 7, and 10 (from 2001 to 2008). Support for the failure model emerged in conventional non-genetically controlled analyses, but not twin-difference score analyses (which remove shared environmental and genetic contributions). Univariate biometric models attributed minimal variance in failure model variables to shared environmental factors, suggesting that genetic factors play an important unacknowledged role in developmental pathways historically ascribed to nonshared experiences in the failure model.

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.

Genetic and phenotypic evidence of the predictive validity of preschool parent reports of hyperactivity/impulsivity and inattention.

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.

Targeting Peer Contagion Dynamics in Children with ADHD: Effects from a Two-Site Randomized Controlled Trial.

OBJECTIVE: Parental Friendship Coaching (PFC) teaches parents to coach their children in friendship skills. This paper examines whether PFC fosters positive peer contagion processes (i.e. dyadic mutuality) and reduces negative peer contagion processes (i.e. coercive joining) within the friendships of children with attention-deficit/hyperactivity disorder (ADHD). METHOD: Participants were 134 families of children with ADHD and peer problems (age 6-11 years; 69% male; 72% white) at two Canadian sites, randomized to PFC or CARE (an active comparison intervention). Children were observed in the lab at baseline, post-treatment, and at 8-month follow-up during cooperation and competition tasks with a real-life friend. Amount and reciprocity of dyadic mutuality indicators (i.e. positive affect and positive behaviors) and coercive joining indicators (i.e. aggressive, controlling, and rule-breaking behaviors) between friends were coded. RESULTS: Across treatment conditions, children showed an increase in the amount of dyadic mutuality during cooperation and a decrease in the amount of coercive joining during competition over time. Relative to CARE, PFC induced a reduced amount of coercive joining behaviors during cooperation at post-treatment and follow-up. However, PFC led to decreases in the reciprocity of positive affect during cooperation at post-treatment and to increases in the reciprocity of coercive joining during competition at follow-up relative to CARE. Moderation analyses suggest PFC was associated with better outcomes for children with externalizing comorbidity, and for those with a stable or a best friend. CONCLUSIONS: Findings highlight the importance of transactional processes, contextual differences, externalizing comorbidities, and friendship status when assessing the efficacy of PFC.

Differential Association of Preadolescent Risk Factors Across Developmental Patterns of Adolescent Concurrent Gambling Participation and Substance Use.

Early risk factors for gambling participation (GP) and substance use (SU) in adolescents have usually been studied separately, although these disorders were integrated into the same clinical category over a decade ago. This exploratory study aimed to investigate the early individual, parental, familial and social risk factors associated with developmental patterns of adolescent GP and SU in a population-representative cohort (N = 1594, 51.2% boys). Using a person-centered strategy and multiple assessments from age 12 to 17, six developmental patterns describing joint GP and SU courses were revealed. Non-substance users/non-gamblers served as the reference class in an integrated longitudinal-multivariate analysis framework examining 15 distinct risk factors. Results showed that a core of risk factors were common to all trajectory-classes of substance users with or without GP. For a similar level of SU, most of the risk factors associated with non-gambling users also affected their gambling peers. However, additional risk factors were specifically related to GP. Thus, substance users who also gamble were affected by a greater number of risk factors than non-gambling substance users. Findings are consistent with a developmental syndrome of addiction, which posits a shared etiology between different expressions of addiction as well as differences in risk factors that lead to distinct trajectories of addictive behaviors. They highlight the importance of considering both GP and SU for a comprehensive assessment of adolescents' level of risk with regard to addictive behaviors.

Adolescents and Social Media: Longitudinal Links Between Motivations for Using Social Media and Subsequent Internalizing Symptoms.

Knowledge is lacking on whether adolescents' motivations for social media use predict internalizing symptoms, and few studies have considered the moderating role of extraversion. In 2017 (T1) and 2018 (T2), 197 adolescents (49.70% girls, Mage = 13.15, SD = 0.36) from a large metropolitan area participated in this study. Adolescents reported on their social media use motivations and extraversion (at T1) and depressive and anxiety symptoms (T1 and T2). Latent class analysis revealed four motivation profiles at T1: (1) entertainment and fun (30.97%); (2) avoidance and escapism (14.21%); (3) meeting new people, feel involved (16.75%); (4) boredom (38.07%). Social motivations (profile 3) predicted elevated internalizing symptoms at T2. Avoidance and boredom motivations (profile 2 and 4) predicted internalizing symptoms for adolescents with low extraversion. Social media use motivations and extraversion distinguish adolescents who benefit from social media from those who experience difficulties.

Mental health comorbidities following peer victimization across childhood and adolescence: a 20-year longitudinal study.

BACKGROUND: 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.

Uncovering the genetic architecture of broad antisocial behavior through a genome-wide association study meta-analysis.

Despite the substantial heritability of antisocial behavior (ASB), specific genetic variants robustly associated with the trait have not been identified. The present study by the Broad Antisocial Behavior Consortium (BroadABC) meta-analyzed data from 28 discovery samples (N = 85,359) and five independent replication samples (N = 8058) with genotypic data and broad measures of ASB. We identified the first significant genetic associations with broad ASB, involving common intronic variants in the forkhead box protein P2 (FOXP2) gene (lead SNP rs12536335, p = 6.32 × 10-10). Furthermore, we observed intronic variation in Foxp2 and one of its targets (Cntnap2) distinguishing a mouse model of pathological aggression (BALB/cJ strain) from controls (BALB/cByJ strain). Polygenic risk score (PRS) analyses in independent samples revealed that the genetic risk for ASB was associated with several antisocial outcomes across the lifespan, including diagnosis of conduct disorder, official criminal convictions, and trajectories of antisocial development. We found substantial genetic correlations of ASB with mental health (depression rg = 0.63, insomnia rg = 0.47), physical health (overweight rg = 0.19, waist-to-hip ratio rg = 0.32), smoking (rg = 0.54), cognitive ability (intelligence rg = -0.40), educational attainment (years of schooling rg = -0.46) and reproductive traits (age at first birth rg = -0.58, father's age at death rg = -0.54). Our findings provide a starting point toward identifying critical biosocial risk mechanisms for the development of ASB.

Adolescents' internalizing symptoms predict dating violence victimization and perpetration 2 years later.

The aim of this longitudinal study was to examine bidirectional associations of adolescents' internalizing symptoms with dating violence victimization and perpetration. We conducted secondary analyses of the Québec Longitudinal Study of Child Development data (n = 974). Each adolescent completed items from the Conflict Tactics Scale (at ages 15 and 17 years) to assess psychological, physical, and sexual dating violence victimization and perpetration in the past 12 months. Adolescents' symptoms of depression and general anxiety in the past 12 months were self-reported (at ages 15 and 17 years) using The Mental Health and Social Inadaptation Assessment for Adolescents. There were concurrent associations of adolescents' internalizing symptoms with dating violence victimization and perpetration. Internalizing symptoms at age 15 years were positively associated with dating violence victimization and perpetration 2 years later in both males and females, even after adjusting for baseline characteristics. However, neither dating violence victimization nor perpetration at age 15 years was associated with internalizing symptoms 2 years later. For males and females, internalizing symptoms put adolescents at risk for future dating violence victimization and perpetration. Interventions that target internalizing symptoms may have the potential to decrease subsequent dating violence.

The phenotypic associations and gene-environment underpinnings of socioeconomic status and diurnal cortisol secretion in adolescence.

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.

Longitudinal patterns of polysubstance use throughout adolescence: association with adult substance use and psychosocial outcomes controlling for preadolescent risk factors in a male cohort.

PURPOSE: Inconsistent reports raise the question of the extent to which poor adult outcomes are associated with adolescent polysubstance use (PSU: alcohol, marijuana, other illicit drugs) above and beyond earlier risk factors. METHODS: Early adulthood substance-related and psychosocial outcomes were examined in association with age 13 to 17 developmental patterns of PSU in boys from urban, low SES neighborhoods (N = 926). Three classes obtained by latent growth modeling described low/non-users (N = 565, 61.0%), lower risk PSU (later onset, occasional use, 2 ≤ substances; N = 223, 24.1%), and higher risk PSU (earlier onset, frequent use, 3 ≥ substances; N = 138, 14.9%). Preadolescent individual, familial and social predictors of adolescent PSU patterns were used as covariates. RESULTS: Adolescent PSU contributed to both age-24 substance-related outcomes (frequency of alcohol, drug use, and getting drunk, risky behaviors under influence, and use-related problems) and psychosocial outcomes (no high school diploma, professional or financial strain, ASP symptoms, criminal record) over and above preadolescent risk factors. Controlling for preadolescent risk factors, adolescent PSU made a more important contribution to adult substance use outcomes (increasing the risk by about 110%) than to psychosocial outcomes (16.8% risk increase). PSU classes showed poorer adjustment for all age-24 substance use, and for various psychosocial outcomes than low/non-users. Higher risk polysubstance users also reported poorer outcomes than their lower risk peers for most substance use outcomes, and for professional or financial strain and criminal record. CONCLUSION: Findings highlight the contribution of adolescent PSU in a dose-response fashion, over and above preadolescent risk factors, on both homotypic and heterotypic outcomes in early adulthood.

Links between peer victimization, dating violence victimization and depression in adolescence: A genetically-informed study.

OBJECTIVE: The current study aimed to test if individuals with inherent dispositions to depression-related cognitions and behaviors are more at risk of experiencing relational difficulties, such as peer victimization and dating violence victimization. METHOD: This study used a genetically informed design with 806 twins (51.5% girls) to test 1) if at least part of the association between peer victimization in school and dating violence victimization in emerging adulthood can be explained by common underlying heritable factors. Participants provided repeated assessments of their peer victimization in school at ages 13 through 17, their depression symptoms at ages 13 through 19, as well as their victimization in dating relationships at age 19. RESULTS: A Cholesky decomposition based on structural equation modeling supported the hypotheses. Specifically, the association between peer victimization and dating violence victimization was to a significant extent explained by common underlying genetic vulnerabilities that were associated with depression symptoms. No sex moderation was found. CONCLUSIONS: The findings highlight the importance of addressing early indicators of vulnerability toward depression symptoms to prevent victimization by peers or dating partners.

Developmental Patterns of Gambling Participation and Substance use Throughout Adolescence in a Population Birth Cohort.

This study investigated adolescents' single and co-occurring developmental patterns of gambling participation and substance use and their association with gambling and substance use-related issues at age 17, controlling for confounders. Multiple assessments from age 12 to 17 were conducted in a population-based cohort (N=1594, 51.2% boys). Latent growth modeling was used to analyze developmental patterns and Generalized linear models to examine their association with age-17 gambling and substance use-related problems, types and variety of activities, and substance abuse. Results revealed six developmental patterns, including Low- or Non-substance Users or Gamblers (24.2% sample), two trajectory-classes of Later-Onset Increasing (to a moderate level) substance users, either with or without gambling participation (7.8% and 45.5%, respectively), two trajectory-classes of Early-Onset Increasing (to a higher level) substance users, either with or without gambling participation (6.2% and 12.7%, respectively), and a smaller trajectory-class of Slow-Increasing Substance Users and Early-Onset Gamblers, declining to non-gambling after age 13 (3.6%). Gambling participation and substance use did not appear to influence each other with regard to their onset and course throughout adolescence, and to age-17 types and variety of gambling activities or substances used, problems related to gambling participation or substance use, or substance abuse. These findings are consistent with the addictive syndrome model and with both common and individualized approaches to prevention and treatment for adolescent gamblers or substance users.

Link Between Peer Victimization in College and Cortisol Secretion: Roles of Genetic Vulnerabilities and Social Support.

It is unclear whether peer victimization in college interacts with genetic vulnerabilities or social support in predicting cortisol secretion. This issue was addressed using a sample of 162 Monozygotic and 237 Dizygotic twin pairs (54% females; 86% Whites, 6% Blacks, 6% Asians, 0.3% Native North Americans). At age 19, participants provided hair for cortisol extraction and reported about victimization in college and support by the mother, father, and best friend. Biometric modeling revealed that environmental influences on cortisol secretion were reduced and genetic influences exacerbated when victimization was high. Moderate to high maternal support mitigated the association between victimization and high cortisol secretion. The findings suggest that victimization in college contributes to physical "wear-and-tear", which may be counteracted by social support.

Changing genetic architecture of body mass index from infancy to early adulthood: an individual based pooled analysis of 25 twin cohorts.

BACKGROUND: Body mass index (BMI) shows strong continuity over childhood and adolescence and high childhood BMI is the strongest predictor of adult obesity. Genetic factors strongly contribute to this continuity, but it is still poorly known how their contribution changes over childhood and adolescence. Thus, we used the genetic twin design to estimate the genetic correlations of BMI from infancy to adulthood and compared them to the genetic correlations of height. METHODS: We pooled individual level data from 25 longitudinal twin cohorts including 38,530 complete twin pairs and having 283,766 longitudinal height and weight measures. The data were analyzed using Cholesky decomposition offering genetic and environmental correlations of BMI and height between all age combinations from 1 to 19 years of age. RESULTS: The genetic correlations of BMI and height were stronger than the trait correlations. For BMI, we found that genetic correlations decreased as the age between the assessments increased, a trend that was especially visible from early to middle childhood. In contrast, for height, the genetic correlations were strong between all ages. Age-to-age correlations between environmental factors shared by co-twins were found for BMI in early childhood but disappeared altogether by middle childhood. For height, shared environmental correlations persisted from infancy to adulthood. CONCLUSIONS: Our results suggest that the genes affecting BMI change over childhood and adolescence leading to decreasing age-to-age genetic correlations. This change is especially visible from early to middle childhood indicating that new genetic factors start to affect BMI in middle childhood. Identifying mediating pathways of these genetic factors can open possibilities for interventions, especially for those children with high genetic predisposition to adult obesity.

Unique and interactive associations of proactive and reactive aggression with cortisol secretion.

The association between aggressive behaviors and diurnal cortisol levels has been debated over the past two decades, as some studies found a negative link between the two, whereas others reported no or a positive association. One possible explanation for these contradictory results is that past studies failed to distinguish between proactive (PROA) and reactive (REA) aggression. The present study examined the unique and joint associations of PROA and REA with three diurnal cortisol indicators: awakening levels, awakening response, and diurnal change. Participants were 542 youths (55.4% girls) followed longitudinally. Teachers evaluated aggressive behaviors when participants were in Grades 4 and 6. In Grade 8, participants provided four saliva samples (i.e., awakening, 30 min thereafter, late afternoon, and bedtime) on four collection days. Controlling for several confounders, multilevel regression analyses revealed an inverse relation between PROA and the CAR in boys who displayed lower or moderate levels of REA, but not in those who exhibited higher levels of REA. No associations emerged with other cortisol indicators. These results are consistent with reports of lower physiological activity in individuals with PROA and underscore the confounding influence of REA in the association between the CAR and proactive aggression.

Peer contagion dynamics in the friendships of children with ADHD.

BACKGROUND: Friendships in middle childhood carry high developmental significance. The majority of children with attention-deficit/hyperactivity disorder (ADHD) have few friendships, unstable friendships, or poor relationship quality in any friendships they have. The current study used time-window sequential analysis to map the dynamics within the friendships of children with ADHD, specifically the peer contagion processes of dyadic mutuality and coercive joining. METHODS: Participants were 164 dyads consisting of a target child with ADHD and peer problems (age 6-11 years; 68% male; and 73% white) and a reciprocated friend. Dyads were observed in the lab during a cooperative task eliciting verbal negotiation processes to decide how to share a limited resource and during a fast-paced, engrossing, and competitive task. Both tasks were designed to mirror the real-world interactions of friends. Sequences of dyadic mutuality (i.e., reciprocity of positive affect and positive behaviors) and coercive joining (i.e., reciprocity of aggressive, controlling, and rule-breaking behaviors) between target children and friends were coded. RESULTS: Regarding dyadic mutuality, target children reciprocated their friends' positive affect in both tasks. They also reciprocated their friends' positive behaviors but only in the cooperative task. In contrast, they only reciprocated their friends' coercive joining behaviors in the competitive task. Medium to large reciprocity effects was found for 36%-53% (dyadic mutuality) and 38%-55% (coercive joining) of target children. CONCLUSIONS: These results extend findings of peer contagion processes to the friendships of children with ADHD and suggest that contagion may vary according to interaction context (i.e., competition vs. cooperation). Understanding the spread of peer contagion may illuminate how children with ADHD and their friends influence each other's adjustment over time and may guide friendship-focused psychosocial interventions for this population.

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.