Richard Ernest Tremblay’s research while affiliated with Université de Montréal and other places

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 (β = 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 (β = −0.02, p = 0.71, 95% CI = [−0.47–0.32]). Higher BMI variability across development predicted higher cortisol (β = 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.

This paper is a summary of the research I did on the development, prevention and treatment of antisocial behavior over the past half century. It is also a reflection on the intellectual and cultural influences that guided my research, from the classic philosophers to my 21st century peers…including David Farrington.

Executive functions (EF) play an essential role in many spheres of child development. Therefore, it is crucial to get a better understanding of their etiology. Using a genetic design that involved 934 twins (400 monozygotic), this study examined the etiology of cognitive flexibility, a component of EF, at 5 years of age and its phenotypic and etiological associations with maternal control. Cognitive flexibility was measured in a laboratory setting at 5 years of age using a well-known EF-task, i.e. the Dimensional Change Card Sort (DCCS). Maternal control was measured using a self-report questionnaire. The univariate genetic model demonstrated that environmental factors mainly explained individual differences in preschoolers’ performance on the DCCS task. A bivariate genetic model demonstrated that non-shared environmental mechanisms mainly explained the association (r = .−13) between maternal control and children’s performance on the DCCS task. This study represents a preliminary step toward a better understanding of the genetic and environmental contributions underlying the relation between parenting behaviors and children’s EF.

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.

Past research has demonstrated associations between parental personality traits and children's behaviour. However, fathers have been largely excluded from this research, and mothers often rate both their own personality and their child's behaviour, contributing to shared method variance. This study contributes to the literature by examining associations between parental biologically based affective personality traits, analysed separately for mothers and fathers, and seven‐ and eight‐year‐old children's self‐reported internalising and externalising behaviours. Data were analysed for 272 mother‐child dyads and 208 father‐child dyads. A series of multiple linear regressions was utilised to test associations between mothers’ and fathers’ traits of ANGER, SADNESS, FEAR, PLAY, SEEKING and CARE, assessed using the Affective Neuroscience Personality Scales (ANPS), and children's self‐reported internalising and externalising behaviours, assessed using the Berkeley Puppet Interview. Results revealed that higher ANPS ANGER scores amongst mothers were associated with more externalising behaviours in boys. Mothers with higher scores on SEEKING had sons with lower scores on externalising behaviours, while mothers with higher PLAY scores had sons with lower scores on internalising behaviours. Fathers with higher ANPS SADNESS scores had children with greater internalising behaviours, while fathers with greater FEAR traits had children with lower internalising behaviours. Indirect associations through harsh or positive parenting were not significant. Findings demonstrated that ANPS traits of ANGER, PLAY and SEEKING for mothers and FEAR and SADNESS for fathers are associated with children's self‐reported externalising and internalising behaviours. This study adds to the literature on biologically based parental affective personality and children's internalising and externalising behaviours.

High impulsive and aggressive traits associate with poor behavioural self-control. Despite their importance in predicting behavioural negative outcomes including suicide, the molecular mechanisms underlying the expression of impulsive and aggressive traits remain poorly understood. Here, we identified and characterized a novel long noncoding RNA (lncRNA), acting as a regulator of the monoamine oxidase A (MAOA) gene in the brain, and named it MAOA-associated lncRNA (MAALIN). Our results show that in the brain of suicide completers, MAALIN is regulated by a combination of epigenetic mechanisms including DNA methylation and chromatin modifications. Elevated MAALIN in the dentate gyrus of impulsive-aggressive suicides was associated with lower MAOA expression. Viral overexpression of MAALIN in neuroprogenitor cells decreased MAOA expression while CRISPR-mediated knock out resulted in elevated MAOA expression. Using viral-mediated gene transfer, we confirmed that MAALIN in the hippocampus significantly decreases MAOA expression and exacerbates the expression of impulsive-aggressive behavioural traits in CD1 aggressive mice. Overall, our findings suggest that variations in DNA methylation mediate the differential expression of a novel lncRNA that acts on MAOA expression to regulate impulsive-aggressive behaviours.

PurposeTo begin to develop an understanding of knowledge translation of early developmental crime prevention.Methods Involves a narrative review of experiments of early developmental prevention with measures of delinquency and criminal offending, and profiles two leading experiments, the Cambridge-Somerville Youth Study (CSYS) and the Montréal Longitudinal-Experimental Study.ResultsWhile the roots of early developmental crime prevention can be traced to studies of human development, experiments of preventive interventions are at the heart of knowledge translation and policy influence. This can be seen in the form of replications, the process of scaling up effective interventions for wider dissemination, and inspiration for prevention scientists to launch new and innovative experiments—sometimes with the aim to improve upon past results. For example, far from curtailing policy interest in a developmental approach to delinquency prevention or dampening the need for prevention experiments, the harmful effects reported in the 30-year follow-up of the CSYS instead had an influence on some new longitudinal-experimental studies in developmental and life-course criminology.Conclusions New experiments are needed to continue to advance early developmental crime prevention, and further research is needed to add to our understanding of knowledge translation in this area.

Objective: Traumatic brain injuries (TBIs) are sustained by approximately 17% of males in the general population, many whom subsequently present mental disorders, cognitive, and physical problems. Little is known about predictors of TBIs and how to prevent them. The present study aimed to determine whether inattention-hyperactivity and/or all externalizing problems presented by boys at age 10 predict subsequent TBIs to age 34 after taking account of previous TBIs and family social status (FSS). Method: 742 Canadian males were followed, prospectively, from age 6 to 34. Diagnoses of TBIs were extracted from health files, parents reported socio-demographic and family characteristics at participants’ age 6, and teachers rated participants’ behaviors at age 10. Separate logistic regression models predicted TBIs sustained from age 11 to 17, and from age 18 to 34. For each age period, two models were computed, one included previous TBIs, inattention-hyperactivity, FSS, and interaction terms, the second included previous TBIs, externalizing problems, FSS, and interaction terms. Results: In models that included inattention-hyperactivity: TBIs sustained from age 11 to 17 were predicted by age 10 inattention-hyperactivity (OR=1.46, 1.05-2.05) and by TBIs prior to age 11 (OR=3.50, 1.48-8.24); TBIs sustained from age 18 to 34 were predicted by age 10 inattention-hyperactivity (OR=1.31, 1.01-170). In models that included all externalizing problems: TBIs from age 11 to 17 were predicted by prior TBIs (OR=3.66, 1.51-8.39); TBIs sustained from age 18 to 34 were predicted by age 10 externalizing problems (OR=1.45, 1.12-1.86). Neither FSS nor interaction terms predicted TBIs in any of the models. Conclusions: Among males, using evidence-based treatments to reduce inattention-hyperactivity and externalizing problems among boys could, potentially, decrease the risk of TBIs to age 34. Further, boys who sustain TBIs in childhood require monitoring to prevent recurrence in adolescence.