Frank Vitaro

Université de Montréal, Montréal, Quebec, Canada

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Publications (321)941.16 Total impact

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    ABSTRACT: In the current prospective study, we investigated (1) whether high and low BMI in early childhood puts a child at risk of victimization by their peers, and (2) whether being victimized increases BMI over the short- and long-term, independent of the effect of BMI on victimization. We also examined whether gender moderated these prospective associations. Participants were 1,344 children who were assessed yearly from ages 3 to 10 years as part of the Québec Longitudinal Study of Child Development (QLSCD). BMI predicted annual increases in victimization for girls aged 6 years and over; for boys aged 7 and 8 years of age, higher BMI reduced victimization over the school year. Further, victimization predicted annual increases in BMI for girls after age 6 years. When these short-term effects were held constant, victimization was also shown to have a three and 5-year influence on annual BMI changes for girls from age 3 years. These short- and long-term cross-lagged effects were evident when the effects of family adversity were controlled. The findings support those from previous prospective research showing a link between higher BMI and victimization, but only for girls. Further, being victimized increased the likelihood that girls would put on weight over time, which then increased future victimization. The implications of these prospective findings for interventions are considered. Aggr. Behav. 9999:XX–XX, 2015. © 2015 Wiley Periodicals, Inc.
    Aggressive Behavior 01/2015; · 2.25 Impact Factor
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    ABSTRACT: Background Antisocial personality disorder (ASPD) is characterised by elevated impulsive aggression and increased risk for criminal behaviour and incarceration. Deficient activity of the monoamine oxidase A (MAOA) gene is suggested to contribute to serotonergic system dysregulation strongly associated with impulsive aggression and antisocial criminality. Aims To elucidate the role of epigenetic processes in altered MAOA expression and serotonin regulation in a population of incarcerated offenders with ASPD compared with a healthy non-incarcerated control population. Method Participants were 86 incarcerated participants with ASPD and 73 healthy controls. MAOA promoter methylation was compared between case and control groups. We explored the functional impact of MAOA promoter methylation on gene expression in vitro and blood 5-HT levels in a subset of the case group. Results Results suggest that MAOA promoter hypermethylation is associated with ASPD and may contribute to downregulation of MAOA gene expression, as indicated by functional assays in vitro, and regression analysis with whole-blood serotonin levels in offenders with ASPD. Conclusions These results are consistent with prior literature suggesting MAOA and serotonergic dysregulation in antisocial populations. Our results offer the first evidence suggesting epigenetic mechanisms may contribute to MAOA dysregulation in antisocial offenders. Royal College of Psychiatrists.
    The British journal of psychiatry: the journal of mental science 12/2014; · 6.62 Impact Factor
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    ABSTRACT: DNA methylation patterns are characterized by highly conserved developmental programs, but allow for divergent gene expression resulting from stochastic epigenetic drift or divergent environments. Genome-wide methylation studies in monozygotic (MZ) twins are providing insight into the extent of epigenetic variation that occurs, irrespective of genotype. However, little is known about the variability of DNA methylation patterns in adolescence, a period involving significant and rapid physical, emotional, social, and neurodevelopmental change. Here, we assessed genome-wide DNA methylation using the 450 K Illumina BeadChip in a sample of 37 MZ twin pairs followed longitudinally since birth to investigate: 1) the extent of variation in DNA methylation in identical genetic backgrounds in adolescence and; 2) whether these variations are randomly distributed or enriched in particular functional pathways. We also assessed stability of DNA methylation over 3-6 months to distinguish stable trait-like and variable state-like genes. A pathway analysis found high within-pair variability in genes associated with development, cellular mechanisms, tissue and cell morphology, and various disorders. Test-retest analyses performed in a sub-sample of 8 twin pairs demonstrated enrichment in gene pathways involved in organismal development, cellular growth and proliferation, cell signaling, and particular disorders. The variability found in functional gene pathways may plausibly underlie phenotypic differences in this adolescent MZ twin sample. Furthermore, we assessed stability of methylation over 3-6 months and found that some genes were stable while others were unstable, suggesting that the methylome remains dynamic in adolescence and that dynamic sites tend to be organized in certain gene pathways.
    Epigenetics: official journal of the DNA Methylation Society 10/2014; 9(10):1410-22. · 5.11 Impact Factor
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    ABSTRACT: Background Little is known about the associations between self-reported offending and official offending whilst considering different types of offences.AimsThe aims of the present study are to identify developmental trajectories of self-reported violent and nonviolent offending (SRVO; SRNVO) and to examine their associations with official violent and nonviolent offences (as juveniles and adults).Methods Developmental trajectories of SRVO and SRNVO from 11 to 17 years of age were estimated with data from the Montreal Longitudinal and Experimental Study, a prospective longitudinal study of 1037 boys from disadvantaged neighbourhoods.ResultsFive trajectories of SRVO (i.e. Chronic, Desisting, Delayed, Moderate and Low) and three trajectories of SRNVO (Chronic, Moderate and Low) were identified. Chronic, Desisting and Delayed trajectories of SRVO were associated with violent and nonviolent official offending in adolescence and early adulthood, over and above the trajectories of SRNVO. In comparison, trajectories of SRNVO were weakly and inconsistently associated with official offending, once controlling for their overlap with trajectories of SRVO.Conclusions Individuals on high trajectories of violent offending during adolescence are most at risk for being exposed to the justice system both concurrently and longitudinally. Differentiating violent and nonviolent offending can help resolve part of the discordance between self-reported and official offending. Copyright © 2014 John Wiley & Sons, Ltd.
    Criminal Behaviour and Mental Health 10/2014; 24(4). · 1.28 Impact Factor
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    ABSTRACT: Proactive aggression (PA) describes an instrumental behavior that is goal-oriented, whereas reactive aggression (RA) refers to an angry or frustrated aggressive response to a real or perceived threat. Little is known about the respective roles of genetic (G) and environmental (E) factors associated with PA and RA during childhood. The objectives of this study were to investigate a) the G-E etiology of the commonality between PA and RA and b) the presence of G or E components specific to PA or RA throughout childhood (i.e., from 6 to 12 years of age). Participants were 254 monozygotic and 413 dizygotic pairs. Teacher reports of PA and RAwere obtained at 6, 7, 9, 10 and 12 years of age. Throughout childhood, genetic factors accounted for most of the common variance between PAand RA, as well as their specificity. Shared environment played no role. Specifically, genetic factors common to PA and RA explained between 39% and 45% of the variance in PA, and between 27% and 42% of the variance in RA. Genetic factor also uniquely accounted for only but a small percentage (9% at 6 years and 3% at 9 years old) of the variation in PA. As for RA, three distinctive genetic factors contributed to phenotypic variation throughout childhood and explained between 12% and 22% of variance. Dynamic genetic factors accounted for the commonality in PA and RA, and for the specificity of RA. Few genetic factors were unique to PA; in contrast, for RA, an early, specific and persistent genetic factor was found alongside new genetic factors that appeared at later ages. These results challenge theoretical models that focus primarily on the effects of environmental factors in the etiology of reactive and proactive aggression.
    Monatsschrift fûr Kriminologie und Strafrechtsreform. 10/2014; 97.
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    ABSTRACT: The goal of the study was to identify a group of adolescent "slow readers" and retrospectively test which ADHD symptoms and neuropsychological processes were affected at 8 years of age.
    Archives of Clinical Neuropsychology 09/2014; 29(6):546. · 1.92 Impact Factor
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    ABSTRACT: This study examined sibling influence over gambling involvement and delinquency in a sample of 628 twins (151 male dyads, 163 female dyads). Self-reports of gambling involvement and delinquency were collected for each twin at ages 13, 14 and 15 years. Results revealed evidence of between-twin influence. Higher levels of an adolescent's delinquency predicted an increase in his or her co-twin's delinquency from age 13 to age 14 and from age 14 to age 15. In contrast, gambling behavior was unaffected by the co-twin's gambling involvement. Within-twins, higher initial levels of delinquency predicted a subsequent increase in gambling behavior from age 13 to age 14 and again from age 14 to age 15, and higher initial levels of gambling involvement predicted an increase in delinquency from age 14 to age 15. Between and within siblings effects are discussed in light of the scant literature on (a) sibling influence on gambling, and (b) the links between gambling and delinquency.
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    ABSTRACT: In this 16-year longitudinal study, a new trajectory estimation approach was used to verify whether the developmental course of childhood inattention significantly predicted functional impairment. A rising childhood inattention trajectory significantly predicted graduation failure (OR: 1.76 [1.32-2.34]) independently of averaged inattention levels. Rising inattention is, in itself, important for prognosis.
    Psychiatry Research 06/2014; · 2.68 Impact Factor
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    ABSTRACT: This study examined the genetic and environmental architecture of early gambling involvement and substance use to determine whether genetic or environmental factors that contribute to substance use also put young adolescents at risk for early involvement in gambling. Self-reports of substance use and gambling involvement were collected at age 13 years from 279 Monozygotic and Dizygotic twin pairs. Univariate ACE modeling revealed that genetic and nonshared environmental factors almost equally accounted for gambling involvement, with no contribution from shared environmental factors. In contrast, both shared and nonshared environmental factors played important roles in substance use; the contribution of genetic factors was also substantial. Bivariate analyses identified a significant, albeit modest, overlap between the genetic influence on gambling involvement and the genetic influence on substance use. The results shed light on the etiology of early gambling involvement and substance use, suggesting that preventive interventions targeting common risk factors may also need to be complemented by modules that are specific to each behavior.
    Behavior Genetics 05/2014; · 2.84 Impact Factor
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    ABSTRACT: Several authors consider high and frequent conflicts between friends during childhood as a serious risk for subsequent conduct problems such as generalized physical aggression toward others (e.g., Kupersmidt, Burchinal, & Patterson, 1995; Sebanc, 2003). Although it seems logical to assume that friendship conflict could have some negative consequences on children's behaviors, some scholars have suggested that a certain amount of conflict between friends may actually promote social adjustment (e.g., Laursen & Pursell, 2009). The aim of this study was to investigate the role of friendship conflict in regard to the development of generalized physical aggression toward others in the early school years (i.e., from kindergarten to Grade 1), as well as the moderating role of relational (i.e., shared positive affect and dyadic conflict resolution skills) and personal (i.e., children's sex and genetic liability for aggression) characteristics in this context. The sample included 745 twins assessed through teacher, peer, child, and friend ratings in kindergarten and Grade 1. Friendship conflict in kindergarten was linearly related to an increase in boys' but not girls' generalized physical aggression. However, shared positive affect and conflict resolution skills mitigated the prospective associations between friendship conflict and generalized physical aggression. These results were independent of children's sex, genetic risk for physical aggression, and initial levels of generalized physical aggression in kindergarten. Fostering a positive relationship between friends at school entry may buffer against the risk associated with experiencing friendship conflict. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
    Developmental Psychology 03/2014; · 3.21 Impact Factor
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    ABSTRACT: 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.
    Journal of Clinical Child & Adolescent Psychology 03/2014; · 1.92 Impact Factor
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    ABSTRACT: Peer antisocial behavior robustly predicts adolescents' own behavior but not all adolescents are equally vulnerable to their peers' influence and genetic factors may confer vulnerability. This study used data of n = 3081 adolescents from the Avon Longitudinal Study of Parents and Children (ALSPAC) to examine whether BDNF, a polymorphism that affects psychological functioning, moderates the association between affiliation with aggressive peers at age 10 and own aggression at age 15. A significant gene-environment interaction was found, where those who affiliated with aggressive peers in childhood showed increased risk for being aggressive in adolescence if they carried the BDNF met-met variant compared to val-val carriers. Our findings underline the importance of both biological and social factors for adolescent development.
    Journal of Research on Adolescence 03/2014; 24(1):177-185. · 1.99 Impact Factor
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    ABSTRACT: High frequency of physical aggression is the central feature of severe conduct disorder and is associated with a wide range of social, mental and physical health problems. We have previously tested the hypothesis that differential DNA methylation signatures in peripheral T cells are associated with a chronic aggression trajectory in males. Despite the fact that sex differences appear to play a pivotal role in determining the development, magnitude and frequency of aggression, most of previous studies focused on males, so little is known about female chronic physical aggression. We therefore tested here whether or not there is a signature of physical aggression in female DNA methylation and, if there is, how it relates to the signature observed in males. Methylation profiles were created using the method of methylated DNA immunoprecipitation (MeDIP) followed by microarray hybridization and statistical and bioinformatic analyses on T cell DNA obtained from adult women who were found to be on a chronic physical aggression trajectory (CPA) between 6 and 12 years of age compared to women who followed a normal physical aggression trajectory. We confirmed the existence of a well-defined, genome-wide signature of DNA methylation associated with chronic physical aggression in the peripheral T cells of adult females that includes many of the genes similarly associated with physical aggression in the same cell types of adult males. This study in a small number of women presents preliminary evidence for a genome-wide variation in promoter DNA methylation that associates with CPA in women that warrant larger studies for further verification. A significant proportion of these associations were previously observed in men with CPA supporting the hypothesis that the epigenetic signature of early life aggression in females is composed of a component specific to females and another common to both males and females.
    PLoS ONE 01/2014; 9(1):e86822. · 3.53 Impact Factor
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    ABSTRACT: Background. Physical aggression (PA) tends to have its onset in infancy and to increase rapidly in frequency. Very little is known about the genetic and environmental etiology of PA development during early childhood. We investigated the temporal pattern of genetic and environmental etiology of PA during this crucial developmental period.
    Psychological Medicine 01/2014; · 5.43 Impact Factor
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    ABSTRACT: Enriched environments may moderate the effect of genetic factors on prosocial leadership (gene–environment interaction, G × E). However, positive environmental experiences may also themselves be influenced by a genetic disposition for prosocial leadership (gene–environment correlation, rGE). Relating these processes to friendships, the present study examined (a) whether children with a genetic disposition for prosocial leadership possess a greater number of reciprocal friends (rGE) and (b) whether the number of reciprocal friends interacts with the effect of genetic factors on children’s prosocial leadership (G × E). The sample comprised 275 twin pairs assessed in Grade 1 (mean age 84.7 months). Reciprocal friendship and prosocial leadership behavior were measured via peer nominations. Consistent with rGE, a genetic disposition for prosocial leadership was related to an increased likelihood of friendship. Moreover, consistent with a compensation process, environmental influences played a stronger role than genetic influences in prosocial leadership when children had many friends.
    Merrill-Palmer Quarterly 01/2014; 60(2):110-141. · 1.26 Impact Factor
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    ABSTRACT: The goal of this study was to test the impact of two interventions designed to promote social competence in aggressive kindergartners. A sample of 182 aggressive students (69% boys) were randomly assigned to three conditions: a) an intervention promoting social competence in classrooms (PSC); b) PSC intervention combined with a dyadic peer intervention (PSC + DPI), and c) control. The impact of these interventions were assessed using parent and teacher ratings, direct observations of behaviours and individual interviews with the children. After the end of the interventions, children in the two experimental conditions showed better social problem solving skills compared to control children. Direct observations indicated that boys in the PSC condition and girls in the PSC + DPI condition were more incline to propose an idea to their peers. A marginal increase is also found for cooperation in the two experimental conditions. Overall, the impact of the PSC + DPI condition is not superior to the PSC only condition. These findings are discussed in the context of other similar prevention programs and the characteristics of effectiveness studies. (PsycINFO Database Record (c) 2014 APA, all rights reserved)
    Canadian Journal of Behavioural Science / Revue canadienne des sciences du comportement. 01/2014; 46(2):301.
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    ABSTRACT: Chronic physical aggression (CPA) is characterized by frequent use of physical aggression from early childhood to adolescence. Observed in approximately 5% of males, CPA is associated with early childhood adverse environments and long-term negative consequences. Alterations in DNA methylation, a covalent modification of DNA that regulates genome function, have been associated with early childhood adversity. To test the hypothesis that a trajectory of chronic physical aggression during childhood is associated with a distinct DNA methylation profile during adulthood. We analyzed genome-wide promoter DNA methylation profiles of T cells from two groups of adult males assessed annually for frequency of physical aggression between 6 and 15 years of age: a group with CPA and a control group. Methylation profiles covering the promoter regions of 20 000 genes and 400 microRNAs were generated using MeDIP followed by hybridization to microarrays. In total, 448 distinct gene promoters were differentially methylated in CPA. Functionally, many of these genes have previously been shown to play a role in aggression and were enriched in biological pathways affected by behavior. Their locations in the genome tended to form clusters spanning millions of bases in the genome. This study provides evidence of clustered and genome-wide variation in promoter DNA methylation in young adults that associates with a history of chronic physical aggression from 6 to 15 years of age. However, longitudinal studies of methylation during early childhood will be necessary to determine if and how this methylation variation in T cells DNA plays a role in early development of chronic physical aggression.
    PLoS ONE 01/2014; 9(4):e89839. · 3.53 Impact Factor
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    ABSTRACT: L’objectif de cette étude est triple : 1- déterminer le nombre, la forme et le degré de chevauchement des trajectoires types de participation à des jeux de hasard et d’argent (JHA) et de consommation de substances psychotropes (SUP) chez un échantillon de jumeaux au début de l’adolescence ; 2- vérifier les ressemblances et les différences au niveau de l’architecture génétique et environnementale des trajectoires de JHA et de SUP ; 3- déterminer la présence de facteurs de risque associés de manière prédictive aux trajectoires simples ou mixtes de JHA et de SUP. L’échantillon final est composé de 213 (122 paires monozygotes et 91 paires dizygotes de même sexe) paires de jumeaux élevés au sein de la même famille. Les données relatives aux JHA et aux SUP ont été recueillies à 13, 14 et 15 ans à l’aide d’instruments de mesure autoadministrés. Les données relatives aux facteurs de risque touchent un facteur d’ordre personnel (c.-à-d., impulsivité) et des facteurs d’ordre familial mesurés à la préadolescence. Des analyses de trajectoires ont permis de dégager deux trajectoires de participation aux JHA et deux trajectoires de consommation de SUP. Des analyses génétiquement informatives ont permis, par ailleurs, de montrer que les trajectoires de participation à des JHA et de consommation de SUP sont majoritairement sous contrôle génétique. Finalement, des analyses de régression ont révélé des différences au plan des variables associées de façon prédictive aux trajectoires simples ou mixtes de JHA et de SUP. Ces résultats sont abordés à la lumière des changements dans le DSM-V qui établissent un rapprochement entre les problèmes de JHA et les problèmes de SUP.
    Drogues, santé et société. 12/2013; 12(1):20-46.
  • Semaine Santé et Société, Institut Santé et Société, Montreal; 11/2013

Publication Stats

7k Citations
941.16 Total Impact Points


  • 1991–2014
    • Université de Montréal
      • School of Psycho-Education
      Montréal, Quebec, Canada
  • 2013
    • King's College London
      Londinium, England, United Kingdom
  • 1999–2013
    • Laval University
      • • École de Psychologie
      • • Département d'études sur l'enseignement et l'apprentissage
      Québec, Quebec, Canada
    • Université du Québec à Montréal
      • Department of Psychology
      Montréal, Quebec, Canada
  • 1995–2013
    • McGill University
      • • Department of Psychology
      • • Department of Psychiatry
      Montréal, Quebec, Canada
  • 2008–2012
    • Radboud University Nijmegen
      • Behavioural Science Institute
      Nijmegen, Provincie Gelderland, Netherlands
  • 2011
    • CHU Sainte-Justine
      Montréal, Quebec, Canada
  • 2010
    • University College Dublin
      Dublin, Leinster, Ireland
  • 2008–2010
    • University of Alabama
      • Department of Psychology
      Tuscaloosa, AL, United States
  • 2006–2010
    • VU University Amsterdam
      • Department of Developmental Psychology
      Amsterdam, North Holland, Netherlands
  • 2008–2009
    • University College London
      • Division of Psychology and Language Sciences
      London, ENG, United Kingdom
  • 2005–2009
    • Università degli Studi di Genova
      Genova, Liguria, Italy
    • Bishop's University
      Sherbrooke, Quebec, Canada
    • The University of Winnipeg
      • Department of Economics
      Winnipeg, Manitoba, Canada
  • 2005–2006
    • University Medical Center Utrecht
      • Department of Child and Adolescent Psychiatry
      Utrecht, Provincie Utrecht, Netherlands
  • 2003
    • University of New Mexico
      • Department of Sociology
      Albuquerque, NM, United States
  • 2002–2003
    • Carnegie Mellon University
      • School of Public Policy & Management
      Pittsburgh, PA, United States
  • 2000–2001
    • Hôpital du Sacré-Coeur de Montréal
      Montréal, Quebec, Canada
    • University of Jyväskylä
      • Department of Psychology
      Jyväskylä, Province of Western Finland, Finland
  • 1996
    • Gannon University
      Erie, Pennsylvania, United States
  • 1989
    • University of Hull
      Kingston upon Hull, England, United Kingdom
  • 1988
    • Université du Québec
      Québec, Quebec, Canada