Alain Girard
Université de Montréal
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Featured researches published by Alain Girard.
Development and Psychopathology | 2008
Mara Brendgen; Michel Boivin; Frank Vitaro; Alain Girard; Ginette Dionne; Daniel Pérusse
Although peer victimization places children at serious risk for aggressive behavior, not all victimized children are aggressive. The diathesis-stress hypothesis of disease proposes that an environmental stressor such as peer victimization should to lead to maladjustment mostly in those individuals with preexisting genetic vulnerabilities. Accordingly, this study examined whether the link between peer victimization and child aggression is moderated by childrens genetic risk for such behavior. Using a sample of 506 6-year-old twins, peer victimization was assessed through peer nominations and aggressive behavior was assessed through peer and teacher reports. Childrens genetic risk for aggression was estimated as a function of their co-twins aggression and the pairs zygosity. Genetic modeling showed that peer victimization is an environmentally driven variable that is unrelated to childrens genetic disposition. Results also provided support for the notion of a gene-environment interaction between peer victimization and childs genetic risk for aggressive behavior, albeit only in girls. For boys, peer victimization was related to aggression regardless of the childs genetic risk for such behavior. Different socialization experiences in girls compared to boys peer groups may explain the different pattern of results for girls and boys.
Child Development | 2011
Mara Brendgen; Michel Boivin; Ginette Dionne; Edward D. Barker; Frank Vitaro; Alain Girard; Richard E. Tremblay; Daniel Pérusse
Aggressive behavior in middle childhood is at least partly explained by genetic factors. Nevertheless, estimations of simple effects ignore possible gene-environment interactions (G × E) or gene-environment correlations (rGE) in the etiology of aggression. The present study aimed to simultaneously test for G × E and rGE processes between aggression, on the one hand, and peer victimization and the teacher-child relationship in school, on the other hand. The sample comprised 124 MZ pairs and 93 DZ pairs assessed in Grade 1 (mean age = 84.7 months). Consistent with rGE, children with a presumed genetic disposition for aggression were at an increased risk of peer victimization, whereas in line with G × E, a positive relationship with the teacher mitigated the genetically mediated expression of aggression.
Journal of Child Psychology and Psychiatry | 2009
Mara Brendgen; Frank Vitaro; Michel Boivin; Alain Girard; William M. Bukowski; Ginette Dionne; Richard E. Tremblay; Daniel Pérusse
BACKGROUNDnGenetic risk for depressive behavior may increase the likelihood of exposure to environmental stressors (gene-environment correlation, rGE). By the same token, exposure to environmental stressors may moderate the effect of genes on depressive behavior (gene-environment interaction, GxE). Relating these processes to a peer-related stressor in childhood, the present study examined (1) whether genetic risk for depressive behavior in children is related to higher levels of rejection by the peer group (rGE) and (2) whether peer rejection moderates the effect of genetic factors on childrens depressive behavior (GxE).nnnMETHODSnThe sample comprised 336 twin pairs (MZ pairs = 196, same-sex DZ pairs = 140) assessed in kindergarten (mean age 72.7 months). Peer acceptance/rejection was measured via peer nominations. Depressive behavior was measured through teacher ratings.nnnRESULTSnConsistent with rGE, a moderate overlap of genetic effects was found between peer acceptance/rejection and depressive behavior. In line with GxE, genetic effects on depressive behavior varied across levels of peer acceptance/rejection.nnnCONCLUSIONSnAn increased genetic disposition for depressive behavior is related to a higher risk of peer rejection (rGE). However, genes play a lesser role in explaining individual differences in depressive behavior in rejected children than in accepted children (GxE).
Human Brain Mapping | 2007
Catherine Côté; Mario Beauregard; Alain Girard; Boualem Mensour; Adham Mancini-Marïe; Daniel Pérusse
Functional neuroimaging studies show substantial individual variation in brain activation accompanying the experience of emotion, including sadness. Here we used functional magnetic resonance imaging (fMRI) in 104 pairs of 8‐year‐old twins (47 MZ, 57 DZ) to assess genetic‐environmental contributions to individual differences in neural activation in two prefrontal cortex (PFC) areas previously shown to be involved in sadness. No genetic effects were found for any area, individual environmental factors entirely accounting for individual variation in brain activation related to sadness. Sadness being the prevailing mood in depression, these findings may be of relevance to the etiology of childhood depressive disorders. Hum Brain Mapp 2007.
Child Development | 2011
Frank Vitaro; Mara Brendgen; Michel Boivin; Stéphane Cantin; Ginette Dionne; Richard E. Tremblay; Alain Girard; Daniel Pérusse
This study used the monozygotic (MZ) twin difference method to examine whether differences in friends aggression increased the differences in MZ twins aggression and depressive symptoms from kindergarten to Grade 1 and whether perceived victimization by the friend played a mediating role in this context. Participants were 223 MZ twin pairs. Results showed that differences in kindergarten friends aggression significantly predicted an increased difference in MZ twins aggression from kindergarten (mean age = 6.7 years) to Grade 1 (mean age = 7.5 years) for both boys and girls. Differences in perceived victimization by the friend mediated this association, albeit only in boys. Differences in perceived victimization by the friend also predicted an increase in MZ twins differences in depressive symptoms. These results support the importance of friendship experiences during early childhood.
Child Development | 2013
Michel Boivin; Mara Brendgen; Frank Vitaro; Ginette Dionne; Alain Girard; Daniel Pérusse; Richard E. Tremblay
This study assessed the genetic and environmental contributions to peer difficulties in the early school years. Twins peer difficulties were assessed longitudinally in kindergarten (796 twins, Mage = 6.1 years), Grade 1 (948 twins, Mage = 7.1 years), and Grade 4 (868 twins, Mage = 10 years) through multiple informants. The multivariate results revealed that genetic factors accounted for a strong part of both yearly and stable peer difficulties. At the univariate level, the genetic contributions emerged progressively, as did a growing consensus among informants with respect to those who experienced peer difficulties. These results underline the need to intervene early and persistently, and to target the child and the peer context to prevent peer difficulties and their consequences.
Infant Behavior & Development | 2009
Robert Soussignan; Michel Boivin; Alain Girard; Daniel Pérusse; Xuecheng Liu; Richard E. Tremblay
The study investigated the genetic and environmental contributions to individual differences in measures of socioemotional reactivity and emotion regulation with a sample of 115 monozygotic (MZ) and 156 dizygotic (DZ) 5-month-old twin pairs. Twins zygosity was determined by a combination of DNA typing and physical similarity. Twins behaviors (motor activity level, social gaze, gaze aversion, positive expression, negative expression, and self-comfort) were videotaped in a laboratory while infants were presented televised sequences of neutral and happy emotional expressions posed by their mother (familiar condition) and a female stranger (unfamiliar condition). Regardless of the social context, the findings based on model-fitting analyses indicated that nonshared environmental influences explained most of the variance of behavioral data. However, there was evidence that motor activity level (an index of emotional arousal) and the latency and frequency of gaze aversion (an index of emotional regulation) were best represented by a model incorporating both additive genetic and nonshared environmental (i.e., AE) influences when infants were exposed to the unfamiliar adult (heritability estimates ranging from 19% to 31%). The results suggest the importance of nonshared environmental influences during early infancy and stress the role of social context for revealing moderate genetic contributions to individual differences in emotional arousal and emotion regulation.
International Journal of Behavioral Development | 2016
Frank Vitaro; Mara Brendgen; Alain Girard; Ginette Dionne; Richard E. Tremblay; Michel Boivin
Exposure to deviant friends has been found to be a powerful source of influence on children’s and adolescents’ aggressive behavior. However, the contribution of deviant friends may have been overestimated because of a possible non-accounted gene-environment correlation (rGE). In this study, we used a cross-lagged design to test whether friends’ physical aggression at age 10 predicts an increase in participants’ physical aggression from age 10 to age 13 years. Participants were 201 pairs of monozygotic twins who are part of the Quebec Longitudinal Twin Study. We performed two sets of analyses. In the first set of analyses, using twins as singletons, we found that teacher-rated friends’ physical aggression predicted an increase in each twin’s self-reported physical aggression from age 10 to age 13, above and beyond auto-regressive and concurrent links. Second, we used within-pair differences in regard to friends’ physical aggression to predict an increase in within-pair differences in physical aggression, thus accounting for family-wide influences, including a likely rGE at age 10. No significant association was found, however. These results suggest that part of the influence attributed to friends in past studies may have been due to common underlying genetic effects on both physical aggression and association with physically aggressive friends.
Journal of Youth and Adolescence | 2015
Frank Vitaro; Mara Brendgen; Alain Girard; Michel Boivin; Ginette Dionne; Richard E. Tremblay
Numerous studies have shown that aggressive and non-aggressive antisocial behaviors are important precursors of later adjustment problems. There is also strong empirical evidence that both types of antisocial behavior are partially influenced by genetic factors. However, despite its important theoretical and practical implications, no study has examined the question whether environmental factors differentially moderate the expression of genetic influences on the two types of antisocial behavior. Using a genetically informed design based on 266 monozygotic and dizygotic twin pairs, this study examined whether the expression of genetic risk for aggressive and non-aggressive antisocial behavior varies depending on the peer group’s injunctive norms (i.e., the degree of acceptability) of each type of antisocial behavior. Self-reported aggressive and non-aggressive antisocial behavior and classroom-based sociometric nominations were collected when participants were 10xa0years old. Multivariate genetic analyses revealed some common genetic factors influencing both types of antisocial behavior (i.e., general antisocial behavior) as well as genetic influences specific to non-aggressive antisocial behavior. However, genetic influences on general antisocial behavior, as well as specific genetic influences on non-aggressive antisocial behavior, vary depending on the injunctive classroom norms regarding these behaviors. These findings speak to the power of peer group norms in shaping aggressive and non-aggressive antisocial behavior. They also contribute further to understanding the distinctive development of both types of antisocial behavior. Finally, they may have important implications for prevention purposes.
Journal of Clinical Child and Adolescent Psychology | 2016
Catherine Serra Poirier; Mara Brendgen; Alain Girard; Frank Vitaro; Ginette Dionne; Michel Boivin
This study examined (a) whether, in line with a gene-environment correlation (rGE), a genetic disposition for anxiety puts children at risk of having anxious friends or having no reciprocal friends; (b) to what extent these friendship experiences are related to anxiety symptoms, when controlling for sex and genetic disposition for this trait; and (c) the additive and interactive predictive links of the reciprocal best friends anxiety symptoms and of friendship quality with childrens anxiety symptoms. Using a genetically informed design based on 521 monozygotic and ic twins (264 girls; 87% of European descent) assessed in Grade 4 (M age = 10.04 years, SD = .26), anxiety symptoms and perceived friendship quality were measured with self-report questionnaires. Results indicated that, in line with rGE, children with a strong genetic disposition for anxiety were more likely to have anxious friends than nonanxious friends. Moreover, controlling for their genetic risk for anxiety, children with anxious friends showed higher levels of anxiety symptoms than children with nonanxious friends but did not differ from those without reciprocal friends. Additional analyses suggested a possible contagion of anxiety symptoms between reciprocal best friends when perceived negative features of friendship were high. These results underline the importance of teaching strategies such as problem solving that enhance friendship quality to limit the potential social contagion of anxiety symptoms.