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Objective: This study examined whether (a) a genetic disposition for physical health problems increases the risk of peer victimization and (b) peer victimization interacts with genetic vulnerability in explaining physical health problems., Methods: Participants were 167 monozygotic and 119 dizyogtic twin pairs. Physical symptoms were assessed in early childhood and early adolescence. Peer victimization was assessed in middle childhood., Results: Genetic vulnerability for physical health problems in early childhood was unrelated to later peer victimization, but genetic vulnerability for physical health problems during early adolescence increased the risk of victimization. Victimization did not interact with genetic factors in predicting physical symptoms. Environmental, not genetic, factors had the greatest influence on the development of physical symptoms in victims., Conclusion: Genetic vulnerability for physical health problems in early adolescence increases the risk of peer victimization. Whether victims suffer a further increase in physical symptoms depends on the presence of protective environmental factors.

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., (© 2012 The Authors. Child Development © 2012 Society for Research in Child Development, Inc.)

Objective: To examine the genetic and environmental influences on variances in weight, height, and BMI, from birth through 19 years of age, in boys and girls from three continents., Design and Settings: Cross-sectional twin study. Data obtained from a total of 23 twin birth-cohorts from four countries: Canada, Sweden, Denmark, and Australia. Participants were Monozygotic (MZ) and dizygotic (DZ) (same- and opposite-sex) twin pairs with data available for both height and weight at a given age, from birth through 19 years of age. Approximately 24,036 children were included in the analyses., Results: Heritability for body weight, height, and BMI was low at birth (between 6.4 and 8.7% for boys, and between 4.8 and 7.9% for girls) but increased over time, accounting for close to half or more of the variance in body weight and BMI after 5 months of age in both sexes. Common environmental influences on all body measures were high at birth (between 74.1-85.9% in all measures for boys, and between 74.2 and 87.3% in all measures for girls) and markedly reduced over time. For body height, the effect of the common environment remained significant for a longer period during early childhood (up through 12 years of age). Sex-limitation of genetic and shared environmental effects was observed., Conclusion: Genetics appear to play an increasingly important role in explaining the variation in weight, height, and BMI from early childhood to late adolescence, particularly in boys. Common environmental factors exert their strongest and most independent influence specifically in pre-adolescent years and more significantly in girls. These findings emphasize the need to target family and social environmental interventions in early childhood years, especially for females. As gene-environment correlation and interaction is likely, it is also necessary to identify the genetic variants that may predispose individuals to obesity.

Home environment quality is a well-known predictor of school readiness (SR), although the underlying processes are little known. This study tested two hypotheses: (a) child language mediates the association between home characteristics (socioeconomic status and exposure to reading) and SR, and (b) genetic factors partly explain the association between language and SR. Data were collected between 6 and 63 months in a large sample of twins. Results showed that home characteristics had direct effects on SR and indirect effects through child language. No genetic correlation was found between language and SR. These results suggest that home characteristics affect SR in part through their effect on early language skills, and show that this process is mainly environmental rather than genetic in nature.

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.

Attention deficit hyperactivity disorder (ADHD) is the most prevalent psychiatric disorder emerging during childhood. Psychostimulant medications (e.g., methylphenidate) noticeably reduce ADHD symptoms in most children. Since methylphenidate inhibits dopamine transporter activity, the dopamine transporter gene (DAT1) was considered to be the prime candidate risk gene in ADHD. Several studies found evidence for an association between the 10-repeat allele of the variable number of tandem repeat (VNTR) located in the 3' untranslated region and ADHD and/or ADHD symptoms in clinical and population-based samples. However, this finding was not replicated in all samples. In this study, we investigated the association between the DAT1 gene and ADHD symptoms in a population-based twin sample from Québec (Canada). We used two polymorphisms, the VNTR and rs27072, the last providing the most significant results in a clinical sample from Toronto (Ontario, Canada). No association was noted between the VNTR and ADHD symptoms in children at 6 and 7 years of age, as reported by teachers. However, a significant association was found for the rs27072 polymorphism and symptoms of inattention and hyperactivity/impulsivity. These findings indicate that the DAT1 gene contributes to ADHD symptoms in this sample and further suggest that the VNTR may not be the optimal polymorphism for study in all populations., (Copyright 2007 Wiley-Liss, Inc.)

Objective: There is growing evidence that genetic factors are involved in the occurrence of sleep terrors. Twin studies provide invaluable information regarding genetic and environmental factors that can affect the manifestation of the disease; however, most previous twin studies on sleep terrors were performed retrospectively or with a sample that was too small to yield conclusive results. The aim of this large prospective study was to clarify the genetic and environmental contributions to sleep terrors in childhood., Methods: In all, 390 pairs of monozygotic and dizygotic twins were recruited at birth for a longitudinal study. The prevalence and frequency of sleep terrors were assessed at 18 and 30 months of age with a questionnaire administered to the biological mother of the twins. Zygosity was determined by a questionnaire and genotyping. The prevalence and polychoric correlation for each type of twins were calculated. Structural-equation modeling was used to determine the proportion of variance attributable to additive genetic, shared, and nonshared environmental factors., Results: The prevalence of sleep terrors was 36.9% at 18 months and 19.7% at 30 months; 49% of affected children were boys, and 51% were girls. At 18 months, the polychoric correlations were 0.63 for monozygotic and 0.36 for the dizygotic twins. These were 0.68 (monozygotic) and 0.24 (dizygotic) at 30 months. Our model-fitting analysis showed that sleep terrors were explained by a 2-component model at 18 months (43.7% additive genetic effects and 56.3% nonshared environment) and at 30 months (41.5% additive genetic effects and 58.5% nonshared environment)., Conclusions: These results strongly support the heritability of sleep terrors. There also seems to be continuity in genetic effects with the persistence of sleep-terror symptoms.

Using a genetic design of 840 60-month-old twins, this study investigated the genetic and environmental contributions to (a) individual differences in four components of cognitive school readiness, (b) the general ability underlying these four components, and (c) the predictive association between school readiness and school achievement. Results revealed that the contribution of the shared environment for cognitive school readiness was substantial. Genetic effects were more important for the core abilities underlying school readiness than for each specific skill, although shared environment remained the largest factor overall. Genetic, shared, and nonshared environmental factors all accounted for the predictive association between school readiness and early school achievement. These results contribute to a better understanding of the early determinants of school readiness.

This study examined (a) the predictive link between peer victimization and children's reactive and proactive aggression, and (b) the potential moderating effect of reciprocal friends' reactive and proactive aggression in this context. The study also examined whether these potential moderating effects of friends' characteristics were stronger with respect to more recent friends compared to previous friends. Based on a convenience sample of 658 twin children (326 boys and 332 girls) assessed in kindergarten and first grade, the results showed that peer victimization uniquely predicted an increase in children's teacher-rated reactive aggression, but not teacher-rated proactive aggression. The relation of peer victimization to increased reactive aggression was, however, moderated by recent not previous reciprocal friends' similarly aggressive characteristics. These findings, however, tended to be mostly true for boys, but not for girls. The findings are discussed in terms of their theoretical and practical implications for victimized children's risk of displaying reactive and proactive aggressive behaviors.

Children's negative characteristics are thought to be a factor in evoking hostile parenting responses. This can result in genotype/environment correlations (rGE) in which children's heritable traits influence the parenting they experience. We did genetic analyses on 292 mothers' self-reported hostile-reactive behaviors toward each of their twins at 5, 18 and 30 months. Finding heritability for a parenting behavior analyzed as a child phenotype is evidence of rGE correlation. The heritability of maternal behavior was modest (29% at 5 months, 0% at 18 months, and 25% at 30 months) and longitudinal analyses indicated that genetic factors at 5 and 30 months were uncorrelated. Common environment factors, probably reflecting characteristics of the mothers, were the main source of variance at the three ages and were highly correlated through time. We concluded that children's heritable characteristics evoked maternal negative response at specific times, but were not responsible for the stability of maternal hostility from infancy to toddlerhood.

Objective: To examine whether kindergarten children's genetic liability to physically aggress moderates the contribution of friends' aggression to their aggressive behaviors., Method: Teacher and peer reports of aggression were available for 359 6-year-old twin pairs (145 MZ, 212 DZ) as well as teacher and peer reports of aggression of the two best friends of each twin. Children's genetic risk for aggression was based on their cotwin's aggression status and the pair's zygosity., Results: Children's aggression was highly heritable. Unique environment accounted for most of the variance in friends' aggression, although there was also a small genetic contribution (15%). Both genetic liability to aggression and having aggressive friends predicted twins' aggression. However, the contribution of aggressive friends to children's aggression was strongest among genetically vulnerable children. This result was similar for boys and girls, despite sex differences in both aggression and the level of aggression of friends., Conclusions: Affiliation with aggressive friends at school entry is a significant environmental risk factor for aggression, especially for children genetically at risk for aggressive behaviors. Developmental models of aggression need to take into account both genetic liability and environmental factors in multiple settings, such as the peer context, to more precisely describe and understand the various developmental pathways to aggression. The implications for early prevention programs are discussed.

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., ((c) 2007 Wiley-Liss, Inc.)

Using a genetic design of 234 six-year-old twins, this study examined (a) the contribution of genes and environment to social versus physical aggression, and (b) whether the correlation between social and physical aggression can be explained by similar genetic or environmental factors or by a directional link between the phenotypes. For social aggression, substantial (shared and unique) environmental effects but only weak genetic effects were found. For physical aggression, significant effects of genes and unique environment were found. Bivariate modeling suggests that social and physical aggression share most of their underlying genes but only very few overlapping environmental factors. The correlation between the two phenotypes can also be explained by a directional effect from physical to social aggression.

Background: Given the importance of parenting for the child's early socio-emotional development, parenting perceptions and behaviours, and their correlates, should be assessed as early as possible in the child's life. The goals of the present study were 1) to confirm, in two parallel population-based samples, including a large sample of twins, the factor structure of a new self-administered questionnaire assessing both parents' specific parenting perceptions and behaviours toward their 5-month-old infants (i.e., parental self-efficacy, perceived parental impact, parental hostile-reactive behaviours and parental overprotection), 2) to identify the specific risk factors associated with the negative side of these parenting dimensions, 3) to document the genetic-environmental etiology of these parenting dimensions through the twin method., Methods: Parents (2,122 mothers and 1,829 fathers) of 5-month-old infants, and parents of 5-month-old infant twins (510 families) completed the questionnaire (28 items). The data were submitted to a series of confirmatory factor analyses. The contribution to parenting of a variety of risk factors was examined in the two samples using regression analyses. A series of quantitative genetic analyses were performed to quantify the different sources of variation in parenting., Results: A consistent factor structure was found across informants and across samples. There were significant mean differences in parenting between mothers and fathers, as well as between parents of twins and parents of singletons. A differentiated pattern of association with risk factors was found for each dimension of parenting. The twin analyses revealed that shared environment accounted for each parenting dimension. Maternal hostile-reactive behaviours were also moderately related to genetic factors in the child and this association was mainly mediated by the infant difficultness., Conclusions: The overall pattern of results was consistent with Belsky's (1984) view of parenting as multiply determined. The longitudinal follow-up of these families should provide the means for testing developmental models about the determinants and outcomes of these parenting dimensions.

In the prevention of physical aggression, possible etiological links with language development are rarely taken into account. Indeed, little is known about when language and aggressive behavior become linked during development and which mechanisms are responsible for this association. This study investigated the association between physical aggression and language in late infancy with a genetic design that involved 562 19-month-old twins. A modest but significant correlation (r = -.20) was found between physical aggression and expressive vocabulary. Substantial heritability was found for physical aggression. Quantitative genetic modeling suggests that the correlation between expressive vocabulary and physical aggression cannot be explained by shared etiologies. However, phenotype-to-phenotype models indicate that the covariation can be entirely accounted for by a significant phenotypic path from expressive vocabulary to physical aggression. The implications of these results for early prevention of chronic physical aggression are discussed.

Genetic and environmental contributions to body size from birth to 5 years in a population-based twin cohort were studied. Sex differences in gene-environment etiology were also explored. Analyses used data from the Quebec Newborn Twin Study (QNTS), a population-based birth cohort of 672 twin pairs. The final sample consisted of 177 complete twin pairs. Heritability of weight was moderate at birth while common environmental factors accounted for almost half of the variance. Influence of family environment disappeared by 5 months and genetic effects were high (approximately 90%) for both sexes at 5 months and 5 years. Adjustment of weight for height yielded similar results as for weight alone. Slight but significant sex-limitation of genetic effects was observed at 5 months. Overall, genetic factors accounted for 40% of birthweight variance, with intrauterine environment influences explaining almost half. However, genetic factors accounted for most of the variance in weight. These results do not imply a lack of environmental effects on body weight, but rather a lack of: (1) environmental effects that are independent from genetic liability, and/or (2) a lack of significant environmental variation in the population (e.g., uniform nutritional habits) that leaves genetic differences between children to generate most of the variance in weight. [ABSTRACT FROM AUTHOR]

The Quebec Newborn Twin Study (QNTS) is 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 bio-social determinants, as well as their putative role in later social-emotional adjustment, school and health 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 has 14 waves of data collected or planned, including 5 in preschool. Over the past 15 years, a broad range of physiological, cognitive, behavioral, school, and health phenotypes were documented longitudinally through multi-informant and multi-method measurements. QNTS also entails extended and detailed multi-level assessments of proximal (e.g., parenting behaviors, peer relationships) and distal (e.g., family income) features of the child's environment. This detailed longitudinal information makes QNTS uniquely suited for the study of the role of the early years and gene-environment transactions in development. [ABSTRACT FROM AUTHOR]

Background Eating behaviors during childhood are related both to children's diet quality and to their weight status. A better understanding of the determinants of eating behavior during childhood is essential for carrying out effective dietary interventions. Methods We assessed the contribution of genetic and environmental factors to variations in selected eating behaviors in early and late childhood. Information on eating behaviors came from questionnaires administered to parents of children participating in the Quebec Newborn Twin Study when the twins were 2.5 and 9 years old (n = 692 children). Dichotomous variables were derived and analyzed using structural equation modeling, as part of a classic twin study design. We performed univariate and bivariate longitudinal analyses to quantify sources of variation and covariation across ages, for several eating behavior traits. Results We found moderate to strong heritability for traits related to appetite such as eating too much, not eating enough and eating too fast. Univariate analysis estimates varied from 0.71 (95% CI: 0.49, 0.87) to 0.89 (0.75, 0.96) in younger children and from 0.44 (0.18, 0.66) to 0.56 (0.28, 0.78) in older children. Bivariate longitudinal analyses indicated modest to moderate genetic correlations across ages (rA varying from 0.34 to 0.58). Common genetic influences explained 17% to 43% of the phenotypic correlation between 2.5 and 9 years for these appetite-related behaviors. In 9-year-old children, food acceptance traits, such as refusing to eat and being fussy about food, had high heritability estimates, 0.84 (0.63, 0.94) and 0.85 (0.59, 0.96) respectively, while in younger children, the shared environment (i.e., common to both twins) contributed most to phenotypic variance. Variances in meal-pattern-related behaviors were mostly explained by shared environmental influences. Conclusions Genetic predispositions explain a large part of the variations in traits related to appetite during childhood, though our results suggest that as children get older, appetite-related behaviors become more sensitive to environmental influences outside the home. Still, for several traits environmental influences shared by twins appear to have the largest relative importance. This finding supports the notion that familial context has considerable potential to influence the development of healthy eating habits throughout childhood. [ABSTRACT FROM AUTHOR]

The present study examined the association between theory of mind and indirect versus physical aggression, as well as the potential moderating role of prosocial behavior in this context. Participants were 399 twins and singletons drawn from two longitudinal studies in Canada. At five years of age, children completed a theory of mind task and a receptive vocabulary task. A year later, teachers evaluated children's indirect and physical aggression and prosocial behavior. Indirect aggression was significantly and positively associated with theory of mind skills, but only in children with average or low levels of prosocial behavior. Physical aggression was negatively associated with prosocial behavior but not with theory of mind. Each analysis included gender, receptive vocabulary, and the respective other subtype of aggression as control variables. These results did not differ between girls and boys or between twins and singletons. Theoretical and clinical implications of these findings are discussed. [ABSTRACT FROM AUTHOR]

Background: Genetic 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, G×E). 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 children’s depressive behavior (G×E). Methods: The 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. Results: Consistent with rGE, a moderate overlap of genetic effects was found between peer acceptance/rejection and depressive behavior. In line with G×E, genetic effects on depressive behavior varied across levels of peer acceptance/rejection. Conclusions: An 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 (G×E). [ABSTRACT FROM AUTHOR]

This study investigated the understanding of false belief and emotion in monozygotic (MZ) and same-sex dizygotic (DZ) twin pairs compared to non-twin children. Aged 3;9 to 5;1 years, the children (N=123) were administered three false belief and three emotion understanding tasks. Age, family socioeconomic status, mother's level of education and language abilities were controlled. Results showed no difference between the three groups in false belief understanding. On emotion tasks, non-twin children and DZ twins did not differ from each other, but they both performed better than MZ twins. Results are discussed in terms of the Peterson's (2000) variety hypothesis and suggest that the affective closeness experienced by MZ twins might interfere with their understanding of others' emotions. [ABSTRACT FROM AUTHOR]

An abstract of the article "Sleep Terrors in Children: A Prospective Study of Twins," by Bich Hong Nguyen, Daniel Pérusse, Jean Paquet, Dominique Petit, Michel Boivin, Richard E. Tremblay, and Jacques Montsplair is presented.

Background: Dysregulation of daytime cortisol activity has been associated with stress-related pathologies. Research suggests that early environmental adversity might shape cortisol activity. However, little is known about the genetic and environmental contributions to early cortisol and how this varies as a function of environmental circumstances. The goals of the study were to estimate the genetic and environmental contributions to daytime cortisol secretion in infant twins and to investigate whether these contributions varied as a function of familial adversity (FA). Methods: Participants were 517 6-month-old twins. Salivary cortisol was collected when the infants woke up at home and in the morning, upon arrival at the laboratory. Familial adversity was defined by seven perinatal and postnatal risk factors: maternal smoking during pregnancy, low birth weight, low family income, low maternal education, single parenthood, young motherhood, and maternal hostile/reactive behaviors. Genetic and environment contributions to cortisol activity were estimated for high (three risk factors or more: 21.3% of the sample) versus low FA. Results: Genetic factors accounted for cortisol levels in different ways: a moderate “main effect” of genes was found for home-based awakening cortisol, whereas the contribution of genes to morning cortisol was conditional to FA. Genetic factors accounted for most of the variance in morning cortisol in high family adversity but not in low family adversity. Conclusions: Early FA modulates the heritability of morning cortisol in infants. The results are consistent with the diathesis-stress model, with genetic factors more likely to be expressed in adverse settings. [Copyright &y& Elsevier]

Abstract: Background: Few twin studies have examined nutrition-related phenotypes among children, and none has investigated energy and macronutrient intakes. Objective: The objective was to quantify genetic and environmental influences on variations in energy and macronutrient intakes among children aged 9years. Design: We conducted a nutrition study among children participating in the Quebec Newborn Twin Study, a population-based birth cohort of twins. We derived dietary data from two multiple-pass 24-hour dietary recalls with a parent and his or her child. The analysis employed a classic twin study design and used data from 379 twin pairs. Results: Univariate analyses indicate that heritability for mean daily energy (kcal) and macronutrient (g) intakes was moderate, ranging from 0.34 (95% CI: 0.22, 0.46) to 0.42 (0.31, 0.53). Genetic effects also accounted for 0.28 (0.16, 0.40) of the variance in percent of energy from lipids, while only environmental (shared and unique) effects accounted for the variance in percent of energy from proteins and carbohydrates. The shared environment did not contribute to variations in daily intakes for most of the nutritional variables under study. Multivariate analyses suggest the presence of macronutrient-specific genetic influences for lipids and carbohydrates, estimated at 0.12 (0.04, 0.19) and 0.20 (0.11, 0.29) respectively. Conclusions: The unique environment (i.e., not shared by family members) has the largest influence on variances in daily energy and macronutrient intakes in 9-year-old children. This finding underscores the need to take obesogenic environments into account when planning dietary interventions for younger populations. [Copyright &y& Elsevier]

Abstract: Glucocorticoids (GCs) have been related to social rank in many studies across species, a particular rank giving rise to a particular stress-related physiological profile. Our aim was to examine the hypothesis that GCs levels in toddlers would be related to social dominance in a competitive resource situation. Subjects were 376 toddlers from the Quebec Newborn Twin Study. At 19months of age, each subject was exposed to 2 unfamiliar situations known to be moderately stressful at that age. Saliva was collected before and after the unfamiliar situations, to assess pre-test and reactive cortisol. Then the toddler reaction to a competitive situation for a toy with an unfamiliar peer was assessed and we measured the proportion of time the child controlled the resource. In girls, no association between cortisol levels and the proportion of time the child got the toy was found. On the other hand, in boys, increased cortisol levels before the unfamiliar situation were significantly related to a decreased proportion of time they got the toy in the competitive situation (r 174 =−0.17, P =0.02). These results show that even in toddlers with limited social experience, association between GCs levels and social dominance can be found, an association that is specific to boys. [Copyright &y& Elsevier]

This study compared the contribution of genes and environment to teacher-rated reactive and proactive aggression in 6-year-old twin pairs (172 pairs: 55 monozygotic girls, 48 monozygotic boys, 33 dizygotic girls, 36 dizygotic boys). Genetic effects accounted for 39% of the variance of reactive aggression and for 41% of the variance of proactive aggression. The remainder of the variance was explained by unique environmental effects. Genetic as well as unique environmental effects were significantly correlated across reactive and proactive aggression (genetic correlation = .87, environmental correlation = .34), but this overlap was largely due to a common underlying form of aggression (i.e., teacher-rated physical aggression). Once common etiological factors due to physical aggression were accounted for, reactive and proactive aggression shared no other genes and only a few environmental influences, although additional specific genetic and environmental effects were observed for both reactive and proactive aggression. These specific effects indicate that both reactive and proactive aggression may be influenced mostly by socialization experiences that are specific to each type of aggression and only to a very small degree by specific genes. [ABSTRACT FROM AUTHOR]