Developmental structure of genetic influences on antisocial behavior across childhood and adolescence (original) (raw)
Related papers
The Genetic and Environmental Etiology of Antisocial Behavior from Childhood to Emerging Adulthood
Behavior Genetics, 2011
Previous research suggests that both genetic and environmental influences are important for antisocial behavior across the life span, even though the prevalence and incidence of antisocial behavior varies considerably across ages. However, little is known of how genetic and environmental effects influence the development of antisocial behavior. A total of 2,600 male and female twins from the population-based Swedish Twin Registry were included in the present study. Antisocial behavior was measured on four occasions, when twins were 8-9, 13-14, 16-17, and 19-20 years old. Longitudinal analyses of the data were conducted using structural equation modeling. The stability of antisocial behavior over time was explained by a common latent persistent antisocial behavior factor. A common genetic influence accounted for 67% of the total variance in this latent factor, the shared environment explained 26%, and the remaining 7% was due to the nonshared environment. Significant age-specific shared environmental factors were found at ages 13-14 years, suggesting that common experiences (e.g., peers) are important for antisocial behavior at this age. Results from this study show that genetic as well as shared environmental influences are important in antisocial behavior that persists from childhood to emerging adulthood.
Intergenerational transmission of antisocial behavior: How do kids become antisocial adults?
Applied and Preventive Psychology, 2006
Exposure to many potential environmental risk factors for child antisocial behavior is associated with one of the strongest predictors of antisocial behavior, a family history of antisociality. Because most studies of putative environmental factors do not take into account genetic propensities for antisocial behavior shared between parent and child, the possibility of genetic contributions to these "environmental" markers is typically not evaluated. In this paper, we review research on the environmental correlates of antisociality, their association with parental antisociality, and highlight findings from studies that have controlled for either genetic propensities or parental antisociality.
Journal of Child Psychology and Psychiatry, 2003
Background: Early childhood antisocial behaviour is a strong prognostic indicator for poor adult mental health. Thus, information about its etiology is needed. Genetic etiology is unknown because most research with young children focuses on environmental risk factors, and the few existing studies of young twins used only mothersÕ reports of behaviour, which may be biased. Method: We investigated genetic influences on antisocial behaviour in a representative-plus-high-risk sample of 1116 pairs of 5year-old twins using data from four independent sources: mothers, teachers, examiner-observers previously unacquainted with the children, and the children themselves. Results: Children's antisocial behaviour was reliably measured by all four informants; no bias was detected in mothersÕ, teachersÕ, examinersÕ, or children's reports. Variation in antisocial behaviour that was agreed upon by all informants, and thus was pervasive across settings, was influenced by genetic factors (82%) and experiences specific to each child (18%). Variation in antisocial behaviour that was specific to each informant was meaningful variation, as it was also influenced by genetic factors (from 33% for the children's report to 71% for the teachersÕ report). Conclusions: This study and four others of very young twins show that genetic risks contribute strongly to population variation in antisocial behaviour that emerges in early childhood. In contrast, genetic risk is known to be relatively modest for adolescent antisocial behaviour, suggesting that the early-childhood form has a distinct etiology, particularly if it is pervasive across situations.
Genetic and Environmental Bases of Childhood Antisocial Behavior: A Multi-Informant Twin Study
Genetic and environmental influences on childhood antisocial and aggressive behavior (ASB) during childhood were examined in 9-to 10-year-old twins, using a multi-informant approach. The sample (605 families of twins or triplets) was socioeconomically and ethnically diverse, representative of the culturally diverse urban population in Southern California. Measures of ASB included symptom counts for conduct disorder, ratings of aggression, delinquency, and psychopathic traits obtained through child self-reports, teacher, and caregiver ratings. Multivariate analysis revealed a common ASB factor across informants that was strongly heritable (heritability was .96), highlighting the importance of a broad, general measure obtained from multiple sources as a plausible construct for future investigations of specific genetic mechanisms in ASB. The best fitting multivariate model required informant-specific genetic, environmental, and rater effects for variation in observed ASB measures. The results suggest that parent, children, and teachers have only a partly "shared view" and that the additional factors that influence the "rater-specific" view of the child's antisocial behavior vary for different informants. This is the first study to demonstrate strong heritable effects on ASB in ethnically and economically diverse samples.
Psychological Medicine, 2007
ABSTRACTBackgroundLongitudinal, genetically informed, prospective data collected on a large population of male twins (n=1037) were used to examine developmental differences in the etiology of antisocial behavior.MethodAnalyses were carried out on both mother- and child-reported symptoms of conduct disorder (CD) in 10- to 17-year-old twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) and self-reported antisocial behavior by the twins as young adults from the Young Adult Follow-Up (YAFU) study.ResultsThe following trends were identified: (1) a single genetic factor influencing antisocial behavior beginning at age 10 through young adulthood (‘life-course persistent’); (2) a shared-environmental effect beginning in adolescence (‘adolescent-onset’); (3) a transient genetic effect at puberty; and (4) a genetic influence specific to adult antisocial behavior.ConclusionsOverall, these etiological findings are consistent with predictions from Moffitt's devel...
Journal of Child Psychology and Psychiatry, 1998
In adolescence, antisocial and depressive symptoms are moderately stable and modestly correlated with each other. We examined the genetic and environmental origins of the stability and change of antisocial and depressive symptoms and their co-occurrence crosssectionally and longitudinally in a national sample of 405 adolescents. Monozygotic (MZ) and dizygotic (DZ) twins and full, half, and unrelated siblings 10-18 years of age from nondivorced and stepfamilies were studied over a 3-year period. Composite measures of adolescent self-reports, parent reports, and observational measures of antisocial and depressive symptoms were analysed in multivariate behavioural genetic models. Results indicated that the majority of the stability in and co-occurrence between dimensions could be accounted for by genetic factors. Nonshared environmental risks and, for antisocial symptoms, shared environmental risks also contributed to the stability. Genetic influences on change were observed, but only for antisocial behaviour. In addition, the longitudinal association between antisocial behavioural and later depressive symptoms was also found to be genetically mediated, but this effect was nonsignificant after controlling for stability. Results are discussed in light of the potential contributions of developmental behavioural genetic research in understanding individual differences in the stability and change of maladjustment.
Purpose: This study investigated genetic and environmental commonalities and differences between aggressive and non-aggressive antisocial behavior (ASB) in male and female child and adolescent twins, based on a newly developed self-report questionnaire with good reliability and external validitythe Self-Report Delinquency Interview (SR-DI). Methods: Subjects were 780 pairs of twins assessed through laboratory interviews at three time points in a longitudinal study, during which the twins were: (1) ages 9-10 years; (2) age 11-13 years, and (3) age 16-18 years. Results: Sex differences were repeatedly observed for mean levels of ASB. In addition, diverse change patterns of genetic and environmental emerged, as a function of sex and form of ASB, during the development from childhood to adolescence. Although there was some overlap in etiologies of aggressive and non-aggressive ASB, predominantly in shared environmental factors, their genetic overlap was moderate and the non-shared environmental overlap was low. Conclusions: Taken together, these results reinforced the importance of differentiating forms of ASB and further investigating sex differences in future research. These results should be considered in future comparisons between youth self-report and parental or teacher report of child and adolescent behavior, and may help elucidate commonalities and differences among informants.
Child Psychiatry & Human Development
The developmental course of antisocial behavior is often described in terms of qualitatively distinct trajectories. However, the genetic etiology of various trajectories is not well understood. We examined heterogeneity in the development of delinquent and aggressive behavior in 1532 twin youth using four waves of data collection, spanning ages 9-10 to 16-18. A latent class growth analysis was used to uncover relevant subgroups. For delinquent behavior, three latent classes emerged: Non-Delinquent, Low-Level Delinquent, and Persistent Delinquent. Liability for persistent delinquency had a substantial genetic origin (heritability = 67%), whereas genetic influences were negligible for lower-risk subgroups. Three classes of aggressive behavior were identified: Non-Aggressive, Moderate, and High. Moderate heritability spanned the entire continuum of risk for aggressive behavior. Thus, there are differences between aggressive behavior and non-aggressive delinquency with respect to heterogeneity of etiology. We conclude that persistent delinquency represents an etiologically distinct class of rule-breaking with strong genetic roots.
BEHAVIORAL GENETICS: THE SCIENCE OF ANTISOCIAL BEHAVIOR
Social scientists generally agree that a paradigm shift has occurred over the course of the last three decades of research in human behavior: the zeitgeist has moved away from a culturally centered, social learning model towards a more balanced perspective in which both genetic and environmental factors are understood to explain the wide variations observed in human behavior. This perspective now applies in the areas of mental health and illness, as well as across several domains of normal, varying psychological constructs, such as intelligence, personality, interests, and attitudes. The study of antisocial behavior is no exception to this paradigm shift. There is now abundant evidence that both genetic and environmental influences —and probably their interaction—are of major importance in explaining individual differences in antisocial behavior, including differences in criminal behavior. Evidence for a genetic basis of antisocial behavior stems from several different lines of research. First, behavioral genetic studies of twins and adoptees have demonstrated that heredity plays a role in antisocial behavior, including various forms of aggression and criminality, by finding greater concordance for such behavior in genetically related individuals compared to nonrelatives living in the same environment. Second, various correlates of antisocial behavior, including personality factors such as impulsivity, sensation-seeking, risk-taking, and callous-unemotional traits, are known to be at least partly genetically influenced. Third, psychiatric outcomes related to antisocial behavior, including antisocial personality disorder, gambling, and substance use and abuse, have also been investigated in genetically informative designs, and each of these has demonstrated significant genetic influence. This paper summarizes the heritability of each of these aspects or correlates of antisocial behavior and discusses research attempting to unpack the genetic and environmental " black boxes " involved in antisocial behavior, including studies investigating the influence of both biological and social risk factors and how they might be mediated by genetic and environmental factors. Examples of biological risk factors could be neurotransmitters, physiological arousal, frontal lobe function, and hormones, while social risk factors would include socioeconomic status, peer characteristics, and parental monitoring and discipline. Biological risk factors may not necessarily be entirely genetically based, and social risk factors may not be purely environmental in origin; this highlights the complexity of the relationships between risk factors and antisocial behavior. This paper also reports studies that have identified specific genetic associations with antisocial behavior. Yet genetic predispositions, though important, are more deleterious in the presence of adverse environments. This view dovetails with other biosocial theories of antisocial behavior in which the effects of biological risk factors have been found to be moderated by social circumstances. An overarching biosocial model of antisocial behavior is presented here,
Journal of Child Psychology and Psychiatry, 2011
Background-A critical issue in devising effective interventions for the treatment of children's behavioral and emotional problems rests upon identifying genuine family environmental factors that place children at risk. In most twin and family studies, environmental factors are confounded with both direct genetic risk from parents and the indirect effect of genes influencing parents' ability to provide an optimal rearing environment. The present study was undertaken to determine whether parental psychopathology, specifically parental antisocial behavior (ASP), is a genuine environmental risk factor for juvenile conduct disturbance, depression, and hyperactivity, or whether the association between parental ASP and children's behavioral and emotional problems can be explained as a secondary consequence of the intergenerational transmission of genetic factors Methods-An extended Children of Twins design (E-COT) comprised of data collected on 2,674 adult female and male twins, their spouses, and 2,454 of their children was used to test whether genetic and/or family environmental factors best accounted for the association between parental antisocial behavior children's behavioral problems. An age matched sample of 2,826 juvenile twin pairs from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) was also included to examine developmental differences in gene expression by partitioning child specific transmissible effects from those effects that persist into adulthood. The fit of alternative models was evaluated using the statistical program Mx Results-We found distinct patterns of transmission between parental antisocial behavior and juvenile conduct, depression, and hyperactivity. Genetic and family environmental factors accounted for the resemblance between parents' ASP and children's conduct disturbance. Family environmental factors alone explained the association between child depression and parental ASP, and the impact of parental ASP on hyperactivity was entirely genetic. Conclusions-These findings underscore differences in the contribution of genetic and environmental factors on the patterns of association between parental antisocial behavior and juvenile psychopathology, having important clinical implications for the prevention and amelioration of child behavioral and emotional problems.