Genetic and environmental influences on conduct and antisocial personality problems in childhood, adolescence, and adulthood.
ABSTRACT: Conduct problems in children and adolescents can predict antisocial personality disorder and related problems, such as crime and conviction. We sought an explanation for such predictions by performing a genetic longitudinal analysis. We estimated the effects of genetic, shared environmental, and unique environmental factors on variation in conduct problems measured at childhood and adolescence and antisocial personality problems measured at adulthood and on the covariation across ages. We also tested whether these estimates differed by sex. Longitudinal data were collected in the Netherlands Twin Register over a period of 27 years. Age appropriate and comparable measures of conduct and antisocial personality problems, assessed with the Achenbach System of Empirically Based Assessment, were available for 9783 9-10-year-old, 6839 13-18-year-old, and 7909 19-65-year-old twin pairs, respectively; 5114 twins have two or more assessments. At all ages, men scored higher than women. There were no sex differences in the estimates of the genetic and environmental influences. During childhood, genetic and environmental factors shared by children in families explained 43 and 44% of the variance of conduct problems, with the remaining variance due to unique environment. During adolescence and adulthood, genetic and unique environmental factors equally explained the variation. Longitudinal correlations across age varied between 0.20 and 0.38 and were mainly due to stable genetic factors. We conclude that shared environment is mainly of importance during childhood, while genetic factors contribute to variation in conduct and antisocial personality problems at all ages, and also underlie its stability over age.
Project description:Childhood behavior problems predict subsequent educational achievement; however, little research has examined the etiology of these links using a longitudinal twin design. Moreover, it is unknown whether genetic and environmental innovations provide incremental prediction for educational achievement from childhood to adolescence.We examined genetic and environmental influences on parental ratings of behavior problems across childhood (age 4) and adolescence (ages 12 and 16) as predictors of educational achievement at age 16 using a longitudinal classical twin design.Shared-environmental influences on anxiety, conduct problems, and peer problems at age 4 predicted educational achievement at age 16. Genetic influences on the externalizing behaviors of conduct problems and hyperactivity at age 4 predicted educational achievement at age 16. Moreover, novel genetic and (to a lesser extent) nonshared-environmental influences acting on conduct problems and hyperactivity emerged at ages 12 and 16, adding to the genetic prediction from age 4.These findings demonstrate that genetic and shared-environmental factors underpinning behavior problems in early childhood predict educational achievement in midadolescence. These findings are consistent with the notion that early-childhood behavior problems reflect the initiation of a life-course persistent trajectory with concomitant implications for social attainment. However, we also find evidence that genetic and nonshared-environment innovations acting on behavior problems have implications for subsequent educational achievement, consistent with recent work arguing that adolescence represents a sensitive period for socioaffective development.
Project description:The present study tested specific hypotheses advanced by the developmental propensity model of the etiology of conduct problems in the Colorado Longitudinal Twin Study, a prospective, longitudinal, genetically informative sample. High negative emotionality, low behavioral inhibition, low concern and high disregard for others, and low cognitive ability assessed during toddlerhood (age 14 to 36 months) were examined as predictors of conduct problems in later childhood and adolescence (age 4 to 17 years). Each hypothesized antisocial propensity dimension predicted conduct problems, but some predictions may be context specific or due to method covariance. The most robust predictors were observed disregard for others (i.e., responding to others' distress with active, negative responses such as anger and hostility), general cognitive ability, and language ability, which were associated with conduct problems reported by parents, teachers, and adolescents, and change in observed negative emotionality (i.e., frustration tolerance), which was associated with conduct problems reported by teachers and adolescents. Furthermore, associations between the most robust early predictors and later conduct problems were influenced by the shared environment rather than genes. We conclude that shared environmental influences that promote disregard for others and detract from cognitive and language development during toddlerhood also predispose individuals to conduct problems in later childhood and adolescence. The identification of those shared environmental influences common to early antisocial propensity and later conduct problems is an important future direction, and additional developmental behavior genetic studies examining the interaction between children's characteristics and socializing influences on conduct problems are needed. (PsycINFO Database Record
Project description:BACKGROUND:Diverse behaviour problems in childhood correlate phenotypically, suggesting a general dimension of psychopathology that has been called the p factor. The shared genetic architecture between childhood psychopathology traits also supports a genetic p. This study systematically investigates the manifestation of this common dimension across self-, parent- and teacher-rated measures in childhood and adolescence. METHODS:The sample included 7,026 twin pairs from the Twins Early Development Study (TEDS). First, we employed multivariate twin models to estimate common genetic and environmental influences on p based on diverse measures of behaviour problems rated by children, parents and teachers at ages 7, 9, 12 and 16 (depressive traits, emotional problems, peer problems, autism traits, hyperactivity, antisocial behaviour, conduct problems and psychopathic tendencies). Second, to assess the stability of genetic and environmental influences on p across time, we conducted longitudinal twin modelling of the first phenotypic principal components of childhood psychopathological measures across each of the four ages. Third, we created a genetic p factor in 7,026 unrelated genotyped individuals based on eight polygenic scores for psychiatric disorders to estimate how a general polygenic predisposition to mostly adult psychiatric disorders relates to childhood p. RESULTS:Behaviour problems were consistently correlated phenotypically and genetically across ages and raters. The p factor is substantially heritable (50%-60%) and manifests consistently across diverse ages and raters. However, residual variation in the common factor models indicates unique contributions as well. Genetic correlations of p components across childhood and adolescence suggest stability over time (49%-78%). A polygenic general psychopathology factor derived from studies of psychiatric disorders consistently predicted a general phenotypic p factor across development (0.3%-0.9%). CONCLUSIONS:Diverse forms of psychopathology generally load on a common p factor, which is highly heritable. There are substantial genetic influences on the stability of p across childhood. Our analyses indicate genetic overlap between general risk for psychiatric disorders in adulthood and p in childhood, even as young as age 7. The p factor has far-reaching implications for genomic research and, eventually, for diagnosis and treatment of behaviour problems.
Project description:Anger is among the earliest occurring symptoms of mental health, yet we know little about its developmental course. Further, no studies have examined whether youth with persistent anger are at an increased risk of exhibiting antisocial personality features in adulthood, or how cognitive control abilities may protect these individuals from developing such maladaptive outcomes. Trajectories of anger were delineated among 503 boys using annual assessments from childhood to middle adolescence (ages ?7-14). Associations between these trajectories and features of antisocial personality in young adulthood (age ?28) were examined, including whether cognitive control moderates this association. Five trajectories of anger were identified (i.e., childhood-onset, childhood-limited, adolescent-onset, moderate, and low). Boys in the childhood-onset group exhibited the highest adulthood antisocial personality features (e.g., psychopathy, aggression, criminal charges). However, boys in this group were buffered from these problems if they had higher levels of cognitive control during adolescence. Findings were consistent across measures from multiple informants, replicated across distinct time periods, and remained when controlling for general intelligence and prior antisocial behavior. This is the first study to document the considerable heterogeneity in the developmental course of anger from childhood to adolescence. As hypothesized, good cognitive control abilities protected youth with persistent anger problems from developing antisocial personality features in adulthood. Clinical implications and future directions are discussed.
Project description:BACKGROUND AND AIMS:The DSM-IV personality disorders (PDs) are comorbid with alcohol use disorder (AUD) and with each other. It remains unclear which PD criteria are most likely to drive onset and recurrence of AUD and which are merely confounded with those criteria. We determine which individual PD criteria predict AUD and the degree of underlying genetic and/or environmental aetiology. DESIGN:A prospective observational twin study. SETTING:Norway 1999-2011. PARTICIPANTS:A total of 2528 and 2275 Norwegian adult twins in waves 1 and 2 variable-selection analyses, and 2785 in biometric analyses. MEASUREMENTS:DSM-IV PDs and their 80 criteria were assessed using a structured personal interview, and AUD using the World Health Organization's Composite International Diagnostic Interview. FINDINGS:In a variable-selection analysis, two PD criteria were associated with AUD even after taking all the other criteria into account: criterion 8 of antisocial PD (childhood conduct disorder) and criterion 4 of borderline PD (self-damaging impulsive behaviours). Adjusting for each other, their respective odds ratios were 3.4 [confidence interval (CI) = 2.1-5.4] and 5.0 (CI = 3.3-7.7). Endorsement strength of the criteria was associated with AUD in a dose-response manner and they explained 5.5% of variation in AUD risk-more than the full diagnoses of antisocial and borderline PDs together (0.5%). The association between borderline criterion 4 and AUD 10 years later derived mainly from their overlapping genetic factors, whereas the association between antisocial criterion 8 and AUD 10 years later was due to both genetic and non-genetic factors. CONCLUSIONS:Conduct disorder and self-harming impulsivity are the foremost risk traits for alcohol use disorder among the 80 personality disorder criteria of DSM-IV, predicting alcohol use disorder more effectively than personality disorder diagnoses. The twin-study analysis suggested that conduct disorder represents a joint genetic and developmental risk for alcohol use disorder and that impulsivity is a genetic risk.
Project description:OBJECTIVE:Childhood conduct problems are associated with poor functioning in early adulthood. We tested a series of hypotheses to understand the mechanisms underlying this association. METHOD:We used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a birth cohort of 2,232 twins born in England and Wales in 1994 and 1995, followed up to age 18 years with 93% retention. Severe conduct problems in childhood were assessed at ages 5, 7, and 10 years using parent and teacher reports. Poor functioning at age 18 years, including cautions and convictions, daily cigarette smoking, heavy drinking, and psychosocial difficulties, was measured through interviews with participants and official crime record searches. RESULTS:Participants 18 years old with versus without a childhood history of severe conduct problems had greater rates of each poor functional outcome, and they were more likely to experience multiple poor outcomes. This association was partly accounted for by concurrent psychopathology in early adulthood, as well as by early familial risk factors, both genetic and environmental. Childhood conduct problems, however, continued to predict poor outcomes at age 18 years after accounting for these explanations. CONCLUSION:Children with severe conduct problems display poor functioning at age 18 years because of concurrent problems in early adulthood and familial risk factors originating in childhood. However, conduct problems also exert a lasting effect on young people's lives independent of these factors, pointing to early conduct problems as a target for early interventions aimed at preventing poor functional outcomes.
Project description:The oxytocin receptor gene (OXTR) influences human behavior. The G allele of OXTR rs53576 has been associated with both prosocial and maladaptive behaviors but few studies have taken account of environmental factors. The present study determined whether the association of childhood maltreatment with conduct problems was modified by OXTR rs53576 genotypes. In a general population sample of 1591 teenagers, conduct problems as well as maltreatment were measured by self-report. DNA was extracted from saliva samples. In males, there was a significant positive association between maltreatment and conduct problems independent of the genotype. In females, among G allele carriers, the level of conduct problems was significantly higher among those who had been maltreated as compared to those not maltreated. By contrast, among female AA carriers, conduct problems did not vary between those who were, and who were not, maltreated. The results indicate that OXTR rs53576 plays a role in antisocial behavior in females such that the G allele confers vulnerability for antisocial behavior if they experience maltreatment, whereas the A allele has a protective effect.
Project description:A longstanding hypothesis is that some alcohol use problems (AUP) develop and are maintained through the "self-medication" of internalizing (INT; depression and anxiety) problems. However, their high rate of co-occurrence with one another and with externalizing (EXT; antisocial behavior and impulse control) problems obscures any causal association because EXT may account for the INT-AUP link. Using a large community sample, we estimated prospective effects of INT and EXT on AUP via latent cross-lagged mediation panel spanning 14 years from childhood (ages 9-11) to young adulthood (ages 21-23). After adjusting for the cross-lagged, concurrent, and stability effects across factors, INT decreased AUP risk through its direct and indirect effects and increased AUP risk through shared variance with EXT. Between childhood and young adulthood, unique aspects of INT reduced risk for AUP while aspects of INT shared with EXT increased risk for AUP. (PsycINFO Database Record
Project description:The genetic and environmental influences on human personality and behaviour are a complex matter of ongoing debate. Accumulating evidence indicates that short tandem repeats (STRs) in regulatory regions are good candidates to explain heritability not accessed by genome-wide association studies.We tested for associations between the genotypes of four selected repeats and 18 traits relating to personality, behaviour, cognitive ability and mental health in a well-studied longitudinal birth cohort (n?=?458-589) using one way analysis of variance. The repeats were a highly conserved poly-AC microsatellite in the upstream promoter region of the T-box brain 1 (TBR1) gene and three previously studied STRs in the activating enhancer-binding protein 2-beta (AP2-?) and androgen receptor (AR) genes. Where significance was found we used multiple regression to assess the influence of confounding factors.Carriers of the shorter, most common, allele of the AR gene's GGN microsatellite polymorphism had fewer anxiety-related symptoms, which was consistent with previous studies, but in our study this was not significant following Bonferroni correction. No associations with two repeats in the AP2-? gene withstood this correction. A novel finding was that carriers of the minor allele of the TBR1 AC microsatellite were at higher risk of conduct problems in childhood at age 7-9 (p?=?0.0007, which did pass Bonferroni correction). Including maternal smoking during pregnancy (MSDP) in models controlling for potentially confounding influences showed that an interaction between TBR1 genotype and MSDP was a significant predictor of conduct problems in childhood and adolescence (p?<?0.001), and of self-reported criminal behaviour up to age 25 years (p???0.02). This interaction remained significant after controlling for possible confounders including maternal age at birth, socio-economic status and education, and offspring birth weight.The potential functional importance of the TBR1 gene's promoter microsatellite deserves further investigation. Our results suggest that it participates in a gene-environment interaction with MDSP and antisocial behaviour. However, previous evidence that mothers who smoke during pregnancy carry genes for antisocial behaviour suggests that epistasis may influence the interaction.
Project description:OBJECTIVE:There is substantial evidence of a link between parental substance use disorders and antisocial behavior and childhood disruptive disorders in offspring, but it is unclear whether this transmission is specific to particular disorders or if a general liability accounts for familial resemblance. The authors examined whether the association between parental externalizing disorders and childhood disruptive disorders in preadolescent offspring is a result of the transmission of general or disorder-specific liabilities and estimated the genetic and environmental contributions to variation in these general and specific liability indicators. METHOD:Participants were 1,069 families consisting of 11-year-old twins and their biological mother and father. Structural equation modeling was used to simultaneously estimate the general and specific transmission effects of four parental externalizing disorders (conduct disorder, adult antisocial behavior, alcohol dependence, and drug dependence) on childhood disruptive disorders (attention deficit hyperactivity disorder, conduct disorder, and oppositional defiant disorder). RESULTS:Parent-child resemblance was accounted for by the transmission of a general liability to externalizing disorders, and this general liability was highly heritable. Specific effects were also detected, but for sibling rather than parental transmission. Specific genetic and nonshared environmental effects were detected for each childhood disruptive disorder, but only conduct disorder exhibited a significant shared environmental effect. CONCLUSIONS:A highly heritable general liability accounts for the parent-child transmission of externalizing psychopathology from parents to their preadolescent offspring. This general liability should be a focus of research for both etiology and intervention.