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The study of psychopathic traits in youth is in its nascent stages and the nature and the structure of these traits is still poorly understood. In one of the most comprehensive analyses to date of the construct validity of the widely used Antisocial Processing Screening Device (APSD), we used two independent samples of youth, one community ( N = 2203) and one clinic-referred ( N = 534), ages 4 to 19 (51% female), to investigate the external correlates of the Callous-unemotionality (CU), Narcissism, and Impulsivity dimensions of youth psychopathy. We used parent reports of externalizing and internalizing psychopathology, personality, and aggressive behavior to examine the pattern of associations between psychopathic trait dimensions and relevant external correlates. Across both samples, CU was positively related to all forms of externalizing psychopathology and aggression, mostly unrelated to internalizing psychopathology, and negatively related to agreeableness and conscientiousness. Narcissism and Impulsivity were positively related to externalizing psychopathology, and aggression, negatively related to agreeableness and conscientiousness, and weakly positively related to internalizing psychopathology. In most cases, each dimension of the APSD manifested statistically significantly different relations with these external correlates. Many of our findings replicate and extend work conducted with both youth and adults, although others suggest that these dimensions do not distinguish among psychopathological domains in conceptually expected ways. Broadly speaking, these findings provide evidence that psychopathic traits in youth are best characterized by a multidimensional model and bear implications for models integrating normative with pathological personality. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Evidence suggests that the Oxytocin Receptor Gene (OXTR) influences human social cognition and behavior. OXTR has been investigated in relation to antisocial behavior, but studies examining this association have produced varying results in terms of the magnitude and significance of the association as well as which SNPs are implicated. This meta-analysis, based on 15 samples in 12 studies with a total sample of 12,236 individuals, examined the overall effects and consistency of associations between eight SNPs in OXTR and antisocial behavior. Random effects models identified a significant association between rs237887 and antisocial behavior (r = 0.06, p = 0.002) based on six studies that included a total of 6278 individuals. Sensitivity analyses suggest that these results were robust to exclusion of any individual study and publication bias. Nevertheless, the high levels of heterogeneity and quality control concerns with the original publications lead us to interpret this one significant finding with caution. We conclude that the available literature does not rule out, nor strongly support, an effect of OXTR on antisocial behavior.

The past several decades have witnessed a proliferation of research on the dark triad (DT), a set of traits comprising Machiavellianism, narcissism, and psychopathy. The bulk of DT research has been marked by several core assumptions, most notably that each DT construct is a monolithic entity that is clearly separable from its counterpart DT constructs. To examine the tenability of these assumptions, we pooled data from 2 samples of North American community members (ns = 312 and 351) to explore (a) the external validity and profile similarities of DT indicators and (b) the factor structure of the DT. Using general personality dimensions as external criteria, we demonstrated that each DT measure is multidimensional and that subdimensions within DT measures often display sharply different and at times even opposing relations with personality domains; these opposing relations were largely obscured at the total score level adopted in most of the DT literature. In both samples, confirmatory factor analyses and exploratory structural equation models provided no clear support for the traditional tripartite DT structure delineated in the literature. Instead, various aspects of the DT constructs fractionated across a number of factors that represented more basic personality elements (e.g., emotional stability, grandiosity). Taken together, our findings raise serious questions regarding the standard model of DT research and suggest that the questions posed regarding the correlates of DT constructs hinge crucially on the specific DT measure and subdimension examined. (PsycINFO Database Record, ((c) 2017 APA, all rights reserved).)

Previous research suggests that fussy temperament in infancy predicts risk for later antisocial behavior (ASB) in childhood and adolescence. It remains unclear, however, to what extent infant fussiness is related to later ASB through causal processes or if they both reflect the same family risk factors for ASB. The current study used two approaches, the comparison of siblings and bivariate biometric modeling, to reduce familial confounding and examine genetic and environmental influences on associations between fussiness in the first 2 years of life and ASB in childhood and late adolescence. Analyses were conducted on data from a prospective cohort (9237 at 4-9 years and 7034 at 14-17 years) who are the offspring of a nationally representative sample of US women. In the full sample, fussiness predicted both child and adolescent ASB to small but significant extents, controlling for a wide range of measured child and family-level covariates. When siblings who differed in their fussiness were compared, fussiness predicted ASB in childhood, but not ASB during adolescence. Furthermore, results from a bivariate Cholesky model suggested that even the association of fussiness with childhood ASB found when comparing siblings is attributable to familial factors. That is, although families with infants who are higher in fussiness also tend to have children and adolescents who engage in greater ASB, the hypothesis that infant fussiness has an environmentally mediated impact on the development of future ASB was not strongly supported.

Psychopathy is often associated with heightened intelligence in the eyes of clinicians and laypersons despite mixed research support for this possibility. We adopted a fine-grained approach to studying the relations among psychopathy and multiple indices of intelligence, including both cognitively based intelligence (CBI) and emotional intelligence (EI), in a large sample of undergraduates (N = 1,257, 70% female, 82% Caucasian). We found no clear support for marked associations between psychopathy and CB I measures, with the magnitudes of these relations being small. With the exception of the dimensions of Fearless Dominance (FD) and Coldheartedness (C), psychopathy dimensions were negatively associated with (EI). In contrast, we found some support for the hypothesis that intelligence served as a protective factor against antisocial behavior among individuals with high levels of psychopathy. On balance, our findings show weak relations between psychopathy and intelligence, suggesting that the link between them may be less robust than theoretical models portray, at least among undergraduates. (PsycINFO Database Record, ((c) 2016 APA, all rights reserved).)

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, ((c) 2016 APA, all rights reserved).)

Variation in central serotonin levels due to genetic mutations or experimental modifications has been associated with the manifestation of aggression in humans and animals. Many studies have examined whether common variants in serotonergic genes are implicated in aggressive or antisocial behaviors (ASB) in human samples. The two most commonly studied polymorphisms have been the serotonin transporter linked polymorphic region of the serotonin transporter gene (5HTTLPR) and the 30 base pair variable number of tandem repeats of the monoamine oxidase A gene (MAOA-uVNTR). Despite the aforementioned theoretical justification for these polymorphisms, findings across studies have been mixed and are thus difficult to interpret. A meta-analysis of associations of the 5HTTLPR and MAOA-uVNTR with ASB was conducted to determine: (1) the overall magnitude of effects for each polymorphism, (2) the extent of heterogeneity in effect sizes across studies and the likelihood of publication bias, and (3) whether sample-level or study-level characteristics could explain observed heterogeneity across studies. Both the 5HTTLPR and the MAOA-uVNTR were significantly associated with ASB across studies. There was also significant and substantial heterogeneity in the effect sizes for both markers, but this heterogeneity was not explained by any sample-level or study-level characteristics examined. We did not find any evidence for publication bias across studies for the MAOA-uVNTR, but there was evidence for an oversampling of statistically significant effect sizes for the 5HTTLPR. These findings provide support for the modest role of common serotonergic variants in ASB. Implications regarding the role of serotonin in antisocial behavior and the conceptualization of antisocial and aggressive phenotypes are discussed.

Despite increasing study of psychopathic traits in children and adolescents, evidence regarding the factor structure of these traits has been inconsistent across community, clinic-referred, and incarcerated samples. Empirical support exists for both 2-factor (Impulsivity-Conduct Problems and Callous-Unemotional) and 3-factor (Narcissism, Callous-Unemotional, and Impulsivity) models, and factorial invariance across various samples has not been either tested or supported in the extant literature. We conducted confirmatory factor analyses of the Antisocial Process Screening Device (APSD; Frick & Hare, 2001) in 838 nonreferred twin pairs (M = 10.57 years, SD = 3.19 years) and 251 clinic-referred children (M = 10.82 years, SD = 3.39 years). Factorial invariance was tested across zygosity (monozygotic vs. dizygotic twins), sex (males vs. females), and age (younger vs. older children, divided by median age of 10.37 years) in the community sample and across sample type in both the community and clinic-referred samples. Results suggested that the 3-factor model fit better than did the 2-factor model in both community and clinic-referred samples. Using the best fitting 3-factor model, full measurement and structural invariance were found across zygosity, sex, and age in the community sample. Full measurement and structural invariance were also found across sample type except for differences in factor means across samples, suggesting excellent psychometric properties of the APSD. These results strongly support the robustness of the 3-factor model of psychopathic traits in children as well as the generalizability of the APSD across samples.

Few studies have examined the etiology of psychopathic traits in youth, and even fewer have tested whether the genetic and environmental influences underlying these traits differ for boys and girls. We tested for sex differences in the etiology of 3 trait dimensions-impulsivity, narcissism, and callous-unemotionality (CU)-previously found to underlie youth psychopathy in our sample. Using biometric modeling we tested whether constraining the genetic and environmental influences for each dimension across sex reduced model fit. We also tested for qualitative sex differences in the influences underlying these dimensions by allowing the genetic and environmental correlations between opposite sex dizygotic twins to be less than their respective values in same-sex dizygotic twins. Although the magnitudes of the genetic and environmental influences underlying the CU and narcissistic trait dimensions did not differ for boys and girls, nonshared environmental influences contributed significantly greater variance to impulsive traits in boys. No qualitative sex differences were found in the influences underlying any of the 3 trait dimensions, suggesting that the same genes and environments contribute to these psychopathic traits in males and females.

Background: Prediction of antisocial behavior is important, given its adverse impact on both the individuals engaging in antisocial behavior and society. Additional research identifying early predictors of future antisocial behavior, or antisocial propensity, is needed. The present study tested the hypothesis that both concern for others and active disregard for others in distress in toddlers and young children predict antisocial behavior during middle childhood and adolescence., Methods: A representative sample of same-sex twins (N=956) recruited in Colorado was examined. Mother-rated and researcher-observed concern and disregard for others assessed at age 14-36 months were examined as predictors of parent- (age 4-12), teacher- (age 7-12), and self-reported (age 17) antisocial behavior., Results:   Observed disregard for others predicted antisocial behavior assessed by three different informants (parents, teachers, and self), including antisocial behavior assessed 14 years later. It also predicted a higher order antisocial behavior factor (β=.58, p<.01) after controlling for observed concern for others. Mother-rated disregard for others predicted parent-reported antisocial behavior. Contrary to predictions, neither mother-rated nor observed concern for others inversely predicted antisocial behavior. RESULTS of twin analyses suggested that the covariation between observed disregard for others and antisocial behavior was due to shared environmental influences., Conclusions: Disregard for others in toddlerhood/early childhood is a strong predictor of antisocial behavior in middle childhood and adolescence. The results suggest the potential need for early assessment of disregard for others and the development of potential interventions., (© 2012 The Author. Journal of Child Psychology and Psychiatry © 2012 Association for Child and Adolescent Mental Health.)

Although psychopathic personality (psychopathy) is marked largely by maladaptive traits (e.g., poor impulse control, lack of guilt), some authors have conjectured that some features of this condition (e.g., fearlessness, interpersonal dominance) are adaptive in certain occupations, including leadership positions. We tested this hypothesis in the 42 U.S. presidents up to and including George W. Bush using (a) psychopathy trait estimates derived from personality data completed by historical experts on each president, (b) independent historical surveys of presidential leadership, and (c) largely or entirely objective indicators of presidential performance. Fearless Dominance, which reflects the boldness associated with psychopathy, was associated with better rated presidential performance, leadership, persuasiveness, crisis management, Congressional relations, and allied variables; it was also associated with several largely or entirely objective indicators of presidential performance, such as initiating new projects and being viewed as a world figure. Most of these associations survived statistical control for covariates, including intellectual brilliance, five factor model personality traits, and need for power. In contrast, Impulsive Antisociality and related traits of psychopathy were generally unassociated with rated presidential performance, although they were linked to some largely or entirely objective indicators of negative job performance, including Congressional impeachment resolutions, tolerating unethical behavior in subordinates, and negative character. These findings indicate that the boldness associated with psychopathy is an important but heretofore neglected predictor of presidential performance, and suggest that certain features of psychopathy are tied to successful interpersonal behavior.

It is necessary to determine if causal influences on developing antisocial behavior change with age to guide both research and theory on its origins. The extent to which the same genetic factors influence antisocial behavior across 4-17 years of age was estimated using 2,482 sibling pairs of varying genetic relatedness. Assessments of antisocial behavior by mothers (4-9 years), mothers and youth (10-13 years), and youth (14-17 years) reflected the changing validity of informants across development. Genetic influences on antisocial behavior at 14-17 years were entirely shared with those on antisocial behavior at 10-13 years according to both informants. Genetic influences on antisocial behavior at 14-17 years were distinct from those at 4-9 years, however. These age differences in genetic influences cannot be fully distinguished from informant differences across age, but the present findings indicate that youth reported to be persistently antisocial during childhood and adolescence are influenced by one set of genetic factors influencing parent-report conduct problems in childhood and a second set of genetic influences on youth-reported delinquency that come into play around the time of the pubertal transition., (PsycINFO Database Record 2009 APA, all rights reserved.)

Although the study of relational aggression is gaining attention in the literature, little is known about the underlying causes of this behavior and the relative validity of various informants. These issues were addressed in a sample of 1,981 6- to 18-year-old twin pairs (36% female, 34% male, 30% opposite-sex). Relational aggression was assessed via maternal and self-report using a structured interview. Univariate models estimated genetic and environmental influences by informant and examined evidence for gender differences. A psychometric model combined data from both informants to estimate etiologic influences that were both common to the informants and informant specific. In both sexes, the latent variable reflecting the mother's and child's shared perception of the child's relational aggression was substantially influenced by both additive genetic (63%) and shared environmental (37%) influences, although this latent variable accounted for much greater variance in the maternal report (66%) than it did in the youth report (9%). In addition, informant-specific additive genetic and shared environmental influences were found only for the youth report, with all remaining variance in the mother's report attributed to nonshared environmental influences. Results are discussed in the context of measuring relational aggression and the importance of multiple informants., (PsycINFO Database Record 2009 APA, all rights reserved.)

Theoretical models concerning how neighborhood contexts adversely influence juvenile antisocial behavior frequently focus on urban neighborhoods; however, previous studies comparing urban and rural areas on the prevalence of youth antisocial behavior have yielded mixed results. The current study uses longitudinal data on the offspring of a nationally representative sample of mothers (N = 4,886) in the US. There was no relation between density and mother-reported child conduct problems across ages 4-13 years, but youth living in areas of greater population density exhibited more youth self-reported delinquency across 10-17 years. Families often moved to counties with greater or lesser population density, but longitudinal analyses treating population density as a time-varying covariate did not support the hypothesis that living in densely populated counties influenced youth delinquency. Rather, the association between population density and delinquency appears to be due to unmeasured selection variables that differ between families who live in more or less densely populated counties.

A meta-analysis of 51 twin and adoption studies was conducted to estimate the magnitude of genetic and environmental influences on antisocial behavior. The best fitting model included moderate proportions of variance due to additive genetic influences (.32), nonadditive genetic influences (.09), shared environmental influences (.16), and nonshared environmental influences (.43). The magnitude of familial influences (i.e., both genetic and shared environmental influences) was lower in parent-offspring adoption studies than in both twin studies and sibling adoption studies. Operationalization, assessment method, zygosity determination method, and age were significant moderators of the magnitude of genetic and environmental influences on antisocial behavior, but there were no significant differences in the magnitude of genetic and environmental influences for males and females.

Similar to many domains in the psychopathology literature, overlap and covariation between antisocial behavior (ASB) and alcohol dependence (AD) are oft documented but little understood. Although the relation between ASB and AD is reliably found and of substantial magnitude, it is not possible given the extant research to discriminate among alternative causal models that could give rise to this relation (e.g., ASB-->AD, AD-->ASB, reciprocal causation between ASB and AD, common causes of ASB and AD). In our opinion, true comorbidity among disorders can only be demonstrated and understood in the context of considerable knowledge regarding the disorders' underlying causes (viz., pathology and etiology). In this article, we present a number of behavior genetic models that may be useful for illuminating the causes of comorbidity among two or more disorders, as well as for understanding the etiology of each disorder individually. Using these behavior genetic approaches, psychopathology researchers can directly test alternative models for the comorbidity among disorders, as well as estimate the magnitude of different etiological factors (i.e., genetic and environmental influences) on comorbidity. Although not a panacea and somewhat demanding technically, behavior genetic approaches can shed new light on the comorbidity among disorders.

In this paper we have described an integrative causal model of the development of antisocial behavior in children and adolescents. The present model primarily integrates several previous models, but offers some new testable hypotheses. We believe that stable individual differences in propensity to antisocial behavior reflect variations in a number of dimensions of predisposing temperament and cognitive ability, each with its own genetic and environmental influences. The dimensions of predisposing temperament include oppositionality, harm avoidance, and callousness. Genetic influences are predicted to have only indirect effects on antisocial behavior via their influence on predisposition and on the youth's social environment. Environmental influences are expected to be important contributors to antisocial propensity, but these environmental influences reflect, in part, the genetic influences on the dimensions of predisposition (i.e. genotype-environment covariance). We also hypothesize that the levels of influence of the factors that determine individual differences in antisocial propensity change with development, such that genetic influences are of greater magnitude in early childhood and social influences contribute more strongly during later childhood and adolescence (both through independent effects and genotype-environment covariance). However, low levels of heritable predisposing child characteristics may protect against peer influences at all ages.