Psychopathic personality traits: heritability and genetic overlap with internalizing and externalizing psychopathology

BACKGROUND: Little research has examined genetic and environmental contributions to psychopathic personality traits. Additionally, no studies have examined etiological connections between psychopathic traits and the broad psychopathological domains of internalizing (mood and anxiety) and externalizing (antisocial behavior, substance abuse). The current study was designed to fill these gaps in the literature. METHOD: Participants were 626 pairs of 17-year-old male and female twins from the community. Psychopathic traits were indexed using scores on the Multidimensional Personality Questionnaire (MPQ). Symptoms of internalizing and externalizing psychopathology were obtained via structured clinical interviews. Structural equation modeling was used to estimate genetic and environmental influences on psychopathic personality traits as well as the degree of genetic overlap between these traits and composites of internalizing and externalizing. RESULTS: Twin analyses revealed significant genetic influence on distinct psychopathic traits (Fearless Dominance and Impulsive Antisociality). Moreover, Fearless Dominance was associated with reduced genetic risk for internalizing psychopathology, and Impulsive Antisociality was associated with increased genetic risk for externalizing psychopathology. CONCLUSIONS: These results indicate that different psychopathic traits as measured by the MPQ show distinct genetically based relations with broad dimensions of DSM psychopathology.     

The Genetic and Environmental Etiology of Antisocial Behavior from Childhood to Emerging Adulthood

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 non-shared 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.     

Genetic and environmental influences on coping styles: a twin study.

OBJECTIVE: Coping styles are generally considered to be environmentally driven, primarily by family influences. However, because personality traits are commonly influenced by genetic effects, we hypothesized that heredity is also important for coping. METHODS: We tested this hypothesis by assessing 19 coping styles, as well as four secondary coping factors, by questionnaire in 212 pairs of monozygotic and dizygotic twins. We then examined heredity by structural equation modeling. RESULTS: All coping styles showed evidence of genetic influences. The coping styles shared one common genetic factor. In addition, each coping style was also influenced by other separate genetic factors. Shared environment had no significant influence on coping styles. Three of 19 more specific coping styles showed shared environmental effects as well as genetic influences, 14 were solely under genetic influences, and two showed only shared environment effects. CONCLUSIONS: We suggest that hereditary effects on certain coping style preferences cannot be explained solely by genetic influences on major personality traits and temperament. An analysis of the relationships between coping and personality in twin subjects may elucidate the distinction between genetic and environmental effects.     

Shared Environmental Influences on Personality: A Combined Twin and Adoption Approach

In the past, shared environmental influences on personality traits have been found to be negligible in behavior genetic studies (e.g., Bouchard and McGue, J Neurobiol 54:4–45, 2003). However, most studies have been based on biometrical modeling of twins only. Failure to meet key assumptions of the classical twin design could lead to biased estimates of shared environmental effects. Alternative approaches to the etiology of personality are needed. In the current study we estimated the impact of shared environmental factors on adolescent personality by simultaneously modeling both twin and adoption data. We found evidence for significant shared environmental influences on Multidimensional Personality Questionnaire Absorption (15 % variance explained), Alienation (10 %), Harm Avoidance (14 %), and Traditionalism (26 %) scales. Additionally, we found that in most cases biometrical models constraining parameter estimates to be equal across study type (twins vs. adoptees) fit no worse than models allowing these parameters to vary; this suggests that results converge across study design despite the potential (sometimes opposite) biases of twin and adoption studies. Thus, we can be more confident that our findings represent the true contribution of shared environmental variance to personality development.     

A longitudinal study of personality and major depression in a population-based sample of male twins

BACKGROUND: The relationship between personality and psychiatric illness is complex. It is not clear whether one directly causes the other. METHOD: In a population-based sample of male twins (n=3030), we attempted to predict major depression (MD) from neuroticism (N) and extraversion (E) and vice versa, to evaluate the causal, scar, state, and prodromal hypotheses. In a longitudinal, structural equation twin model, we decomposed the covariation between N and MD into (a) genetic and environmental factors that are common to both traits, as well as specific to each one and (b) direct causal effects of N at time 1 on subsequent MD, as well as between MD and subsequent N. RESULTS: E was negatively correlated with lifetime and one-year prevalence of MD. N predicted the new onset of MD, and was predicted by both current and past MD. It did not predict the time to onset of MD. All of the covariation between N and MD was due to additive genetic and individual-specific environmental factors shared by both traits and a direct causal path between MD and N assessed later. No genetic factors were unique to either trait. CONCLUSIONS: In men, N may be a vulnerability factor for MD but does not cause it directly. However, MD may have a direct causal effect on N. The genetic overlap between N and MD in men may be greater than in women.     

Genetic and environmental influences on behavioral disinhibition

Comorbidity among childhood disruptive behavioral disorders is commonly reported in both epidemiologic and clinical studies. These problems are also associated with early substance use and other markers of behavioral disinhibition. Previous twin research has suggested that much of the covariation between antisocial behavior and alcohol dependence is due to common genetic influences. Similar results have been reported for conduct problems and hyperactivity. For the present study, an adolescent sample consisting of 172 MZ and 162 DZ twin pairs, recruited through the Colorado Twin Registry and the Colorado Longitudinal Twin Study were assessed using standardized psychiatric interviews and personality assessments. DSM-IV symptom counts for conduct disorder and attention deficit hyperactivity disorder, along with a measure of substance experimentation and novelty seeking, were used as indices of a latent behavioral disinhibition trait. A confirmatory factor model fit to individual-level data showed a strong common factor accounting for 16-42% of the observed variance in each measure. A common pathway model evaluating the genetic and environmental architecture of the latent phenotype suggested that behavioral disinhibition is highly heritable (a(2) = 0.84), and is not influenced significantly by shared environmental factors. A residual correlation between conduct disorder and substance experimentation was explained by shared environmental effects, and a residual correlation between attention deficit hyperactivity disorder and novelty seeking was accounted for by genetic dominance. These results suggest that a variety of adolescent problem behaviors may share a common underlying genetic risk.     

Are there meaningful etiological differences within antisocial behavior? Results of a meta-analysis

There is mounting evidence of etiologically driven distinctions between aggressive (AGG) and non-aggressive rule-breaking (RB) forms of antisocial behavior. To date, however, these differences remain somewhat speculative. The current meta-analysis of twin and adoption studies sought to clarify these distinctions by comparing meta-analytic estimates of genetic, shared environmental, and non-shared environmental influences across AGG and RB to more clearly ascertain whether they evidence differential patterns of genetic and environmental influence. A comprehensive literature search resulted in the collection of 103 twin and adoption studies, of which 15 RB samples and 19 AGG samples were ultimately included in the analyses. Results reveal clear evidence of etiological distinctions between AGG and RB. Namely, AGG appears to be a highly heritable condition (genetic factors account for 65% of the variance), with little role for the shared or common environment, particularly after childhood. By contrast, while genetic influences also contribute to RB (48% of the variance), there is an important role for shared environmental effects as well (18% of the variance). Such findings are indicative of meaningful etiologic distinctions between aggressive and rule-breaking forms of antisocial behavior, and underscore the advantage of differentiating between these behavioral subtypes when studying the causal processes that underlie antisocial behavior.     

Sex differences in the genetic and environmental influences on the development of antisocial behavior

The present study uses a population-based sample of 6.806 adult twins from same-sex and opposite-sex twin pairs to examine sex differences in the underlying genetic and environmental architecture of the development of antisocial behavior (AB). Retrospective reports of AB during three different developmental periods were obtained: prior to age 15 years (childhood), age 15-17 years (adolescent), and age 18 years and older (adult). Structural equation modeling analyses revealed that there was no evidence for sex-specific genetic or sex-specific shared family environmental influences on the development of AB; that is, the types of genetic and environmental influence were similar for males and females. For both sexes, a model that allowed for genetic influences on adolescent and adult AB that were not shared with childhood AB fit better than a model with a single genetic factor. In contrast, shared environmental influences on adolescent and adult AB overlapped entirely with shared environmental influences on childhood AB. Genetic factors played a larger role in variation in childhood AB among females, whereas shared environmental factors played a larger role among males. However, heritability of AB increased from childhood to adolescence and adulthood for both sexes, and the magnitude of genetic and environmental influences on adolescent and adult AB was approximately equal across sex. We speculate that sex differences in timing of puberty may account for the earlier presence of genetic effects among females.     

Genetic and Environmental Sources of Individual Religiousness: The Roles of Individual Personality Traits and Perceived Environmental Religiousness

In the current study, we examined the genetic and environmental sources of the links between individual religiousness and individual personality traits, perceived parental religiousness, and perceived peer religiousness. Data from 870 individuals (incl. 394 twin pairs) were analyzed. Variance in individual religiousness was significantly influenced by genetic effects, environmental influences shared by twins reared together, and individual-specific environmental influences. Individual religiousness showed significant associations with age, sex, specific personality traits (e.g., agreeableness, openness to values), and perceived religiousness of important social interaction partners, such as parents, best friends, and spouses. The links to personality traits were relatively small and primarily genetically mediated. The associations between individual religiousness and parental religiousness were substantial and mediated by shared environmental effects. These links significantly decreased across age accompanying a significant decrease of shared environmental influences on individual religiousness. The correlations between individual religiousness and perceived religiousness of spouses and best friends were relatively moderate but increased with age. These associations were mediated by genetic as well as nonshared environmental sources accompanying an increase of nonshared environmental influences on individual religiousness with age. The results suggest that inter-individual differences in religiousness are due to multiple sources.     

Rural environments reduce the genetic influence on adolescent substance use and rule-breaking behavior

BACKGROUND: There is increasing evidence that certain environmental factors can modify genetic effects. This is an important area of investigation as such work will help to guide the development of new intervention programs. In this paper, we address whether rural environments moderate the genetic influence on adolescent substance use and rule-breaking behavior (i.e. externalizing psychopathology).MethodOver 1200 Minnesotan 17-year-old twins were classified as either urban or rural. Externalizing behavior was operationalized as the use and abuse of alcohol and drugs along with symptoms of conduct, oppositional defiant, and antisocial personality disorders. Biometric factor modeling estimated whether the relative contribution of genetic and shared environmental factors varied from urban to rural settings. RESULTS: Residency effects reached statistical significance in the male sample only. In urban environments, externalizing behavior was substantially influenced by genetic factors, but in rural environments, shared environmental factors became more influential. This was apparent at both the individual-variable and factor levels. CONCLUSIONS: These findings suggest a gene-environment interaction in the development of male adolescents' problem behaviors, including substance use. The results fit within an expanding literature demonstrating both the contextual nature of the heritability statistic and how certain environments may constrain the expression of genetic tendencies.     

Genetic and neurocognitive contributions to the development of psychopathy

An overview is provided of recent twin, molecular genetic, and magnetic resonance imaging studies that are helping to inform a model of developmental vulnerability to adult psychopathy. Although the current evidence base suggests that children with high levels of callous-unemotional traits are genetically and neurocognitively vulnerable to developing psychopathic and antisocial behaviors, existing research also clearly indicates that environmental influences play an important role. One potential implication is that interventions for children with antisocial behavior and callous-unemotional traits may need to be tailored to take into account their distinct pattern of neurocognitive vulnerability, as revealed by developmental neuroimaging studies. Specifically, interventions that pursue punishment-oriented or explicit empathy induction strategies may be less effective with this group of antisocial children. By contrast, preliminary evidence suggests that enhancing positive parenting and parental involvement, as well as applying consistent rewards may represent more promising intervention approaches.     

Genetic and environmental influences on juvenile antisocial behaviour assessed on two occasions

BACKGROUND: There is conflicting evidence concerning the magnitude of genetic and shared environmental influences on juvenile antisocial behaviour (AB). The use of more than one assessment of AB may yield more accurate estimates of these influences. METHODS: Retrospective reports of antisocial behaviour prior to age 18 were obtained on two occasions from a population-based sample of 3522 adult males from male-male twin pairs: phone interviews (wave 1) and self-report questionnaires obtained 19 months later (wave 2). Structural equation modelling estimated the genetic and environmental influences on reliably-measured AB. Factors related to participation of co-twin at wave 1, attrition between waves 1 and 2, and reliability of wave 1 and wave 2 assessments were also investigated. RESULTS: Twin analyses revealed that genetic, shared environmental, and non-shared environmental influences accounted for approximately 33% (95% CI = 9-57%), 31% (95% CI = 10-51%) and 36% (95% CI = 29-44%) of the variance of reliably measured AB, respectively. We also found significant occasion-specific genetic influences on wave 1 AB. Wave 1 AB did not predict wave 1 participation of co-twin or attrition, but was related to reliability. Co-twins of MZ twins and younger twins were more likely to participate at wave 1; attrition was predicted by being a DZ twin, lack of initial participation of co-twin, fewer years of education, and fewer children. Being older, being unmarried, and having less psychopathology were associated with greater reliability. CONCLUSIONS: When measurement error is taken into account, both genetic and shared environmental factors are significant influences on juvenile AB, accounting for approximately one-third of variation. The origin of the specific genetic influences on wave 1 AB is unclear, but may be due to factors related to measurement.     

Heritability and Longitudinal Stability of Schizotypal Traits During Adolescence

The study investigated the genetic and environmental etiology of schizotypal personality traits in a non-selected sample of adolescent twins, measured on two occasions between the ages of 11 and 16 years old. The 22-item Schizotypal Personality Questionnaire- Child version (SPQ-C) was found to be factorially similar to the adult version of this instrument, with three underlying factors (Cognitive-Perceptual, Interpersonal-Affective, and Disorganization). Each factor was heritable at age 11–13 years (h ² = 42–53%) and 14–16 years old (h ² = 38–57%). Additive genetic and unique environmental influences for these three dimensions of schizotypal personality acted in part through a single common latent factor, with additional genetic effects specific to both Interpersonal-Affective and Disorganization subscales at each occasion. The longitudinal correlation between the latent schizotypy factor was r = 0.58, and genetic influences explained most of the stability in this latent factor over time (81%). These longitudinal data demonstrate significant genetic variance in schizotypal traits, with moderate stability between early to middle adolescence. In addition to common influences between the two assessments, there were new genetic and non-shared environmental effects that played a role at the later assessment, indicating significant change in schizotypal traits and their etiologies throughout adolescence.     

Sleep duration and personality in Croatian twins

The objective of this study was to examine which genetic and environmental influences contribute to individual differences in sleep duration in a sample of Croatian adolescent/early adult twins, as well as to investigate the relationship between personality and sleep duration. Participants included 339 twin pairs (105 monozygotic and 234 dizygotic) aged between 15 and 22 years. They reported on their average sleep duration and personality. The broad heritability estimate (additive and non‐additive genetic influences) for sleep duration was 0.63, while personality estimates ranged between 0.47 and 0.62. Significant negative phenotypic associations with neuroticism and openness were mainly genetically mediated 100 and 80%, respectively. Only 6% of the sleep duration variance was explained by genetic influences shared with neuroticism and openness. In regression analysis, age, gender and five personality traits explained 5% of sleep duration variance, with neuroticism and openness as significant predictors. Comparison of short, moderate and long sleepers showed that participants in the short sleepers group had significantly higher neuroticism scores than groups of moderate and long sleepers, as well as a significantly higher openness score than the group of long sleepers. This indicates that personality traits of neuroticism and openness contribute to the prediction of sleep duration due to overlapping genetic influences that contribute to both these personality traits and sleep duration. However, as phenotypic overlap of personality and sleep duration is relatively weak, heritability of sleep duration is not only related to individual differences in personality traits, so future research needs to examine other phenotypic correlates of sleep duration.     

Genetic and environmental influences on the association between smoking and panic attacks in females: a population-based twin study

BACKGROUND: Clinical and epidemiological studies have reported an association between lifetime cigarette-smoking and panic attacks. Several explanations for this relationship have been proposed, mostly focusing on direct causal pathways. The objective of this study was to investigate a hypothesis of shared vulnerability by examining whether panic attacks and cigarette-smoking share genetic or environmental liability factors. METHOD: Questionnaire data on 3172 female-female twins (1409 complete pairs), aged 18-31 years, from a population-based Norwegian twin registry, were used to calculate the correlation between genetic factors and the correlation between environmental factors that influence lifetime measures of panic attacks and daily smoking. RESULTS: The best-fitting biometrical twin model suggested that genetic factors influencing panic and smoking were uncorrelated. Shared or familial environmental factors were perfectly correlated, and accounted for 75 % of the association between the phenotypes. The correlation between individual environmental factors influencing the phenotypes was 0.25 (0.07-0.44). In the full model, the genetic correlation was 0.17 (0.00-1.00), and genetic and shared environmental factors respectively accounted for 18 % and 61 % of the co-variance between panic and smoking. CONCLUSION: The results suggest that panic attacks and lifetime smoking have few or no genetic liability factors in common. The shared environmental factors that influence the two phenotypes are identical. Liability to panic attacks in females appears to be more influenced by shared environmental factors than previously indicated by univariate studies.     

Heritability and Longitudinal Stability of Impulsivity in Adolescence

Impulsivity is a multifaceted personality construct that plays an important role throughout the lifespan in psychopathological disorders involving self-regulated behaviors. Its genetic and environmental etiology, however, is not clearly understood during the important developmental period of adolescence. This study investigated the relative influence of genes and environment on self-reported impulsive traits in adolescent twins measured on two separate occasions (waves) between the ages of 11 and 16. An adolescent version of the Barratt Impulsiveness Scale (BIS) developed for this study was factored into subscales reflecting inattention, motor impulsivity, and non-planning. Genetic analyses of these BIS subscales showed moderate heritability, ranging from 33-56% at the early wave (age 11-13 years) and 19-44% at the later wave (age 14-16 years). Moreover, genetic influences explained half or more of the variance of a single latent factor common to these subscales within each wave. Genetic effects specific to each subscale also emerged as significant, with the exception of motor impulsivity. Shared twin environment was not significant for either the latent or specific impulsivity factors at either wave. Phenotypic correlations between waves ranged from r = 0.25 to 0.42 for subscales. The stability correlation between the two latent impulsivity factors was r = 0.43, of which 76% was attributable to shared genetic effects, suggesting strong genetic continuity from mid to late adolescence. These results contribute to our understanding of the nature of impulsivity by demonstrating both multidimensionality and genetic specificity to different facets of this complex construct, as well as highlighting the importance of stable genetic influences across adolescence.     

Genetic and environmental contributions to allergen sensitization in a Chinese twin study

Background Allergic disease is on the rise worldwide. Effective prevention of allergic disease requires comprehensive understanding of the factors that contribute to its intermediate phenotypes, such as sensitization to common allergens. Objective To estimate the degree of genetic and environmental contributions to sensitization to food and aeroallergens. Methods Sensitization was defined as a positive skin prick test to an allergen. We calculated the zygosity‐specific concordance rates and odds ratios (ORs) for sensitization to food and aeroallergens in 826 Chinese twin pairs [472 monozygotic (MZ) and 354 dizygotic (DZ)] aged 12–28 years. We also applied structural equation modelling procedures to estimate genetic and environmental influences on sensitization. Results The concordance rates and risk of sensitization in one twin given the presence vs. the absence of sensitization in the other twin were higher in MZ twins than those in DZ twins. However, a large number of MZ twins were discordant in sensitization to common allergens. These observations suggest both genetic and environmental factors influence sensitization. Consistently, the estimated heritability and individual environmental components of the liability to sensitization ranged from 0.51 to 0.68 and 0.32 to 0.49, respectively, based on the best‐fitted structural equation model. We also observed high phenotypic correlations between sensitization to two aeroallergens (cockroach and dust mite: 0.83) and two food allergens (peanut and shellfish: 0.58), but only moderate correlations for the pairs between sensitization to a food and an aeroallergen (0.31–0.46). The shared genetic and environmental factors between paired sensitizations contribute to the observed correlations. Conclusion We demonstrated that sensitization to common food and aeroallergens were influenced by both genetic and environmental factors. Moreover, we found that paired allergen sensitizations might share some common sets of genes and environmental factors. This study underscores the need to further delineate unique and/or pleiotropic genetic and environmental factors for allergen sensitization.     

Genetic and Cultural Transmission of Smoking Initiation: An Extended Twin Kinship Model

BACKGROUND: Considerable evidence from twin and adoption studies indicates that genetic and shared environmental factors play a significant role in the initiation of smoking behavior. Although twin and adoption designs are powerful to detect genetic and environmental influences, they do not provide information on the processes of assortative mating and parent-offspring transmission and their contribution to the variability explained by genetic and/or environmental factors. METHODS: We examined the role of genetic and environmental factors for smoking initiation using an extended kinship design. This design allows the simultaneous testing of additive and non-additive genetic, shared and individual-specific environmental factors, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A dichotomous lifetime smoking measure was obtained from twins and relatives in the Virginia 30,000 sample. RESULTS: Results demonstrate that both genetic and environmental factors play a significant role in the liability to smoking initiation. Major influences on individual differences appeared to be additive genetic and unique environmental effects, with smaller contributions from assortative mating, shared sibling environment, twin environment, cultural transmission and resulting genotype-environment covariance. The finding of negative cultural transmission without dominance led us to investigate more closely two possible mechanisms for the lower parent-offspring correlations compared to the sibling and DZ twin correlations in subsets of the data: (i) age x gene interaction, and (ii) social homogamy. Neither mechanism provided a significantly better explanation of the data, although age regression was significant. CONCLUSIONS: This study showed significant heritability, partly due to assortment, and significant effects of primarily non-parental shared environment on smoking initiation.     

Familial association between allergic disorders and depression in adult Finnish twins

Clinical studies have shown a relationship between allergic disorders and depression, panic disorder, attention deficit/hyperactivity disorder, and social anxiety for a significant subset of patients with these disorders. The nature of the relationship, whether due to shared environmental or biologic vulnerabilities or as a result of the stress of chronic illness, has been less clear. By examining the covariance of atopic disorders and depressive symptoms in a community sample of monozygotic (MZ) and dizygotic (DZ) twins, the contribution of genetic and/or shared environmental etiological factors can be established. A Finnish sample of 1337 MZ and 2506 DZ twin pairs, ages 33-60 years, was sent questionnaires inquiring about history of asthma, eczema, and atopic rhinitis, as well as the Beck Depression Inventory (BDI). The nature of the covariation between twins of these symptoms was investigated by fitting competing genetic and environmental models. Within-person correlation between atopic symptoms and BDI was 0.103 (P < 0.001) for the total sample. Using the Mx statistical modeling program to fit the data to competing quantitative genetic models, the best fitting model estimated that 64% of the association between atopy and BDI was due to shared familial vulnerability, primarily additive genetic influences. Although the measures for allergic disorders and depression are crude, this study supports the hypothesis that there is a small shared genetic risk for atopic and depressive symptoms, and if replicated, may open research for common mechanisms between allergic and depressive disorders. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:146-153, 2000.     

A longitudinal behavioral genetic analysis of the etiology of aggressive and nonaggressive antisocial behavior

Developmental studies of antisocial behavior (ASB) have found two subgroups of behaviors, roughly described as aggressive and nonaggressive ASB. Theoretical accounts predict that aggressive ASB, which shows greater stability, should have high heritability. In contrast, nonaggressive ASB is very common in adolescence, shows less continuity, and should be influenced both by genes and shared environment. This study explored the genetic and environmental influences on aggressive and nonaggressive ASB in over 1,000 twin pairs aged 8-9 years and again at 13-14 years. Threshold models were fit to the data to incorporate the skew. In childhood, aggressive ASB was highly heritable and showed little influence of shared environment, whereas nonaggressive ASB was significantly influenced both by genes and shared environment. In adolescence, both variables were influenced both by genes and shared envirnmment. The continuity in aggressive antisocial behavior symptoms from childhood to adolescence was largely mediated by genetic influences, whereas continuity in nonaggressive antisocial behavior was mediated both by the shared environment and genetic influences. These data are in agreement with the hypothesis that aggressive ASB is a stable heritable trait as compared to nonaggressive behavior, which is more strongly influenced by the environment and shows less genetic stability over time.