Antisocial behavior from a developmental psychopathology ...labs.uno.edu/developmental-psychopathology/APSD/DP_2009_Frick_… · Antisocial behavior from a developmental psychopathology

Antisocial behavior from a developmentalpsychopathology perspective

PAUL J. FRICKaAND ESSI VIDINGb

aUniversity of New Orleans; and bUniversity College London

Abstract

This paper reviews research on chronic patterns of antisocial behavior and places this research into a developmentalpsychopathology framework. Specifically, research suggests that there are at least three important pathways through whichchildren and adolescents can develop severe antisocial behaviors. One group of youth shows antisocial behavior thatbegins in adolescence, and two groups show antisocial behavior that begins in childhood but differ on the presence orabsence of callous–unemotional traits. In outlining these distinct pathways to antisocial behavior, we have tried toillustrate some key concepts from developmental psychopathology such as equifinality and multifinality, the importanceof understanding the interface between normal and abnormal development, and the importance of using multiplelevels of analyses to advance causal theories. Finally, we discuss how this development model can be used to enhanceexisting interventions for antisocial individuals.

The study of antisocial, criminal, and aggres-sive behaviors has a long and rich research his-tory (Binder, 1987). This intensive focus fromresearch is not surprising given that these be-haviors often operate at a very high cost tosociety, such as costs to victims of these behav-iors and the costs associated with detainingindividuals in an effort to protect potential fu-ture victims (Krug, Dahlberg, Mercy, Zwi, &Lozano, 2002; Loeber & Farrington, 2001).Of importance, these behaviors have been stud-ied from a number of different perspectives,including anthropological, evolutionary, soci-ological, psychological, and biological per-spectives, to name a few. Research from eachof these disciplines provides a unique perspec-tive for understanding the course, causes, andmost effective interventions for individualswho show severe antisocial behaviors. In thispaper, and in fitting with this special section,we take a developmental psychopathology ap-

proach for integrating the large and diverse re-search literature on antisocial behavior, usedbroadly to refer to criminal and aggressive be-haviors, as well as other behaviors that violatethe rights of others or major societal norms.

We think that a developmental psychopathol-ogy approach for integrating this research couldbe important for at least two reasons. First, a devel-opmental psychopathology framework provides avery useful way for integrating the diverse researchliteratures into a coherent causal model. This canhelp us to understand the developmental mecha-nisms that can lead to antisocial behavior patternsand to translate this research into implications forprevention and treatment. Second, research on an-tisocial behavior provides a clear way of illustratingthe importance of several key developmental psy-chopathology concepts, such as equifinality andmultifinality, the importance of integrating researchon both normal and abnormal development, and theimportance of integrating multiple level of analyses(e.g., neurological, social, cognitive, behavioral)for understanding psychopathological conditions.

One broad question that is often raised intaking a developmental psychopathology per-spective on antisocial behavior is whether or

Address correspondence and reprint requests to: PaulJ. Frick, Department of Psychology, University of NewOrleans, 2001 Geology and Psychology Building, NewOrleans, LA 70148; E-mail: [email protected].

Development and Psychopathology 21 (2009), 1111–1131Copyright # Cambridge University Press, 2009doi:10.1017/S0954579409990071

1111

not patterns of antisocial behavior should orshould not be considered a psychopathologicalcondition, psychiatric disorder, or mental ill-ness (Richters & Cicchetti, 1993; Wakefield,Pottick, & Kirk, 2002). We think that a devel-opmental psychopathology perspective cannotcompletely address this question because theanswer is largely dependent on how one defines“mental disorder” (Lilienfeld, & Marino, 1995;Wakefield, 1992). This is, if a mental disorderis defined solely as a pattern of behavior thatcauses harm for a person (e.g., leads to orputs him or her at risk for impairments in psy-chological, social, or occupational functioningor for violating the rights of others), then im-pairing levels of antisocial behavior would fitwell within such a definition of a disorder. Incontrast, other definitions, such as those thatrequire the disruption of some internal mecha-nism in the person (e.g., Wakefield, 1992),may fit for some antisocial individuals but notothers. A developmental psychopathological per-spective can help to define the various differentcausal pathways that may lead to antisocial be-havior, some of which fit particular definitionsof mental disorders and others that do not.Further, this perspective can uncover factors(e.g., biological, social) that can disrupt a per-son’s normal development and lead to the prob-lematic behavior, again defining some patternsthat may fit with certain definitions of mentaldisorders and others that do not. Thus, the de-velopmental psychopathology perspective canprovide a way of conceptualizing antisocial be-havior and its causes that informs the debateregarding criteria for a disorder, but it cannotdetermine the “best” method for differentiatingdisordered and nondisordered individuals. Thisissue is largely dependent on the purpose formaking this distinction.

Another broad classification issue relates tothe great diversity of behaviors subsumed underthe rubric of antisocial behavior (Frick et al.,1993). This large and heterogeneous set of be-haviors has led to numerous attempts to definemeaningful subtypes of antisocial youth basedon the particular pattern of behaviors they ex-hibit (for a review, see Frick & Marsee, 2006).Some examples include the distinction madein the Diagnostic and Statistical Manual ofMental Disorders—Fourth Edition, Text Revi-

sion (DSM-IV-TR; American Psychiatric Asso-ciation, 2000) between argumentative, noncom-pliant, and oppositional behaviors subsumedunder the diagnosis of oppositional defiant dis-order and the aggressive, destructive, deceitful,and norm-violating behaviors of conduct disor-der. Other distinctions have been made betweenovert conduct problems involving direct con-frontation (e.g., arguing, fighting, stealing withconfrontation) and covert conduct problemsthat do not involve confrontation (e.g., lying,stealing without confrontation; Snyder et al.,2008) or between aggressive behavior that is re-active (e.g., in response to real or perceived pro-vocation) or proactive (e.g., premeditated or forinstrumental gain) in nature (Card & Little,2006; Marsee & Frick, 2007). Still other methodsclassify youth based on the trajectory of theirantisocial behavior over time, such as whetherthe behavior is high and stable, low and stable,high and declining, or low and increasing (Broidyet al., 2003; LaCourse, Depere, & Loeber, 2008).

A further classification concern, and one thatis particularly relevant to the focus of this specialissue, is the relationship between antisocial be-havior patterns and personality disorders. Forsome classification systems, including the mostrecent versions of the DSM (American Psychiat-ric Association, 1980, 1987, 2000), chronic pat-terns of severe antisocial behavior and antisocialpersonality disorder are considered synonymousconcepts (Robins, 1978). However, there havebeen several alternative approaches to classify-ing antisocial individuals that focus on the per-sonality traits that may underlie the chronic anti-social behavior. For example, individuals withchronic patterns of antisocial behavior can beclassified based on their pattern of scores onthe Big Five personality dimensions. Specifi-cally, antisocial individuals often are low onthe personality dimensions of agreeablenessand conscientiousness (Lynam & Widiger, 2001).Another example of this approach using per-sonality features focuses on the affective (e.g.,lack of empathy and guilt) and interpersonal(e.g., callous use of others and narcissism)characteristics that have been hallmarks of theconstruct of psychopathy (Cleckley, 1976;Hare, 1993; Lykken, 1995). This research hasindicated that not all individuals who showchronic antisocial and criminal behavior show

P. J. Frick and E. Viding1112

elevated levels of psychopathic traits. In fact, itis only a minority of antisocial individuals whodo so. However, the subgroup of antisocialindividuals with psychopathic traits show a par-ticularly severe and violent pattern of behavior(Hemphill, 2007; Leistico, Salekin, DeCoster,& Rogers 2008; Porter & Woodworth, 2006)and distinct cognitive and emotional deficitscompared with other antisocial individuals(Blair, Mitchell, & Blair, 2005; Patrick, 2007).

A common theme of all of these issues in-volved in the classification of antisocial indi-viduals is the recognition that there are importantsubgroups of antisocial individuals that need tobe defined by any classification system. Further,most of the approaches that have been used to de-fine more homogeneous subgroups of antisocialindividuals have relied on differences in the be-havioral manifestations (e.g., type of behavior,trajectory of behavior over time) or differencesin personality traits (e.g., Big Five dimensions;presence of psychopathic traits) to make distinc-tions within antisocial youth. We would arguethat a developmental psychopathology approachshould emphasize potential differences in thedevelopmental mechanisms that may underliethese behavioral manifestations or personality fea-tures. The reason for this emphasis is that some-times different behavioral manifestations mayreflect different development processes under-lying the behavior. However, it is also possiblethat the same behavioral pattern (e.g., high andstable levels of antisocial behavior) can comeabout through very different developmentalmechanisms. Thus, in the following sections,we outline a model for understanding patternsof severe antisocial behavior that focuseslargely on the developmental processes thatcan explain some of the differences in the be-havioral manifestations or associated personal-ity traits displayed by antisocial individuals.

The Concepts of Equifinality andMultifinality and Subgroupsof Antisocial Youth

The childhood- versus adolescent-onsetdistinction

A number of reviews of the literature have sum-marized research supporting the distinction

between children who begin showing severeconduct problems and antisocial behavior inchildhood versus those whose onset of antiso-cial behavior does not emerge until adolescence(Moffitt, 1993, 2003; Patterson, 1996). Childrenin the childhood-onset group often begin show-ing mild conduct problems as early as preschoolor early elementary school, and their behavioralproblems tend to increase in rate and severitythroughout childhood and into adolescence(Lahey & Loeber, 1994). In contrast, the ado-lescent-onset group does not show significantbehavioral problems in childhood, but they be-gin exhibiting significant antisocial and delin-quent behavior coinciding with the onset of ado-lescence (Moffitt, 2003). In addition to thedifferent patterns of onset, the childhood-onsetgroup is more likely to show aggressive behav-iors in childhood and adolescence, and is morelikely to continue to show antisocial and criminalbehavior into adulthood (for a review, see Frick& Loney, 1999).

For example, Farrington, Gallagher, Morley,St. Ledger, and West (1988) reported that boyswho were arrested prior to age 12 showed al-most twice as many convictions at two laterpoints in time (between the ages of 16 and 18and between the ages of 22 and 24). Similarly,Robins (1966) reported that boys referred to amental health clinic for antisocial behaviorprior to age 11 were twice as likely to receivea diagnosis of an antisocial personality disorderas an adult, compared to boys who began show-ing antisocial behavior after age 11. As a finalexample, Moffitt, Caspi, Harrington, and Milne(2002) reported that, within a birth cohort of539 males born in New Zealand and followedthrough age 26, the 45 men who had displayedsignificant conduct problems prior to adoles-cence were more likely to have had a criminalconviction (55%) and to have a greater numberof convictions (M ¼ 6.9, SD ¼ 11.5) as adultsthan the 121 men who showed significant con-duct problems starting in adolescence (34%;M ¼ 3.5, SD ¼ 10.8). Both groups, however,differed from controls without histories of con-duct problems (17%; M ¼ 0.6, SD ¼ 3.1). Thedifference was more dramatic when the focuswas on convictions for violent offenses, withthe early-onset group being much more likely(38%) to be convicted as an adult than either

Developmental psychopathology and antisocial 1113

the adolescent-onset (14%) or control (5%)groups.

Thus, the childhood and adolescent sub-types of antisocial youth show very differenttrajectories of antisocial behavior, both in termsof their patterns of onset and life-course trajec-tory. However, if these were the only differ-ences between groups, this method for subtyp-ing would not be much different from otherapproaches that have focused on the different be-havioral trajectories of antisocial behavior overtime. Of importance, there is now a rather ex-tensive body of research to suggest that thetwo groups also differ on a number of disposi-tional and contextual risk factors that seem toimplicate different developmental processesin the disruptive behaviors of the two groups(Moffitt, 2002). To summarize these findings,childhood-onset conduct problems seem to bemore strongly related to neuropsychological(e.g., deficits in executive functioning) and cogni-tive (e.g., low intelligence) deficits (Fergusson,Lynsky, & Horwood, 1996; Kratzer & Hodgins,1999; Piquero, 2001; Raine, Yaralian, Reynolds,Venables, & Mednick, 2002). Further, the child-hood-onset group has been reported to show moretemperamental and personality risk factors,such as impulsivity (McCabe, Hough, Wood,& Yeh, 2001; Silverthorn, Frick, & Reynolds,2001), attention deficits (Fergusson et al., 1996),and problems in emotional regulation (Moffitt,Caspi, Dickson, Silva, & Stanton, 1996). Thisgroup has also been shown to come from homeswith greater family instability, more family con-flict, and with parents who use less effectiveparenting strategies (Aguilar, Sroufe, Egeland,& Carlson, 2000; McCabe et al., 2001; Patter-son & Yoerger, 1997; Woodward, Fergusson, &Horwood, 2002). When children within theadolescent-onset group differ from control chil-dren without conduct problems, it is often inshowing higher levels of rebelliousness andbeing more rejecting of conventional values(Dandreaux & Frick, 2009; Moffitt et al.,1996).

The different outcomes and risk factors forthe two subtypes of antisocial individuals haveled to theoretical models that propose verydifferent causal mechanisms operating acrossthe two groups. For example, Moffitt (2003)has proposed that children in the childhood-

onset group develop their problem behaviorthrough a transactional process involving a dif-ficult and vulnerable child (e.g., impulsive,with verbal deficits) who experiences an inade-quate rearing environment (e.g., poor parentalsupervision, poor quality schools). This dys-functional transactional process disrupts thechild’s socialization leading to poor social rela-tions with persons both inside (e.g., parents andsiblings) and outside the family (e.g., peers andteachers). These disruptions lead to enduring vul-nerabilities that can negatively affect the child’spsychosocial adjustment across multiple devel-opmental stages.

In contrast, children in the adolescent-onsetpathway have problems that are more likely tobe limited to adolescence and show fewer riskfactors. Thus, this group is conceptualized asshowing an exaggeration of the normative pro-cess of adolescent rebellion (Moffitt, 2003).That is, all adolescents show some level of re-belliousness to parents and other authorityfigures (Brezina & Piquero, 2007). This rebel-liousness is part of a process by which the ad-olescent begins to develop his or her autono-mous sense of self and his or her uniqueidentity. According to Moffitt (2003), the childin the adolescent-onset group engages in anti-social and delinquent behaviors as a misguidedattempt to obtain a subjective sense of maturityand adult status in a way that is maladaptive(e.g., breaking societal norms) but encouragedby an antisocial peer group. Given that their be-havior is viewed as an exaggeration of a processspecific to adolescence, and not because of anenduring vulnerability, their antisocial behavioris less likely to persist beyond adolescence.However, they may still have impairments thatpersist into adulthood because of the conse-quences of their adolescent antisocial behavior(e.g., a criminal record, dropping out of school,substance abuse; Moffitt & Caspi, 2001).

Callous–unemotional (CU) traits andsubgroups of antisocial youth

This distinction between the childhood andadolescent-onset patterns of antisocial behav-iors illustrates a subgrouping approach for anti-social individuals that proposes different devel-opmental mechanisms underlying the problem


behavior across groups. Thus, this is an exam-ple of the important concept in developmentalpsychopathology of equifinality, which pro-poses that the same developmental outcome(e.g., antisocial behavior) can result from verydifferent developmental processes (Cicchetti& Rogosch, 1996). It is important that researchhas begun extending the concept of equifinalityfor understanding antisocial youth by exploringwhether additional distinctions can be madewithin groups who show a childhood onset totheir antisocial behavior.

This distinction is based on the presenceof a callous and unemotional interpersonal stylecharacterized by a lack of guilt and empathy anda callous use of others. It is similar to the distinc-tion made within samples of antisocial adultsusing the construct of psychopathy that was de-scribed previously. As noted previously, withinincarcerated adults, the presence of psychopathictraits has proven to designate an important sub-group of antisocial individual who show a moresevere, violent, and difficult to treat pattern ofantisocial behavior (Hemphill, 2007; Leisticoet al., 2008; Porter & Woodworth, 2006).They also show a number of different back-ground and emotional characteristics thatseem to suggest a unique etiology to their anti-social behavior (Blair et al., 2005; Patrick,2007). There is growing evidence that thesame may be true for antisocial youth whoshow CU traits.

Specifically, youth who show the childhoodonset to their antisocial behavior tend to scorehigher on measures of CU traits than thosewho show an adolescent onset (Dandreaux& Frick, 2009; Moffitt et al., 1996; Silverthornet al., 2001). Further, several recent qualitative(Frick & Dickens, 2006; Frick & White, 2008)and quantitative (Edens, Campbell, & Weir,2007; Leistico et al., 2008) reviews have beenpublished showing that CU traits are predictiveof a more severe, stable, and aggressive patternof behavior in antisocial youth. For example,Edens et al. (2007) conducted a quantitativemeta-analyses of 21 nonoverlapping samplesshowing that measures that include CU traitswere associated with general or violent recidivismwith effect sizes of r ¼ .24 or .25, respectively.Frick and Dickens (2006) reported on a qualita-tive review of 24 published studies using 22 in-

dependent samples. Ten of these studies showeda concurrent association between CU traits andmeasures of aggressive, antisocial, or delinquentbehavior and 14 studies showed a predictive re-lationship with follow-up intervals rangingfrom 6 months to 10 years. These authors furtherreported on 5 studies showing that CU traits wereassociated with poorer treatment outcomes. Ofimportance, these studies included community(n¼ 6), clinic-referred (n¼ 4), and forensic (n¼13) samples, and they included samples rangingin age from 4 to 20.

One important issue in interpreting this bodyof research is that CU traits seem to predict laterantisocial behavior even after controlling forother risk factors (e.g., past criminal offenses,drug use, delinquent peers; Salekin, 2008). Fur-ther, the association between CU traits and ag-gressive behavior could explain some of thetypologies proposed for understanding aggres-sive individuals. That is, youth with CU traitsnot only show a more severe and pervasive pat-tern of aggressive behavior but they also tend toshow aggression that is both reactive and proac-tive in nature (Enebrink, Andershed, & Lang-strom, 2005; Frick, Cornell, Barry, Bodin, &Dane, 2003; Kruh, Frick, & Clements, 2005).In contrast, antisocial youth without CU traitstend to show less aggression overall and,when they do show aggressive behavior, ittends to be largely reactive in nature. Further,many of the social–cognitive and affective dif-ferences that have been found between reactiveand proactive aggression may be due to the dif-ferences in their association with CU traits (Mu-noz, Frick, Kimonis, & Aucoin, 2008; Pardini,Lochman, & Frick, 2003; Waschbusch, Walsh,Andrade, King, & Carrey, 2007).

For example, Pardini et al. (2003) studieddetained adolescents’ (ages 11–18) responsesto eight vignettes depicting peers involved inaggressive acts in various age-appropriate so-cial contexts. Youth were asked to respond toquestions asking how likely and how importantvarious possible outcomes to the aggressive in-terpersonal situations were. In this ethnicallydiverse sample of boys and girls, CU traitswere associated with responses indicating a ten-dency to emphasize the positive and rewardingaspects of aggression, to value the importanceof being dominant in aggressive interactions,


and to minimize the potential for punishmentfor being aggressive. All of these social cog-nitive factors have been associated with proac-tive aggression in past research (Dodge & Pettit,2003). Similarly, Munoz et al. (2008) studied85 boys (ages 13–18) who had been detainedfor delinquent behavior. They reported thatthose who showed high rates of both reactiveand proactive aggression showed lower levelsof emotional reactivity to provocation, consis-tent with past research on adolescents whoshow proactive aggression (e.g., Pitts, 1997).However, this reduced reactivity to provocationwas only found for those who were also high onCU traits. Finally, Frick, Cornell, Bodin, Dane,Barry, and Loney (2003) reported that a ten-dency to attribute hostile intent to the actionsof others (i.e., a hostile attribution biase) thathas been associated with reactive forms of ag-gression was only found in boys with conductproblems who did not show CU traits.

Frick and White (2008) provided a compre-hensive review of this research on the social,cognitive, and emotional characteristics of anti-social youth with and without CU traits. First,they reviewed four studies showing that theconduct problems in youth without CU traitsare more strongly related to dysfunctional par-enting practices (see also Edens, Skopp, & Ca-hill, 2008). Second, they reviewed 10 studiesshowing differences in how antisocial youthwith and without CU traits process emotionalstimuli, with youth high on CU traits showingdeficits in the processing of negative emotionalstimuli and, even more specifically, deficits tosigns of fear and distress in others. Third, an-other 10 studies were reviewed showing distinctcognitive characteristics of antisocial youthwith CU traits, such as being less sensitive topunishment cues, especially when a rewardoriented response set is primed, showing morepositive outcome expectancies in aggressivesituations with peers, and being more likelyto exhibit verbal deficits than other antisocialyouth. Fourth, they reviewed seven studiesshowing that youth with CU traits have uniquepersonality characteristics, such as showingmore fearless or thrill seeking behaviors andless trait anxiety or neuroticism.

Thus, taken together, there is now a fairlysubstantial body of research to suggest that

CU traits designate an important subgroup ofantisocial youth, that differ both in the severityand stability of their behavior but also on impor-tant emotional, cognitive, and social charac-teristics. These latter findings could suggestdistinct etiological mechanisms leading to theirantisocial behavior. As a result, like the researchreviewed on the childhood and adolescent-onset distinction, this research provides addi-tional evidence supporting the concept of equi-finality in understanding the development ofantisocial behavior in youth.

Before discussing the different etiologicalmechanisms and their relationship with normaldevelopmental processes, it is also importantto note that research on CU traits also supportsthe related concept of multifinality, which recog-nizes that the same risk factors can have multipledevelopmental outcomes. Specifically, as notedpreviously, one characteristic of youth with CUtraits is the presence of a fearless, thrill seeking,and behaviorally uninhibited temperament. Con-sistent with the importance of this temperamentfor the development of CU traits, Cornell andFrick (2007) reported that preschool childrenwho were rated by their teachers as being behav-iorally uninhibited were more at risk for show-ing problems in empathy and guilt than otherchildren. However, they also reported that unin-hibited preschoolers showed enhanced con-science development if they experienced con-sistent discipline and a parenting style thatemphasized a strong and obedience-oriented(i.e., authoritarian) approach to parenting. Theseauthors suggested that the underarousal exhibitedby fearless children may require parents toincorporate stronger methods of socializationthat bring arousal levels into an optimal rangefor the child to internalize parental norms forprosocial behavior (Fowles & Kochanska,2000; Kochanska, DeVet, Goldman, Murray,& Putnam, 1994). Thus, the same temperamen-tal risk factor (i.e., fearless and uninhibited)could have different outcomes (i.e., normal ordeficient conscience development) dependingon the type of parenting the child experiences.A similar possibility has been proposed by Pat-rick (in press) who suggests that the same tem-perament of fearlessness can lead some childrento become “bold” and others “mean” dependingon the presence of other temperamental traits or


depending on the presence of certain types of so-cializing environments.

The Interface Between Normal andAbnormal Development

Understanding developmental mechanisms

The research reviewed in the previous sectionclearly suggests that there are important sub-groups of antisocial youth who are at differen-tial risk for continuing their antisocial behaviorinto adulthood and who show different patternsof risk factors that could suggest etiologies in-volving distinct developmental mechanisms.As noted previously, based on the differencesin the course and correlates to antisocial behav-ior for youth with adolescent-onset antisocialbehavior, Moffitt (2003) proposed that thesechildren show an exaggeration of the normativeprocess of adolescent rebellion. In contrast,children in the childhood-onset group show sig-nificant problems in adjustment across multipledevelopmental stages. Further, as also notedabove, they also show more numerous and moresevere dispositional and environmental riskfactors associated with their behavior problems.However, within this group, those who showCU traits seem to show different characteristicsthat could suggest some differences in whichdevelopmental mechanisms may be involvedin their antisocial propensities.

Specifically, the research reviewed pre-viously suggests that children with CU traitsdesignate a group of children with severe con-duct problems who show a distinct tempera-mental style, characterized by a preference fordangerous and novel stimuli, a reward-orientedresponse style, and a lack of reactivity to emo-tional stimuli that signify distress in others.The bold and fearless temperamental style hasbeen variously labeled as low fearfulness(Rothbart & Bates, 1998), low behavioral inhi-bition (Kagan & Snidman, 1991), low harmavoidance (Cloninger, 1987), or high daring(Lahey & Waldman, 2003). Of importance,there have been a number of studies of normallydeveloping children documenting both concur-rent (e.g., Fowles & Kochanska, 2000; Ko-chanska, Gross, Lin, & Nichols, 2002) and pre-dictive (Rothbart, Ahadi, & Hershey, 1994)

associations between a fearless temperamentand lower scores on measures of conscience de-velopment. Further, this research has led to anumber of theories to explain this link. For ex-ample, fearless children may be less likely toexperience transgression-related arousal in re-sponse to behavior that has been punished byothers (Kochanska, 1993; Newman, 1987). Inaddition, children with this temperament maybe less likely to experience empathic arousallinked to the distress in others (Blair, 1999).In short, the temperamental deficits in differentaspects of emotional reactivity could makeit more difficult for a child to develop appropri-ate levels of guilt, empathy, and other dimen-sions of conscience that, at its extreme, couldresult in CU traits and severe patterns of anti-social behavior. Consistent with this theoreticalmodel, Pardini (2006) reported that the asso-ciation between fearlessness and violent delin-quency was mediated by the presence of CUtraits in a sample of adjudicated adolescents.

As noted previously, children with child-hood-onset antisocial behavior but withoutCU traits show very different dispositional (e.g.,impulsivity, low verbal intelligence, poor emo-tional regulation) and contextual (e.g., higherrates of family dysfunction) risk factors. Mostimportantly, the children in this group showhigh rates of anxiety (Andershed, Gustafson,Kerr & Stattin, 2002; Frick, Lilienfeld, Ellis,Loney, & Silverthorn, 1999; Pardini, Lochman,& Powell, 2007), they do not typically showproblems in empathy and guilt (Pardini et al.,2003), and they appear to be distressed by the ef-fects of their behavior on others (Loney, Frick,Clemens, Ellis, & Kerlin, 2003; Pardini et al.,2003). Thus, the antisocial behavior in this groupdoes not seem to be easily explained by deficits inconscience development.

Given the many different types of risk fac-tors that are found in this group, it is likelythat there are a number of different causal pro-cesses that could lead to the impulsive and anti-social behavior exhibited by these youth (Frick& Morris, 2004). For example, in this group,there is a strong association between ineffectiveparenting practices and their antisocial behav-ior. Thus, it is possible that children in thisgroup are not socialized adequately and, as a re-sult, do not learn to appropriately regulate their


behavior in response to environmental contin-gencies (Kochanska et al., 2002). Another con-sistent finding for antisocial youth without CUtraits is that they often have problems regulatingtheir emotions. That is, children in this groupappear to show a temperament characterizedby strong emotional reactivity, a deficit in theskills needed to adequately regulate their emo-tional reactivity, or both (Frick & Morris,2004). These problems in emotional regulationcan result in the child committing impulsiveand unplanned aggressive and antisocial actsfor which he or she may be remorseful after-ward but may still have difficulty controllingin the future (Pardini et al., 2003). Such prob-lems in regulating emotion would also explainthe findings that the aggressive behavior dis-played by this group tends to be confined to re-active forms of aggression (Frick, Kimonis,Dandreaux, & Farrell, 2003; Kruh et al., 2005).

Different types of deviations from normaldevelopment

Thus, this developmental model of antisocialbehavior specifies three subgroups of antisocialindividuals that differ on the developmental tra-jectory of their antisocial behavior and on thedevelopmental mechanisms that seem to be in-volved in their problem behavior. Like symp-toms of most forms of psychopathology, somelevel of antisocial and aggressive behavior isnormal in children and adolescents (Moffittet al., 1996). Therefore, it is critical to deter-mine the relationship between normal and ab-normal patterns of antisocial behavior. The de-velopmental models outlined above illustratetwo ways that abnormal antisocial behaviorcan differ from normal development. Specifi-cally, the problems in adjustment experiencedby the adolescent-onset group seem to bemore specific to a single developmental stage(i.e., adolescence) and result from a failure toadequately adjust to the developmental demands(e.g., separation and individuation from parents)of that stage. In contrast, both groups who showa childhood onset to their antisocial behaviorshow risk factors (e.g., emotional and cognitivedeficits) that negatively affect developmentacross multiple stages, albeit in different waysfor the two groups.

Potential gender differences

In general, the majority of research on antisocialbehavior in youth has focused on the samples ofboys. Thus, the applicability of these develop-mental models to girls is open to question. Oneconsistent finding is that a childhood onset to se-vere antisocial and aggressive behavior is muchrarer in girls than in boys (Hipwell et al., 2002;Moffitt & Capsi, 2001; White & Piquero,2004). However, despite the predominance ofadolescent onset in antisocial girls, there is evi-dence that girls with severe conduct problemsshow poor outcomes in adulthood and show alarge number of the dispositional and contextualrisk factors that are more characteristic of child-hood-onset antisocial behavior in boys (Frick &Dickens, 2006).

To reconcile these findings, Silverthorn andFrick (1999) proposed a modification of the de-velopmental model outlined above which theylabeled as a delayed-onset pathway to antisocialbehavior for girls. These authors proposed thatantisocial and aggressive behavior in girls showthe same causal mechanisms as those outlinedpreviously for childhood-onset boys. However,their severe antisocial behavior is often delayeduntil adolescence coinciding with biological(e.g., hormonal changes associated with pu-berty) and psychosocial (e.g., less parentalmonitoring and supervision; greater contactwith deviant peers) changes that encourage an-tisocial behavior in girls with predisposing vul-nerabilities (e.g., CU; problems in emotionalregulation). In an initial test of this theory, adju-dicated adolescent girls who largely showed anadolescent onset to their antisocial behavioralso showed high levels of CU traits, problemswith impulse control, and a number of othersocial and temperamental vulnerabilities thatwere more similar to childhood-onset boys thanto adolescent-onset boys (Silverthorn et al.,2001). Despite this initial positive finding, addi-tional tests of this model have been more mixed(Lahey et al., 2006; McCabe et al., 2001; Moffitt& Caspi, 2001; White & Piquero, 2004).

As a result of these conflicting findings, thepredictions made from the delayed-onset theoryrequire further testing. Also, it is possible that,although many girls may not show the overtantisocial and aggressive behavior prior to ado-


lescence, they may show other forms of antiso-cial behavior such as relational aggression. Re-lational aggression can be defined as behaviorsthat seek to harm another child’s social relation-ships (e.g., telling lies about them, excludingthem from social events) rather than physicallyharming the child (Crick & Grotpeter, 1996)Several studies have shown that when girlsbehave aggressively, they are more likely tochoose relational aggression (rather than physi-cal or overt aggression) as a strategy for usewithin the peer group (Crick, 1996; Crick, Ca-sas, & Mosher, 1997; Crick & Grotpeter, 1995;Lagerspetz, Bjorkqvist, & Peltonen, 1988; Os-trov & Keating, 2004). Of importance, rela-tional aggression shares some of the same riskfactors as those reviewed previously as beingassociated with antisocial behavior, includingimpulsivity (Zalecki & Hinshaw, 2004) andCU traits (Marsee & Frick, 2007). Therefore,it may be that girls with risk factors for antiso-cial behavior display relational aggressive be-haviors prior to adolescence, giving them theappearance of showing an adolescent onset, ifsuch behaviors are not assessed.

Stable personality traits versusdevelopmental transitions

As noted previously, there is some debate as towhether antisocial personality should be de-fined solely by a consistent pattern of antisocialbehavior or by the underlying personality traitsthat can lead to this pattern of behavior. In ei-ther case, there is some assumption of stabilityacross development. In fact, many definitionsof antisocial personality disorder require thepresence of antisocial behavior starting in child-hood or adolescence (American Psychiatric As-sociation, 2000). Prospective studies of eitherclinic referred (Lahey, Loeber, Burke, & Apple-gate, 2005; Robins, 1966) or community partic-ipants (Moffitt et al., 2002) have suggested thatbetween 14 and 54% of children with severeconduct problems will show an antisocial per-sonality disorder as adults. Further, as notedpreviously, children with a childhood onset totheir conduct problems (Moffitt, 2003) andthose with CU traits (Frick & Dickens, 2006;Frick & White, 2008) seem to show a morestable pattern of antisocial behavior. Thus,

this research suggests that some patterns of an-tisocial behavior are more stable than others.Unfortunately, there are no clear guidelines tosuggest what level of stability in antisocial be-havior would be sufficient to warrant designa-tion as a personality disorder. Further, even ifa pattern of behavior is not highly stable, suchas adolescent-onset conduct problems, it maystill lead to significant impairments and warranttreatment (Dandreaux & Frick, 2009; Moffittet al., 1996).

The issue of stability may be even moreimportant if one focuses on the personalitytraits that may lead to antisocial behavior.That is, an important consideration is whetherCU traits are stable enough in children or ado-lescents to warrant the designation of “traits”that implies some level of continuity across de-velopment (Edens, Skeem, Cruise, & Cauf-mann, 2001; Seagrave & Grisso, 2002). Thereare now a number of studies showing that thesetraits are relatively stable from late childhood toearly adolescence both when assessed by self-report (Munoz & Frick, 2007) or by parent re-port (Frick, Kimonis, et al., 2003). For exam-ple, Frick, Kimonis, et al. (2003) reported astability estimate of .71 using an intraclasscorrelation coefficient across 4 years for CUtraits in a sample of children with an averageage of 10.65 at the initial assessment. This levelof stability for parent report is much higherthan is typically reported for parent ratings ofothers aspects of children’s adjustment (Ver-hulst, Koot, & Berden, 1990). With respect toyounger children, Dadds, Frazer, Frost, andHawes (2005) found moderate 1-year stabilityestimates for parent-reported CU traits (r ¼.55) in a community sample of Australian chil-dren who were 4 to 9 years of age. Using a moreextended follow-up period (i.e., 9 years), Obra-dovic, Pardini, Long, and Loeber (2007) re-ported relatively high rates of stability for par-ent (r ¼ .50) but modest levels of stability forteacher ratings (r ¼ .27) ratings of CU traitsfor boys between the ages of 8 and 16. Bloni-gen, Hicks, Kruger, Patrick, and Iacono(2006) reported that CU traits were relativelystable (r ¼ .60) from late adolescence (age17) into early adulthood (age 24). Further,Loney, Taylor, Butler, and Iacono (2007) re-ported that CU traits in adolescence (ages 16–


18) were significantly stable (intraclass correla-tion coefficient ¼ .40) over a 6-year follow-upperiod. Finally, two studies have shown thatmeasures of CU traits assessed prior to adoles-cence were significantly associated with similarmeasures in adulthood, even after controllingfor other childhood risk factors (Burke, Loeber,& Lahey, 2007; Lynam, Caspi, Moffitt, Loeber,& Stouthamer-Loeber, 2007).

Based on these findings, the stability of CUratings across development appears to be betteror equivalent to other trait indices across child-hood to adolescence and early adulthood. How-ever, there is no agreed on metric regardingwhat level of stability would warrant the classi-fication of a “stable trait.” Critically, even rea-sonably high levels of stability would not implythat CU traits are unchangeable. For example,Frick, Kimonis, et al. (2003) reported that,despite the high level of stability in these traitsacross their 4-year study period, there were asignificant number of youth who decreased intheir level of CU traits over the course of thestudy (for a similar pattern of change over alonger period of development, see also Lynamet al., 2007). Further, this decrease in the levelof CU traits was related to the level of conductproblems displayed by the child, the socioeco-nomic status of the child’s parents, and thequality of parenting the child received. Thus,CU traits do appear to be at least somewhat mal-leable and changes in their level across devel-opment seem to be influenced by factors inthe child’s psychosocial environment.

The Importance of Multiple Levelsof Analysis

From the review provided above, it is clear thatsubgroups of antisocial youth differ in a numberof important ways behaviorally. That is, they candiffer in their timing of onset, the stability of theirbehavior, and the level and type of aggressionthat is displayed. Further, we have also notedseveral ways that these subgroups differ in theiremotional, cognitive, social, and interpersonalfunctioning. Understanding differences on eachof these levels provides important informationfor charting the varied mechanisms (e.g., deficitsin conscience; poor emotional regulation) thatmay be involved in the development of antisocial

traits. In recent years, there have been substantialincreases in the number of studies exploringbiological vulnerabilities to antisocial behav-ior (Raine & Yang, 2006). In this section, we pro-vide a selective review of genetic and brainimaging (focusing on functional magnetic reso-nance imaging [fMRI]) studies with antisocialindividuals and, in particular, reviewing severalareas of research that could advance our under-standing of the different developmental path-ways to antisocial behavior.

Behavioral genetic studies

There have been a large number of studiesshowing moderate heritability and nonsharedenvironmental influence, as well as modestshared environmental influence on antisocialbehavior (e.g., Mason & Frick, 1994; Rhee &Waldman, 2002). In other words, individualdifferences in susceptibility to antisocial behav-ior have both a heritable and environmentalcomponent. In recent years, there have beenseveral lines of research that have attempted togo beyond this basic partitioning of geneticand environmental influences to antisocial be-havior that could be especially important forunderstanding the different developmental path-ways that may lead to severe patterns of antiso-cial behavior.

First, twin and adoption studies have demon-strated several important types of gene–envi-ronment correlations and gene–environment in-teractions. For example, risk factors that havebeen traditionally conceptualized as environ-mental (e.g., parenting reactions) may actuallybe evoked partly by the heritable temperamentalfeatures of the child (gene–environment corre-lation; Larsson, Viding, Rijsdijk, & Plomin,2008). Further, genetically influenced individualdifferences in the sensitivity to environmentalrisk factors such as maltreatment (gene–environ-ment interaction) are also important in explain-ing variance in antisocial behavior. Specifically,research has suggested that genes regulatingserotonergic neurotransmission, in particularmonoamine oxidase A (MAOA), are importantfor explaining individual differences in antiso-cial behavior (Buckholtz & Meyer-Lindenberg,2008). However, the genetic vulnerability toantisocial behavior conferred by the MAOA


low-activity allele (MAOA-L) may only becomeevident in the presence of an environmentaltrigger, such as maltreatment (Caspi et al.,2002; Kim-Cohen et al., 2006).

Second, and more directly related to the differ-ent developmental pathways to antisocial behav-ior, several studies have begun studying differ-ences in the heritability of antisocial behavioracross subtypes. For example, Taylor, Iacono,and McGue (2000) reported greater genetic influ-ence for childhood-onset delinquency, comparedto adolescence-onset delinquency. A recent studyby Silberg, Rutter, Tracy, Maes, and Eaves (2007)extended these findings with a larger sampleof twins. They reported that a single genetic factorwas important in influencing antisocial behaviorthat started in childhood and was persistent intoadulthood. They also found that there were ado-lescent-onset shared environmental factors thatwere not influencing individual differences inantisocial behavior before adolescence. Finally,they reported a transient genetic effect at pubertyand argued that this finding is consistent with anotion of genetically mediated influence on thetiming of puberty affecting the expression of ge-netic differences in antisocial outcomes.

Directly related to the model of the CU traitsdifferentiating subtypes within the childhood-onset group, antisocial behavior in childrenwith CU traits has been found to be understrong genetic influence (heritability of .81)with little influence of shared environment(Viding, Blair, Moffitt, & Plomin, 2005). Incontrast, antisocial behavior in children withoutelevated levels of CU shows more modest ge-netic influence (heritability of .30) and substantialenvironmental influence (shared environmentalinfluence ¼ .34, nonshared environmental influ-ence¼ .26). It was important that the differencesin heritability could not be attributed to differ-ences in the severity of conduct problems inthis sample of 7-year-old twins. These findingswere replicated when the children were 9 yearsold, and this latter study also demonstrated thatthe difference in heritability magnitude holdseven after hyperactivity scores of the childrenwere controlled (Viding, Jones, Frick, Moffitt,& Plomin, 2008).

Thus, these behavioral genetic studies pro-vide strong support for differences in the etiol-ogy for the different patterns of antisocial be-

havior (childhood vs. adolescence onset; CUvs. non-CU), again supporting the importanceof recognizing equifinality in causal models.Further, these findings are also consistent withsome of the findings on behavioral, cognitive,affective, and social correlates reported pre-viously. For example, the finding of persistentgenetic influences being associated with child-hood-onset antisocial behavior and new envi-ronmental influences coming to play in ado-lescence is consistent with the emphasis onbiological and temperamental vulnerabilitiesfor the early starters and greater emphasis onsocial causes for the adolescent-onset group.The finding of differences in etiological factorsfor antisocial behavior in children high and lowon CU traits also is consistent with previousfindings. For example, stronger environmentalinfluences on antisocial behavior in childrenwho are low on CU traits support those studiesreviewed previously showing that parentingfactors were more strongly associated with con-duct problems in these children (Frick & White,2008).

Third, although no molecular genetic studieshave directly compared different subtypes ofchildren with conduct problems, some imagingstudies have suggested that the MAOA-L riskpolymorphism may relate specifically to chil-dren who show primarily impulsive and reac-tive types of conduct problems (for a review,see Buckholtz & Meyer-Lindenberg, 2008).Buckholtz and Meyer-Lindenberg (2008) pro-pose that MAOA-L causes an ontogentic excessof serotonin and influences the brain’s affectivecircuitry in a way that amplifies the effects ofenvironmental risk, such as maltreatment. It isinteresting to note that some studies have re-ported an increased vulnerability to antisocialbehavior in the presence of the MAOA high(as opposed to low) activity allele (e.g., Man-uck et al., 2000). Thus, it is possible that differ-ent alleles of the same gene may predispose todifferent types of conduct problems by havingopposite effects on the affective lability of anindividual. This would be consistent with ourdevelopmental model specifying different pat-terns of emotional responding across subgroupsof antisocial youth. However, this possibility ishighly speculative at present. As for any psychi-atric outcome, the genetic influences on any


subtype of conduct problems will not be limitedto a single candidate gene. However, these find-ings also nicely illustrate the concept of multifi-nality. That is, it is unlikely that specific genesthat increase the likelihood for antisocial behav-ior would conform to diagnostic boundaries.For example, different levels of MAOA activityhave been linked to a wide range of psychiatricdisorders such as depression, autism, bipolardisorder, and alcoholism (Cicchetti, Rogosch,& Sturge-Apple, 2007; Rende & Waldman,2006; Shin, Chen, & Ridd, 1999). The multi-finality of outcomes suggests that any geneticrisk conferred by MAOA-L is likely to bemoderated by both distinct environmental riskfactors and other genes, as already outlinedabove.

Fourth, twin studies have not only begun tocompare genetic and environmental influencesin subgroups of antisocial youth, they havealso begun to explore whether antisocial behav-ior, CU traits, and other related traits (e.g., sub-stance abuse) co-occur because of commongenetic and/or environmental factors (Kruegeret al., 2002; Taylor, Loney, Bobadilla, Iacono,& McGue, 2003; Viding et al., 2007). In muchthe same way as a comparison of identical andfraternal twins enables the partitioning of var-iance into genetic, shared, and nonshared envi-ronmental components, the twin design canalso be used to partition covariance betweentraits into different etiological components.Such multivariate behavioral genetic analysesare ideal for investigating different phenotypicmanifestations of shared genetic or environ-mental risk. In general, these types of analyseshave suggested that the overlap among antiso-cial behavior and other externalizing symptomsor personality traits (e.g., CU) has a substantialgenetic component (e.g., Viding et al., 2007).In addition, these studies have found that thenonshared environmental factors (i.e., thoseenvironmental risk factors that are not sharedby two family members) are often phenotypespecific. Such findings suggest that nonshared,phenotype specific, environmental risk factorsare critical for differentiating the eventual be-havioral outcome, even if the same geneticrisk factors are important for two different be-havioral patterns. It is also possible that somedifferentiation of behavioral outcome is be-

cause of those risk genes that are not commonbetween two distinct outcomes.

Fifth, behavior genetic studies have begun toaddress the issue of whether severe antisocialbehavior is better thought of as being on a con-tinuum with normal behavior or whether it isbetter considered a qualitatively distinct taxon(Beauchaine, 2003; Vasey, Kotov, Frick, &Loney, 2005). One possibility is that commonbehavioral disorders are the quantitative ex-treme of the same genetic effects that operatethroughout the distribution of the trait (Plomin,Owen, & McGuffin, 1994). In this quantitativetrait loci model, several genes (rather than a fewrogue mutations) are hypothesized to act in aprobabilistic manner to increase risk for the de-velopment of maladaptive behavioral outcome.Each gene is thought to account for only a min-iscule proportion of variance for any risk out-come (Plomin, DeFries, McClearn, & McGuf-fin, 2008). It is thus unsurprising that evenwhen environmental risk factors increase the“penetrance” of genetic risk, the interaction be-tween any specific gene and an environmentalrisk factor does not account for all of the var-iance in a maladaptive behavioral outcome(Caspi et al., 2002). Twin studies have gener-ally documented similar heritability (and envi-ronmental) estimates across the continuum ofconduct problem scores, as well as at the ex-treme trait level (e.g., Slutske et al., 1997; Vid-ing et al., 2005, 2007). For example, Slutskeet al. (1997) found that a multiple-thresholdmodel of severe antisocial behavior fit theirdata well, suggesting that antisocial behaviorseems to be an extreme of the normal variationin conduct problems, rather than a discrete en-tity. Similar heritability estimates for normal/subclinical and extreme forms of behavior arein line with the quantitative trait loci model.

It is important to note that such a model doesnecessarily contradict the possibility that theremay be different subgroups of antisocial youthwith qualitatively different causal processes.That is, heritability and environmental esti-mates obtained at different cutoffs of any uni-variate distribution could be based on datafrom a heterogeneous group of individualswho could have a distinct set of genetic andenvironmental risk factors. In addition, theremay be different normal to abnormal continua


in terms of the relative importance of certaingenes and environments for different subtypes.Thus, it is still possible that different subtypesof antisocial individuals could have distinctetiologies, even if their vulnerability profileon a single indicator (e.g., specific behavior orneurocognitive measure) is not qualitativelydifferent from the rest of the population.

fMRI Brain imaging studies

Despite the demonstration of genetic influenceson individual differences in antisocial behavior,it is important to emphasize that risk genes forantisocial behavior do not act deterministically.Instead, genes code for neurocognitive vulner-abilities that may, in turn, increase a child’srisk for antisocial behavior in certain environ-mental contexts. For example, individual differ-ences in several brain areas and cognitive func-tions associated with perception and regulationof emotions have been found to correlate withantisocial and violent behavior and could alsomediate genetic influences (Davidson, Putnam,& Larson, 2000). In particular, the orbitofron-tal/ventromedial prefrontal cortex, anterior cin-gulate, amygdala, and interconnected regionshave shown both structural and functional ab-normalities in antisocial populations (Blair et al.,2005).

fMRI is a relatively new tool for studying an-tisocial behavior in children and, as a result,only a handful of studies exist to date. Hence,to date, there are no fMRI studies contrastingchildhood-onset with adolescent-onset sub-types or antisocial youth with and without CUtraits. Instead, published studies have eitherfocused on an undifferentiated group of chil-dren with antisocial behavior or on the CU sub-type alone. However, these studies do providesome at least speculative support for the devel-opmental model that has been outlined in thispaper. Specifically, reduced anterior cingulateresponsivity to threatening emotional scenesunder passive viewing conditions has beenreported for antisocial youth, possibly reflect-ing poor emotional regulation (Stadler et al.,2007; Sterzer, Stadler, Krebs, Kleinschmidt,& Poutska, 2005). The same studies also re-ported amygdala hypoactivation to negativeand threatening pictures for antisocial youth,

but this result emerged only when anxietyscores were used as a covariate. A more recentstudy using an almost identical passive viewingparadigm found increased amygdala activation,partly related to comorbid anxiety, in chil-dren with antisocial behavior (Herpertz et al.,2008). These functional deficits would be con-sistent with some of the abnormalities in howchildren with CU traits process emotionalstimuli.

In support of this possibility, two studieshave directly measured CU traits and explicitlytested the hypothesis that this group wouldshow amygdala hyporeactivity to others’ dis-tress (Jones, Laurens, Herbs, Baker, & Viding,2009; Marsh et al., 2008). Both studies em-ployed an implicit emotion processing task(gender recognition) and found amygdala hy-poreactivity to fearful faces in antisocial youthwith CU traits compared to typically develop-ing children and children with attention-defi-cit/hyperactivity disorder. Another study docu-mented an abnormal ventromedial prefrontalcortex response to punishment in childrenwith CU traits (Finger et al., 2008). This studyemployed a task in which the participants had tolearn that a stimulus that used to be rewardingwas subsequently associated with loss andthat they should stop responding to that stimu-lus. This finding is consistent with previouslyreviewed findings showing abnormalities inhow youth with CU traits respond to rewardand punishment contingencies.

Thus, although much more work in this areais needed, these initial findings from brainimaging studies are promising in providing pos-sible neurological bases to some of the cog-nitive and affective differences found acrossthe different developmental pathways to antiso-cial behaviors, and could help in uncoveringsome of the neurocognitive mechanismsthrough which inherited predispositions canplace a child at risk for the development antiso-cial traits (Viding & Jones, 2008). Of impor-tance, these promising studies demonstrate theimportance of integrating findings across multi-ple levels of analyses. That is, the unique func-tional neurological deficits were documentedwhen CU traits were used to form experimentalgroups and when tasks tapping the specificemotional and cognitive deficits that have


been associated with these traits were used totest functional brain differences.

It is important to bear in mind that althoughour selective review focused on fMRI studies,such studies do not by any means representthe only avenue of investigation for chartingneurobiological vulnerabilities that can mediatethe genetic influences on antisocial behavior.For example, several studies have shown thatyouth with CU traits show differences in theirautonomic reactivity to certain types of stimuli(Blair, 1999; Kimonis et al., 2008) and theyshow differences in both their resting (Loney,Butler, Lima, Counts, & Eckel, 2006) andstress-induced (O’Leary, Loney, & Eckel,2007) cortisol levels. Thus, some of the geneticrisk for this group of antisocial youth could bedue to inherited individual differences in thefunctioning of their autonomic nervous systemor in the reactivity of their hypothalamic–pitui-tary–adrenal axis as indexed by the hormonecortisol. Combining across all of these levelsprovides the greatest likelihood of advancingour knowledge of the different pathways tothe equifinal outcome of antisocial behavior(Viding & Frith, 2006).

Implications for Prevention and Treatment

The research on different subgroups of antiso-cial youth, and the developmental model thatwe have used to organize it, has several impor-tant applied implications. One key implicationof this approach is an emphasis on prevention.As noted previously, the most aggressive youth,and the youth most likely to continue their anti-social behavior into adulthood, tend to show achildhood onset to their antisocial behavior.Further, there are a number of interventionsthat have proven effective in treating earlyemerging conduct problems, with a great de-crease in their effectiveness in older childrenand adolescents (Eyberg, Nelson, & Boggs,2008). Thus, intervening early in the develop-mental trajectory of childhood-onset conductproblems is an important goal for preventinglater serious aggression and antisocial behavior.However, even these interventions require achild to have already shown serious and impair-ing conduct problems, albeit at an early age. Byfocusing on the developmental processes that

can precede even these early conduct problems,it opens the possibility of prevention programsthat promote optimal development in childrenwith certain risk factors (e.g., an fearless tem-perament, poor emotional regulation) even be-fore serious behavioral problems emerge.

A second implication of the developmentalapproach to understanding antisocial behaviorthat was outlined in this paper is that interventionsneed to be comprehensive and target multiple riskfactors. As noted throughout this paper, no gene,no temperamental risk factor, no environmentalrisk factor operates in isolation. Thus, it is not sur-prising that some of the most effective interven-tions for antisocial behavior involve multiplecomponents, rather than targeting only a singlerisk factor (e.g., Conduct Problems PreventionResearch Group, 2004).

A third implication of the developmentalmodel is that interventions not only need to becomprehensive, but they also need to be indi-vidualized. That is, given that the causal pro-cesses leading to antisocial behavior appear tobe different across subgroups, it is also quitelikely that treatments will need to be differentacross these groups as well. For example,Hawes and Dadds (2005) reported that clinic-referred boys (ages 4 to 9) with conduct prob-lems and CU traits were less responsive to aparenting intervention than boys with conductproblems who were low on CU traits. However,this differential effectiveness was not consis-tently found across all phases of the treatment.That is, children with and without CU traitsseemed to respond equally well to the firstpart of the intervention that focused on teachingparents methods of using positive reinforce-ment to encourage prosocial behavior. In con-trast, only the group without CU traits showedadded improvement with the second part ofthe intervention that focused on teaching par-ents more effective discipline strategies. Thisoutcome would be consistent with the reward-oriented response style that, as reviewed pre-viously, appears to be characteristic of childrenwith CU traits. In another study of the differen-tial response to treatment of youth with CUtraits, Waschbusch, Carrey, Willoughby, King,and Andrade (2007) reported that children(ages 7–12) with conduct problems and CUtraits responded less well to behavior therapy


alone than children with conduct problemswithout CU traits. However, these differenceslargely disappeared when stimulant medicationwas added to the behavior therapy, although thechildren with CU traits were still less likely toscore in the normative range than those withoutthese traits.

These findings support the contention thatinterventions may be more effective if theyare specifically tailored to the unique needs ofchildren within the different developmentalpathways. This focus on a comprehensive andindividualized approach to treatment may beparticularly important for enhancing the effec-tiveness of existing treatments for older childrenand adolescents who show severe antisocial anddelinquent behavior. For example, a studygroup commissioned by the Office of JuvenileJustice and Delinquency Prevention of theUnited States Department of Justice reviewedfour juvenile justice programs that provided in-dividualized and comprehensive services to ad-judicated youth who were under the age of 13(Burns et al., 2003). This summary outlinedseveral features of such comprehensive modelsthat appeared critical to their success. One crit-ical feature is that there was a system for ensur-ing that an array of mental health, medical,child welfare, and educational services wereavailable to adjudicated youth. In addition,there was a system for providing a comprehen-sive assessment to determine the specific needsof the adjudicated youth and a strong case-management system for ensuring that serviceswere provided in an integrated and coherentmanner. Similar models of comprehensiveand individualized interventions have provento be effective for older youth with severe anti-social behavior (Henggeler, Schoenwald, Bor-duin, Rowland, & Cunningham, 1998).

Research on the various developmentalpathways to antisocial behavior could be quiteimportant for guiding these comprehensiveand individualized approaches to treatment.That is, knowledge of the different develop-mental processes that may be operating in thevarious subgroups of antisocial youth couldhelp in determining the most effective combi-nation of services for an individual child (Frick,2006). For example, interventions that focus onenhancing identity development in adolescents

and increasing contact with prosocial peers,such as mentoring programs (Grossman & Tier-ney, 1998) or programs that provide structuredafterschool activities (Mahoney & Stattin,2000), may be particularly effective for youthwithin the adolescent-onset pathway. In con-trast, interventions that focus on anger controlmay be more effective for children within thechildhood-onset pathway who do not exhibitCU traits but who often show problems withemotional regulation (Larson & Lochman,2003). Further, interventions that interveneearly in the parent–child relationship to teachparents ways to foster empathic concern in theiryoung child or that help the child developcognitive perspective taking skills may bemore effective for children with CU traits(Chi-Ming, Greenberg, & Walls, 2003). Laterin development, intervening in ways that em-phasize the reward-oriented response style ofthis group and attempt to motivate childrenthrough appealing to their self-interest, ratherthan through interventions that solely focuson punishment-oriented strategies, may bemore effective for this group of youth (Frick,2006).

An important note of caution relates to thebehavioral genetic research reviewed above.That is, such research could lead some to con-sider gene therapy for antisocial behavior.Genes that have variants that are common inthe population are likely to have multiple func-tions, some of which are desirable, others not.For example, the genetic variants that increasethe probability of CU traits may also be protec-tive against excessive anxiety. When this infor-mation is combined with the fact that genes in-teract in complex systems, as well as withenvironmental risk factors, it quickly becomesevident that removing the effects of one genevia gene therapy is unlikely to be effective(Nuffield Council on Bioethics, 2002).

This does not mean that genotype informa-tion is irrelevant to prevention and treatment.For example, demonstrating that there are ge-netically heterogeneous subtypes of childhood-onset antisocial behavior suggests the possibil-ity of subtype-specific risk gene variants thatindex vulnerability for specific neurocognitivedeficits. An early knowledge of such riskgenes, particularly in the context of certain


environmental factors, could also be used toguide prevention efforts prior to the emergenceof severe conduct problems.

Summary and Conclusions

In this paper, we have outlined a developmentalpsychopathology framework for understandingthe etiology of severe patterns of antisocial be-havior or antisocial personality. In this frame-work, we outline three important pathwaysthrough which children and adolescents can de-velop severe antisocial behaviors. Unlike pastattempts to define important subgroups of anti-social individuals, this approach does not relysolely on differences in the types of behaviors,timing of onset of behaviors, the stability ofbehaviors, or personality traits. Instead, an em-phasis is placed on the developmental processesthat may place a child at risk for acting in an an-tisocial and aggressive manner. Specifically,the model defines a group of youth whose anti-social behavior begins in adolescence and whoseem to be showing an exaggeration of normaladolescent rebellion. Further, the model definestwo groups of youth whose antisocial behaviorbegins prior to adolescence and who seem toshow problems in adjustment across multipledevelopmental stages. One group is character-ized by the presence of CU traits that seem re-lated to a temperamental deficit in how theyprocess emotional stimuli and respond to pun-ishment cues that interfere with the normal de-velopment of empathy, guilt, and other aspectsof conscience. The second group of early-onsetantisocial youths show problems more relatedto cognitive deficits and ineffective sociali-zation that lead to problems in the normal de-velopment of behavioral and emotional regula-tion.

In outlining these distinct pathways to anti-social behavior, we have tried to illustratesome key concepts from developmental psy-chopathology. First, we have used these path-ways to illustrate the concepts of equifinalityand multifinality, by showing how severe pat-terns of antisocial behavior can result fromvery different causal processes (i.e., equifinal-ity) and how the same risk factors can lead tomany different outcomes (i.e., multifinality).Second, we have illustrated how understanding

the interface between normal and abnormal de-velopment is crucial for understanding thecauses of antisocial behavior. That is, each pat-tern of antisocial behavior involves somewhatunique developmental processes and they eachdeviate from normative patterns of antisocialbehavior in different ways. Third, we haveused this model to show how using multiplelevels of analyses can advance causal theories.Specifically, children in all three pathwaysshow unique behavioral, social, emotional,cognitive, and neurological correlates that,when combined, provide an integrated causaltheory that is not possible when research is re-stricted to any single level of analysis. Fourth,and potentially most importantly, we have high-lighted how this development model can beused to enhance existing interventions for anti-social individuals, particularly by highlightingavenues for early intervention and by guidingcomprehensive and individualized approachesto treatment.

Thus, we think that developmental modelssuch as the one we have outlined in this paperneed to guide etiological theories of conductproblems, aggression, and antisocial behavior.Further, this body research points the way toseveral potentially important directions forfuture research. First, a key aspect to the devel-opmental models outlined in this manuscript isthe different temperaments that may place achild at risk for showing severe antisocial andaggressive behavior. However, the vast major-ity of research has focused on studying the tem-peramental characteristics of children and ado-lescents who already show problem behavior.As a result, it will be critical for future researchto study children with the hypothesized tem-peramental risk factors (e.g., low levels of fear-fulness; high levels of emotional reactivity)early in development to see if the temperamen-tal risk factors predict later conduct problemsand, even more importantly, predict the specificdevelopmental mechanisms (e.g., lack of guiltand empathy; poorly regulated emotions) thatare proposed to underlie the conduct problemsacross the different causal pathways. Such pro-spective research is not only important for pro-viding strong tests of the predictive utility of thedevelopmental model but also could help to un-cover protective factors that may reduce the


likelihood that a child with a temperamentalrisk factor will show severe behavior problems.A better understanding of protective factorscould be quite helpful for guiding future pre-vention programs. Second, we have outlinedthe potential importance of studying the differ-ent pathways at many different levels of analy-ses (e.g., behavioral, affective/cognitive, neuro-logical). Unfortunately, only very few studieshave tested predictions made by this develop-mental model on the neurological level, whichis likely because of the type of expertise neededto conduct such studies and the great expenseinvolved in conducting such research. How-ever, the promising findings from the neuro-imaging studies that have been conducted to

date clearly illustrate the great potential of fu-ture studies in this area. Third, and potentiallymost important, very few intervention studieshave used this developmental model to tailortheir interventions to the unique needs ofantisocial youths in the different causal path-ways. In this paper, we have made some edu-cated hypotheses as to what types of interven-tions may be most effective for the differentgroups of antisocial youth. However, thesehypotheses remain largely untested. Such testsshould be a critical goal for future research,given that the few existing studies clearlysuggest that youth in all three pathways canrespond to interventions, albeit to differentones.

References

American Psychiatric Association. (1980). The diagnosticand statistical manual of mental disorders (3rd ed.).Washington, DC: Author.

American Psychiatric Association. (1987). The diagnosticand statistical manual of mental disorders (3rd ed.,rev.). Washington, DC: Author.

American Psychiatric Association. (2000). The diagnosticand statistical manual of mental disorders (4th ed.,text revision). Washington, DC: Author.

Aguilar, B., Sroufe, A., Egeland, B., & Carlson, E. (2000).Distinguishing the early-onset/persistent and adoles-cence-onset antisocial behavior types: From birth to16 years. Development and Psychopathology, 12,109–132.

Andershed, H., Gustafson, S. B., Kerr, M., & Stattin, H.(2002). The usefulness of self-reported psychopathy-like traits in the study of antisocial behaviour amongnon-referred adolescents. European Journal of Person-ality, 16, 383–402.

Beauchaine, T. P. (2003). Taxometrics and developmentalpsychopathology. Development and Psychopathology,15, 501–527.

Binder, A. (1987). An historical and theoretical introduc-tion. In H. C. Quay (Ed.), Handbook of juvenile delin-quency (pp. 1–33). New York: Wiley.

Blair, R. J. R. (1999) Responsiveness to distress cues in thechild with psychopathic tendencies. Personality and In-dividual Differences, 27, 135–145.

Blair, R. J. R., Mitchell, D., & Blair, K. (2005). Thepsychopath: Emotion and the brain. Malden, MA:Blackwell.

Blonigen, D. M., Hicks, B. M., Kruger, R. F., Patrick, C. P.,& Iacono, W. G. (2006). Continuity and change in psy-chopathic traits as measured via normal-range personal-ity: A longitudinal-biometric study. Journal of Abnor-mal Psychology, 115, 85–95.

Brezina, T., & Piquero, A. R. (2007). Moral beliefs, isola-tion from peers, and abstention from delinquency. Devi-ant Behavior, 28, 433–465.

Broidy, L. M., Nagin, D. S., Tremblay, R. E., Bates, J. E.,Brame, B. U, Dodge, K. A., et al. (2003). Develop-mental trajectories of childhood disruptive behaviors

and adolescent delinquency: A six-site, cross-nationalstudy. Developmental Psychology, 39, 222–245.

Buckholtz, J. W., & Meyer-Lindenberg, A. (2008). MAOAand the neurogenetic architecture of human aggression.Trends in Neurosciences, 31, 120–129.

Burke, J. D., Loeber, R., & Lahey, B. B. (2007). Adolescentconduct disorder and interpersonal callousness as pre-dictors of psychopathy in young adults. Journal of Clin-ical Child and Adolescent Psychology, 36, 334–346.

Burns, B., Howell, J. C., Wiig, J. K., Augimeri, L. K.,Welsh, B. C., Loeber, R., et al. (2003). Treatment, ser-vices, and intervention programs for child delinquents.Office of Juvenile Justice and Delinquency Child Delin-quency Bulletin Series, March, 1–15.

Card, N. A., & Little, T. D. (2006). Proactive and reactiveaggression in childhood and adolescence: A meta-anal-ysis of differential relations with psychosocial adjust-ment. International Journal of Behavioral Develop-ment, 30, 466–480.

Caspi, A., McClay, J., Moffitt, T., Mill, J., Martin, J., Craig,I. W., et al. (2002). Role of genotype in the cycle of vio-lence in maltreated children. Science, 297, 851–854.

Chi-Ming, K., Greenberg, M. T., & Walls, C. T. (2003). Ex-amining the role of implementation quality in school-based prevention using the PATH curriculum. Preven-tion Science, 4, 55–63.

Cicchetti, D., & Rogosch, F. A. (1996). Equifinality andmultifinality in developmental psychopathology. De-velopment and Psychopathology, 8, 597–600.

Cicchetti, D., Rogosch, F. A., & Sturge-Apple, M. L.(2007). Interactions of child maltreatment and serotonintransporter and monoamine oxidase A polymorphisms:Depressive symptomatology among adolescents fromlow socioeconomic status backgrounds. Developmentand Psychopathology, 19, 1161–1180.

Cleckley (1976). The mask of sanity. St. Louis, MO:Mosby.

Cloninger, C. R. (1987). A systematic method for clinicaldescription and classification of personality variants.Archives of General Psychiatry, 44, 573–588.

Conduct Problems Prevention Research Group. (2004). Theeffects of the Fast Track Program on serious problem


outcome at the end of elementary school. Journal ofClinical Child and Adolescent Psychology, 33, 650–661.

Cornell, A. H., & Frick, P. J. (2007). The moderating effectsof parenting styles in the association between behavioralinhibition and parent-reported guilt and empathy in pre-school children. Journal of Clinical Child and Adoles-cent Psychology, 36, 305–318.

Crick, N. R. (1996). The role of overt aggression, relationalaggression, and prosocial behavior in the prediction ofchildren’s future social adjustment. Child Development,67, 2317–2327.

Crick, N. R., Casas, J. F., & Mosher, M. (1997). Relationaland overt aggression in preschool. Developmental Psy-chology, 33, 579–588.

Crick, N. R., & Grotpeter, J. K. (1995). Relational aggres-sion, gender, and social–psychological adjustment.Child Development, 66, 710–722.

Dadds, M. R., Fraser, J., Frost, A., & Hawes, D. (2005).Disentangling the underlying dimensions of psychopa-thy and conduct problems in childhood: A communitystudy. Journal of Consulting and Clinical Psychology,73, 400–410.

Dandreaux, D. M., & Frick, P. J. (2009). Developmentalpathways to conduct problems: A further test of thechildhood and adolescent-onset distinction. Journal ofAbnormal Child Psychology, 37, 375–385.

Davidson, R. J., Putnam, K. M., & Larson, C. L. (2000).Dysfunction in the neural circuitry of emotion regula-tion: A possible prelude to violence. Science, 289, 591–594.

Dodge, K. A., & Pettit, G. S. (2003). A biopsychosocialmodel of the development of chronic conduct problemsin adolescence. Developmental Psychology, 39, 349–371.

Edens, J. F., Campbell, J. S., & Weir, J. M. (2007). Youthpsychopathy and criminal recidivism: A meta-analysisof the psychopathy checklist measures. Law and HumanBehavior, 31, 53–75.

Edens, J. F., Skeem, J. L., Cruise, K. R., & Cauffman, E.(2001). Assessment of “juvenile psychopathy” and itsassociation with violence: A critical review. BehavioralSciences and the Law, 19, 53–80.

Edens, J. F., Skopp, N. A., & Cahill, M. A. (2008). Psycho-pathic features moderate the relationship between harshand inconsistent parental discipline and adolescent anti-social behavior. Journal of Clinical Child and Adoles-cent Psychology, 37, 472–476.

Enebrink, P., Anderson, H., & Langstrom, N. (2005). Cal-lous–unemotional traits are associated with clinical se-verity in referred boys with conduct problems. NordicJournal of Psychiatry, 59, 431–440.

Eyberg, S. M., Nelson, M. M., & Boggs, S. R. (2008).Evidence-based psychosocial treatments for childrenand adolescents with disruptive behavior. Journal ofClinical Child and Adolescent Psychology, 37, 215–237.

Farrington, D. P., Gallagher, B., Morley, L., St. Ledger, R. J.,& West, D. (1988). Are there any successful men fromcriminogenic backgrounds? Psychiatry: Journal for theStudy of Interpersonal Processes, 51, 116–130.

Fergusson, D. M., Lynsky, M. T., & Horwood, L. J. (1996).Factors associated with continuity and changes in dis-ruptive behavior patterns between childhood and ado-lescence. Journal of Abnormal Child Psychology, 24,533–553.

Finger, E. C., Marsh, A. A., Mitchell, D. G., Reid, M. E.,Sims, C., Budhani, S., Kosson, D. S., et al. (2008). Ab-

normal ventromedial prefrontal cortex function in chil-dren with psychopathic traits during reversal learning.Archives of General Psychiatry, 65, 586–594.

Fowles, D. C., & Kochanska, G. (2000). Temperament as amoderator of pathways to conscience in children: Thecontribution of electrodermal activity. Psychophysiol-ogy, 37, 788–795.

Frick, P. J. (2006). Developmental pathways to conduct dis-order. Child and Adolescent Psychiatric Clinics ofNorth America, 15, 311–331.

Frick, P. J., Cornell, A. H., Barry, C. T., Bodin, S. D., &Dane, H. E. (2003). Callous–unemotional traits andconduct problems in the prediction of conduct problemseverity, aggression, and self-report of delinquency.Journal of Abnormal Child Psychology, 31, 457–470.

Frick, P. J., Cornell, A. H., Bodin, S. D., Dane, H. A., Barry,C. T., & Loney, B. R. (2003). Callous–unemotionaltraits and developmental pathways to severe conductproblems. Developmental Psychology, 39, 246–260.

Frick, P. J., & Dickens, C. (2006). Current perspectives onconduct disorder. Current Psychiatry Reports, 8, 59–72.

Frick, P. J., Kimonis, E. R., Dandreaux, D. M., & Farrell, J. M.(2003). The 4-year stability of psychopathic traits in non-referred youth. Behavioral Sciences and the Law, 21,713–736.

Frick, P. J., Lahey, B. B., Loeber, R., Tannenbaum, L. E.,Van Horn, Y., Christ, M. A. G., et al. (1993). Opposi-tional defiant disorder and conduct disorder: A meta-analytic review of factor analyses and cross-validationin a clinic sample. Clinical Psychology Review, 13,319–340.

Frick, P. J., Lilienfeld, S. O., Ellis, M., Loney, B., & Silver-thorn, P. (1999). The association between anxiety andpsychopathy dimensions in children. Journal of Abnor-mal Child Psychology, 27, 383–392.

Frick, P. J., & Loney, B. R. (1999). Outcomes of childrenand adolescents with conduct disorder and oppositionaldefiant disorder. In H. C. Quay & A. Hogan (Eds.), Hand-book of disruptive behavior disorders (pp. 507–524).New York: Plenum Press.

Frick, P. J., & Marsee, M. A. (2006). Psychopathy and de-velopmental pathways to antisocial behavior in youth.In C. J. Patrick (Ed.), The handbook of psychopathy(pp. 353–375). New York: Guilford Press.

Frick, P. J., & Morris, A. S. (2004). Temperament and de-velopmental pathways to conduct problems. Journalof Clinical Child and Adolescent Psychology, 33, 54–68.

Frick, P. J., & White, S. F. (2008). Research review: The im-portance of callous–unemotional traits for develop-mental models of aggressive and antisocial behavior.Journal of Child Psychology and Psychiatry, 49, 359–375.

Grossman, J. B., & Tierney, J. P. (1998). Does mentoringwork? An impact study of the Big Brothers/Big Sistersprogram. Evaluation Review, 22, 403–426.

Hare, R. D. (1993). Without conscience: The disturbingworld of the psychopaths among us. New York: Guil-ford Press.

Hawes, D. J., & Dadds, M. R. (2005). The treatment of con-duct problems in children with callous–unemotionaltraits. Journal of Consulting and Clinical Psychology,73, 737–741.

Hemphill, J. F. (2007). The Hare Psychopathy Checklistand recidivism: Methodological issues and criticallyevaluating empirical evidence. In H. Herve & J. C.Yuille (Eds.), The psychopath: Theory, research, andpractice (pp. 141–172). Mahwah, NJ: Erlbaum.


Henggeler, S. W., Schoenwald, S. K., Borduin, C. M., Row-land, M. D., & Cunningham, P. B. (1998). Multisys-temic treatment of antisocial behavior in children andadolescents. New York: Guilford Press.

Herpertz, S. C., Huebner, T., Marx, I., Vloet, T. D., Fink, G.R., Stoecker, T., et al. (2008). Emotional processingin male adolescents with childhood-onset conductdisorder. Journal Child Psychology and Psychiatry,49, 781–791.

Hipwell, A. E., Loeber, R., Stouthamer-Loeber, M.,Keenan, K., White, H. R., & Kroneman, L. (2002).Characteristics of girls with early onset disruptive andantisocial behaviour. Criminal Behavior and MentalHealth, 12, 99–118.

Jones, A. P., Laurens, K. L., Herba, C., Barker, G., & Vid-ing, E. (2009). Amygdala hypoactivity to fearful facesin boys with conduct problems and callous–unemo-tional traits. American Journal of Psychiatry, 166,95–102.

Kagan, J., & Snidman, N. (1991). Tempermental factors inhuman development. American Psychologist, 46, 856–862.

Kim-Cohen, J., Caspi, A., Taylor, A., Williams, B., New-combe, R., Craig, I. W., et al. (2006). MAOA, maltreat-ment, and gene–environment interaction predictingchildren’s mental health: New evidence and a meta-analysis. Molecular Psychiatry, 11, 903–913.

Kimonis, E. R., Frick, P. J., Skeem, J., Marsee, M. A.,Cruise, K., Munoz, L. C., et al. (2008). Assessing cal-lous–unemotional traits in adolescent offenders: Vali-dation of the Inventory of Callous–Unemotional Traits.Journal of the International Association of Psychiatryand Law, 31, 241–251.

Kochanska, G. (1993). Toward a synthesis of parental so-cialization and child temperament in early developmentof conscience. Child Development, 64, 325–347.

Kochanska, G., DeVet, K., Goldman, M., Murray, K., &Putnam, S. P. (1994). Maternal reports of consciencedevelopment and temperament in young children. ChildDevelopment, 65, 852–868.

Kochanska, G., Gross, J. N., Lin, M., & Nichols, K. E.(2002). Guilt in young children: Development, determi-nants, and relations with a broader system of standards.Child Development, 73, 461–482.

Kratzer, L., & Hodgins, S. (1999). A typology of offenders:A test of Moffitt’s theory among males and femalesfrom childhood to age 30. Criminal Behaviour andMental Health, 9, 57–73.

Krueger, R. F., Hicks, B. M., Patrick, C. J., Carlson, S. R.,Iacono, W. G., & McGue, M. (2002). Etiologic connec-tions among substance dependence, antisocial behavior,and personality: modeling the externalizing spectrum.Journal of Abnormal Psychology, 111, 411–424.

Krug, E. G., Dahlberg, L. L., Mercy, J. A., Zwi, A. B., &Lozano, R. (2002). World report on violence andhealth. Geneva: World Health Organisation.

Kruh, I. P., Frick, P. J., & Clements, C. B. (2005). Historicaland personality correlates to the violence patterns of ju-veniles tried as adults. Criminal Justice and Behavior,32, 69–96.

Lacourse, E., Dupere, V., & Loeber, R. (2008). Develop-mental trajectories of violence and theft. In R. Loeber,D. P. Farrington, M. Stouthamer-Loeber, & H. R. White(Eds.), Violence and serious theft: Development andprediction from childhood to adulthood (pp. 231–268). New York: Routledge.

Lagerspetz, K. M. J., Bjorkqvist, K., & Peltonen, T. (1988).Is indirect aggression typical of females? Gender differ-

ences in aggressiveness in 11-to 12-year-old children.Aggressive Behavior, 14, 403–414.

Lahey, B. B., & Loeber, R. (1994). Framework for a devel-opmental model of oppositional defiant disorder andconduct disorder. In D. K. Routh (Ed.), Disruptivebehavior disorders in childhood (pp. 139–180). NewYork: Plenum Press.

Lahey, B. B., Loeber, R., Burke, J. D., & Applegate, B.(2005). Predicting future antisocial personality disorderin males from a clinical assessment in childhood. Journalof Consulting and Clinical Psychology, 73, 389–399.

Lahey, B. B., Van Hulle, C. A., Waldman, I. D., Rodgers, J. L,D’Onofrio, B. M., Pedlow, S., et al. (2006). Testing de-scriptive hypotheses regarding sex differences in the de-velopmentofconduct problemsand delinquency. Journalof Abnormal Child Psychology, 34, 737–755.

Lahey, B. B., & Waldman, I. D. (2003). A developmentalpropensity model of the origins of conduct problemsduring childhood and adolescence. In B. B. Lahey, T. E.Moffitt, & A. Caspi (Eds.), Causes of conduct disorderand juvenile delinquency (pp. 76–117). New York: Guil-ford Press.

Larson, J., & Lochman, J. E. (2003). Helping schoolchil-dren cope with anger. New York: Guilford Press.

Larsson, H., Viding, E., Rijsdijk, F., & Plomin, R. (2008).Relationships between a parental negativity and child-hood antisocial behavior over time: A bidirectional ef-fect model in a longitudinal genetically informativedesign. Journal of Abnormal Child Psychology, 36,633–645.

Lilienfeld, S. O., & Marino, L. (1995). Mental disorder as aRoschian concept: A critique of Wakefield’s “harmfuldysfunction” analysis. Journal of Abnormal Psychol-ogy, 104, 411–420.

Leistico, A. R., Salekin, R. T., DeCoster, J., & Rogers, R.(2008). A large-scale meta-analysis related the Haremeasures of psychopathy to antisocial conduct. Lawand Human Behavior, 32, 28–45.

Loeber, R., & Farrington, D. P. (2001). The significance ofchild delinquency. In R. Loeber & D. Farrington (Eds.),Child delinquents: Development, intervention, and ser-vice needs (pp. 1–24). Thousand Oaks, CA: Sage.

Loney, B. R., Butler, M. A., Lima, E. N., Counts, C. A., &Eckel, L. A. (2006). The relation between salivary cor-tisol, callous–unemotional traits, and conduct problemsin an adolescent non-referred sample. Journal of ChildPsychology and Psychiatry, 47, 30–36.

Loney, B. R., Frick, P. J., Clements, C. B., Ellis, M. L., &Kerlin, K. (2003). Callous–unemotional traits, impul-sivity, and emotional processing in adolescents with an-tisocial behavior problems. Journal of Clinical Childand Adolescent Psychology, 32, 66–80.

Loney, B. R., Taylor, J., Butler, M. A., & Iacono, W. G.(2007). Adolescent psychopathy features: 6-year stabil-ity and the prediction of externalizing symptoms duringthe transition to adulthood. Aggressive Behavior, 33,242–252.

Lykken, D. (1995). The antisocial personalities. Hillsdale,NJ: Erlbaum.

Lynam, D. R., Caspi, A., Moffitt, T. E., Loeber, R., & Stout-hamer-Loeber, M. (2007). Longitudinal evidence thatpsychopathy scores in early adolescence predict adultpsychopathy. Journal of Abnormal Psychology, 116,155–165.

Lynam, D. R., & Widiger, T. A. (2001). Using the five-fac-tor model to represent the DSM-IV personality disor-ders: An expert consensus approach. Journal of Abnor-mal Psychology, 110, 401–412.


Mahoney, J. L., & Stattin, H. (2000). Leisure activities andadolescent antisocial behavior: The role of structure andsocial context. Journal of Adolescence, 23, 113–127.

Manuck, S. B., Flory, J. D., Ferrell, R. E., Mann, J. J., &Muldoon, M. F. (2000). A regulatory polymorphismof the monoamine oxidase: A gene may be associatedwith variability in aggression, impulsivity, and centralnervous system serotonergic responsivity. PsychiatryResearch, 95, 9–23.

Marsee, M. A., & Frick, P. J. (2007). Exploring the cog-nitive and emotional correlates to proactive and reactiveaggression in a sample of detained girls. Journal ofAbnormal Child Psychology, 35, 969–981.

Marsh, A. A., Finger, E. C., Mitchell, D. G., Reid, M. E.,Sims, C., Kosson, D. S., et al. (2008). Reduced amyg-dala response to fearful expressions in children and ado-lescents with callous–unemotional traits and disruptivebehavior disorders. American Journal of Psychiatry,165, 712–720.

Mason, D. A., & Frick, P. J. (1994). The heritabilty of anti-social behavior: A meta-analysis of twin and adoptionstudies. Journal of Psychopathology and BehavioralAssessment, 16, 301–323.

McCabe, K. M., Hough, R., Wood, P. A., & Yeh, M.(2001). Childhood and adolescent onset conduct disor-der: A test of the developmental taxonomy. Journal ofAbnormal Child Psychology, 29, 305–316.

Moffitt, T. E. (1993). Adolescence-limited and life-coursepersistent antisocial behavior: A developmental taxon-omy. Psychological Review, 100, 674–701.

Moffitt, T. E. (2003). Life-course persistent and adoles-cence-limited antisocial behavior: A 10-year researchreview and research agenda. In B. B. Lahey, T. E. Mof-fitt, & A. Caspi (Eds.), Causes of conduct disorder andjuvenile delinquency (pp. 49–75). New York: GuilfordPress.

Moffitt, T. E., & Caspi, A. (2001). Childhood predictorsdifferentiate life-course persistent and adolescence-lim-ited antisocial pathways in males and females. Develop-ment and Psychopathology, 13, 355–376.

Moffitt, T. E., Caspi, A., Dickson, N., Silva, P., & Stanton,W. (1996). Childhood-onset versus adolescent-onsetantisocial conduct problems in males: Natural historyfrom ages 3 to 18 years. Development and Psycho-pathology, 8, 399–424.

Moffitt, T. E., Caspi, A., Harrington, H., & Milne, B. J.(2002). Males on the life-course-persistent and adoles-cence-limited antisocial pathways: Follow-up at age26 years. Development and Psychopathology, 14, 179–207.

Munoz, L. C., & Frick, P. J. (2007). The reliability, stability,and predictive utility of the self-report version of theAntisocial Process Screening Device. ScandinavianJournal of Psychology, 48, 299–312.

Munoz, L. C., Frick, P. J., Kimonis, E. R., & Aucoin, K. J.(2008). Types of aggression, responsiveness to provoca-tion, and callous–unemotional traits in detained adoles-cents. Journal of Abnormal Child Psychology, 36, 15–28.

Newman, J. P. (1987). Reaction to punishment in extravertsand psychopaths: Implications for the impulsive behav-ior of disinhibited individuals. Journal of Research inPersonality, 21, 464–480.

Nuffield Council on Bioethics. (2002). Genetics and humanbehaviour: The ethical context. London: NuffieldCouncil on Bioethics.

Obradovic, J., Pardini, D., Long, J. D., & Loeber, R. (2007).Measuring interpersonal callousness in boys from child-hood to adolescence: An examination of longitudinal

invariance and temporal stability. Journal of ClinicalChild and Adolescent Psychology, 36, 276–292.

O’Leary, M. M., Loney, B. R., & Eckel, L. A. (2007). Gen-der differences in the association between psychopathicpersonality traits and cortisol response to induced stress.Psychoneuroendocrinology, 32, 183–191.

Ostrov, J. M., & Keating, C. F. (2004). Gender differencesin preschool aggression during free play and structuredinteractions: An observational study. Social Develop-ment, 13, 255–275.

Pardini, D. A. (2006). The callousness pathway to severeviolent delinquency. Aggressive Behavior, 32, 1–9.

Pardini, D. A., Lochman, J. E., & Frick, P. J. (2003). Cal-lous/unemotional traits and social–cognitive processesin adjudicated youths. Journal of the American Acad-emy of Child & Adolescent Psychiatry, 42, 364–371.

Pardini, D. A., Lochman, J. E., & Powell, N. (2007). Thedevelopment of callous–unemotional traits and antiso-cial behavior in children: Are there shared and/or uniquepredictors? Journal of Clinical Child and AdolescentPsychology, 36, 319–333.

Patrick, C. J. (in press). The construct of psychopathy. In D. R.Lynam & R. T. Salekin (Eds.), Handbook of child andadolescent psychopathy. New York: Guilford Press.

Patrick, C. J. (2007). Getting to the heart of psychopathy. InH. Herves & J. C. Yuille (Eds.), The psychopathy: The-ory, research, and practice (pp. 207–252). Mahwah,NJ: Erlbaum.

Patterson, G. R. (1996). Performance models for antisocialboys. American Psychologist, 41, 432–444.

Patterson, G. R., & Yoerger, K. (1997). A developmentalmodel for late-onset delinquency. In D. W. Osgood(Ed.), Motivation and delinquency (pp. 119–177). Lin-coln, NE: University of Nebraska Press.

Piquero, A. (2001). Testing Moffitt’s neuropsychologicalvariation hypothesis for the prediction of life-coursepersistent offending. Psychology, Crime, and Law, 7,193–215.

Pitts, T. B. (1997). Reduced heart rate levels in aggressivechildren. In A. Raine, P. A. Brennan, D. P. Farrington,& S. A. Mednick (Eds.), Biosocial bases of violence(pp. 317–320). New York: Plenum Press.

Plomin, R., DeFries, J., McClearn, G., & McGuffin, P.(2008). Behavioral genetics (5th ed.). New York: Worth.

Plomin, R., Owen, M. J., & McGuffin, P. (1994). The ge-netic basis of complex human behaviors. Science,264, 1733–1739.

Porter, S., & Woodworth, M. (2006). Psychopathy and ag-gression. In C. J. Patrick (Ed.), Handbook of psychopa-thy (pp. 481–494). New York: Guilford Press.

Raine, A., & Yang, Y. (2006). Neural foundations to moralreasoning and antisocial behavior. Social Cognitive andAffective Neuroscience, 1, 203–213.

Raine, A., Yaralian, P. S., Reynolds, C., Venables, P. H., &Mednick, S. A. (2002). Spatial but not verbal cognitivedeficits at age 3 years in persistently antisocial indi-viduals. Development and Psychopathology, 14, 25–44.

Rende, R., & Waldman, I. (2006). Behavioral and molecu-lar genetics and developmental psychopathology. In D.Cicchetti & D. Cohen (Eds.), Developmental psychopa-thology (Vol. 2, 2nd ed., pp. 427–464). New York:Wiley.

Rhee, S. H., & Waldman, I. D. (2002). Genetic and environ-mental influences on antisocial behavior: A meta-anal-ysis of twin and adoption studies. Psychological Bulle-tin, 128, 490–529.

Richters, J. E., & Cicchetti, D. (1993). Mark Twain meetsDSM-III-R: Conduct disorder, development, and the


concept of harmful dysfunction. Development and Psy-chopathology, 5, 5–29.

Robins, L. N. (1966). Deviant children grown up. Balti-more, MD: Williams & Wilkins.

Robins, L. N. (1978). Aetiological implications in studiesof childhood histories related to antisocial personality.In R. D. Hare & D. Schalling (Eds.), Psychopathic be-havior: Approaches to research (pp. 255–271). Chi-chester: Wiley.

Rothbart, M. K., Ahadi, S. A., & Hershey, K. (1994). Tem-perament and social behavior in childhood. Merrill–Palmer Quarterly, 40, 21–39.

Rothbart, M. K., & Bates, J. E. (1998). Temperament. InW. Damon & N. Eisenberg (Eds.), Handbook of childpsychology: Social, emotional, and personality devel-opment (pp. 105–176). New York: Wiley.

Salekin, R. T. (2008). Psychopathy and recidivism formmid-adolescence to young adulthood: Cumulating legalproblems and limiting life opportunities. Journal ofAbnormal Psychology, 117, 386–395.

Seagrave, D., & Grisso, T. (2002). Adolescent developmentand the measurement of juvenile psychopathy. Law andHuman Behavior, 26, 219–239.

Shin, J. C., Chen, K., & Ridd, M. J. (1999). Monoamineoxidase: From genes to behavior. Annual Review ofNeuroscience, 22, 197–217.

Silberg, J. L., Rutter, M., Tracy, K., Maes, H. H., & Eaves, L.(2007). Etiological heterogeneity in the development ofantisocial behavior: The Virginia Twin Study of Adoles-cent Behavioral Development and the Young AdultFollow-Up. Psychological Medicine, 37, 1193–1202.

Silverthorn, P., & Frick, P. J. (1999). Developmental path-ways toantisocialbehavior: The delayed-onset pathway ingirls. Development and Psychopathology, 11, 101–126.

Silverthorn, P., Frick, P. J., & Reynolds, R. (2001). Timingof onset ad correlates of severe conduct problems in ad-judicated girls and boys. Journal of Psychopathologyand Behavioral Assessment, 23, 171–181.

Slutske, W. S., Heath, A. C., Dinwiddie, S. H., Madden,P. A., Bucholz, K. K., Dunne, M. P., et al. (1997).Modeling genetic and environmental influences in theetiology of conduct disorder: A study of 2,682 adulttwin pairs. Journal of Abnormal Psychology, 106,266–279.

Snyder, J., Schrepferman, L., McEachern, A., Barner, S.,Johnson, K., & Provines, J. (2008). Peer deviancy train-ing and peer coercion: Dual processes associated withearly-onset conduct problems. Child Development, 79,252–268.

Stadler, C., Sterzer, P., Schmeck, K., Krebs, A., Klein-schmidt, A., & Poustka, F. (2007). Reduced anteriorcingulate activation in aggressive children and adoles-cents during affective stimulation: association with tem-perament traits. Journal of Psychiatry Research, 41,410–417.

Sterzer, P., Stadler, C., Krebs, A., Kleinschmidt, A., &Poutska, F. (2005). Abnormal neural responses to emo-tional visual stimuli in adolescents with conduct disor-der. Biological Psychiatry, 57, 7–15.

Taylor, J., Iacono, W. G., & McGue, M. (2000). Evidencefor a genetic etiology of early-onset delinquency. Jour-nal of Abnormal Psychology, 109, 634–643.

Taylor, J., Loney, B. R., Bobadilla, L., lacono, W. G., &McGue, M. (2003). Genetic and environmental influ-

ences on psychopathy trait dimensions in a communitysample of male twins. Journal of Abnormal Child Psy-chology, 3, 633–645.

Vasay, M. W., Kotov, R., Frick, P. J., & Loney, B. R.(2005). The latent structure of psychopathy in youth:A taxometric investigation. Journal of Abnormal ChildPsychology, 33, 411–429.

Verhulst, F. C., Koot, H. M., & Berden, G. F. (1990). Four-year follow-up of an epidemiological sample. Journalof American Academy of Child & Adolescent Psychia-try, 29, 440–448.

Viding, E., Blair, R. J. R., Moffitt, T. E., & Plomin, R.(2005). Evidence for substantial genetic risk for psy-chopathy in 7-year-olds. Journal of Child Psychologyand Psychiatry, 46, 592–597.

Viding, E., & Frith, U. (2006). Genes for violence lurk inthe brain. Commentary. Proceedings of the NationalAcademy of Sciences of the United States of America,103, 6085–6086.

Viding, E., Frick, P. J., & Plomin, R. (2007). Aetiology ofthe relationship between callous–unemotional traits andconduct problems in childhood. British Journal of Psy-chiatry, 49, s33–s38.

Viding, E., & Jones, A. P. (2008). Cognition to genesvia the brain in the study of conduct disorder. QuarterlyJournal of Experimental Psychology, 61, 171–181.

Viding, E., Jones, A. P., Frick, P. J., Moffitt, T. E., & Plo-min, R. (2008). Heritability of antisocial behaviour atnine-years: Do callous–unemotional traits matter? De-velopmental Science, 11, 17–22.

Wakefield, J. C. (1992). Disorder as a harmful dysfunction:A conceptual critique of DSM-III-R’s definition of men-tal disorder. Psychological Review, 99, 232–247.

Wakefield, J. C., Pottick, K. J., & Kirk, S. A. (2002). Shouldthe DSM-IV diagnostic criteria for conduct disorder con-sider social context? American Journal of Psychiatry,159, 380–386.

Waschbusch, D. A., Carrey, N. J., Willoughby, M. T., King,S., & Andrade, B. F. (2007). Effects of methylphenidateand behavior modification on the social and academicbehavior of children with disruptive behavior disorders:The moderating role of callous/unemotional traits. Jour-nal of Clinical Child and Adolescent Psychology, 36,629–644.

Waschbusch, D. A., Walsh, T. M., Andrade, B .F., King, S.,& Carrey, N. J. (2007). Social problem solving, conductproblems, and callous–unemotional traits in children.Child Psychiatry and Human Development, 37, 293–305.

White, N. A., & Piquero, A. R. (2004). A preliminary em-pirical test of Silverthorn and Frick’s delayed-onsetpathway in girls using an urban, African-American,US-based sample. Criminal Behavior and MentalHealth, 14, 291–309.

Woodward, L. J., Fergusson, D. M., & Horwood, L. J.(2002). Romantic relationships of young people withchildhood and adolescent onset antisocial behaviorproblems. Journal of Abnormal Child Psychology, 30,231–244.

Zalecki, C. A., & Hinshaw, S. P. (2004). Overt and rela-tional aggression in girls with attention deficit hyperac-tivity disorder. Journal of Clinical Child and Adoles-cent Psychology, 33, 125–137.


Antisocial behavior from a developmental psychopathology ...labs.uno.edu/developmental-psychopathology/APSD/DP_2009_Frick_… · Antisocial behavior from a developmental psychopathology

Documents