Antisocial behavior from a developmental psychopathology perspective

Department of Psychology, University of New Orleans, 2001 Geology and Psychology Building, New Orleans, LA 70148, USA.
Development and Psychopathology (Impact Factor: 4.89). 11/2009; 21(4):1111-31. DOI: 10.1017/S0954579409990071
Source: PubMed
ABSTRACT
This paper reviews research on chronic patterns of antisocial behavior and places this research into a developmental psychopathology framework. Specifically, research suggests that there are at least three important pathways through which children and adolescents can develop severe antisocial behaviors. One group of youth shows antisocial behavior that begins in adolescence, and two groups show antisocial behavior that begins in childhood but differ on the presence or absence of callous-unemotional traits. In outlining these distinct pathways to antisocial behavior, we have tried to illustrate some key concepts from developmental psychopathology such as equifinality and multifinality, the importance of understanding the interface between normal and abnormal development, and the importance of using multiple levels of analyses to advance causal theories. Finally, we discuss how this development model can be used to enhance existing interventions for antisocial individuals.

Full-text

Available from: Paul J Frick
Antisocial behavior from a developmental
psychopathology perspective
PAUL J. FRICK
a
AND ESSI VIDING
b
a
University of New Orleans; and
b
University College London
Abstract
This paper reviews research on chronic patterns of antisocial behavior and places this research into a developmental
psychopathology framework. Specifically, research suggests that there are at least three important pathways through which
children and adolescents can develop severe antisocial behaviors. One group of youth shows antisocial behavior that
begins in adolescence, and two groups show antisocial behavior that begins in childhood but differ on the presence or
absence of callous–unemotional traits. In outlining these distinct pathways to antisocial behavior, we have tried to
illustrate some key concepts from developmental psychopathology such as equifinality and multifinality, the importance
of understanding the interface between normal and abnormal development, and the importance of using multiple
levels of analyses to advance causal theories. Finally, we discuss how this development model can be used to enhance
existing 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 from
research is not surprising given that these be-
haviors often operate at a very high cost to
society, such as costs to victims of these behav-
iors and the costs associated with detaining
individuals 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 each
of these disciplines provides a unique perspec-
tive for understanding the course, causes, and
most effective interventions for individuals
who show severe antisocial behaviors. In this
paper, 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, used
broadly to refer to criminal and aggressive be-
haviors, as well as other behaviors that violate
the rights of others or major societal norms.
W e think that a developmental psychopa thol-
ogy approach for integra ting this r esear ch could
be important for at least two reasons. First, a devel-
opmental psychopa thology fr ame work pr o vides a
very useful wa y for integra ting the diverse research
litera tur es into a coher ent causal model. This can
help us to understand the dev elopmental mecha-
nisms that can lead to antisocial beha vior patterns
and to tr anslat e this r esearch i nto implica tions for
prev ention and tr ea tment. Second, r esear ch on an-
tisocial beha vior pr o vides a clear wa y of illus tr a ting
the importance of sever al ke y developmental psy-
chopathology concepts, such as equifinality and
multifinality, the importance of integra ting research
on both normal and abnormal development, and the
importance of integra ting multiple level of analyses
(e.g., neurological, social, cognitive, behavior al)
for understanding psychopa thological conditions.
One broad question that is often raised in
taking a developmental psychopathology per-
spective on antisocial behavior is whether or
Address correspondence and reprint requests to: Paul
J. Frick, Department of Psychology, University of New
Orleans, 2001 Geology and Psychology Building, New
Orleans, LA 70148; E-mail: pfrick@uno.edu.
Development and Psychopathology 21 (2009), 1111–1131
Copyright
#
Cambridge University Press, 2009
doi:10.1017/S0954579409990071
1111
Page 1
not patterns of antisocial behavior should or
should not be considered a psychopathological
condition, psychiatric disorder, or mental ill-
ness (Richters & Cicchetti, 1993; Wakefield,
Pottick, & Kirk, 2002). We think that a devel-
opmental psychopathology perspective cannot
completely address this question because the
answer is largely dependent on how one defines
“mental disorder” (Lilienfeld, & Marino, 1995;
Wakefield, 1992). This is, if a mental disorder
is defined solely as a pattern of behavior that
causes harm for a person (e.g., leads to or
puts him or her at risk for impairments in psy-
chological, social, or occupational functioning
or for violating the rights of others), then im-
pairing levels of antisocial behavior would fit
well within such a definition of a disorder. In
contrast, other definitions, such as those that
require the disruption of some internal mecha-
nism in the person (e.g., Wakefield, 1992),
may fit for some antisocial individuals but not
others. A developmental psychopa thological per-
spective c an help to define the various different
causal pathways that may lead to antisocial be-
havior, some of which fit particular definitions
of 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 patterns
that may fit with certain definitions of mental
disorders and others that do not. Thus, the de-
velopmental psychopathology perspective can
provide a way of conceptualizing antisocial be-
havior and its causes that informs the debate
regarding criteria for a disorder, but it cannot
determine the “best” method for differentiating
disordered and nondisordered individuals. This
issue is largely dependent on the purpose for
making this distinction.
Another broad classification issue relates to
the great diversity of behaviors subsumed under
the rubric of antisocial behavior (Frick et al.,
1993). This large and heterogeneous set of be-
haviors has led to numerous attempts to define
meaningful subtypes of antisocial youth based
on the particular pattern of behaviors they ex-
hibit (for a review, see Frick & Marsee, 2006).
Some examples include the distinction made
in the Diagnostic and Sta tis tical Manual of
Mental Disorders—Fourth Edition, Text Revi-
sion (DSM-IV-TR; American Psychiatric Asso-
ciation, 2000) between argumentativ e, noncom-
pliant, and oppositional behaviors subsumed
under 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 between
overt conduct problems involving direct con-
frontation (e.g., arguing, fighting, stealing with
confrontation) and cov ert conduct problems
that do not involv e confronta tion (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., premedita ted or for
instrumental gain) in natur e (Card & Little,
2006; Marsee & Frick, 2007). Still other methods
classify youth based on the trajectory of their
antisocial behavior o ver time, such as whether
the behavior is high and stable, low and stable,
high and declining, or low and increasing (Broidy
et al., 2003; LaCourse, Deper e, & Loeber, 2008).
A further classification concern, and one that
is particularly relevant to the focus of this special
issue, is the relationship between antisocial be-
havior patterns and personality disorders. For
some classification systems, including the most
recent versions of the DSM (American Psychiat-
ric Association, 1980, 1987, 2000), chronic pat-
terns of severe antisocial behavior and antisocial
personality disorder are considered synonymous
concepts (Robins, 1978). However, there have
been 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 with
chronic patterns of antisocial behavior can be
classified based on their pattern of scores on
the Big Five personality dimensions. Specifi-
cally, antisocial individuals often are low on
the personality dimensions of agreeableness
and conscientiousness (Lynam & W idiger, 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 the
construct of psychopathy (Cleckley, 1976;
Hare, 1993; Lykken, 1995). This research has
indicated that not all individuals who show
chronic antisocial and criminal behavior show
P. J. Frick and E. Viding1112
Page 2
elevated levels of psychopathic traits. In fact, it
is only a minority of antisocial individuals who
do so. However, the subgroup of antisocial
individuals 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 deficits
compared 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 important
subgroups of antisocial individuals that need to
be defined by any classification system. Further,
most of the approaches that have been used to de-
fine more homogeneous subgroups of antisocial
individuals have relied on differences in the be-
havioral manifesta tions (e.g., type of behavior,
trajectory of behavior over time) or differences
in personality traits (e.g., Big Five dimensions;
presence of psychopathic traits) to make distinc-
tions within antisocial youth. We would argue
that a developmental psychopathology approach
should emphasize potential differences in the
developmental mechanisms that may underlie
these behavior al manifesta tions or personality fea-
tures. The r eason for this emphasis is tha t some-
times different behavioral manifestations may
reflect different development processes under-
lying the behavior. However, it is also possible
that the same behavioral pattern (e.g., high and
stable levels of antisocial behavior) can come
about through very different developmental
mechanisms. Thus, in the following sections,
we outline a model for understanding patterns
of severe antisocial behavior that focuses
largely on the developmental processes that
can explain some of the differences in the be-
havioral manifestations or associated personal-
ity traits displayed by antisocial individuals.
The Concepts of Equifinality and
Multifinality and Subgroups
of Antisocial Youth
The childhood- versus adolescent-onset
distinction
A number of reviews of the literature have sum-
marized research supporting the distinction
between children who begin showing severe
conduct problems and antisocial behavior in
childhood versus those whose onset of antiso-
cial behavior does not emerge until adolescence
(Moffitt, 1993, 2003; Patterson, 1996). Children
in the childhood-onset group often begin show-
ing mild conduct problems as early as preschool
or early elementary s chool, and their behavioral
problems tend to increase in rate and severity
throughout childhood and into adolescence
(Lahey & Loeber, 1994). In contrast, the ado-
lescent-onset group does not show significant
behavioral 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 the
different patterns of onset, the childhood-onset
group is more likely to show aggressive behav-
iors in childhood and adolescence, and is more
likely to continue to show antisocial and criminal
behavior into adulthood (for a review, see Frick
& Loney, 1999).
For example, Farrington, Ga llagher, Morley,
St. Ledger, and West (1988) reported that boys
who were arrested prior to age 12 showed al-
most twice as many convictions at two later
points in time (between the ages of 16 and 18
and between the ages of 22 and 24). Similarly,
Robins (1966) reported that boys referred to a
mental health clinic for antisocial behavior
prior to age 11 were twice as likely to receive
a diagnosis of an antisocial personality disorder
as an adult, compared to boys who began show-
ing antisocial behavior after age 11. As a final
example, Moffitt, Caspi, Harrington, and Milne
(2002) reported that, within a birth cohort of
539 males born in New Zealand and followed
through age 26, the 45 men who had displayed
significant conduct problems prior to adoles-
cence were more likely to have had a criminal
conviction (55%) and to have a greater number
of conv ictions (M ¼ 6.9, SD ¼ 11.5) as adults
than 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). The
difference was more dramatic when the focus
was on convictions for violent offenses, with
the early-onset group being much more likely
(38%) to be convicted as an adult than either
Developmental psychopathology and antisocial 1113
Page 3
the adolescent-onset (14%) or control (5%)
groups.
Thus, the childhood and adolescent sub-
types of antisocial youth show very different
trajectories of antisocial behavior, both in terms
of 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 other
approaches that have focused on the different be-
havioral trajectories of antisocial behavior over
time. Of importance, there is now a rather ex-
tensive body of research to suggest that the
two groups also differ on a number of disposi-
tional and contextual risk factors that seem to
implicate different developmental processes
in the disruptive behaviors of the two groups
(Moffitt, 2002). To summarize these findings,
childhood-onset conduct problems seem to be
more stro ngly related to neurops ychologica l
(e.g., deficits in executive functioning) and cogni-
tive (e.g., low intelligence) deficits (Fergusson,
Lynsky, & Horwood, 1996; Kratzer & Hodgins,
1999; Piquero, 2001; Raine, Yar alian, Reynolds,
Venables, & Mednick, 2002). F urther, the child-
hood-onset group has been reported to show more
temperamental and personality risk factors,
such as impulsivity (McCabe, Hough, Wood,
& Yeh, 2001; Silv erthorn, Frick, & R e yno lds,
2001), attention deficits (Fergusson et al., 1996),
and pr oblems in emotional regula tion (Moffitt,
Caspi, Dickson, Silva, & Stanton, 1996). This
gr oup has also been sho wn to come from homes
with grea ter family ins tability , mor e family con-
flict, and with parents who use less effective
par enting str a tegies (Aguilar, Sroufe, Egeland,
& Carlson, 2000; McCabe et al., 2001; Pa tter-
son & Y oerger, 1997; Woodw ard, Fergusson, &
Horwood, 2002). When children within the
adolescent-onset group differ from control chil-
dren without conduct problems, it is often in
showing higher levels of rebelliousness and
being more rejecting of conventional values
(Dandreaux & Frick, 2009; Moffitt et al.,
1996).
The different outcomes and risk factors for
the two subtypes of antisocial individuals have
led to theoretical models that propose very
different causal mechanisms operating across
the two groups. For example, Moffitt (2003)
has proposed that children in the childhood-
onset group develop their problem behavior
through 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 parental
supervision, poor quality schools). This dys-
functional transactional process disrupts the
child’s socialization leading to poor social rela-
tions with persons both inside (e.g., parents and
siblings) and outside the family (e.g., peers and
teachers). These disruptions lead to enduring vul-
nera bilities tha t can negativ ely affect the child’s
psyc hosocial adjustment across multiple devel-
opmental stages.
In contrast, children in the adolescent-onset
pathway have problems that are more likely to
be limited to adolescence and show fewer risk
factors. Thus, this group is conceptualized as
showing 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 authority
figures (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 unique
identity. According to Moffitt (2003), the child
in the adolescent-onset group engages in anti-
social and delinquent behaviors as a misguided
attempt to obtain a subjective sense of maturity
and adult status in a way that is maladaptive
(e.g., breaking societal norms) but encouraged
by an antisocial peer group. Given that their be-
havior is viewed as an exaggeration of a process
specific to adolescence, and not because of an
enduring vulnerability, their antisocial behavior
is less likely to persist beyond adolescence.
However, they may still have impairments that
persist 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 and
subgroups of antisocial youth
This distinction between the childhood and
adolescent-onset patterns of antisocial behav-
iors illustrates a subgrouping approach for anti-
social individuals that proposes different devel-
opmental mechanisms underlying the problem
P. J. Frick and E. Viding1114
Page 4
behavior across groups. Thus, this is an exam-
ple of the important concept in developmental
psychopathology of equifinality, which pro-
poses that the same developmental outcome
(e.g., antisocial behavior) can result from very
different developmental processes (Cicchetti
& Rogosch, 1996). It is important that research
has begun extending the concept of equifinality
for understanding antisocial youth by exploring
whether additional distinctions can be made
within groups who show a childhood onset to
their antisocial behavior.
This distinction is based on the presence
of a callous and unemotional interpersonal style
chara cterized by a lack of guilt and empathy and
a callous use of others. It is similar to the distinc-
tion made within samples of antisocial adults
using the construct of psychopathy that was de-
scribed previously. As noted previously, within
incarcerated adults, the presence of psychopathic
traits has proven to designate an important sub-
grou p of antisocial individual who show a more
severe, violent, and difficult to treat pattern of
antisocial behavior (Hemphill, 2007; Leistico
et al., 2008; Porter & Woodworth, 2006).
They also show a number of different back-
ground and emotional characteristics that
seem to suggest a unique etiology to their anti-
social behavior (Blair et al., 2005; Patrick,
2007). There is growing evidence that the
same may be true for anti social youth who
show CU traits.
Specifically, youth who show the childhood
onset to their antisocial behavior tend to score
higher on measures of CU traits than those
who show an adolescent onset (Dandreaux
& Frick, 2009; Moffitt et al., 1996; Silverthorn
et al., 2001). Further, several recent qualitative
(Frick & Dickens, 2006; Frick & White, 2008)
and quantitative (Edens, Campbell, & Weir,
2007; Leistico et al., 2008) reviews have been
published showing that CU traits are predictive
of a more severe, stable, and aggressive pattern
of behavior in antisocial yout h. For example,
Edens et al. (2007) conducted a quantitativ e
meta-analyses of 21 nonoverlapping samples
showin g that measures that include CU traits
w er e associated with general or violent recidivism
with effect sizes of r ¼ .24 or .25, respectiv ely .
Frick and Dickens (2006) reported on a qualita-
tive review of 24 published studies using 22 in-
dependent samples. Ten of these studies showed
a concurrent association between CU traits and
measures of aggressive, antisocial, or delinquent
behavior and 14 studies showed a predictive re-
lationship with follow-up intervals ranging
from 6 months to 10 years. These authors further
reported on 5 studies showing that CU traits were
associated with poorer treatment outcomes. Of
importance, these studies included community
(n ¼ 6), clinic-referred (n ¼ 4), and forensic ( n ¼
13) samples, and they included samples ranging
in age from 4 to 20.
One important issue in interpreting this body
of research is that CU traits seem to predict later
antisocial behavior even after controlling for
other 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 the
typologies proposed for understanding aggres-
sive individuals. That is, youth with CU traits
not only show a more severe and pervasive pat-
tern of aggressive behavior but they also tend to
show 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 traits
tend to show less aggression overall and,
when they do show aggressive behavior, it
tends to be largely reactive in nature. Further,
many of the social–cognitive and affective dif-
ferences that have been found between reactive
and 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) studied
detained adolescents’ (ages 11–18) responses
to eight vignettes depicting peers involved in
aggressive acts in various age-appropriate so-
cial contexts. Youth were asked to respond to
questions asking how likely and how important
various possible outcomes to the aggressive in-
terpersonal situations were. In this ethnically
diverse sample of boys and girls, CU traits
were associated with responses indicating a ten-
dency to emphasize the positive and rewarding
aspects of aggression, to value the importance
of being dominant in aggressive interactions,
Developmental psychopathology and antisocial 1115
Page 5
and to minimize the potential for punishment
for 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) studied
85 boys (ages 13–18) who had been detained
for delinquent behavior. They reported that
those who showed high rates of both reactive
and proactive aggression showed lower levels
of emotional reactivity to provocation, consis-
tent with past research on adolescents who
show proactive aggression (e.g., Pitts, 1997).
However, this reduced reactivity to provocation
was only found for those who were also high on
CU traits. Finally, Frick, Cornell, Bodin, Dane,
Barry, and Loney (2003) reported that a ten-
dency to attribute hostile intent to the actions
of others (i.e., a hostile attribution biase) that
has been associated with reactive forms of ag-
gression was only found in boys with conduct
problems 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 witho ut CU traits. First,
they reviewed four studies showing that the
conduct problems in youth without CU traits
are more strongly related to dysfunctional par-
enting practices (see also Edens, Skopp, & Ca-
hill, 2008). Second, they reviewed 10 studies
showing differences in how antisocial youth
with and without CU traits process emotional
stimuli, with youth high on CU traits showing
deficits in the processing of negative emotional
stimuli and, even more specifically, deficits to
signs of fear and distress in others. Third, an-
other 10 studies were reviewed showing distinct
cognitive characteristics of antisocial youth
with CU traits, such as being less sensitive to
punishment cues, especially when a reward
oriented response set is primed, showing more
positive outcome expectancies in aggressive
situations with peers, and being more likely
to exhibit verbal deficits than other antisocial
youth. Fourth, they reviewed seven studies
showing that youth with CU traits have unique
personality characteristics, such as showing
more fearless or thrill seeking behaviors and
less trait anxiety or neuroticism.
Thus, taken together, there is now a fairly
substantial body of research to suggest that
CU traits designate an important subgroup of
antisocial youth, that differ both in the severity
and stability of their behavior but also on impor-
tant emotional, cognitive, and social charac-
teristics. These latter findings could suggest
distinct etiological mechanisms leading to their
antisocial behavior. As a result, like the research
reviewed on the childhood and adolescent-
onset distinction, this research provides addi-
tional evidence supporting the concept of equi-
finality in understanding the development of
antisocial behavior in youth.
Before discussing the different etiological
mechanisms and their relationship with normal
developmental processes, it is also important
to note that research on CU traits also supports
the related concept of multifinality, which recog-
nizes that the same risk factors can have multiple
developmental outcomes. Specifically, as noted
previously, one characteristic of youth with CU
traits is the presence of a fearless, thrill seeking,
and behaviorally uninhibited temperament. Con-
sistent with the importance of this temperament
for the development of CU traits, Cornell and
Frick (2007) reported that preschool children
who were rated by their teachers as being behav-
iorally uninhibited were more at risk for show-
ing problems in empathy and guilt than other
children. However, they also reported that unin-
hibited preschoolers showed enhanced con-
science development if they experienced con-
sistent discipline and a parenting style that
emphasized a strong and obedienc e-oriented
(i.e., authoritarian) approa ch to parenting. These
authors suggested that the underar ousal exhibited
by fearless children may require parents to
incorporate stronger methods of socialization
that bring arousal levels into an optimal range
for the child to internalize parental norms for
prosocial 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 or
deficient conscience development) depending
on 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 children
to become “bold” and others “mean depending
on the presence of other temperamental traits or
P. J. Frick and E. Viding1116
Page 6
depending on the presence of certain types of so-
cializing environments.
The Interface Between No rmal and
Abnormal Development
Understanding developmental mechanisms
The research reviewed in the previous section
clearly suggests that there are important sub-
groups of antisocial youth who are at differen-
tial risk for continuing their antisocial behavior
into adulthood and who show different patterns
of risk factors that could suggest etiologies in-
volving distinct developmental mechanisms.
As noted previously, based on the differences
in the course and correlates to antisocial behav-
ior for youth with adolescent-onset antisocial
behavior, Moffitt (2003) proposed that these
children show an exaggeration of the normative
process of adolescent rebellion. In contrast,
children in the childhood-onset group show sig-
nificant problems in adjustment across multiple
developmental stages. Further, as also noted
above, the y also show more numerous and more
sever e dispositional and environmental risk
factors associated with their behavior problems.
How ever, within this group, those who show
CU traits seem to show different chara cteris tics
that could suggest some differences in which
developmen tal mechanisms may be inv olv ed
in their antisocial pr opensities.
Specifically, the research reviewed pre-
viously suggests that children with CU traits
designate a group of children with severe con-
duct problems who show a distinct tempera-
mental style, characterized by a preference for
dangerous and novel stimuli, a reward-oriented
response style, and a lack of reactivity to emo-
tional stimuli that signify distress in ot hers.
The bold and fearless temperamental style has
been variously labeled as low fearfulness
(Rothbart & Bates, 1998), low behavioral inhi-
bition (Kagan & Snidman, 1991), low harm
avoidance (Cloninger, 1987), or high daring
(Lahey & Waldman, 2003). Of importance,
there have been a number of studies of normally
developing 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 temperament
and lower scores on measures of conscience de-
velopment. Further, this research has led to a
number of theories to explain this link. For ex-
ample, fearless children may be less likely to
experience transgression-related arousal in re-
sponse to behavior that has been punished by
others (Kochanska, 1993; Newman, 1987). In
addition, children with this temperament may
be less likely to experience empathic arousal
linked to the distress in others (Blair, 1999).
In short, the temperamental deficits in different
aspects of emotional reactivity could make
it more difficult for a child to develop appropri-
ate levels of guilt, empathy, and other dimen-
sions of conscience that, at its extreme, could
result in CU traits and severe patterns of anti-
social behavior. Consistent with this theoretical
model, Pardini (2006) reported that the asso-
ciation between fearlessness and violent delin-
quency was mediated by the presence of CU
traits in a sample of adjudicated adolescents.
As noted previously, children with child-
hood-onset antisocial behavior but without
CU traits sho w very differ ent dispositional (e.g.,
impulsivity, low verbal intelligence, poor emo-
tional regulation) and contextual (e.g., higher
rates of family dy sfunctio n) risk fa ctors. Most
importantly, the childr en in this group show
high ra tes of anxiety (Andershed, Gusta fson,
Kerr & Stattin, 2002; Frick, Lilienfeld, Ellis,
Loney, & Silverth orn, 1999; Pardini, Lochman,
& Powell, 2007), they do not typically show
problems in empathy and guilt (Pardini et al.,
2003), and they appear to be distr e ssed 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 group
does not seem to be easily explained by deficits in
conscience development.
Given the many different types of risk fac-
tors that are found in this group, it is likely
that 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 ineffective
parenting practices and their antisocial behav-
ior. Thus, it is possible that children in this
group are not socialized adequately and, as a re-
sult, do not learn to appropriately regulate their
Developmental psychopathology and antisocial 1117
Page 7
behavior in response to environmental contin-
gencies (Kochanska et al., 2002). Another con-
sistent finding for antisocial youth without CU
traits is that they often have problems regulating
their emotions. That is, children in this group
appear to show a temperament characterized
by strong emotional reactivity, a deficit in the
skills needed to adequately regulate their emo-
tional reactivity, or both (Frick & Morris,
2004). These problems in emotional regulation
can result in the child committing impulsive
and unplanned aggressive and antisocial acts
for which he or she may be remorseful after-
ward but may still have difficulty controlling
in the future (Pardini et al., 2003). Such prob-
lems in regulating emotion would also explain
the 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 normal
development
Thus, this developmental model of antisocial
behavior specifies three subgroups of antisocial
individuals that differ on the developmental tra-
jectory of their antisocial behavior and on the
developmental mechanisms that seem to be in-
volved in their problem behavior. Like symp-
toms of most forms of psychopathology, some
level of antisocial and aggressive behavior is
normal in children and adolescents (Moffitt
et 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 illustrate
two ways that abnormal antisocial behavior
can differ from normal development. Specifi-
cally, the problems in adjustment experienced
by the adolescent-onset group seem to be
more specific to a single developmental stage
(i.e., adolescence) and result from a failure to
adequately adjust to the developmental demands
(e.g., separation and individuation from parents)
of that stage. In contrast, both groups who show
a childhood onset to their antisocial behavior
show risk factors (e.g., emotional and cognitive
deficits) that negatively affect development
across multiple stages, albeit in different ways
for the two groups.
Potential gender differences
In gener al, the majority of research on antisocial
behavior in youth has focused on the samples of
boys. Thus, the applicability of these dev elop-
mental models to girls is open to question. One
consistent finding is that a childhood onset to se-
vere antisocial and aggressive behavior is much
rarer in girls than in boys (Hipwell et al., 2002;
Moffitt & Capsi, 2001; White & Piquero,
2004). How ev er, despite the predominance of
adolescent onset in antisocial girls, ther e is evi-
dence that girls with sever e conduct problems
show poor outcomes in adulthood and show a
large number of the dispositional and contextual
risk factors tha t are more chara cteris tic of child-
hood-onset antisocial behavior in boys (Frick &
Dickens, 2006).
To reconcile these findings, Silverthorn and
Frick (1999) proposed a modification of the de-
velopmental model outlined above which they
labeled as a delayed-onset pathway to antisocial
behavior for girls. These authors proposed that
antisocial and aggressive behavior in girls show
the same causal mechanisms as those outlined
previously for childhood-onset boys. However,
their severe antisocial behavior is often delayed
until adolescence coinciding with biological
(e.g., hormonal changes associated with pu-
berty) and psychosocial (e.g., less parental
monitoring and supervision; greater contact
with deviant peers) changes that encourage an-
tisocial behavior in girls with predisposing vul-
nerabilities (e.g., CU; problems in emotional
regulation). In an initial test of this theory, adju-
dicated adolescent girls who largely showed an
adolescent onset to their antisocial behavior
also showed high levels of CU traits, problems
with impulse control, and a number of other
social and temperamental vulnerabilities that
were more similar to childhood-onset boys than
to 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, the
predictions made from the delayed-onset theory
require further testing. Also, it is possible that,
although many girls may not show the overt
antisocial and aggressive behavior prior to ado-
P. J. Frick and E. Viding1118
Page 8
lescence, they may show other forms of antiso-
cial behavior such as relational aggression. Re-
lational aggression can be defined as behaviors
that seek to harm another child’s social relation-
ships (e.g., telling lies about them, excluding
them from social events) rather than physically
harming the child (Crick & Grotpeter, 1996)
Several studies have shown that when girls
behave aggressively, they are more likely to
choose relational aggression (rather than physi-
cal or overt aggression) as a strategy for use
within the peer group (Crick, 1996; Crick, Ca-
sas, & Mosher, 1997; Crick & Grotpeter, 1995;
Lagerspetz, Bjo
¨
rkqvist, & Peltonen, 1988; Os-
trov & Keating, 2004). Of importance, rela-
tional aggression shares some of the same risk
factors as those reviewed previously as being
associated with antisocial behavior, including
impulsivity (Zalecki & Hinshaw, 2004) and
CU 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 the
appearance of showing an adolescent onset, if
such behaviors are not assessed.
Stable personality traits versus
developmental transitions
As noted previously, there is some debate as to
whether antisocial personality should be de-
fined solely by a consistent pattern of antisocial
behavior or by the underlying personality traits
that can lead to this pattern of behavior. In ei-
ther case, there is some assumption of stability
across development. In fact, many definitions
of antisocial personality disorder require the
presence of antisocial behavior starting in child-
hood or adolescence (American Psychiatric As-
sociation, 2000). Prospective studies of either
clinic referred (Lahey, Loeber, Burke, & Apple-
gate, 2005; Robins, 1966) or community partic-
ipants (Moffitt et al., 2002) have suggested that
between 14 and 54% of children with severe
conduct problems will show an antisocial per-
sonality disorder as adults. Further, as noted
previously, children with a childhood onset to
their conduct problems (Moffitt, 2003) and
those with CU traits (Frick & Dickens, 2006;
Frick & White, 2008) seem to show a more
stable 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 to
suggest what level of stability in antisocial be-
havior would be sufficient to warrant designa-
tion as a personality disorder. Further, even if
a pattern of behavior is not highly stable, such
as adolescent-onset conduct problems, it may
still lead to significant impairments and warrant
treatment (Dandreaux & Frick, 2009; Moffitt
et al., 1996).
The issue of stability may be even more
important if one focuses on the personality
traits that may lead to antisocial behavior.
That is, an important consideration is whether
CU 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). There
are now a number of studies showing that these
traits are relatively stable from late childhood to
early 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 a
stability estimate of .71 using an intraclass
correlation coefficient across 4 years for CU
traits in a sample of children with an average
age of 10.65 at the initial assessment. This level
of stability for parent report is much higher
than is typically reported for parent ratings of
others aspects of children’s adjustment (Ver-
hulst, Koot, & Berden, 1990). With respect to
younger children, Dadds, Frazer, Frost, and
Hawes (2005) found moderate 1-year stability
estimates 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 more
extended 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 for
teacher ratings ( r ¼ .27) ratings of CU traits
for boys between the ages of 8 and 16. Bloni-
gen, Hicks, Kruger, Patrick, and Iacono
(2006) reported that CU traits were relatively
stable (r ¼ .60) from late adolescence (age
17) into early adulthood (age 24). Further,
Loney, Taylor, Butler, and Iacono (2007) re-
ported that CU traits in adolescence (ages 16–
Developmental psychopathology and antisocial 1119
Page 9
18) were significantly stable (intraclass correla-
tion coefficient ¼ .40) over a 6-year follow-up
period. Finally, two studies have shown that
measures of CU traits assessed prior to adoles-
cence were significantly associated with similar
measures in adulthood, even after controlling
for other childhood risk factors (Burke, Loeber,
& Lahey, 2007; Lynam, Caspi, Moffitt, Loeber,
& Stouthamer-Loeber, 2007).
Based on these findings, the stability of CU
ratings across development appears to be better
or equivalent to other trait indices across child-
hood to adolescence and early adulthood. How-
ever, there is no agreed on metric regarding
what level of stability would warrant the classi-
fication of a “stable trait.” Critically, even rea-
sonably high levels of stability would not imply
that CU traits are unchangeable. For example,
Frick, Kimonis, et al. (2003) reported that,
despite the high level of stability in these traits
across their 4-year study period, there were a
significant number of youth who decreased in
their level of CU traits over the course of the
study (for a similar pattern of change over a
longer period of development, see also Lynam
et al., 2007). Further, this decrease in the level
of CU traits was related to the level of conduct
problems displayed by the child, the socioeco-
nomic status of the child’s parents, and the
quality 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 in
the child’s psychosocial environment.
The Importance of Multiple Levels
of Analysis
From the review provided above, it is clear that
subgroups of antisocial youth differ in a number
of important ways behaviorally. That is, they can
differ in their timing of onset, the stability of their
behavior, and the level and type of aggression
that is displayed. Further, we have also noted
several ways that these subgroups differ in their
emotional, cognitive, social, and interpersonal
functioning. Understanding differences on each
of these levels provides important information
for charting the varied mechanisms (e.g., deficits
in conscience; poor emotional regulation) that
may be involved in the development of antisocial
traits. In recent years, there have been substantial
increases in the number of studies exploring
biological vulnerabilities to antisocial behav-
ior (Raine & Yang, 2006). In this section, we pr o-
vide a selective review of genetic and brain
imaging (focusing on functional magnetic reso-
nance imaging [fMRI]) studies with antisocial
individuals and, in particular, reviewing several
areas 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 studies
showing moderate heritability and nonshared
environmental influence, as well as modest
shared environmental influence on antisocial
behavior (e.g., Mason & Frick, 1994; Rhee &
Waldman, 2002). In other words, individual
differences in susceptibility to antisocial behav-
ior have both a heritable and environmental
component. In recent years, there have been
several lines of research that have attempted to
go beyond this basic partitioning of genetic
and environmental influences to antisocial be-
havior that could be especially important for
understanding 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 have
been traditionally conceptualized as environ-
mental (e.g., parenting reactions) may actually
be evoked partly by the heritable temperamental
features of the child (gene–environment corre-
lation; Larsson, Viding, Rijsdijk, & Plomin,
2008). Further, genetically influenced individual
differences in the sensitivity to environmental
risk factors such as maltreatment (gene–environ-
ment interaction) are also important in explain-
ing variance in antisocial behavior. Specifically,
research has suggested that genes regulating
serotonergic neurotransmission, in particular
monoamine oxidase A (MAOA), are important
for explaining individual differences in antiso-
cial behavior (Buckholtz & Meyer-Lindenberg,
2008). However, the genetic vulnerability to
antisocial behavior conferred by the MAOA
P. J. Frick and E. Viding1120
Page 10
low-activity allele (MAOA-L) may only become
evident in the presence of an environmental
trigger, such as maltreatment (Caspi et al.,
2002; Kim-Cohen et al., 2006).
Second, and more directly related to the differ-
ent developmental pa thw a ys to antisocial behav-
ior, several s tudies hav e begun studying differ-
ences in the heritability of antisocial behavior
acr oss subtypes. For example, Ta ylor, Iacono,
and McGue (2000) reported greater genetic influ-
ence for childhood-onset delinquency, compared
to adolescence-onset delinquency. A recent study
by Silberg, Rutter, Tracy, Maes, and Eav es (2007)
extended these findings with a larger sample
of twins. They reported that a single genetic factor
was important in influencing antisocial behavior
that started in childhood and was persistent into
adulthood. They also found that ther e wer e ado-
lescent-onset shared environmental factors that
wer e not influencing individual differences in
antisocial behavior before adolescence. Finally,
they reported a transient genetic effect a t puberty
and argued that this finding is consistent with a
notion of genetically mediated influence on the
timing of puberty a ffecting the expression of ge-
netic differences in antisocial outcomes.
Directly related to the model of the CU traits
differentiating subtypes within the childhood-
onset group, antisocial behavior in children
with CU traits has been found to be under
strong genetic influence (heritability of .81)
with little influence of shared environment
(Viding, Blair, Moffitt, & Plomin, 2005). In
contrast, antisocial behavior in children without
elevated levels of CU shows more modest ge-
netic influence (heritability of .30) and subs tanti al
environmental influence (shared environmental
influence ¼ .34, nonshared environmental influ-
ence ¼ .26). It w as important that the differ ences
in heritability could not be attributed to differ-
ences in the severity of conduct problems in
this sample of 7-year-old twins. These findings
were replica ted when the children were 9 years
old, and this latter study also demonstr a ted that
the difference in heritability magnitude holds
even after hypera ctivity scor es of the children
were 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; CU
vs. non-CU), again supporting the importance
of recognizing equifinality in causal models.
Further, these findings are also consistent with
some of the findings on behavioral, cognitive,
affective, and social correlates reported pre-
viously. For example, the finding of persistent
genetic 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 on
biological and temperamental vulnerabilities
for the early starters and greater emphasis on
social causes for the adolescent-onset group.
The finding of differences in etiological factors
for antisocial behavior in children high and low
on CU traits also is consistent with previous
findings. For example, stronger environmental
influences on antisocial behavior in children
who are low on CU traits support those studies
reviewed previously showing that parenting
factors were more strongly associated with con-
duct problems in these children (Frick & White,
2008).
Third, although no molecular genetic studies
have directly compared different subtypes of
children with conduct problems, some imaging
studies have suggested that the MAOA-L risk
polymorphism 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 excess
of serotonin and influences the brain’s affective
circuitry in a way that amplifies the effects of
environmental risk, such as maltreatment. It is
interesting to note that some studies have re-
ported an increased vulnerability to antisocial
behavior 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 to
different types of conduct problems by having
opposite effects on the affective lability of an
individual. This would be consistent with our
developmental model specifying different pat-
terns of emotional responding across subgroups
of antisocial youth. However, this possibility is
highly speculative at present. As for any psychi-
atric outcome, the genetic influences on any
Developmental psychopathology and antisocial 1121
Page 11
subtype of conduct problems will not be limited
to a single candidate gene. However, these find-
ings also nicely illustrate the concept of multifi-
nality. That is, it is unlikely that specific genes
that increase the likelihood for antisocial behav-
ior would conform to diagnostic boundaries.
For example, different levels of MAOA activity
have been linked to a wide range of psychiatric
disorders such as depression, autism, bipolar
disorder, and alcoholism (Cicchetti, Rogosch,
& Sturge-Apple, 2007; Rende & Waldman,
2006; Shin, Chen, & Ridd, 1999). The multi-
finality of outcomes suggests that any genetic
risk conferred by MAOA-L is likely to be
moderated by both distinct environmental risk
factors and other genes, as already outlined
above.
Fourth, twin studies have not only begun to
compare genetic and environmental influences
in subgroups of antisocial youth, they have
also begun to explore whether antisocial behav-
ior, CU traits, and other related traits (e.g., sub-
stance abuse) co-occur because of common
genetic and/or environmental factors (Krueger
et al., 2002; Taylor, Loney, Bobadilla, Iacono,
& McGue, 2003; Viding et al., 2007). In much
the same way as a comparison of identical and
fraternal twins enables the partitioning of var-
iance into genetic, shared, and nonshared envi-
ronmental components, the twin design can
also be used to partition covariance between
traits into different etiological components.
Such multivariate behavioral genetic analyses
are ideal for investigating different phenotypic
manifestations of shared genetic or environ-
mental risk. In general, these types of analyses
have suggested that the overlap among antiso-
cial behavior and other externalizing symptoms
or personality traits (e.g., CU) has a substantial
genetic component (e.g., Viding et al., 2007).
In addition, these studies have found that the
nonshared environmental factors (i.e., those
environmental risk factors that are not shared
by two family members) are often phenotype
specific. Such findings suggest that nonshared,
phenotype specific, environmental risk factors
are critical for differentiating the eventual be-
havioral outcome, even if the same genetic
risk factors are important for two different be-
havioral patterns. It is also possible that some
differentiation of behavioral outcome is be-
cause of those risk genes that are not common
between two distinct outcomes.
Fifth, behavior genetic studies have begun to
address the issue of whether severe antisocial
behavior is better thought of as being on a con-
tinuum with normal behavior or whether it is
better considered a qualitatively distinct taxon
(Beauchaine, 2003; Vasey, Kotov, Frick, &
Loney, 2005). One possibility is that common
behavioral disorders are the quantitative ex-
treme of the same genetic effects that operate
throughout the distribution of the trait (Plomin,
Owen, & McGuffin, 1994). In this quantitative
trait loci model, several genes (rather than a few
rogue mutations) are hypothesized to act in a
probabilistic 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 even
when environmental risk factors increase the
“penetrance” of genetic risk, the interaction be-
tween any specific gene and an environmental
risk 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 of
conduct 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, Slutske
et al. (1997) found that a multiple-threshold
model of severe antisocial behavior fit their
data well, suggesting that antisocial behavior
seems to be an extreme of the normal variation
in conduct problems, rather than a discrete en-
tity. Similar heritability estimates for normal/
subclinical and extreme forms of behavior are
in line with the quantitative trait loci model.
It is important to note that such a model does
necessarily contradict the possibility that there
may be different subgroups of antisocial youth
with qualitatively different causal processes.
That is, heritability and environmental esti-
mates obtained at different cutoffs of any uni-
variate distribution could be based on data
from a heterogeneous group of individuals
who could have a distinct set of genetic and
environmental risk factors. In addition, there
may be different normal to abnormal continua
P. J. Frick and E. Viding1122
Page 12
in terms of the relative importance of certain
genes and environments for different subtypes.
Thus, it is still possible that different subtypes
of antisocial individuals could have distinct
etiologies, even if their vulnerability profile
on a single indicator (e.g., specific behavior or
neurocognitive measure) is not qualitatively
different from the rest of the population.
fMRI Brain imaging studies
Despite the demonstration of genetic influences
on individual differences in antisocial behavior,
it is important to emphasize that risk genes for
antisocial behavior do not act deterministically.
Instead, genes code for neurocognitive vulner-
abilities that may, in turn, increase a child’s
risk 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 regulation
of emotions have been found to correlate with
antisocial and violent behavior and could also
mediate genetic influences (Davidson, Putnam,
& Larson, 2000). In particular, the orbitofron-
tal/ventromedial prefrontal cortex, anterior cin-
gulate, amygdala, and interconnected regions
have shown both structural and functional ab-
normalities in antisocial popula tions (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 contrasting
childhood-onset with adolescent-onset sub-
types or antisocial youth with and without CU
traits. Instead, published studies have either
focused on an undifferentiated group of chil-
dren with antisocial behavior or on the CU sub-
type alone. However, these studies do provide
some at least speculative support for the devel-
opmental model that has been outlined in this
paper. Specifically, reduced anterior cingulate
responsivity to threatening emotional scenes
under passive viewing conditions has been
reported 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 negative
and threatening pictures for antisocial youth,
but this result emerged only when anxiety
scores were used as a covariate. A more recent
study using an almost id entical passive viewing
paradigm 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 how
children with CU traits process emotional
stimuli.
In support of this possibility, two studies
have directly measured CU traits and explicitly
tested the hypothesis that this group would
show 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 youth
with CU traits compared to typically develop-
ing children and children with attention-defi-
cit/hyperactivity disorder. Another study docu-
mented an abnormal ventromedial prefrontal
cortex response to punishment in children
with CU traits (Finger et al., 2008). This study
employed a task in which the participants had to
learn that a stimulus that used to be rewarding
was subsequently associated with loss and
that they should stop responding to that stimu-
lus. This finding is consistent with previously
reviewed findings showing abnormalities in
how youth with CU traits respond to reward
and punishment contingencies.
Thus, although much more work in this area
is needed, these initial findings from brain
imaging studies are promising in providing pos-
sible neurological bases to some of the cog-
nitive and affective differences found across
the different developmental pathways to antiso-
cial behaviors, and could help in uncovering
some of the neurocognitive mechanisms
through which inherited predispositions can
place a child at risk for the development anti so-
cial traits (Viding & Jones, 2008). Of impor-
tance, these promising studies demonstrate the
importance of integrating findings across multi-
ple levels of analyses. That is, the unique func-
tional neurological deficits were documented
when CU traits were used to form experimental
groups and when tasks tapping the specific
emotional and cognitive deficits that have
Developmental psychopathology and antisocial 1123
Page 13
been associated with these traits were used to
test functional brain differences.
It is important to bear in mind that although
our selective review focused on fMRI studies,
such studies do not by any means represent
the only avenue of investigation for charting
neurobiological vulnerabilities that can mediate
the genetic influences on antisocial behavior.
For example, several studies have shown that
youth with CU traits show differences in their
autonomic reactivity to certain types of stimuli
(Blair, 1999; Kimonis et al., 2008) and they
show differences in both their resting (Loney,
Butler, Lima, Counts, & Eckel, 2006) and
stress-induced (O’Leary, Loney, & Eckel,
2007) cortisol levels. Thus, some of the genetic
risk for this group of antisocial youth could be
due to inherited individual differences in the
functioning of their autonomic nervous system
or in the reactivity of their hypothalamic–pitui-
tary–adrenal axis as indexed by the hormone
cortisol. Combining across all of these levels
provides the greatest likelihood of advancing
our knowledge of the different pathways to
the 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 that
we have used to organize it, has several impor-
tant applied implications. One key implication
of 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 a
childhood onset to their antisocial behavior.
Further, there are a number of interventions
that have proven effective in treating early
emerging conduct problems, with a great de-
crease in their effectiveness in older children
and adolescents (Eyberg, Nelson, & Boggs,
2008). Thus, intervening early in the develop-
mental trajectory of childhood-onset conduct
problems is an important goal for preventing
later serious aggression and antisocial behavior.
However, even these interventions require a
child to have already shown serious and impair-
ing conduct problems, albeit at an early age. By
focusing on the developmental processes that
can precede even these early conduct problems,
it opens the possibility of prevention programs
that promote optimal development in children
with certain risk factors (e.g., an fearless tem-
perament, poor emotional regulation) even be-
fore serious behavioral problems emerge.
A second implica tion of the developmental
approa ch to understanding antisocial behavior
that was outlined in this paper is that interventions
need to be comprehensiv e and target multiple risk
factors. As noted thr oughout this paper, no gene,
no temperamental risk factor, no envir onmental
risk factor opera tes in isolation. Thus, it is not sur-
prising that some of the mos t effectiv e interven-
tions for antisocial behavior involv e multiple
components, ra ther than targeting only a single
risk factor (e.g., Conduct Problems Prev ention
Resear ch Group, 2004).
A third implication of the developmental
model is that interventions not only need to be
comprehensive, but they also need to be indi-
vidualized. That is, given that the causal pro-
cesses leading to antisocial behavior appear to
be different across subgroups, it is also quite
likely that treatments will need to be different
across 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 a
parenting intervention than boys with conduct
problems 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 traits
seemed to respond equally well to the first
part of the intervention that focused on teaching
parents methods of using positive reinforce-
ment to encourage prosocial behavior. In con-
trast, only the group without CU traits showed
added improvement with the second part of
the intervention that focused on teaching par-
ents more effective discipline strategies. This
outcome would be consistent with the reward-
oriented response style that, as reviewed pre-
viously, appears to be characteristic of children
with CU traits. In another study of the differen-
tial response to treatment of youth with CU
traits, Waschbusch, Carrey, Willoughby, King,
and Andrade (2007) reported that children
(ages 7–12) with conduct problems and CU
traits responded less well to behavior therapy
P. J. Frick and E. Viding1124
Page 14
alone than children with conduct problems
without CU traits. However, these differences
largely disappeared when stimulant medication
was added to the behavior therapy, although the
children with CU traits were still less likely to
score in the normative range than those without
these traits.
These findings support the contention that
interventions may be more effective if they
are specifically tailored to the unique needs of
children within the different developmental
pathways. This focus on a comprehensive and
individualized approach to treatment may be
particularly important for enhancing the effec-
tiveness of existing treatments for older children
and adolescents who show severe antisocial and
delinquent behavior. For example, a study
group commissioned by the Office of Juvenile
Justice and Delinquency Prevention of the
United States Department of Justice reviewed
four 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 outlined
several features of such comprehensive models
that 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 were
available to adjudicated youth. In addition,
there was a system for providing a comprehen-
sive assessment to determine the specific needs
of the adjudicated youth and a strong case-
management system for ensuring that services
were provided in an integrated and coherent
manner. Similar models of comprehensive
and individualized interventions have proven
to be effective for older youth with severe anti-
social behavior (Henggeler, Schoenwald, Bor-
duin, Rowland, & Cunningham, 1998).
Research on the various developmental
pathways to antisocial behavior could be quite
important for guiding these comprehensive
and individualized approaches to treatment.
That is, knowledge of the different develop-
mental processes that may be operating in the
various subgroups of antisocial youth could
help in determining the most effective combi-
nation of services for an individual child (Frick,
2006). For example, interventions that focus on
enhancing identity development in adolescents
and increasing contact with prosocial peers,
such as mentoring programs (Grossman & Tier-
ney, 1998) or programs that provide structured
afterschool activities ( Mahoney & Stattin,
2000), may be particularly effective for youth
within the adolescent-onset pathway. In con-
trast, interventions that focus on anger control
may be more effective for children within the
childhood-onset pathway who do not exhibit
CU traits but who often show problems with
emotional regulation (Larson & Lochman,
2003). Further, interventions that intervene
early in the parent–child relationship to teach
parents ways to foster empathic concern in their
young child or that help the child develop
cognitive perspective taking skills may be
more effective for children with CU traits
(Chi-Ming, Greenberg, & Walls, 2003). Later
in development, intervening in ways that em-
phasize the reward-oriented response style of
this group and attempt to motivate children
through appealing to their self-interest, rather
than through interventions that solely focus
on punishment-oriented strategies, may be
more effective for this group of youth (Frick,
2006).
An important note of caution relates to the
behavioral 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 in
the population are likely to have multiple func-
tions, some of which are desirable, others not.
For example, the genetic variants that increase
the 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 with
environmental risk factors, it quickly becomes
evident that removing the effects of one gene
via 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 that
index vulnerability for specific neurocognitive
deficits. An early knowledge of such risk
genes, particularly in the context of certain
Developmental psychopathology and antisocial 1125
Page 15
environmental factors, could also be used to
guide prevention efforts prior to the emergence
of severe conduct problems.
Summary and Conclusions
In this paper, we have outlined a developmental
psychopathology framework for understanding
the etiology of severe patterns of antisocial be-
havior or antisocial personality. In this frame-
work, we outline three important pathways
through which children and adolescents can de-
velop severe antisocial behaviors. Unlike past
attempts to define important subgroups of anti-
social individuals, this approach does not rely
solely on differences in the types of behaviors,
timing of onset of behaviors, the stability of
behaviors, or personality traits. Instead, an em-
phasis is placed on the developmental processes
that may place a child at risk for acting in an an-
tisocial and aggressive manner. Specifically,
the m odel defines a group of youth whose anti-
social behavior begins in adolescence and who
seem to be showing an exaggeration of normal
adolescent rebellion. Further, the model defines
two groups of youth whose antisocial behavior
begins prior to adolescence and who seem to
show problems in adjustment across multiple
developmental stages. One group is character-
ized by the presence of CU traits that seem re-
lated to a temperamental deficit in how they
process emotional stimuli and respond to pun-
ishment cues that interfere with the normal de-
velopment of empathy, guilt, and other aspects
of conscience. The second group of early-onset
antisocial youths show problems more related
to 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 illustrate
some key concepts from developmental psy-
chopathology. First, we have used these path-
ways to illustrate the concepts of equifinality
and multifinality, by showing how severe pat-
terns of antisocial behavior can result from
very different causal processes (i.e., equifinal-
ity) and how the same risk factors can lead to
many different outcomes (i.e., multifinality).
Second, we have illustrated how understanding
the interface between normal and abnormal de-
velopment is crucial for understanding the
causes of antisocial behavior. That is, each pat-
tern of antisocial behavior involves somewhat
unique developmental processes and they each
deviate from normative patterns of antisocial
behavior in different ways. Third, we have
used this model to show how using multiple
levels of analyses can advance causal theories.
Specifically, children in all three pathways
show unique behavioral, social, emotional,
cognitive, and neurological correlates that,
when combined, provide an integrated causal
theory 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 be
used to enhance existing interventions for anti-
social individuals, particularly by highlighting
avenues for early intervention and by guiding
comprehensive and individualized approaches
to treatment.
Thus, we think that developmental models
such as the one we have outlined in this paper
need to guide etiological theories of conduct
problems, aggression, and antisocial behavior.
Further, this body research points the way to
several potentially important directions for
future research. First, a key aspect to the devel-
opmental models outlined in this manuscript is
the different temperaments that may place a
child at risk for showing severe antisocial and
aggressive 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 research
to 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 problems
and, even more importantly, predict the specific
developmental mechanisms (e.g., lack of guilt
and empathy; poorly regulated emotions) that
are proposed to underlie the conduct problems
across the different causal pathways. Such pro-
spective research is not only important for pro-
viding strong tests of the predictive utility of the
developmental model but also could help to un-
cover protective factors that may reduce the
P. J. Frick and E. Viding1126
Page 16
likelihood that a child with a temperamental
risk factor will show severe behavior problems.
A better understanding of protective factors
could be quite helpful for guiding future pre-
vention programs. Second, we have outlined
the 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 studies
have tested predictions made by this develop-
mental model on the neurological level, which
is likely because of the type of expertise needed
to conduct such studies and the great expense
involved 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 potentially
most important, very few intervention studies
have used this developmental model to tailor
their interventions to the unique needs of
antisocial 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 different
groups of antisocial youth. However, these
hypotheses remain largely untested. Such tests
should be a critical goal for future research,
given that the few existing studies clearly
suggest that youth in all three pathways can
respond to interventions, albeit to different
ones.
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    • "Accordingly, CU traits have been incorporated into the Diagnostic and Statistical Manual–5th Edition as the " with limited prosocial emotions " specifier for Conduct Disorder (American Psychiatric Association, 2013). Although the majority of work examining CU traits has involved adolescents and youth in middle to late childhood, there is increasing evidence that CU traits may be identifiable early in life (Frick & Viding, 2009; Kotler & McMahon, 2005; Nichols et al., 2014; Waller, Hyde, Grabell, Alves, & Olson, 2015). Testing theoretical assumptions regarding developmental trajectories of the behavioral problems associated with CU traits (Blair, 2013; Frick & White, 2008; Wakschlag, Tolan, & Leventhal, 2010) requires tools to assess the expression of these traits in a developmentally sensitive manner. "
    [Show abstract] [Hide abstract] ABSTRACT: Introduction: Callous-unemotional (CU) traits in the presence of conduct problems are associated with increased risk of severe antisocial behavior. Developmentally sensitive methods of assessing CU traits have recently been generated, but their construct validity in relation to neurocognitive underpinnings of CU has not been demonstrated. The current study sought to investigate whether the fear-specific emotion recognition deficits associated with CU traits in older individuals are developmentally expressed in young children as low concern for others and punishment insensitivity. Method: A subsample of 337 preschoolers (mean age 4.8 years, SD = 0.8) who completed neurocognitive tasks was taken from a larger project of preschool psychopathology. Children completed an emotional recognition task in which they were asked to identify the emotional face from the neutral faces in an array. CU traits were assessed using the Low Concern (LC) and Punishment Insensitivity (PI) subscales of the Multidimensional Assessment Profile of Disruptive Behavior (MAP-DB), which were specifically designed to differentiate the normative misbehavior of early childhood from atypical patterns. Results: High LC, but not PI, scores were associated with a fear-specific deficit in emotion recognition. Girls were more accurate than boys in identifying emotional expressions but no significant interaction between LC or PI and sex was observed. Conclusions: Fear recognition deficits associated with CU traits in older individuals were observed in preschoolers with developmentally defined patterns of low concern for others. Confirming that the link between CU-related impairments in empathy and distinct neurocognitive deficits is present in very young children suggests that developmentally specified measurement can detect the substrates of these severe behavioral patterns beginning much earlier than prior work. Exploring the development of CU traits and disruptive behavior disorders at very early ages may provide insights critical to early intervention and prevention of severe antisocial behavior.
    No preview · Article · Apr 2016 · Journal of Clinical and Experimental Neuropsychology
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    • "Frick & Hare, 2001). The APSD and the CU subscale in particular have been extensively validated in developmental and clinical research (Frick & Viding, 2009; Sylvers et al., 2011; van Zwieten et al., 2013) and have been shown to predict subsequent outcomes, for example, (Wymbs et al., 2012), including the prediction to adult arrests, e.g., (McMahon et al., 2010). Given the focus on CU in research on sensitivity or susceptibility to parenting influence, analyses below focus on the CU scale; select analyses of the total scale are reported in Supplementary Analysis. "
    [Show abstract] [Hide abstract] ABSTRACT: Children and adolescents with callous-unemotional (CU) traits have been distinguished as a subset of individuals with disruptive behavioral disorders who may be less sensitive to parenting influence; we test this hypothesis using multiple methods and assessment paradigms. Two hundred seventy-one adolescents (mean age = 12.6 years) from 3 samples at elevated risk for disruptive behavior disorders were studied. Symptoms of CU behavior were derived from standard questionnaire; assessments of behavioral adjustment were derived from clinical interview with parent, and parent-report, teacher-report, and self-report questionnaire. Parent-child relationship quality was based on observational assessments in which adolescent and parent behaviors were rated in 3 interaction tasks: (a) low conflict planning task; (b) problem-solving conflict task; (c) puzzle challenge task; parent interview and parent-report and child-report questionnaires of parenting were also assessed. Results indicated that the associations between parent-child relationship quality and behavioral adjustment were comparable in adolescents with and without CU traits. More notably, observational data indicated that adolescents with elevated CU traits showed comparatively greater within-individual variability in observed angry/irritable behavior across interaction tasks, suggesting greater sensitivity to and emotional dysregulation in challenging interpersonal contexts. The findings suggest that adolescents with CU are not less sensitive to parental influence and may in contrast show greater context-sensitive disturbances in emotional regulation. The results have implications for family-based assessment and treatment for adolescents with disruptive behavior disorders. (PsycINFO Database Record
    Full-text · Article · Apr 2016 · Journal of Abnormal Psychology
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    • "Certainly the most frequent finding (7/15 studies) was that outcomes, as measured by recidivism or post treatment antisocial behavior, were worse among high-CU children. This appears in keeping with the extant research that these children exhibit a distinct risk profile and are more likely to persist in antisocial behavior (Frick & Viding, 2009). However, it is important to note that only a minority of studies examining whether CU traits were related to treatment outcomes adopted an RCT design, which is required to establish whether CU traits moderate the effectiveness of a treatment. "
    [Show abstract] [Hide abstract] ABSTRACT: Background: Children and adolescents with callous unemotional (CU) traits are at risk of severe and persistent antisocial behavior. It is commonly assumed that these children are difficult to treat but it has been proposed that they may benefit from being involved in interventions that go beyond typical parent training programs. Aim: This systematic review sought to answer two previously unanswered questions: do interventions involving young people reduce levels of CU traits? Do CU traits predict the effectiveness of interventions for antisocial behavior involving young people? Method: Studies were included that adopted an randomized controlled trial, controlled or open trial design and that had examined whether treatment was related to reductions in CU traits or whether CU traits predicted or moderated treatment effectiveness. Results: Treatments used a range of approaches, including behavioral therapy, emotion recognition training, and multimodal interventions. 4/7 studies reported reductions in CU traits following treatment. There was a mixed pattern of findings in 15 studies that examined whether CU traits predicted treatment outcomes following interventions for antisocial behavior. In 7/15 studies, CU traits were associated with worse outcomes, although three of these studies did not provide data on baseline antisocial behavior, making it difficult to evaluate whether children with high CU traits had shown improvements relative to their own behavioral baseline, despite having the worst behavioral outcomes overall. CU traits did not predict outcomes in 7/15 studies. Finally, a single study reported that CU traits predicted an overall increased response to treatment. Conclusions: Overall, the evidence supports the idea that children with CU traits do show reductions in both their CU traits and their antisocial behavior, but typically begin treatment with poorer premorbid functioning and can still end with higher levels of antisocial behavior. However, there is considerable scope to build on the current evidence base.
    Full-text · Article · Dec 2015 · Journal of Child Psychology and Psychiatry
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