Behavior Genetics of Aggression in Children

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Behavior genetics of aggression inchildren: Review and future directions

Lisabeth Fisher DiLalla*

Department of Family and Community Medicine, Southern Illinois University School of Medicine,

Mail Code 6517, Carbondale, IL 62901-6517, USA

Received 20 September 2000; received in revised form 18 November 2001

Abstract

A thorough understanding of factors that influence aggression in children cannot

be achieved without including behavior genetic studies that allow us to examine the

effects of shared versus non-shared environment, as well as genes, on aggressive be-

haviors. This review details the growing body of evidence on the genetic effects on

aggression. The majority of twin and adoption studies on antisocial behavior in chil-

dren suggest that genetic effects are important influences, but most of these studies

utilize parent reports rather than observational data. Some recent studies of non-

parent raters are beginning to suggest that aggression in childhood may indeed be

heritable and that this may not be a function simply of parent reporting bias. Future

studies will need to focus on geneenvironment correlations and interactions to begin

to disentangle the myriad ways that children and the people in their environments

inter-relate and mutually affect each other.

2002 Elsevier Science (USA). All rights reserved.

Keywords: Aggression; Behavior genetics; Delinquency; Children

Violent behaviors are becoming alarmingly commonplace in our societyand have been described as a public health problem as perilous as any dis-

ease (Human Capital Initiative Coordinating Committee, 1997). In an

Developmental Review 22 (2002) 593622www.academicpress.com

* Fax: 1-618-453-5861.

E-mail address: [email protected]

0273-2297/02/$ - see front matter 2002 Elsevier Science (USA). All rights reserved.

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effort to combat this growing trend, an increasing number of research pro-

jects have been aimed at understanding and intervening in violent behaviors.

Research over the last few decades has yielded developmental theories of theetiology of aggression that approach the problem from different perspectives

(e.g., Crick & Bigbee, 1998; Crick & Dodge, 1996; Dishion, Duncan, Eddy,

& Fagot, 1994; Loeber & Stouthamer-Loeber, 1998; Moffitt, 1993; Patter-

son, Capaldi, & Bank, 1991). An important piece of the puzzle that is only

recently beginning to be adequately explored is the etiology of aggression

from a behavior genetics perspective. That is, what roles do genotype,

shared family environment, and non-shared environment play in the devel-

opmental course of aggression? A thorough understanding of factors that

influence aggression in children cannot be achieved without including be-havior genetic studies that allow us to examine the effects of shared versus

non-shared environment, as well as genes, on aggressive behaviors (Plomin,

1994). Only by including genetic effects in our developmental theories of ag-

gressive behavior can we move this field of research forward to a thorough

understanding of all relevant factors that account for aggressive develop-

ment. Inclusion of genetic effects in our developmental models is necessary

for understanding how environmental influences, such as parental discipline

or peer delinquency, interact with individual differences, such as tempera-

ment or physiological responses to novelty, to lead to aggressive outcomes.

This paper has three goals. First, the importance of the behavior genetic

paradigm for understanding influences on development will be propounded.

Environmental influences typically are studied by examining one child with-

in a family. This method does not allow us to separate the effects of genes

and environment, and it does not allow examination of geneenvironment

correlations which result from children choosing environments, or niches,

that suit their own styles and temperaments. Second, this paper will detail

the growing body of evidence on the genetic effects on aggression. Finally,

the behavior genetic aggression literature will be considered within the

framework of some prevailing developmental theories on aggression. Earlier

reviews of genetic influences on aggression (e.g., Gottesman, Goldsmith, &

Carey, 1997; Miles & Carey, 1997) have greatly enlightened audiences seek-

ing biological explanations. This review seeks to broaden the fields of both

behavior genetics and child development by directly addressing ways in

which prevailing developmental theories might be expanded to include ge-

netic influences on child development, specifically within the framework of

aggression.

The behavior genetic paradigm

The study of development from a behavior genetics perspective allows

consideration of the impact of genotype on behavior, which is complex

594 L.F. DiLalla / Developmental Review 22 (2002) 593622


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because of the ways that genes and environment may correlate, as discussed

below. Early behavior genetic studies partitioned phenotypic variance into

genetic and environmental components, the latter being further separatedinto shared and non-shared environment. This can most easily be done with

twin or adoption studies because these allow systematic comparisons to be

made between groups of family members who differ primarily on the extent

to which they share genetic make-up. These methods are described briefly

below. For more detailed explanations, see Plomin, DeFries, McClearn,

and McGuffin (2000).

The twin method

The twin method relies on the naturally occurring phenomenon that there

are two types of twins: identical or monozygotic (MZ) twins, who are genet-

ically identical, and fraternal or dizygotic (DZ) twins, who share on average

50% of their genetic make-up, as do any two siblings. A comparison between

the two types provides an estimation of heritability by measuring the corre-

lation between identical twins and the correlation between fraternal twins on

a specific trait or behavior. The correlation between identical twins (the de-

gree to which they are similar to each other) is a function of their genetic

make-up (they are genetically identical) and the environmental influences

that they share. These are designated ash2 andc2, respectively. The equation

for this correlation is

rMZ h2 c2:

The correlation between fraternal twins also is a function of their genetic

make-up and the environmental influences that they share. The equation for

this correlation is

rDZ 1=2h2 c2:

A rough estimate of heritability can be achieved by subtracting the two

equations (rMZ rDZ 1=2h2) and then doubling the difference

h2 2rMZ rDZ:

This estimate depends on a particular assumption, the equal environments

assumption, that states that the environments that identical and fraternal

twins share are comparable with respect to the characteristic of interest,

except to the extent that more similar twins evoke or choose more similarenvironments (reflecting evocative or active geneenvironment correlation),

which becomes an effect of genes and not only environment. It is certainly

possible that there are basic differences between the environments of identical

twins and fraternal twins, but the equal environments assumption states that

these differences are not relevant for the psychological traits studied. Al-

though this assumption has serious implications for interpretation of results

L.F. DiLalla / Developmental Review 22 (2002) 593622 595


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from twin studies, most of the research that has explored this assumption

has supported its applicability (Hettema, Neale, & Kendler, 1995; Loehlin

& Nichols, 1976; Scarr & Carter-Saltzman, 1979). Several twin studieshave demonstrated that identical twins share a more similar environment

in terms of dressing similarly, sharing friends more, and maintaining more

frequent contact in adulthood (Kendler, Neale, Kessler, Heath, & Eaves,

1992; Loehlin & Nichols, 1976; Rose, Kaprio, Williams, Viken, &

Obremski, 1990), but these similarities have not led to increased similarity

in the psychological traits that were studied, including personality and

intelligence (Loehlin & Nichols, 1976; Matheny, Wilson, & Dolan, 1976;

Plomin, Willerman, & Loehlin, 1976) and clinical diagnoses of mental

disorders (Kendler et al., 1992, 1994). (However, recent results fromadoption studies may challenge these findings; see section on geneenvi-

ronment correlation below.)

A second possible confound for all behavior genetic studies (with twins as

well as adoptees) is the phenomenon of assortative mating. If parents of

twins mate based in part on similarity of aggressiveness, then fraternal twins

will share more aggression-influencing genes than expected by chance.

(Identical twins, of course, still share 100% of their genetic make-up.) This

would increase the similarity between fraternal twins, thus reducing the dif-

ference between identical and fraternal twin correlations, yielding a deflated

heritability estimate.

The adoption method

The adoption method involves examination of the correlation between

adopted children and adoptive parents and the correlation between adopted

children and biological parents. The adoptive child theoretically shares

genes but no environment with the biological parents and shares environ-

ment but no genetic make-up with the adoptive parents. Very basically,

any similarity between the adopted child and biological parents reflects

the influence of genetic factors. Conversely, any similarity between the

adopted child and adoptive parents reflects the influence of environmental

factors on the trait being measured.

There are some basic assumptions with this paradigm that must be made

and potential confounds that must be considered. One primary assumption

is that there is no selective placement. That is, children are assumed to be

placed with adoptive parents who are not systematically similar to the bio-logical parents on the measure of interest. However, if selective placement

does occur, it can be included in a statistical model to determine whether

it significantly influences the estimates of heritability and environmental ef-

fects. This involves modeling a correlation between the adoptive and biolog-

ical parents to determine whether, in fact, they are correlated on the trait of

interest. This partials out that correlation and allows the partial regressions



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from each parent to the adoptive child to reflect the genetic and environmen-

tal contributions to the trait of interest. Other assumptions particular to the

adoption and twin methods are detailed in Plomin et al. (2000).One potential confound that is more difficult to address is the influence of

the biological mothers prenatal environment on the childs behavior. A

large number of research studies demonstrate effects of such prenatal envi-

ronments as smoking, stress, and cocaine on childrens behaviors (e.g.,

Browne, Colditz, & Dunster, 2000; Swanson, Beckwith, & Howard, 2000),

but these studies may be marred by geneenvironment correlations (e.g.,

the type of woman who feels more stressed during pregnancy may also

transmit the genetic influences of her personality to her offspring as well

as the physiological effects of her stress during pregnancy, making it difficultto determine whether the child is highly reactive because of maternal stress

neonatally or because of shared personality traits inherited from the

mother). Another confound is the possibility of assortative mating. With

twins, this results in an underestimate of heritability. However, with adop-

tees, this can lead to two different outcomes. It can cause biological parents

and offspring to share more than 50% of their genotype for a trait, assuming

that genes influence the behavior, yielding an inflated estimate of genetic in-

fluence, and/or it can cause adoptive parents to provide an environment

more supportive of the trait than if only one parent had it, assuming that

environment influences the behavior, yielding an inflated estimate of envi-

ronmental influence. A third concern is that measures of children and adults

are rarely isomorphic, yet the adoption method assumes they are (Fulker &

DeFries, 1983). Thus, to compute heritability, measures of the types of ag-

gression seen in young children cannot be compared directly to adult aggres-

sion unless a latent variable is created that can be shown to represent the

same measure of aggression in both adults and children. (However, this as-

sumption is not necessary if a method is used to linearly test for genetic me-

diation between parent and child resemblance rather than assess heritability

of the behavior; see Coon, Carey, & Fulker, 1990.)

Behavior genetics and development

This partitioning of variance between genetic and environmental influ-

ences has allowed the enormous leap from believing that all behaviors are

influenced solely by environmental input, as was the prevalent view duringmost of the 20th century, to understanding that genotype also plays an im-

portant role in influencing our behaviors. However, the picture is much more

complicated than these early studies suggested. The interplay between geno-

type and environment is difficult to disentangle conceptually and even more

difficult to measure. For instance, studies have shown that children who play

with more aggressive peers act more aggressively themselves (Rourke,



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Wozniak, & Cassidy, 1999). However, we must ask why these children

choose to play with aggressive peers to begin with. It is possible that they

possess some characteristics that make them more prone to behaving aggres-sively already, or that something about aggression intrigues them. There-

fore, playing with aggressive peers may simply be a reflection of their own

characteristics, or it may trigger pre-existing aggressive tendencies, or it

may increase aggressive behaviors that were already present.

At the basis of this question is the issue of genotypeenvironment (ge)

correlation (Plomin, DeFries, & Loehlin, 1977; Scarr & McCartney,

1983). These correlations probably occur with most of the behaviors that

we study, but they are extremely difficult to measure. They occur: when

the genotype and the environment both come from the same sourcetheparents (passive ge correlation); when childrens environments partly are

reactions to the childrens behaviors, which are influenced by their geno-

types (reactive ge correlation); or when the environments are chosen by

the children (consciously or unconsciously) partly because of their genotypes

(active ge correlation). For example, a child may inherit musical talent

from her parents, and her parents may also play music often and have mu-

sical instruments in the home. Both the genes and the environment may

cause the child to be musically inclined. This is an example of passive ge

correlation. Also, a child who has inherited musical talent may sing often

and well, and therefore her parents may decide to start her at a young

age with piano or singing lessons, which may lead to increased musical tal-

ent (reactive ge correlation). Finally, a child who has inherited a proclivity

for music may always love music and may choose to attend a college with a

music major, where she becomes well trained in music, thus leading to in-

creased musical talent (active ge correlation).

It would be difficult to determine for this child whether it was her geno-

type or her environment that led to her musical success. The same may be

true of aggression. Disentangling the genetic and environmental causes of

aggressive behavior is complex because at any point we can ask whether

the childs environment is a function of his genotype or whether his genotype

is being expressed because of his environment. As we learn more about the

main effects of genotype and environment on aggression, we will become

better able to disentangle these correlations. This is an issue that behavior

genetic research must begin to explore more rigorously if we hope to acquire

a more complete understanding of any effects on behaviors such as aggres-

sion. Because of the complex interplay between genes and behavior, this is avery demanding and difficult endeavor, but as new techniques are developed

for partitioning these effects, our knowledge about the causes of aggression

and other behaviors will expand enormously.

A new crop of research has begun to explore the effects of genes on chil-

drens behaviors which in turn affect how the children are responded to

by people in their environment (DiLalla & Bishop, 1996; Gottesman &



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Goldsmith, 1994; Hur & Bouchard, 1995; OConnor, Hetherington, Reiss, &

Plomin, 1995; Plomin, Reiss, Hetherington, & Howe, 1994; Rowe, 1983).

Most of the research has focused on how parents respond to their childrensbehaviors, thus shaping the parental environment in which the child devel-

ops. However, the responses of peers and teachers to children s behaviors

are just as relevant for understanding childrens environments. The childs

genotype is partially and indirectly responsible for the part of the child s en-

vironment that she shapes for herself. Two adoption studies of antisocial be-

havior have yielded results supporting the hypothesis that aggressive

children elicit more negative environments from their parents (Ge et al.,

1996; OConnor, Deater-Deckard, Fulker, Rutter, & Plomin, 1998). This

is an example of reactive geneenvironment correlation. Ge et al. (1996)found that adoptive childrens antisocial behaviors were predicted by their

biological parentspsychiatric disorders, and in turn the children s behaviors

predicted their adoptive parentsdiscipline practices. Thus, childrens behav-

iors are influenced by their genotype, and these behaviors elicit certain be-

haviors from the people around them. Caution must be exercised in

interpreting these results because the sample size was very small (N 41)for the structural equation modeling analyses that were conducted, but

the method used to attempt to unravel this geneenvironment correlation

is promising. A second study using a similar design also yielded results that

supported the influence of geneenvironment correlations. OConnor et al.

(1998) showed that children whose biological mothers were rated as at least

somewhat antisocial were disciplined by their adoptive parents with more

negative control. Again, their sample size was small (38 at-risk children

and 50 not-at-risk children), and the results did not hold for inconsistent

or positive parenting, stressing the need for replication and a better under-

standing of what contributes to parenting behaviors. But the fact that their

results were consistent with Ge et al.s demonstrates that geneenvironment

correlations may be an important piece of the aggression puzzle.

Geneenvironment interaction also is important to consider as an influ-

ence on aggression. It is possible that children with genotypes that may tend

toward aggression will only express that aggression in certain, aggression-

enhancing environments, whereas children without such genotypes will

not express aggression or will express it to a smaller extent even in negative

environments. A simple test for this would be to assess heritability sepa-

rately for an unselected sample and again for those children in the sample

who fall in the 15% tail as most aggressive. If heritability is significantlyhigher for the extremely aggressive subsample, and if those children also

have been raised in an environment especially conducive to behavior prob-

lems, then geneenvironment interaction can be assumed because if there

was only a main effect for genes, this extreme group would be diverse in

the types of environment they were exposed to. But if they are all exposed

to a negative environment, then it is probable that the combination of a high



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genetic loading plus high environmental deviance led to extreme aggression.

This may also represent a geneenvironment correlation, with the environ-

ment reacting to the childs extreme genetically influenced phenotype, thuscausing the childs environment to be negative. This in turn becomes a

geneenvironment interaction because now the childs extreme genotype

and the negative environment together over time lead to extreme aggression

in the child.

Genetic effects on aggression

A number of twin and adoption studies have documented a genetic influ-ence on adult criminality and violence (Christiansen, 1977; Cloninger &

Gottesman, 1987; Crowe, 1975; DiLalla & Gottesman, 1989; Hutchings &

Mednick, 1975; Mednick, Gabrielli, & Hutchings, 1984, 1987). However,

the literature on child and adolescent delinquency and aggression is much

less consistent. Until very recently, there had been surprisingly few studies

on childhood aggression using the behavior genetics paradigm. Given the

compelling research on adult criminality, it is natural to attempt to extend

those findings to younger children. However, the original studies on delin-

quency in twins yielded results showing virtually no heritability of this be-

havior, and perhaps that is why so little research was conducted after that

time. Only in the last few years are behavior geneticists beginning to study

aggression in children more systematically.

One drawback to all research on aggression is the lack of a consistent def-

inition across research studies. Definitions range from clear acts of interper-

sonal violence to less physically harmful, delinquent behaviors such as

shoplifting. They also differ in the ways that aggressive behaviors are consid-

ered (e.g., covert versus overt, Loeber & Stouthamer-Loeber, 1998; reactive

versus proactive, Crick & Dodge, 1996). For each study, definitions depend

on the sample sex and age and on the theoretical rationale for the study. For

instance, Crick and colleagues (Crick & Bigbee, 1998; Crick & Grotpeter,

1995) have studied relational aggression, which does not involve physical

harm but rather verbal statements that are insulting to others. Their ratio-

nale for including this under the rubric of aggression is that girls more of-

ten engage in this type of action as a substitute for more physical aggression

(although some research suggests that boys do this equally often, Hening-

ton, Hughes, Cavell, & Thompson, 1998; Tomada & Schneider, 1997). Re-lational aggression may have a different etiology than physical aggression.

Other differences in definition depend in part on the method for assessing

aggression. Studies that use parent reports are likely to focus on more minor

aggressive behaviors either because the children in the study are younger or

because older children tend to exhibit most aggression away from the home.

Studies that use teacher reports or school-age peer reports may be able to



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include a greater range of aggressive behaviors because teachers and older

peers are able to report more extreme aggression that occurs at school. Stud-

ies of unselected, very young children tend to include less physically harmfulaggression because even aggressive preschoolers are less often in situations

where extreme aggression is likely to occur. Thus, the studies included in this

review will range in their definitions of aggression, and this will be detailed

as the studies are described.

Research on genetic influences on delinquency and aggression is still in its

infancy. We are beginning to learn about the possible genetic influences on

these behaviors, but we have not yet reached the point where social context

has been included in the models. The macrosystems of influence as outlined

by Bronfenbrenner (1979) in terms of home, school, neighborhood, andoverall culture are known to be relevant to these constructs. At this point

in time, however, behavior genetic studies have focused on determining

whether it is important to include genetic influences on delinquency and ag-

gression before beginning to implement such complicated studies that will

include broader social influences. Behavior genetic research eventually will

be instrumental in determining to what extent these broader influences are

shared or not shared among family members. This type of analysis will be

critical for addressing specific theoretical deficits in our understanding of in-

dividual differences in aggressive development (Coie & Dodge, 1998). One

nationwide study of 2-year-old twins in England and Wales has shown that

neighborhood deprivation does indeed significantly affect general behavior

problems in 2-year-olds above and beyond the effects of genetic influence

(Caspi, Taylor, Moffitt, & Plomin, 2000), demonstrating that this is a critical

area of inquiry to continue in terms of the development of aggression.

Delinquency

Our interest in aggression stems primarily from its consequences to vic-

tims. Therefore, it is reasonable to begin the study of aggression by asking

questions about criminality and delinquency, as these are the obvious behav-

iors in our society that have the most dire consequences for others. There is

clear evidence of the importance of genotype in influencing criminal and vi-

olent behaviors in adults (Christiansen, 1977; Cloninger & Gottesman, 1987;

Mednick et al., 1984, 1987). However, in adolescence the evidence is less com-

pelling. This should not be surprising given that delinquency is so common in

our society, with 80% of adolescents reporting having engaged in some delin-quent act (Gold & Petronio, 1980). This is in part a definitional problem

based on the ways in which delinquency is ascertained. If court records are

used, then generally more serious delinquency is being considered, and if

there is a genetic influence on these more extreme behaviors then the herita-

bility estimate will increase. If all delinquent behaviors are included, then the

base rate will be high and genetic influences will be more difficult to detect.



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Early studies of delinquency among twins showed that genetic influences

account for very little of the variance in the populations studied (Hayashi,

1967; Rosanoff, Handy, & Plesset, 1941; Shields, 1977). The weighted con-cordances across the delinquency studies are 87% for MZ twins and 72%

for DZ twins (DiLalla & Gottesman, 1989). The high concordance rates

for DZ twins, greater than 50%, suggest a fairly large influence of shared

family environment. The MZ and DZ concordances are not sufficiently dif-

ferent to support a strong genetic component for delinquency for most

twins. These studies relied exclusively on court records for the twins. More

recent studies on antisocial behaviors in adolescents have used self reports

or parent reports, and these have yielded different results.

Twin studies by Rowe (1983) and Rowe and Osgood (1984) have sug-gested that delinquency does indeed have a substantial heritable component.

These two studies utilized self-reports of antisocial behavior which in-

cluded both aggressiveness and delinquency, making it impossible to distin-

guish the two behaviors. The data yielded a heritability estimate of about

70% for this scale as well as a significant contribution from shared environ-

mental influences. The discrepancy in heritability estimates between these la-

ter studies and the earlier twin studies might be explained by the different

methods for ascertaining delinquency. The earlier studies relied on court

records, whereas Rowe (1983; Rowe & Osgood, 1984) used self-report mea-

sures and combined aggression and delinquency. Twin studies of self-report

measures typically yield moderate to high heritabilities regardless of the con-

struct under study (Plomin & Fulker, 1987), suggesting that there may be a

genetic influence for responding to questionnaires. Also, there may be a bias

with court records because twins may be more likely to be arrested once a

co-twin is arrested, thus increasing the apparent effect of shared environ-

ment. A delinquency study using more than one measurement method is

necessary for obtaining a more accurate heritability estimate.

A description of three types of offenders was offered by DiLalla and Got-

tesman (1989), with similar ones described later by Moffitt (1993), to high-

light the differences between adolescents passing through a delinquent

phase and those who are beginning or have yet to begin criminal careers.

The three groups are: (1) transitory delinquents, youths who are delin-

quent but do not continue these activities as adults; (2) continuous antiso-

cials, those who commit delinquent acts as adolescents and criminal acts as

adults; and (3) late bloomers, adults who commit criminal acts but were

not delinquent as adolescents. DiLalla and Gottesman (1989) hypothesizedthat the continuous antisocials may have a genetic loading for behaving in

a delinquent/criminal manner, thus maintaining these behaviors from adoles-

cence into adulthood, whereas the transitory delinquents may be responding

simply to environmental pressures that cease as the adolescents mature. Mof-

fitt (1993) similarly described two types of antisocial behavior: adolescent-

limited antisocial behavior, similar to the transitory delinquents, which is



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seen in adolescents who are responding to environmental influences to be-

have in an antisocial manner, but who are unlikely to continue these behav-

iors as they mature; and life-course-persistent antisocial behavior, similar tocontinuous antisocials, which is seen in those individuals who are tempera-

mentally and biologically disposed toward behaving in an antisocial manner

and therefore who maintain this type of behavior across their lifespans.

These distinctions between types of offenders will be useful if each has a dis-

tinct etiology or responds differentially to intervention. The question of ge-

netic etiology of each type is explored in this paper. Other distinctions,

such as those between violent and non-violent offenders and socialized delin-

quents versus loner delinquents, still require behavior genetic research to de-

termine whether these involve genetically distinct etiologies.A huge number of studies have identified factors in the family and the

child that increase the risk of delinquency and that may help to distinguish

the groups defined by DiLalla and Gottesman (1989) and Moffitt (1993).

These have yet to be adequately explored from a behavior genetics perspec-

tive. Many of these factors may have underlying genetic causes so that ge-

notype indirectly leads to delinquency. For instance, harsh parental

attitude and harsh or lax discipline (Baldry & Farrington, 1998; DiLalla,

Mitchell, Arthur, & Pagliocca, 1988; Farrington, 1991; Glueck & Glueck,

1968; Loeber & Hay, 1997; McCord, 1978; Olweus, 1978; Pagani, Tremb-

lay, Vitaro, Kerr, & McDuff, 1998; Patterson, Reid, & Dishion, 1992) have

been linked with increased delinquency. Genotypeenvironment correla-

tions may be occurring here. Unusually harsh or chaotic parents share both

their genotypes and their environments with their children, so their chil-

dren may have genotypes that put them at risk for aggressive or antisocial

behaviors. Thus, these children may already behave in a more difficult

manner. Their parents, who have a difficult time disciplining their children

properly anyway, may then respond to these difficult behaviors in their

children by creating an even more harsh or chaotic environment, thus caus-

ing the children to respond even more strongly in an aggressive or delin-

quent manner.

Other factors related to delinquency include conflict between youths and

their parents (Wirt & Briggs, 1959), criminality and low IQ scores of the par-

ents (Farrington, Gundry, & West, 1975; Hutchings & Mednick, 1975; Os-

born & West, 1979) or siblings (Glueck & Glueck, 1968), and reinforcement

of childrens coercive behaviors (Patterson et al., 1991; Patterson, DeBary-

she, & Ramsey, 1989). Characteristics of the youths themselves also havebeen shown to be related to their chances of being criminal as adults. These

include extroverted and less self-controlled behavior (Glueck & Glueck,

1968), high levels of antisocial behavior at age 18 (Farrington et al., 1975)

or earlier (Loeber, 1982), academic failure and an inability to relate to nor-

mal peers (Dishion et al., 1994; Wirt & Briggs, 1959), and persistent recid-

ivism during adolescence (Osborn & West, 1978; Robins, 1966). All of these



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also could be interpreted from a genetic or a geneenvironment correla-

tional perspective. For example, familial criminality was shown to be high

among boys who were criminal (Farrington et al., 1975). The researchers ru-led out some obvious environmental explanations for this phenomenon: sib-

lings were as likely to be convicted after index subjects as before, and

previously convicted fathers often had no convictions after subjects were

born. Thus, boys imitation of siblings and fathers did not account for the

index boys criminality. Familial attitude toward police and authority did

not differ between subjects who were and were not convicted. Farrington

et al. were reluctant to rely on genetic explanations because their data

were insufficient for this, but such an explanation would help to clarify their

results.One study examined whether genetic differences distinguished delinquents

who were classified as early-onset versus late-onset (Taylor, Iacono, &

McGue, 2000a). The authors found that early starters were more likely to

experience psychological, behavioral, and emotional problems at age 11

years, and greater genetic influence on early starters was evident. This study

lends support to the idea that genetic differences may be one of the factors

leading to early-onset delinquency. This also demonstrates a meaningful dif-

ference between early- and late-onset delinquents; if genetic factors account

for group differences, this implies distinction in terms of typology of delin-

quency. Similarly, temperament was one of several factors that distinguished

early-onset from adolescent-onset antisocial behavior in the Dunedin longi-

tudinal study (Moffitt & Caspi, 2001), suggesting indirectly that genetic fac-

tors play a role in distinguishing the two.

Genetically influenced underlying personality traits may be at the root of

certain delinquent or aggressive acts. Adult criminals have been shown to be

high on Psychoticism, Neuroticism, and Extraversion (Eaves, Eysenck, &

Martin, 1989). Similar patterns may emerge in adolescence or earlier (Caspi,

Henry, McGee, Moffitt, & Silva, 1995; Gjone & Stevenson, 1997). Other

personality characteristics also may be important for the display of delin-

quent and aggressive behaviors. For instance, two uncorrelated types of shy-

ness have been identified: introverted, characterized by a lack of caring for

other people; and neurotic, characterized by a fear of other people, which is

the type of shyness that we most typically consider (Eaves et al., 1989). This

distinction may be related to delinquency and aggression. Introverted ado-

lescents may be more likely to be delinquent or aggressive (e.g., Fischer &

Ayoub (1993) suggest this for adults), whereas neurotic shy adolescentsmay be the least likely to be delinquent or aggressive. Ladd and Burgess

(1999) identified a group of aggressive/withdrawn children as being as or

more aggressive than aggressive/non-withdrawn children and as having few-

er friends, suggesting that it is worthwhile to further study the relation be-

tween withdrawn behaviors and aggression in early childhood. This

underlying personality characteristic may provide one important bridge



13/30

between genotype (which affects personality) and delinquency (which is

affected by personality).

Aggression

Fewer behavior genetic studies have been conducted directly related to

aggression in children, although parent report studies are beginning to flour-

ish. Aggression has been studied separately from delinquency in the belief

that these are distinct behaviors. Behavior genetic studies on both behaviors

as rated by parents and teachers concur, demonstrating that aggression is

more heritable than is delinquency. These studies are described below. How-

ever, the research that has assessed genetic influences on childhood aggres-sion has yielded mixed results. Most of the studies have used parent reports

(Cadoret, Leve, & Devor, 1997; Miles & Carey, 1997). Only three published

studies have actually measured the childrens behaviors in the laboratory.

These three behavioral studies failed to find evidence of genetic influence

on aggression although the parent rating studies have demonstrated signif-

icant heritability. Thus, the issue clearly is not resolved.

Two of the three studies that failed to show heritability for behaviorally

rated aggression in young children used small samples and combined re-

sponses from children across a wide age range. The first (Owen & Sines,

1970) combined twins aged 614 years, a very wide and developmentally di-

verse age range, which could have obscured meaningful results by averaging

developmental differences. Owen and Sines found no heritability for a pro-

jective measure of aggression. A second study (Plomin, Foch, & Rowe,

1981) that did not find significant heritability for aggression examined chil-

dren across the age range of 511 years, again a range that encompasses chil-

dren at very different developmental stages. In this study, twins were

encouraged to hit a large Bobo clown doll. Such behaviors as number

of hits and intensity of hits were scored. Identical and fraternal twins were

similarly correlated on these measures, suggesting that all variability was

due to environmental factors (h2 :00). The third study (OConnor et al.,1995) involved videotaped observational ratings of verbal aggression toward

mothers and fathers by adolescents. Results were extremely similar for

mothers and fathers, suggesting that adolescent behaviors did not depend

on the parent toward whom the aggression was directed. Heritability was

somewhat higher in this study than in the previous two, but it was still

low (h2

:28).The studies that did demonstrate significant heritabilities all utilized pa-rental ratings of the children. Most have used the Child Behavior Checklist

(CBCL; Achenbach, 1991). In one study (Edelbrock, Rende, Plomin, &

Thompson, 1995), parents of 7 to 15-year-old twins completed the CBCL

on each twin. Heritability was found to be 35% for the delinquency subscale,

which was not significantly different from 0, and 60% for the Aggression



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subscale. Shared environmental effects were found to be significant for De-

linquency (37%) but not for Aggression (15%). As Eley, Lichtenstein, and

Stevenson (1999) have suggested, the CBCL Delinquency subscale may rep-resent more adolescent-limited (Moffitt, 1993) or transitory delinquent

(DiLalla & Gottesman, 1989) types of behaviors that are more influenced

by environmental pressures, whereas the Aggression subscale may represent

more life persistent (Moffitt, 1993) or continuous antisocial (DiLalla & Got-

tesman, 1989) types of behaviors that are more temperamentally mediated

and more consistent across the lifespan. If so, higher heritability estimates

would be expected for the Aggression subscale, as was found in the Edel-

brock et al. (1995) study. A second twin study of 7 to 9-year-old Swedish

twins and 8- to 16-year-old British twins also used CBCL parent reportsto measure antisocial behaviors (Eley et al., 1999). They found that genetic

influences were important for Aggression scores for boys (h2 :70) and girls(h2 :70), but that genetic influences were smaller but significant for Delin-quency scores for girls only (h2 :44 averaged across both samples; resultswere inconsistent for boys). Shared environment was influential for Delin-

quency scores for boys (c2 :54), less so for girls (c2 :32). Thus, for boys,aggressive behaviors fit the genetically-influenced, life persistent or continu-

ous antisocial profile, and non-aggressive behaviors fit the environmentally

influenced, adolescent-limited or transitory delinquent profile. A third study

of adoptive and non-adoptive siblings from the Colorado Adoption Project

also demonstrated evidence for genetic influence on aggressive behaviors

based on CBCL scores (h2 :49) and evidence for shared environmental in-fluences (c2 :13) on the CBCL delinquency scores (Deater-Deckard & Plo-min, 1999). A fourth study (van der Valk, Verhulst, Neale, & Boomsma,

1998), also using adoptive and biological siblings, found results similar to

those above; Aggression scores showed heritability estimates of approxi-

mately .57 whereas Delinquency scores showed lower heritability estimates

of about .35. Shared environment was less influential for both behaviors

(c2 :15 for Aggression and c2 :20 for Delinquency) but was strongerfor Delinquency. Although heritability differences between Aggression and

Delinquency are small within studies, a trend emerges suggesting greater

heritability for aggression.

Three twin studies used parent ratings that were different from the CBCL,

but results were similar. Scarr (1966) had parents rate their children using an

adjective checklist to describe aggressiveness. Heritability was found to be

40%. Another study (Ghodsian-Carpey & Baker, 1987) used a novel methodof having mothers of twins check at given intervals whether certain behav-

iors had occurred for each twin over a three day period. The mothers also

completed a problem behavior checklist for each twin. Each of these mea-

sures showed a significantly high heritability (h2 :60 for behavioral rat-ings; h2 :78 for checklist ratings). The researchers used a sample thatspanned the developmental stages from preschooler to early school-age,



15/30

47 years. Their results were age-corrected, occluding developmental differ-

ences. Interestingly, Kuntsi, Gayan, and Stevenson (2000) used the Connors

Rating Scales to assess several behaviors, including conduct problems, andasked both parents and teachers to complete them on 125 same-sex, 7- to 11-

year-old twins. They found that this scale had a significantly heritable com-

ponent. This was higher for teacher (h2 :69; CI .56.79) than for parentratings (h2 :29; CI .00.69), but the parent rating results were equivocal,and a model with comparable fit yielded a heritability estimate of .59

(CI .42.71), which is comparable to the teacher rating estimate.A number of sibling (twins and adoptees) studies of aggression were sum-

marized by Cadoret et al. (1997). Only three studies were reported using par-

ent rating scales at that time (Ghodsian-Carpey & Baker, 1987; OConnor,Foch, Sherry, & Plomin, 1980; van den Oord, Boomsma, & Verhulst, 1994).

All employed small samples and covered somewhat different age ranges, but

the results were fairly similar to those reported in the more recent studies

above. Averaged across all parent report studies, heritability for aggression

as rated by parents is approximately 58%. This involves averaging across a

variety of ages and types of questionnaires, but the range was not huge (40

78%), suggesting that approximately half of the variance in childrens ag-

gression, as reported by parents, can be attributed to heritable influences.

In contrast, observational studies of young children yield an averaged her-

itability estimate of 9% (range of 028%).

One important difference between studies showing that aggression is her-

itable versus those not finding this is in the choice of measures used by the

researchers (Miles & Carey, 1997). Those studies that rated the childrens be-

haviors directly found no heritable effects, whereas those studies that used

parental ratings found high heritabilities. It may be that behavioral observa-

tions tend to have lower internal consistency, which would attenuate herita-

bility estimates because of the inflation in the non-shared environmental

component due to unreliability. Additionally, Plomin (1981) has noted that

parental ratings of any characteristic tend to yield high heritability esti-

mates, suggesting that parents tend to rate identical twins more similarly

than fraternal twins on all measures. Developmental, non-behavior genetic

studies that have contributed most to our understanding of aggressiveness in

children have used a variety of methods for addressing aggression, including

sociometric ratings (Coie, Dodge, & Coppotelli, 1982) and family interviews

and self-reports (Farrington, 1991; Patterson, 1986; Robins, 1966). Behavior

genetic studies have relied primarily on parental questionnaire data that canbe obtained fairly easily and inexpensively by mail because of the large num-

bers of participants necessary for complicated modeling analyses. Sociomet-

ric studies are virtually impossible to conduct with a selected population

such as twins or adoptees because aggressive children must be chosen by

their peers from a classroom, and most of those children will not be twins

or adoptees. Studies utilizing parent reports as well as direct behavioral



16/30

observation are needed, and this may be possible if more resources are used

to collect behavioral data. The study by Deater-Deckard and Plomin (1999)

used teacher ratings (Teacher Report Form, Achenbach, 1991, parallel tothe CBCL parent form) as well as CBCL parent ratings, thus allowing com-

parison between parent and teacher ratings. They found that teacher reports

were consistent with parent reports for the aggression subscale; both demon-

strated heritable influences on aggressive behaviors. However, for the de-

linquency subscale, teacher ratings showed modest effects of shared

environment and no effects of genetic influence, whereas parent reports

showed significant effects of both shared environment and genes. This find-

ing suggests that parent ratings may indeed overestimate genetic influences,

at least for delinquency, because parents may rate siblings who are moresimilar genetically (either MZ twins versus DZ twins or biological siblings

versus adoptive siblings) as more similar behaviorally, as Plomin (1981) sug-

gested earlier. Again, this supports the need for behavioral ratings of chil-

drens behaviors, and ratings by trained coders as children interact would

be an enormous asset to this line of research. Indeed, one preliminary report

(DiLalla & Gehlbach, 2000) with a small sample of preschool twins and sib-

lings used a rating that combined parent reports with trained observersrat-

ings of peer play behaviors with an unfamiliar peer and found that identical

twins were rated as more similar on measures of aggression (rMZ :91,p< :001) than were fraternal twins (rDZ :52,p< :05; significantly differentfrom rMZ) or siblings tested at the same age at different points in time

(rsib :34; significantly different from rMZ).Multiple ratings from multiple sources will yield more reliable assess-

ments of aggressiveness, and the bias due to rater or method effect can be

modeled as a latent variable using structural equation modeling (Loehlin,

1998). This provides an alternative to simply averaging scores across mea-

ures and allows variance shared by measures solely because they share rater

or methodology to be partialled out. This results in a purer latent variable of

aggression.

Additionally, most of the above studies included children across a wide

age range, thus making developmental interpretation impossible. In one

study (Eley et al., 1999), the children were divided into preteen and adoles-

cent groups and heritability was assessed separately for the two groups. No

significant heritability differences between aggressive and non-aggressive an-

tisocial behaviors were found for the two groups, suggesting that the causes

of antisocial behaviors do not differ by age group. However, the researchersdid find that adolescents had higher rates of delinquent behaviors but not of

aggressive behaviors. This is in line with other research suggesting that de-

linquency becomes more prevalent at adolescence but that aggression is

fairly stable (Loeber & Hay, 1997).

To better explore the developmental etiological differences between con-

tinuous antisocials (or life-course-persistent antisocials) and transitory



17/30

delinquents (or adolescent-limited antisocials), adolescents must be followed

into early adulthood to distinguish those who behaved delinquently during

adolescence from those who continue such behaviors into adulthood. On theother end of the developmental continuum, behavior genetic studies of ag-

gression need to include younger children if we are to better understand

the early behaviors that may lead to later aggression and delinquency in ad-

olescence. This is especially true if it turns out that ge correlations are

strong influences on aggression because that would imply that early child be-

haviors that are genetically influenced may have a powerful effect on the

childs environment, and this in turn may increase the level of aggression

that children exhibit as they get older. Behavioral examination of the effects

child behaviors have on the childs environment, and then the effects of thatenvironment on child aggression or delinquency, would help disentangle

geneenvironment correlation effects. This can only be accomplished using

a longitudinal design, first assessing childrens behavior at time 1, then pre-

dicting environment at time 2 from these earlier behaviors, and finally pre-

dicting child aggression at time 3 from the environmental measures,

partialling out the time 1 child behaviors.

A further focus for developmental research on aggression should be on

the developmental skills that are related to aggressive behavior, and how

the heritabilities of these change with age. For instance, the heritability of

cognitive ability has been well documented (Bouchard & McGue, 1981;

McGue, Bouchard, Iacono, & Lykken, 1993), showing near-zero genetic in-

fluence in infancy, increasing throughout childhood, and finally attaining

adult levels of approximately 50% by adolescence. There have been a num-

ber of studies suggesting a relation between IQ and both aggression (Hin-

shaw, 1992) and delinquency (White, Moffitt, & Silva, 1989). If a similar

pattern of increasing heritability is found for aggression or delinquency, it

is possible that IQ is a mediating link that causes an increase in genetic in-

fluence. This could be tested with multivariate models incorporating both

IQ and aggression or delinquency measures in a twin study. Similarly, em-

pathy or inhibition may be important influences on aggressive behaviors

(Greenberg, Kusche, Cook, & Quamma, 1995). Heritabilities have been

shown to be quite high as young as infancy or toddlerhood for both empa-

thy (Davis, Luce, & Kraus, 1994; Emde et al., 1992) and inhibition (Cherny,

Fulker, Corley, Plomin, & DeFries, 1994; DiLalla, Kagan, & Reznick,

1994). If heritability of aggression is shown to be high at very young ages,

it is possible that these processes may account for that genetic effect. Empa-thy has been described as necessary for moral development and prevention

of antisocial behavior (Young, Fox, & Zahn-Waxler, 1999). The fact that it

is fairly stable and moderately heritable in the preschool years suggests that

it may be one mechanism for understanding the development of aggression

in children. If, as Young et al. (1999) suggest, early inhibition as character-

ized by high reactivity is related to empathy, and empathy is related to



18/30

decreased aggression, then understanding the degree to which these behav-

iors share genetic and environmental etiology will greatly increase our

knowledge of the ways that these behaviors are inter-related. Again, thiscould be tested with a twin study examining these measures using multivar-

iate models.

Molecular genetics

There is a large body of molecular genetics research on aggression. The

scope of this paper does not allow an in-depth review of this research, but

it is too important to completely omit. A brief overview touching on afew aspects of this research follows in order to alert the reader to the impor-

tance of this work.

The quest for specific genes that may influence aggression is an intriguing

one. On the one hand, there have been many animal studies that have shown

without a doubt that aggression is genetically mediated because it has been

possible to breed mice for high and low aggressive strains (Cairns, Mac-

Combie, & Hood, 1983). The fact that they can be bred to differ on aggres-

siveness demonstrates that there are genes that influence this behavior.

Developmental effects also have been demonstrated in mice, and mice have

been bred for early and late appearing aggression (Cairns et al., 1983). On

the other hand, this picture appears to be greatly complicated in humans.

There are so many environmental factors that contribute to aggressive be-

haviors that genetic effects become less clearly identifiable. Researchers have

attempted to locate genes that influence dopamine receptors, serotonin re-

ceptors, and the enzyme monoamine oxidase A (MAOA) (Manuck et al.,

1999), and some linkage analyses have suggested that certain genes may re-

late to aggressive behaviors. However, none of this work in humans has

been developmental in focus. The most promising work thus far appears

to suggest that each of the above plays a role in influencing aggression in

both animals and humans. Given that the etiology of aggression is clearly

multifactorial, it is likely that treatments based on dopamine, serotonin,

and MAOA will be differentially effective in different cases. For some peo-

ple, one of these biological mechanisms may be a primary cause of aggres-

sion, whereas for others, the cause will be more environmental in origin.

Studies combining genetic and environmental influences for different sub-

groups of children and adults eventually will disentangle the various influ-ences, but first we must learn more about the individual genetic and

environmental main effects developmentally.

Genetic influences on individual differences in the liability to delinquency

and aggression require that there be some physiological bases for these be-

haviors (Mednick et al., 1987; Virkkunen, 1983), and these may begin to

show effects in adolescence (Olweus, 1978). More studies are needed which



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assess levels of physiological correlates during adolescence. Thus far, studies

examining specific genes that may influence these behaviors have been con-

ducted with adults, therefore not informing developmental theory. This isnecessary for ethical concerns, and these studies provide a beginning for this

search for genes that should lead to useful studies with children in the future.

Developmental behavior genetics and aggression

A number of theories have explained the developmental progression of

aggressive behaviors, each with emphasis on a different aspect of develop-

ment. For instance, Dodge and colleagues have focused on social learningtheory causes of aggression; Patterson and colleagues have demonstrated

links between parental behaviors and childrens coercive cycles as portend-

ing aggression; attachment theorists such as Bowlby and Sroufe have

pointed to the importance of insecure motherchild attachment in the early

years of life as the primary indicator of later child aggression. Each of these

theories can benefit from the additional consideration of biological and her-

itable influences on behavior. As developmental psychologists, we must

question individual differences in responses to aggressive or otherwise nega-

tive environments. For instance, why does one child of abusive parents be-

come a violent, abusive adult whereas another similarly abused child

becomes especially passive or non-aggressive? Understanding genetic differ-

ences that influence temperament, personality, and responses to various en-

vironments will allow us to develop a more complete understanding of the

etiology of aggression. To illustrate, two prominent developmental theories

of aggression are described below, with a behavior genetic component added

to each, thus augmenting and enhancing the theories.

One of the leading current developmental theories of aggression was put

forward by Crick and Dodge (1994) based on social learning theory. They

suggested that aggressive behaviors are a result of a childs encoding of

and interpretation of cues in the environment. It would not be difficult to in-

clude genetic propensities toward aggressive interpretations in this model.

Thus, a childs interpretation of an event as aggression-provoking may be

driven by previously learned experiences but also by a genetic predisposition

to perceive ambiguous situations as aggressive or to be more quick to re-

spond aggressively. This theory has not been addressed by behavioral genetic

researchers yet. A twin study that assesses childrens schematic responding toambiguous or aggressive vignettes would help to tease apart genetic and en-

vironmental influences on aggressive responses. It may be that children de-

velop schemas that they rely on to respond to provocative situations

(Gehlbach, 2000), and these schemas may be developed based on genetic pre-

dispositions to aggressiveness. A twin study that assesses these responses

would shed light on the impact of genotype on aggressive responses.



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Dodge and colleagues (Crick & Dodge, 1996; Dodge & Coie, 1987) also

have distinguished two types of aggression: reactive and proactive. Reactive

aggression involves responding aggressively to provoking situations. Proac-tive aggression involves behaving aggressively in order to get something, not

as a response to provocation. Although these two types of behaviors are re-

lated, they also appear to tap distinct forms of aggression, as evidenced by

two-factor models showing two clear patterns of behavior (Poulin & Boivin,

2000) and predictive models showing that proactive but not reactive aggres-

sion predicted delinquency (Vitaro, Gendreau, Tremblay, & Oligny, 1998).

Crick and Dodge (1996) showed that proactively aggressive children viewed

aggressive acts more positively and were less interested in social relation-

ships in conflict situations (these differences were significant although notlarge). However, the impact of genetic factors on childrens cognitive inter-

pretations of aggressive acts and on social relationships has not been evalu-

ated. A twin study on this would greatly enhance the literature on the

development of aggression. It also would be interesting to determine

whether proactive aggression is more influenced by genotype than is reactive

aggression. Children who exhibit proactive aggression may be temperamen-

tally inclined to engage in aggressive behaviors in general, without provoca-

tion (genetic influence) and they may imitate aggressive people whom they

admire (active geneenvironment correlation). Reactively aggressive chil-

dren, on the other hand, may have learned from their environment (e.g.,

parents, siblings) that the way to respond to bad situations is to fight back

(environmental influence) or they may be temperamentally more volatile

and more likely to respond aggressively to provocation (genetic influence).

Distinguishing between these two types of aggression when studying genetic

influences on aggression may be important because their etiologies may be

different and, subsequently, various intervention techniques may be better

tailored for one type of aggression or the other. For instance, if reactive ag-

gression is more a function of shared environment, such as parental teaching

or discipline, then intervention may be more effective if it is aimed at the

family level because otherwise individual intervention would not be rein-

forced in the home where the aggressive behaviors were first learned to begin

with. If, on the other hand, proactive aggression is more genetically based,

then intervention may need to be aimed more at the individual in order to

teach the child new behavioral responses because behavior at the family le-

vel may not require intervention, although of course teaching parents to

continue to reinforce the new, non-aggressive behaviors is always essential.Work by Patterson and colleagues (Patterson, 1986; Patterson, Dishion, &

Bank, 1984) also lends itself to behavior genetic interpretation. Their coer-

cion model has elegantly demonstrated the important roles of parenting

and peer interactions in predicting antisocial behavior. Specifically, they have

shown that poor parental discipline, monitoring, and family problem solving

as well as interactions with deviant peers in adolescence are predictive of



21/30

child antisocial behavior (Patterson, Forgatch, Yoerger, & Stoolmiller,

1998). Behavior genetic theory can be used to augment this model to better

understand the mechanisms behind the predictive relations and to focusmore on childrens individual differences in terms of both etiology and treat-

ment of problem behaviors. As discussed earlier, it is not sufficient to dis-

cover that children who spend more time with deviant peers are

themselves more deviant. We must also ask why these children choose devi-

ant peers to begin with. It is likely that children who are more prone to be-

having in an antisocial way prefer to spend time with others who are like

themselves, a process we can call assortative friendships (similar to assorta-

tive mating, where mates choose each other non-randomly based on similar-

ities). There is some evidence that adults show assortative mating based onantisocial characteristics, although the strength of this association is unclear

(e.g., Taylor, McGue, & Iacono, 2000b, suggest that it is modest in degree

parents of twins were correlated approximately .3 on a delinquency self-

report measurewhereas Krueger, Moffitt, Caspi, Bleske, & Silva, 1998,

found a slightly higher correlation of .54 for assortative mating based on an-

tisocial behavior, but only a correlation of .17 for the personality measure of

negative emotionality, which includes an aggression subscale). However, the

process by which delinquent adults or children tend to choose each other has

not been investigated. Behavior genetic studies should be used to unravel

this question by examining precursors to friendships, such as temperament

and early childhood friendships, determining how similar identical twins

are on these dimensions versus fraternal twins, and then exploring the sim-

ilarity between identical and fraternal twins in terms of current antisocial

friendships and antisocial behaviors. This would provide some insight into

whether children with antisocial tendencies choose antisocial friends, who

may augment those antisocial tendencies, or whether children happen to find

friends who are antisocial and who then encourage antisociality by this

friendship.

Crick and Grotpeter (1995) distinguished relational aggression as a type

of verbal aggression that is more common among girls. Relational aggres-

sion involves manipulating a persons reputation with peers in a negative

way (e.g., spreading rumors; saying, She likes me more than you!; saying,

You cant come to my birthday party!). We also do not know if there is a

genetic influence on this type of aggression, but again, it can be tested with a

behavior genetic study. Relational aggression may be more typical among

girls (Crick, Casas, & Mosher, 1997), so it is important to have a large sam-ple of females. However, it is unlikely that a large heritability estimate will

be obtained for this type of behavior because it is such a common behavior

among girls that both MZ and DZ correlations are likely to be quite high

(unlike a behavior like extroversion, for example, which has much more var-

iability). More likely, it is a developmentally typical behavior that girls use

to gain power as they discover the fact that they can use verbal, non-physical



22/30


23/30

It also is noteworthy that shared environment shows significant influence

for delinquency but not for aggression in twin studies. This is consistent with

theories of delinquency that point to the influence of deviant peers, and adelinquent co-twin would certainly be included. In fact, to the extent that

co-twins engage in such behaviors together, they would share more peer in-

fluences, thus augmenting the shared environment impact. This shared envi-

ronmental influence has not been shown for aggression, but studies have not

yet been conducted that examine this influence separately for different types

of aggression. It is possible that reactive aggression will be more susceptible

to shared environmental influences than proactive aggression, and the same

may hold for relational aggression, which may be seen as an important part

of fitting in with cliques. Further studies on these and other subtypes ofaggression are necessary before we can assess the influence of shared and

non-shared environment.

Methods such as the adoption design used by Ge et al. (1996) and

OConnor et al. (1998) for examining geneenvironment correlations are

fairly new. Their use with larger adoption samples would be an excellent

way to explore geneenvironment correlations, although large adoption

samples are difficult to obtain. We need to devise similar techniques for

exploring geneenvironment correlations with twin samples, which would

further our understanding of the interwoven effects of genes and environ-

ment on all behaviors. One possibility includes assessing parental treat-

ment of infant twins to determine whether identical twins are treated

more similarly than are fraternal twins (DiLalla & Bishop, 1996). If so,

it would suggest that more genetically similar infants elicit a more similar

environment based on genetic traits, such as temperament, which would

be an example of passive ge correlation. Another possibility is to model

shared genetic and environmental influences on environmental measures

and child measures using multivariate genetic analyses. This would pro-

vide information on the extent to which the same genetic or environmen-

tal influences affect both of these measures. If both environment and child

behavior share these influences, this would suggest the existence of a ge

correlation.

A critical bottom line for understanding behavior and for encouraging de-

velopmental behavior genetic research is the understanding that genes do

not determine behavior any more than do environments. It is the compli-

cated interplay between these influences that leads to specific behavioral out-

comes. If we limit our studies to include only environmental or only geneticinfluences, then we will be incapable of developing a complete understanding

of the ways in which these forces interact to produce behavior. Studies to

date that do limit themselves to studying only main effects of either specific

environmental or genetic influences have been able to identify significant

sources of variance, but the variance accounted for tends to be (sometimes

quite a bit) less than 50%, which means that there are still influences as



24/30

yet unexplained that very likely will be a function of the interactions and cor-

relations between genes and environment. Only by including both sources of

influence and by developing theories to explain how environment and geno-type interact will we be able to advance our understanding of the true causes

of aggression in children.

This opens the door to an entirely new perspective for understanding

childhood aggression. Rather than simply uncovering environmental influ-

ences that may lead to aggression in large groups of children, we can begin

to ask questions about individual differences. By acknowledging the role

that an individual child brings to a situation, and by considering the childs

genotype as an important influence on the childs perceptions and behaviors,

we can begin to interpret childrens behaviors in terms of the intercorrela-tions between their genotypes and their environments. Our understanding

of this complex interweaving is only in its infancy, but we are advancing

by leaps and bounds. The more we know about the genetic and environmen-

tal influences on aggression, the better we can design effective environmental

interventions. Aggression when it is aimed at hurting another person is a se-

rious health threat that we cannot ignore, and as we grapple with unraveling

its causes we will be in a better position to design effective intervention pro-

grams that are aimed more accurately at individuals rather than large, het-

erogeneous groups of children.

Acknowledgments

This paper was written in part while the author was a Visiting Scholar at

Brandeis University, Waltham, MA. Partial support was provided by a

grant from the Central Research Committee of the Southern Illinois Univer-

sity School of Medicine. The author wishes to thank Robert Plomin and

anonymous reviewers for their helpful comments.

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Behavior Genetics of Aggression in Children