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STUDENT PSYCHOLOGY JOURNAL VOLUME I
GENE-ENVIRONMENT INTERACTIONS IN DETERMINING
CRIMINALITY
Laura Mangan
Senior Sophister, Psychology
[email protected]
ABSTRACT
The determination of criminality is multifactorial as it involves the
interaction of several different factors including individual, familial and
social factors. Correlations between antisocial behaviour and impairment
of the prefrontal cortices have been found (Eastman & Campbell, 2006).
Socioeconomic deprivation has a strong link with subsequent criminality
(Ferguson, Swain-Campbell & Horwood, 2004), as those from low SES
backgrounds are three times more likely to engage in antisocial behaviour
than individuals from high SES backgrounds. In contrast, both the Social
Causation Perspective and Control Theories place the burden of criminal
determination firmly on peer relations. Familial factors also have an
important role in shaping whether an individual engages in criminal
activity as they have the potential to exacerbate or moderate criminality
in the developing child (Ferguson et al., 2004). In sum, neither genetic nor
environmental factors alone are sufficient in explaining the determination
of criminality. They must be combined in order to establish any causal
relationship.
INTRODUCTION
Among the most important factors in predicting criminal convictions are
socioeconomic deprivation, poor parenting and an antisocial family
(Farrington, 1990). These factors are necessary but not sufficient alone;
the emergence of the antisocial behavioural phenotype necessarily must
occur as a result of interactions between an individual‟s genetic make-up
and their environment (Beaver & Holtfreter, 2009). Genetic and
environmental factors work separately and in tandem to create criminal
behaviour phenotypes (Moffitt, 2005; Rutter, 2006), for example, if a child
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has both conduct disorder and hyperactivity then he is more likely to
engage in antisocial behaviours (Farrington, 1990). Antisocial conduct
itself has a moderate to strong association with genetic factors (Rhee &
Waldmen, 2002). The importance of delinquent peer association is as such
that it is not only a predictor of antisocial conduct but it is also linked
with fraudulent behaviours (Beaver & Holtfreter, 2009). Children who
suffer abuse or neglect are more likely to have Antisocial Personality
Disorder (ASPD) as adults and are more likely to be arrested in
adolescence (Wisdom, 1989).
From these examples it is clear that criminality should be
approached from a multifactorial perspective. The current essay
endeavours to discuss the determinants of criminality from an individual,
familial and societal level. Firstly, the individual‟s influence over his/her
own criminality will be discussed. Personality disorder and genetic factors
mediate an individual‟s entry into criminality. Secondly, familial influence
is an important determinant of criminality. Factors such as maternal
deprivation, parenting and attachment relationship are prominent
determinants in the literature. Finally, socioeconomic status (SES) and
peer influence are important societal determinants that contribute to the
individual‟s level of criminal involvement.
ADOLESCENT AND ADULT OFFENDING: BIOSOCIAL MODELS
According to Moffitt‟s developmental taxonomy (MDT) there are two
types of offenders; life-course persistent (LCP) and adolescent-limited
offenders (AL) (Moffitt, 1993). Delinquent involvement is quite common
amongst adolescents and it is considered to be age normative (Farrington,
1986). Most adolescents engage in delinquency and only a very small
percentage of adolescents abstain from delinquent involvement (Moffitt,
1993). Thus it could be assumed that delinquency in adolescence is not
just a form of antisocial behaviour but somewhat of a rite of passage.
Even if delinquency is a natural progression, only the minority of
delinquents persist with their misconduct throughout the lifespan whereas
the majority of delinquent adolescents „grow out of it‟ (Boutwell &
Beaver, 2008). LCP offenders account for approximately 6% of the
population but they account for a huge proportion of all crimes committed
(Moffitt et al., 2002). For example, in America LCP offenders account for
50% of all crimes committed (Eme, 2010). Misconduct in these offenders
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emerges in early childhood and it remains stable throughout the lifespan
(Moffitt et al., 2006). LCP offending has a causal relationship with two
interlocking factors; neuropsychological deficits and adverse home life. In
order for LCP offending to develop it is necessary to have
neuropsychological deficits but if an individual has neuropsychological
deficits this does not mean he must be an LCP offender (Boutwell &
Beaver, 2008). Secondly, LCP offending is causally linked with an adverse
home life. A criminogenic family and neuropsychological deficits work in
tandem with each other and are conducive for chronic antisocial conduct.
Thus the cause of LCP offending is biosocial. Biogenic risk factors (e.g.
neuropsychological deficits) coupled with environmental risk factors (e.g.
criminogenic family) creates LCP offenders (Boutwell & Beaver, 2008).
AL offenders constitute the vast majority of delinquent offenders.
They confine their criminal involvement to adolescence; they tend not to
display antisocial behaviour in childhood and they do not offend as adults
(Boutwell & Beaver, 2008). According to Moffitt (1993, 2006) the
„maturity gap‟ is the main cause of AL offending. It occurs when the
adolescent is biologically mature (i.e. physically, they resemble adults),
but they are not permitted to engage in adult behaviours. Adolescents aim
to reduce the disjuncture of the „maturity gap‟ by mimicking adult
behaviours. These behaviours include consuming alcohol, smoking, having
sex and they are expressed in order to portray social maturity. With age
comes the privileges associated with adulthood and thus the maturity gap
diminishes as does delinquent behaviour along with it (Moffitt, 2006). The
cause of AL offending is biosocial because there is an interaction between
biological (i.e. puberty onset) and social factors (i.e. restraints imposed by
society) (Boutwell & Beaver, 2008).
NEURAL AND PERSONALITY FACTORS
According to Eastman and Campbell (2006) there is a correlation between
antisocial behaviour and impairment of the prefrontal cortices (PFC).
Deception, for example, is linked with activation of the PFC and the
anterior cingulate cortices. The PFC has a pivotal role in the regulation of
behaviour. Frontal lobe damage in infancy results in impairments in
decision-making and social and emotional regulation (Anderson, Damasio,
Tranel & Damasio, 2001). PFC deficits are also greatly involved in the
development of disruptive behavioural disorders such as hyperactivity,
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executive functioning and response inhibition deficits (Schachar & Logan,
1990). Specifically, lesions to the ventromedial PFC may result in
impaired ability to adhere to social norms and attitudes (Moll et al., 2005).
The social norms and attitudes affected by PFC impairment are directly
linked to the laws that criminals tend to violate (Knabb, Welsh, Zieball &
Reimer, 2009).
Impairment in the limbic or paralimbic regions will affect moral
behaviour. For example, rage, a lack of empathy or abnormal sexual
behaviours will occur as a result of this type of impairment (Moll et al,
2005). Hence limbic dysfunction may contribute directly to antisocial
behaviour (Knabb et al., 2009).
According to Weber and colleagues (2008, p. 23) the “existing body
of evidence tentatively supports the idea that psychopathy is associated
with brain abnormalities in the prefrontal-tempero-limbic circuit”. Hesse
(2010) has stated that Antisocial Personality Disorder (ASPD) and
psychopathy are two related concepts that are used to describe the
personality problems that may result in antisocial behaviour. In support
of this statement, Coid and Ullrich (2010, p. 432) have found that
psychopathy and ASPD are not distinct clinical syndromes but rather are
both on a continuum of ASPD. Specifically, psychopathic ASPD is “a
more severe form than ASPD alone” with a greater risk of violence (Coid
& Ullrich, 2010, p. 432). In relation to brain abnormalities and ASPD,
Vollm and colleagues (2004) have stated that ASPD suggests dysfunction
of the frontal lobes. Research has found that the frontal lobe volume of
ASPD patients was 11% smaller than that of the control group (Raine et
al., 2000). Damasio and colleagues (1990) have used acquired brain injury
as evidence of the association between PFC damage and antisocial
behaviour. PFC damage is associated with higher rates of impulsivity and
poor self-control which are the characteristics of ASPD. Individuals with
Cluster B personality disorders (especially ASPD) display many different
PFC and memory dysfunctions. Of all the personality disorders Cluster B
is
particularly
associated
with
criminal
activity
(Moran,
1999). Additionally, there is a strong link between Cluster B and the risk
of violence and recidivism (Moran, 2002). ASPD has a prevalence rate of
between 2-3% in most Western countries (Coid, 2003) and at least 50% of
UK prisoners meet DSM criteria for ASPD (Singleton et al., 1998). There
is a strong relationship between ASPD and crime, including violent crime
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(Eronen, Hakola & Tiihonen, 1996). Thus there is a greater chance of
committing a felony if one has ASPD (Thompson & Bland, 1995). There is
little evidence to suggest a definite cause of ASPD but familial factors
including early adverse events (e.g. childhood abuse) are involved in the
development of personality disorders later in life (Farrington, 1993). The
possible causes of personality disorders include genetic and neurobiological
liability and structural brain abnormalities. A criticism would be that in
the DSM-IV the definition of ASPD emphasises antisocial behaviour and
thus there is an overlap between ASPD and criminality, while according
to Robins (1998) the most common symptoms of ASPD include violence
and marital problems but not criminality.
SOCIOECONOMIC FACTORS
There is little doubt that individuals from socio-economically deprived
backgrounds exhibit a greater propensity towards criminal involvement
(Rutter, Giller & Hagell, 1998). According to Ferguson, Swain-Campbell
and Horwood (2004) socioeconomic deprivation has a strong association
with later criminal involvement. For example, they suggested that
socioeconomic deprivation experienced as a child is related to higher rates
of crime later in life. Also individuals with a low socioeconomic status
(SES) are three times more likely to engage in criminal activity than those
with a high SES (Ferguson et al., 2004). There are several theories relating
the causes of crime to SES. Merton‟s (1938) strain theory aims to explain
the relationship between social structures and deviance. Strain theory
states that there is a dichotomy between societal expectations of desirable
achievements and the possibility to actually achieve these within the
society. The link between criminality and socioeconomic disadvantage is
caused by these „strains‟ or imbalances which result in predisposed
individuals engaging in antisocial behaviour in order to balance these
stains. Hence the experience of low SES encourages criminal involvement
(Kelly, 2000). According to the differential association theory of crime the
higher rates of crime amongst individuals from socioeconomically
deprived backgrounds are due to greater exposure to antisocial peers and
environment (Ferguson et al., 2004). Ferguson and colleagues (2004)
suggest that the differential association theory contrasts with strain
theory via an emphasis on peer influence and motivation towards
criminality. On the other hand, the social learning perspective theory
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claims that early exposure to maladaptive parenting and a lack of
supervision encourage the development of crime (Rutter et al., 1998).
Furthermore, Rutter and colleagues posit that differences in crime rates
across differing social strata are directly linked with differing child rearing
practices for each of the social stratum. Finally the social control theory
states that the inclination towards deviance is a characteristic of all
individuals but social bonds mediate these impulses (Gottfredson &
Hirschi, 1990). These social bonds may include attachments to family and
school however, deterioration of these bonds occurs as a result of
socioeconomic disadvantage, thus leading to criminal activity (Kelly,
2000). Ultimately, individuals from low socioeconomic environments are
at an increased risk of later criminal participation because of the
accumulative effects of individual, familial and peer factors (Ferguson et
al., 2004). Other intervening factors between socioeconomic deprivation
and crime include marital conflict, parental hostility and poor parenting
(Conger, Patterson & Ge, 1995).
FAMILIAL FACTORS
Family influences are the greatest contributors to criminal involvement
but conversely also have the greatest propensity to moderate criminal
behaviours (Ferguson et al., 2004). Externalising problem behaviour is
related to poor parenting (Shaw et al., 1998). Farrington (1990) found that
there was a high risk of hyperactivity and conduct disorder as a result of
parenting risk factors discussed below. Morrell and Murray (2003)
postulated that conduct disorder requires environmental risk factors for
the expression of the genetic factors that are associated with conduct
disorder. Patterson‟s coercive family process model states that cycles of
negative reinforcement are a risk factor for criminality. For example, this
occurs when a child does not comply with the parent‟s demands but is still
rewarded by the parent giving in to them (Morrell & Murray, 2003). Poor
quality parenting is a better predictor of poor attention at three to four
years and hyperactivity at five years than biological or temperamental
factors (Carlson, Jacobvitz & Scroufe, 1995). However, a positive
relationship between parent and child is an effective method of prevention
of conduct disorder (Pettit, Bates & Dodge, 1997). Maternal depression is
another significant risk factor in whether the individual develops a
disruptive behavioural disorder. Research has found that five years after
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postnatal depression was experienced there was a higher risk of
behavioural problems in children of postnatally depressed mothers
(Murray et al., 1999). Poor quality of attachment relationships is also
another risk factor for criminality in later life. According to Lyons-Ruth
(1989) the attachment relationship at 18 months is a predictor for an
individual‟s later functioning. Externalizing problem behaviour is
associated with low quality of attachment. Golder, Gillmore, Spieker and
Morrison (2005) suggested that poor attachment security may foster poor
psychosocial development and behavioural problems. Conversely, Stein,
Milburn, Zane and Rotheram-Borus (2009) stated that high quality
attachment, particularly to fathers, was protective against delinquent
behaviour. In relation to the mother, “Primary attachment relationships
provide a protective foundation for the child (and later adult) to explore
his or her environment and to meet developmental changes” (Stein et al.,
2009, p. 40). Stein and colleagues (2009) also found that homeless youths
who engaged in antisocial behaviours lacked a „secure base‟ in the form of
an attachment figure and therefore these problem behaviours developed as
a consequence. In contrast, Robins (1998) criticised poor parenting as a
determinant of criminality because a child‟s own behaviour is a better
predictor of adult antisocial behaviour than rearing, family background or
SES.
PEER FACTORS
Finally, criminal behaviour is correlated with having criminal friends.
Having criminal friends is positively linked with antisocial conduct and
drug-taking (Warr, 2002). There are two opposing theories regarding peer
influence over criminality. The Social Causation Perspective states that
delinquent peers imprint delinquent values onto their friends because their
behaviours‟ and values are mimicked and adopted by the other members
of the social network (Akers, 1998). However, Control Theories state that
delinquents produce traits that may instruct them to join a delinquent
peer network (Gottfredson & Hirschi, 1990). Individuals self-select peers
with similar traits and interests. According to Walsh (2002, p. 173) “We
all seek environments that are compatible with our genetic dispositions”
Interestingly, Beaver et al. (2008) posit that choosing to associate with a
delinquent peer network is influenced by an individual‟s genotype. Hence
the genotype chooses the environment that allows for optimum gene
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expression (Scarr, 1992). The phenomenon gene x environment correlation
(rGE) posits that genotype and environment are inextricably intertwined.
Thus genes that influence particular characteristics also influence the
environment in order to achieve optimal expression (Beaver et al., 2008).
For example, male adolescents with the 10R allele for DAT1 are
significantly more inclined to be associated with delinquent peers than
adolescent males without the allele. In families in high and low risk
backgrounds the 10R allele increases the likelihood that male adolescents
will associate with delinquent peers. However, low risk parents may be
able to control for the effect of the gene via parenting strategies (Beaver et
al., 2008).
CONCLUSIONS
The issue surrounding the determination of criminality is essentially a
nature-nurture debate. Separately, neither genetic nor environmental
factors are sufficient in explaining the determination of criminality and
thus a heuristic approach must be considered. According to Beaver and
Holtfreter (2009) it is the interplay between environmental and genetic
factors which determines expression of an antisocial behavioural
phenotype. In essence, the independent influence of one or the other tends
not to yield a strong causal effect however their combined influence has a
stronger causal link for individual criminal involvement. Specifically, in
the case of LCP offenders a causal relationship exists between
neuropsychological deficits and adverse home life. It is necessary that
these individuals possess neuropsychological deficits and combined with a
criminogenic family, results in chronic antisocial behaviour (Boutwell &
Beaver, 2008). In relation to ASPD, causal factors include familial
influences (Farrington, 1993) and dysfunction of the frontal lobes (Vollm
et al., 2004). These factors work in tandem and are conducive for the
expression of the antisocial phenotype. Similarly, conduct disorders
require environmental risk factors for the expression of the genetic factors
that are associated with the disorder (Morrell & Murray, 2003).
Presently, it is suggested that a positive parent-child relationship is
the most effective preventative measure against conduct disorder (Pettit,
Bates & Dodge, 1997) as high quality attachment relationships have been
found to be protective against delinquent behaviour (Stein et al., 2009).
Beaver and colleagues (2008) found that in families in high and low risk
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backgrounds that although the 10R allele increased the likelihood that
male adolescents associated with antisocial peers, low risk parents may be
able to control for the effect of the gene through appropriate parenting
strategies. Further research is required to understand how to prevent
conduct disorder in those at high risk.
In sum, each determining factor – such as familial, peer and genetic
influences – when assessed independently is insufficient in explaining the
determination of criminality. Analyses of the interactions between genetic
and environmental factors are therefore necessary for understanding who
is at risk for criminal behaviour and how such behaviour arises, and also
for developing and implementing preventative strategies.
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