Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 21

NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING THEORY

It’s Nature and Nurture:


Integrating Biology and Genetics into the Social Learning Theory of Criminal Behavior

Bryanna Fox, Ph.D.


University of South Florida
Department of Criminology
Department of Mental Health, Law & Policy
College of Behavioral and Community Sciences
4202 E. Fowler Avenue, SOC 107
Tampa, FL 33620

Bryanna Fox is an assistant professor in the Department of Criminology and courtesy professor
in the Department of Mental Health, Law, and Policy at the University of South Florida. She is a
former research fellow in the FBI’s Behavioral Science Unit, and the recipient of the 2013
Excellence in Law Enforcement Research Award from the International Association of Chiefs of
Police for her experimental research on statistical behavioral analysis. Her research interests
involve the identification of psychological and developmental risk factors for criminal behavior,
developing evidence-based policing tools, and conducting experimental field research.

Abstract:
Purpose: Major advances in the fields of biology, genetics, neuroscience, and psychiatry
have shown that many human behaviors are impacted by factors other than social influences.
Still, the field of criminology has not incorporated these biological influences into any
mainstream criminological theories, leaving a large divide between theories holding entirely
sociological and entirely biological explanations of criminal behavior.
Method: Two exceptions to this strict “nature versus nurture” dichotomy are social
learning theory, which posits that criminal behavior is learned through peer association, and the
biosocial perspective in criminology, which uses various biological and social factors to explain
the commission of criminal behavior. Given the growing evidence that both biology and
environmental factors contribute to the commission of criminal behavior, it is increasingly
difficult for any theory to ignore the influence of either biology or sociology altogether.
Conclusion: This article illustrates how to incorporate both nature and nurture into a
single theory, by integrating social learning theory and the biosocial perspective into a more
accurate and modern model of criminal behavior.

Key Words: biosocial • social learning • genetics • environment • integrated theory

Published in: Journal of Criminal Justice

Citation:
Fox, B.H. (2017). It’s nature and nurture: Integrating biology and genetics into the Social
Learning Theory of criminal behavior. Journal of Criminal Justice, 49, 22-31.
http://www.sciencedirect.com/science/article/pii/S004723521630143X
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

IT’S NATURE AND NURTURE: INTEGRATING BIOLOGICAL FACTORS INTO


THE SOCIAL LEARNING THEORY OF CRIMINAL BEHAVIOR

INTRODUCTION

Is criminal behavior a product of human nature, or nurture? This has been the enduring
question among many criminologists, and a debate that continues to perplex many theorists and
researchers today. While a variety of notable theories have emerged in criminology, there are
few exceptions to this strict “nature versus nurture” theoretical dichotomy. As the evidence
linking both social and biological risk factors to criminal behavior constantly grows, it is
becoming more difficult for any theory to ignore the influence of either biology or sociology
entirely.
Despite the considerable success biosocial models have shown in predicting criminal
behavior, these findings have not yet been integrated into any “mainstream” theories in
criminology (Barnes, Boutwell, Beaver, Gibson, & Wright, 2014; Barnes, Boutwell, & Beaver,
2016). Rather than positing that one’s biology is a direct determinant of criminal behavior,
biosocial criminology suggests that biology is more of a susceptibility that may be enhanced or
negated depending on different environmental factors (Belsky & Pluess, 2009; DiLalla &
Bersted, 2015; Ishikawa & Raine, 2002; Vaughn, DeLisi, Beaver & Wright, 2009). Moreover, as
biosocial research indicates that our explained variance increases when biological influences are
coupled with environmental factors, and no mainstream criminological theory has yet to explain
100% of the variance in criminal behavior, it stands to reason that by adding biological concepts
into social-based mainstream criminological theories an increase in explanatory power and our
understanding of criminal behavior will occur (Barnes et al., 2014; Schwartz & Beaver, 2014;
Walsh, 2002; Wright & Beaver, 2005; Wright & Boisvert, 2009). It is therefore of great benefit
to our field that a direct integration of biological factors into mainstream criminological theories
takes place.
This article aims to guide such an integration by reviewing the research supporting
biological risk factors for criminality, and proposing the framework for a propositional
integration of biological and genetic features into a mainstream sociological-based model of
criminal behavior.

THE “NATURE” OF CRIME: A BIOSOCIAL PERSPECTIVE


In 1964, Hans Eysenck became one of the first social scientists to subscribe to the idea of
a nonsocial influence on criminal behavior (Rafter, Posick, & Rocque, 2016). Through his bold
research on genetic and neurobiological influences on criminality using twin data, Eysenck
(1964) found a higher concordance in criminal behavior among identical (77%) versus fraternal
(12%) twins. This, and results from follow-up research led Eysenck to conclude that “beyond
any question, heredity plays an important, any possibly vital part, in predisposing a given
individual to crime” (p. 68-69). While these early studies had difficulty measuring genetic
influence, they were the first to identify correlations between inherited genetics and criminal
behavior.
Following this lead, significant research has since been conducted on the interactive
effects of various genetic and biological factors and an individual’s environment on the
development of antisocial and criminal behavior. This cutting-edge research has found support
for the influence of factors ranging from an individual’s genetic make-up, psychophysiology,
autonomic activity, hormones, neurotransmitters, and environmental toxins, to name a few,
making the list of biological factors now known to affect an individual’s behavior is lengthy, and
significant (Raine, 2002). Now called the biosocial perspective of criminal and antisocial
behavior, this perspective relies on two main principles, biological influence and social
environment, as the major processes which individually and interactively prompt or protect a
person from criminality (Beaver, 2008; Rafter et al., 2016, Walsh, 2002a; Walsh & Beaver,
2009).
The Biosocial Perspective in Criminology
Biosocial research examining the relationship between biological factors, sociological
factors, and criminal behavior has grown exponentially over the past decade (Burt & Simons,
2014; Moffitt, Ross, & Raine, 2011), and is the fastest growing line of research in criminology
(Beaver, Nedelec, Costa, & Vidal, 2015). While the number of significant findings stemming

2
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

from biosocial research are far too numerous to discuss in a single review (see Barnes, Boutwell,
& Beaver, 2016; Beaver, Barnes, & Boutwell, 2015; Raine, 2013; Walsh & Beaver, 2009, for
excellent summaries), the following is a brief overview of key findings stemming from the
biosocial perspective in order to highlight the robust and sizable impact of this line of research.
As stated, there are numerous biological factors found to play a role in producing
criminal behavior, such as genetics, hormones and neurotransmitters, neurological deficits,
psychophysiology, and environmental toxins. Of these, the area receiving the greatest amount of
interest among biosocial criminologists is behavioral genetics (Beaver, Boutwell, Barnes &
Cooper, 2009a). Research on behavioral genetics examines the impact of three components,
heritability, shared environment, and nonshared environment, on a given phenotype (i.e.,
criminality) (Wright et al., 2015). Heritability refers to the proportion of variance in a phenotype
for a population that can be attributed to genetic factors.1 The remaining variance is due in part to
the shared environment (i.e. the setting shared by siblings in the same household, such as family
socioeconomic status), and in part to the nonshared environment (i.e. the setting not shared by
siblings, such as peer group) (Beaver et al., 2009a).
Behavioral geneticists aim to uncover the exact proportion these three factors play in
developing our behavior. In general, results of behavioral genetic research indicates that up to
60% of variation in antisocial and criminal behavior is heritable, while shared environmental
factors and nonshared environmental factors explain up to 10% and 50% of variance in criminal
and antisocial behavior, respectively (see meta-analyses by Ferguson, 2010; Mason & Frick,
1994; Miles & Carey, 1997; Rhee & Waldman, 2002; see also Harris, 1998; Moffitt, 2005;
Plomin, Owen, & McGuffin, 1994; Rowe, 1994).
More recent research has aimed to hone in not just on heritability, but the specific
“candidate” genes that contribute to causes of behavior (referred to as molecular genetics) and
the genes that interact with specific social and environmental factors to produce criminal
behavior (referred to as epigenetics) (Walsh & Beaver, 2009). In their landmark study on the
interaction between genetic polymorphism monoamine oxidase A (MAOA) and childhood abuse
on future violent behavior, Caspi and colleagues (2002) found that abuse increased the risk of
future violent behavior, but only for the youth with low levels of MAOA. In fact, while only
12% of the sample had both genetic (low MAOA) and environmental (history of abuse) risk
factors, they were responsible for 44% of all the violent crime committed by the cohort.
Furthermore, 85% of the youth with genetic and environmental risk factors developed some form
of antisocial or criminal behavior (Caspi et al., 2002; see also Kim-Cohen et al., 2006).
Additional research using genetically informed twin data from the National Longitudinal
Study of Adolescent Health (Add Health) (Udry, 2003) suggests that dopamine receptor genes
(DRD2, DRD4), dopamine transport gene (DAT1), serotonin transporter gene (5HTT) and
MAOA all interact with social conditions such as delinquent peers, maternal attachment, parental
criminality, family engagement, marital status, religiosity, and even neighborhood characteristics
to predict criminality, violence, gang membership, desistence, abstention, and victimization
among adult and adolescent males (Barnes & Jacobs, 2013; Beaver & Holtfreter, 2009; Beaver &
Wright, 2005; Beaver, et al., 2007; Beaver, Wright, DeLisi, & Vaughn, 2008b; Beaver et al.,
2009a; Beaver, Gibson, Jennings, & Ward, 2009c; Boutwell & Beaver, 2008; DeLisi, Beaver,
Wright, & Vaughn, 2008; DeLisi, Beaver, Vaughn & Wright, 2009; Guo, Roettger, & Shih,
2007; Guo, Roettger, & Cai, 2008; Vaughn et al., 2009).
In short, while genes certainly do not cause any behavior, they do produce the traits and
tendencies which lead individuals to respond to their environment in one way and not another
(Walsh & Beaver, 2009). For instance, a person in the United States with a genotype for darker
skin tone will often experience a different social environment than a person with lighter skin, and
may therefore display different behaviors due to this combination of biological and social
influences (Burt & Simons, 2014). As research on the role that genes and biology play in the
production of human behavior continues to unfold, it is increasingly clear that criminal behavior
results from a combination of factors, both biological and environmental. As Burt and Simons
(2014) noted, “any claim to the contrary is patently false” (p. 225).
Other biosocial research has investigated the direct and indirect effects of hormones and
neurotransmitters, including testosterone (Banks & Dabbs, 1996; Dabbs & Morris, 1990; Pratt,
Turanovic, & Cullen, 2016; van Honk & Schutter, 2007), cortisol (Cima, Smeets, & Jelicic,
2008; Loney, Butler, Lima, Counts, & Eckel, 2006; Holi, Auvinen-Lintunen, Lindberg, Tani, &
Virkkunen, 2006) and serotonin (Berman & Coccaro, 1998; Moffitt et al., 1997; Moore, Scarpa,
& Raine, 2002; Sadeh et al., 2010), on criminal and antisocial behavior. This line of research
suggests that hormones such as testosterone can help explain important criminological issues
1
A heritability coefficient (h2) of .25 would indicate that 25% of the variance in the phenotype is due to genetic
factors (Beaver et al., 2009a).

3
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

such as the gap in offending rates between males and females, (males typically have higher
testosterone levels than females) (Ellis, 2003), and that these hormones and neurotransmitters
and the environmental factors they interact with can actually be treated to reduce the risk of
antisocial behavior (Brotman et al., 2007; O’Neal et al., 2010).
Advances in brain imaging research have also been extremely helpful in understanding
the role that structural and functional deficiencies in the prefrontal cortex, amygdala, and
hippocampus of the brain play in influencing criminal and antisocial behavior (Raine, 2013). For
instance, psychopaths with criminal convictions have more impaired amygdala-orbitofrontal
connections than control group members (Craig et al., 2009), while murderers and violent
offenders have higher deficits in their prefrontal, orbitofrontal, and superior frontal cortex
compared to normal controls (Raine et al., 1994; Raine et al., 2001). Environmental interactions
with neurological deficiencies have also been uncovered. For instance, Raine and colleagues
(2001) found that murderers from “good” homes had a 14% reduction in prefrontal cortex
functioning compared to non-offenders, while murderers from “bad” homes actually had
relatively higher levels of prefrontal cortex functioning than non-offenders.
Psychophysiological factors such as resting heart rate, skin conductance, and autonomic
arousal have also been found to factor into future criminal behavior (Raine, 2013). Specifically,
adult offenders have lower resting heart rates, lower skin conductance, and lower autonomic
arousal compared to non-offenders (Farrington, 1997; Raine, Venables, & Williams, 1995;
Raine, Venables, & Williams, 1996; Raine, Mellingen, Liu, Venables, & Mednick, 2003). Of
these measures, low resting heart rate is considered one of the strongest biological predictors of
antisocial behavior. Notably, a meta-analysis of 45 studies containing a total of 5,868 children
found an average effect size of d= -.44 for the relationship between resting heart rate and
antisocial behavior, leading researchers to state that “low resting heart rate appears to be the best-
replicated biological correlate to date of antisocial and aggressive behavior” (Ortiz & Raine,
2004, p. 154; see also Lorber, 2004; Portnoy et al., 2014).
Finally, several chemicals and toxins have been shown to directly and indirectly impact
antisocial and criminal behavior. For instance, lead absorption has been linked to higher levels of
psychopathy (Wright, Boisvert, & Vaske, 2009), adolescent delinquency (Bellinger, Leviton,
Alfred, & Rabinowitz, 1994; Needleman, Riess, Tobin, Biesecker, & Greenhouse, 1996;
Needleman, McFarland, Ness, Fienberg, & Tobin, 2002) and violent crime (Stretesky & Lynch,
2001; Wright, Dietrich, Ris, Hornung, & Wessel, 2008). In fact, even when controlling for
relevant covariates, for every 5µg/dl increase in lead exposure, the probability of being arrested
for a violent crime increases about 50% (Wright et al., 2008). Other common toxic substances
children are exposed to are cigarette byproducts and alcohol in utero (Walsh, Taylor & Yun,
2015). Smoking during pregnancy has been linked to aggressive and criminal behavior (Gibson,
Piquero & Tibbetts, 2000; Gibson & Tibbetts, 2000), and a meta-analysis indicates that youth
exposed to maternal cigarette smoking are 150% to 400% more likely to develop antisocial
behavior compared to youth not exposed to cigarette smoke in utero (Wakschlag, Pickett, Cook,
Benowitz, & Levanthal, 2002; Pratt, McGlion, & Fearn, 2006). A similar review of the effects of
prenatal exposure to alcohol found links to low IQ, impulsivity, hyperactivity, and poor social,
emotional, and moral development, which in turn have also been linked to criminal behavior
(May & Gossage, 2008; see also Walsh & Bolen, 2012).
While it is clear that no gene, hormone, toxin, or other biological factor may be held
singly responsible for conduct as complex as criminality, biosocial research consistently
indicates that criminal behavior is largely the result of an interaction between both biological and
social factors (Barnes et al., 2014; Burt & Simons, 2014; Burt & Simons, 2015; Raine, 2002;
Nedelec, 2015; Walsh & Beaver, 2015). Consequently, neither biology, nor environment, alone
accurately explains criminal behavior. In fact, a comprehensive review of biosocial research
analyzed results of 39 studies ranging from areas including genetics, obstetrics, neurology,
hormones, brain imaging, environmental toxins, neuropsychology, neurotransmitters, and
psychophysiology, and found that these factors are equally as important to the development of
criminal activity as sociological and environmental factors (Raine, 2002). While the biosocial
perspective obviously considers biological influences on behavior, environmental factors are
given significant weight by biosocial criminologists. After all, “even the strongest biological
influences still need an environment in which to be expressed” (Raine, 2002, p. 32).
Opportunities for Integration
Unlike previous biological theories in the field of criminology,2 the biosocial perspective
relies heavily on social context as an influence on an individual’s criminal behavior (Rafter et al.,
2016). Specifically, social context serves as triggers or protective factors for any biological
2
Today’s biosocial perspective is in stark contrast to Lombroso’s original biological theory of crime outlined in his
book, The Criminal Man (Lombroso, 1876).

4
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

tendencies an individual may possess (Beaver, DeLisi, Wright, & Vaughn, 2009b). These social
factors generally include measures used in many socially-based theories of criminology,
including peer influence, family structure, socio-economic status, parental attachment, education
level, religiosity, marital status, and neighborhood location. As social learning theory includes
many of these social influences, it allows for the exact measures prescribed by biosocial theory
to be used as the social context factors in the proposed theory integration. Thus, it is through this
inclusion of social context in the biosocial principles that the theory becomes open to social
learning theory integration.
NURTURED BEHAVIOR: SOCIAL LEARNING THEORY OF CRIME
First developed in 1966 by Burgess and Akers, social learning theory (SLT) proposes that
both deviant and conforming behavior are developed through an individual’s learning processes,
with the determinant being the direction and influences on the individual’s behavior. SLT is
already an integrated theory, as Burgess and Akers combined Edwin Sutherland’s (1939)
differential association theory with psychological elements such operant conditioning and
observational learning (Bandura, 1976) to provide a more complete explanation of how social
forces shape an individual’s criminal and deviant behavior.
Social Learning Principles and Support
The first tenet of SLT, differential association, is the interaction and association with
others who engage in, or who express norms, values, and attitudes supportive of certain kinds of
behavior (Sutherland, 1939). SLT hypothesizes that the more association or interaction an
individual has with others engaged in criminal behavior, the greater the probability that person
will engage in criminal behavior as well (Akers, 1998). In fact, the association between criminal
peers and future criminal behavior is among the most replicated and recurrent findings in all of
criminology (Akers, Krohn, Lanza-Kaduce, & Radosevich, 1979; Akers, 1998; Beaver et al.,
2009b; Pratt et al., 2010).
SLT’s second concept, definitions, refers to the attitudes and meanings an individual
attaches to a given behavior (Burgess & Akers, 1966). Learned through socialization and societal
interaction, these definitions are what cause a person to qualify certain acts as right or wrong,
good or bad, moral or immoral. While most of our society’s values and norms provide
definitions favorable to conforming behavior, an individual may still associate with others that
provide, or approve of definitions which support criminal and deviant behavior (Akers & Sellers,
2008). Still, these non-conforming definitions are not a blanket for all an individual’s attitudes
and beliefs. For instance, a person may hold definitions that it is morally wrong to steal or kill
and thus respect the laws against these actions, yet have no issue with illegal drug use and
therefore violate the laws against such behavior.
The third principle, differential reinforcement, refers to the balance of actual or
anticipated rewards and punishments for committing, or not committing, a certain behavior
(Burgess & Akers, 1966). SLT posits that the probability an individual will refrain from, or
commit a crime depends upon the balance of past, present, and anticipated future rewards and
punishments for their actions. While these reinforcers are often socially imposed physical
rewards and punishments as described in operant conditioning, SLT also acknowledges the role
of symbolic reinforcement, self-reinforcement, and other intangible reinforcement as motivating
criminal and deviant behavior (Akers, 1998).
The final concept of SLT, imitation, describes an individual’s engagement in behavior
after the observation of similar behavior in admired others (Burgess & Akers, 1966). Also
commonly referred to as “modeling” or “observational learning”, the likelihood of a person
imitating others’ behavior is affected by the characteristics of the models, the behavior observed,
and the observed consequences of the behavior (Bandura, 1976). SLT posits that if an individual
observes a desired outcome resulting from an admired person’s criminal behavior, the individual
is more likely to model, imitate, and adopt the criminal behavior themselves. While this concept
is generally more important to the initial acquisition of behavior than to the maintenance of it, it
is possible for imitation to affect the desistence of learned behavior as well (Akers & Sellers,
2008). Although imitation may sometimes be difficult to accurately tap in the research, it is still
considered one of the most influential concepts in the SLT model (Akers & Sellers, 2008).
By assessing the magnitude and direction of these four core concepts, this theory has
consistently found moderate to strong relationships between the SLT variables and an
individual’s criminal and delinquent behavior, in the theoretically expected direction (Akers &
Jensen, 2006; Akers & Sellers, 2008; Pratt et al., 2010).
A meta-analysis by Pratt and colleagues (2010) was conducted on 133 studies statistically
evaluating SLT found a moderate mean effect size for the theory in general (similar to mean
effect results for self-control theory, but greater than those for rational choice/deterrence theory).
Moderate to strong mean effect sizes for the four elements of SLT, with differential association

5
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

and definitions showing the strongest effects, and differential reinforcement and modeling
showing lesser effects (Pratt et al., 2010).3 Additionally, when testing the learning variables in a
myriad of populations and settings, the model produced considerable levels of explained
variance in criminal and deviant behavior (see Akers, 1998; Akers & Jensen, 2006; Akers &
Sellers, 2008). Specifically, the SLT model has explained between 31% and 68% of variance in
adolescent alcohol and drug use and abuse, 21% of coerced rape by college males, and 65% of
variance in homicide rates across the globe (Akers & Jensen, 2007; Akers & Sellers, 2008).
Opportunities for Integration
While consistent empirical support for a model is rare, particularly in the field of
criminology, there are several critiques of SLT that must be noted. The first is that SLT does not
take into account the individual differences that may affect the way in which behavior is learned
or expressed by different people (Akers, 1998). These differences may be biological,
psychological, or genetic in nature, and can even directly result in impulses and tendencies that
may cause individual’s criminal behavior in the absence of protective social influence. As a
growing body of biosocial research has aimed to examine how people actively select their own
environments and social contexts based upon their genetic propensities (Christakis & Fowler,
2014; Scarr & McCartney, 1983), genetics may help explain both the individual propensity for
antisocial behavior and the antisocial behavior of the peer group the individual associates with
(Connolly, Schwartz, Nedelec, Beaver, & Barnes, 2015; Kendler, Jacobson, Myers, & Eaves,
2008; TenEyck & Barnes, 2015; Vitaro et al., 2016). So while behavior is learned, biology and
genetics underlie how learning occurs and why certain people learn differently than others.
Therefore, to understand why certain individuals select into delinquent peer groups more than
others, and why the impact of delinquent peers amplifies the behavior of certain individuals more
than others, we need to account for genetic makeup (Beaver et al., 2009d; Connolly et al., 2015;
Lacourse et al., 2006; TenEyck & Barnes, 2015; Vitaro et al., 2016).
As SLT does not specifically bar the inclusion of such “differential predispositions” to
learning,4 the door to a biosocial integration with social learning theory remains open. The
propositional integration of biosocial and social learning models would account for many of
these differences across individuals, and resolve this criticism against SLT.
The second critique is in regard to the temporal sequence and tautology of the learning
variables, particularly in reference to differential association with delinquent peers (Akers &
Sellers, 2008). As SLT aims to explain an individual’s criminal behavior through learning and
social influence processes, there must be an explanation for why some people exhibit criminal
tendencies despite their lack of theoretically expected associations, rewards, or reinforcements.
This criticism has been very well heeded by those in the biosocial camp, as such a non-socialized
“spark” for criminal behavior can be explained by the individual’s genetic or biological factors.5
As SLT does not prohibit such predispositional factors as the impetus behind the sensations that
make criminal behavior more rewarding for an individual than it would typically be, the
explanatory benefits from such theoretical integration are substantial.
Although data to test all aspects of this proposed integrated theory are not currently
available in a single dataset, it is hoped that by proposing this theoretical framework based upon
results of research from a variety of data and fields, future researchers may be able to collect the
data to test the integrated theory proposed as follows.
NATURE AND NURTURE- INTEGRATING BIOLOGY INTO SOCIAL LEARNING
While learning clearly has social origins among peers and conditioning in society, it is
also a biochemical process which involves perception, encoding, and reinforcement (Wright &
Boisvert, 2009). In fact, several prominent biosocial researchers have suggested the biological
roots of learning make it an ideal construct for biosocial research (Connolly et al., 2015; Kendler
et al., 2008; TenEyck & Barnes, 2015; Wright & Boisvert, 2009). For instance, while SLT
suggests that antisocial behavior is often learned, in order to learn one must first observe
behavior from peers or models, or feel rewards for existent antisocial behavior. This begs the
question: why are some individuals more likely to associate or model antisocial peers, or feel
reinforcement and rewards for their antisocial behavior?
It is from this question that the need for theoretical integration, and abolition of the strict
nature versus nurture paradox, arises. While there have been other attempts to meld biological
and sociological variables before in the field of criminology (e.g., Harris, 1998; Moffitt &

3
Pratt et al.’s (2010) meta-analysis indicated that the mean effect sizes (Mz) for the four elements of SLT are as
follows: differential association = .225, definitions = .218, differential reinforcement = .097, modeling = .103.
4
Concept illuminated through personal communication with Dr. Akers (2009).
5
This has been supported by social learning proponents via the creation of a nonsocial reinforcement arm of social
learning. Results show the neurophysiological and psychological high of committing certain crimes can be
“intrinsically rewarding, and reinforce such behavior among criminals” (Wood, Gove, Wilson, & Cochran, 2006).

6
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Walsh, 2003; Wikström, 2004), none have united biological factors into the SLT model
specifically. As biology often precedes the act of learning, a propositional integration of
biosocial factors and the tenets of SLT is suggested as follows.
Peer Association
Significant research has been done on the effect of peer association in relation to an
individual’s criminal and delinquent behavior. While SLT traditionally examines an individual’s
delinquent peer association by assessing socially influenced propensities and preferences,
biosocial researchers simply reduce the unit of analysis from the individual level down to the
biological or genetic level (Cleveland, Wiebe, & Rowe, 2005). As personality, propensities, and
preferences are highly heritable (Bouchard, Lykken, McGue, Segal, & Tellegen, 1990;
Turkheimer, 2000), and individuals tend to select environments that suit his or her personality,
propensities and preferences, then biological factors clearly influence an individual’s social
environment (TenEyck & Barnes, 2015; Vitaro et al., 2016). In other words, an individual’s
genotype will influence the way in which they select, modify, and create their own environment,
including peer group formation (Beaver et al., 2009d; Boisvert, Boutwell, Vaske, & Newsome,
2013; Christakis & Fowler, 2014; Connolly et al., 2015; DiLalla, 2002; Kendler et al., 2008;
Harden, Hill, Turkheimer, & Emery, 2008; Lacourse et al., 2006; TenEyck & Barnes, 2015;
Vaske, 2015; Vitaro et al., 2016; Yun, Cheong, & Walsh, 2011), and ultimately, criminal
behavior (Beaver, Wright, & DeLisi, 2008a; Burt, 2009a; Burt, 2009b; Rhee & Waldman, 2002;
Vaughn et al., 2009).
Specifically, biosocial research has indicated that people actively seek out environments
compatible with their genetic predispositions, resulting in social environments that are partially a
construction and a reflection of each person’s genotype (Beaver & Wright, 2007; Beaver et al.,
2008b; Beaver et al., 2009b; Caspi & Moffitt, 1995; DiLalla, 2002; Moffitt, 2005; Rutter, 2006;
TenEyck & Barnes, 2015; Vaske, 2015; Walsh, 2002a; Walsh, 2002b). It is therefore not random
or accidental which peers an adolescent will choose to associate with. Due to some underlying
genetic or biological influence, individuals actively seek out certain friends and peer groups that
reinforce their particular propensities. Just as athletes are drawn to sports teams, singers join the
choir, and intellectuals enroll in graduate school, delinquents seek out other delinquents to
befriend (Beaver et al., 2009b).
Nevertheless, even these choices about whom an individual wants to associate with are
still partially hemmed in by the social context of family, neighborhood, school, location, and
other factors. For instance, if youth with delinquent propensities is in a neighborhood or school
with few other delinquent prone youth with whom to associate, he may wind up with peer
associations leaning in the conforming direction, and the predisposition to be attracted to other
delinquent youth would have little or no effect.
These caveats aside, numerous studies support the claim of genetic factors influencing
peer associations through the peer group selection process, also known as the active gene
environment (rGE) correlation. In a study by the Colorado Adoption Project, nearly 65% of the
variance in peer delinquency was accounted for by genetic influences (Wadsworth, DeFries,
Fulker, & Plomin, 1995). An analysis of sibling pairs from the Add Health data also showed that
64% of the variance in delinquent peer affiliation was accounted for by genetic factors, while the
remaining 36% was attributable to the nonshared environment (Cleveland et al., 2005). In a
study from the Virginia Twin Registry, inherited genetic factors account for between 30% and
50% of the variance in peer-group deviance (Kendler et al., 2007). To further illustrate the effect
of heritability on peer group selection, longitudinal studies have found that kindergarten boys
who are fearless, hyperactive, and display few prosocial behaviors are at substantially greater
risk of associating with delinquent others in middle to late adolescence than the boys who did not
possess those genetically influenced characteristics (Lacourse et al., 2006; see also Cleveland et
al., 2005; Espelage, Holt, & Henkel, 2003; Iervolino, Pike, Manke, Reiss, Hetherington, &
Plomin, 2002; Pike, McGuire, Hetherington, Reiss, & Plomin, 1996). Finally, in a recent study
examining the impact of peer delinquency on self-reported delinquency after accounting for the
active rGE (i.e. genetic influence on peer group selection), TenEyck and Barnes (2015) found
that without accounting for an individual’s underlying genetic influences, peer association had a
significant influence on self-reported delinquency. However, once the individual’s underlying
genetic influences on the selection of one’s peers was accounted for, the direct influence of peer
groups on delinquency was no longer significant (TenEyck & Barnes, 2015).
In short, these results indicate that there is a considerable genetic contribution to the
personality traits and underlying propensities which later result in the selection of an individual’s
peer groups and peer associations that then lead to criminal and delinquent behavior. The rGE
concept is compatible with both the biosocial and social learning tenets, particularly when the
concept is integrated into SLT “back-to-back”, or propositionally.

7
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

To illustrate this propositional integration, a diagram of the theoretical pathway to


criminal and delinquent behavior via genetic influence on peer group selection is featured below.
<INSERT FIGURE 1 ABOUT HERE>
Definitions
Social learning’s concept of definitions refers to the attitudes or “stigma” attached to a
given behavior. Through personal and societal interaction, an individual develops a set of learned
associations and norms that result in their qualifying a certain act as right or wrong, good or bad,
moral or immoral. As the majority of our society subscribe to the “conventional” values and
definitions of what constitutes correct and incorrect behavior, it is not surprising that the majority
of society tends not to commit criminal or deviant acts. However, there are those who do
develop unconventional definitions, resulting in unconventional, deviant, behavior. As the
majority of this deviant behavior is criminalized by society by being made illegal, this difference
in definitions often results in what is then categorized as criminal behavior.
While SLT posits that these definitions are developed through a learning process which
one responds to those in their surroundings, the theory does not prohibit the attribution of
definitions to come from within an individual as well. Therefore, if there is something inherent
to a person’s make-up that would result in their defining a situation differently than others in
society typically would, it is possible that such underlying disposition may influence what
attitudes an individual attaches to nonconforming, criminal behavior.
Relying on literature in support of sensation-seeking theory, it has been found that an
individual with low arousal levels is not at normal “rest” levels until they reach a mildly stressful
situation (Raine, 2002, p. 315). This low autonomic activity would cause an individual to
interpret their lack of arousal in a stressful situation as unpleasant, thus defining otherwise
stressful and anxiety-ridden situations as acceptable and comfortable to engage in (Portnoy et al.,
2014; Raine, 2002).
This change in definition for certain situations may prove detrimental for future criminal
behavior, as the majority of deviant and criminal acts require an individual to overcome a
significant amount of fear and anxiety to engage in such stressful and dangerous situations. Take
for instance an individual with low blood pressure and resting heart rate. Though the
“discomfort” of this state may not be consciously felt by the underaroused individual, the
positive feelings resulting from increased stimulation would redefine high levels of stimulation
as pleasurable, not fear inducing. As deviant behavior is a well-known form of heightened
stimulation, a person with a biological disposition to underarousal may grow to associate
criminal activity with positive feelings, thus defining deviant and criminal behavior as positive
activity.
Support for this concept comes from research on psychopathic criminal offenders, who
have been shown to experience intense pleasure from thrill-seeking, and not receive the
discomfort of anxiety typically associated with such behavior (Fishbein, 1990). This re-definition
of dangerous activities such as crime and violence as pleasurable would suggest that psychopaths
have an increased likelihood of being involved in deviant and criminal activities, which an
enormous body of literature on psychopaths conclusively supports (DeLisi, 2016; Edens,
Campbell, & Weir, 2007). Thus, the criminal behavior of psychopaths is a result of biological
traits reinforced through social learning principles.
Sensation-seeking theory has also been supported by studies on serial killers and violent
offenders (Blackburn, 1978; Quay, 1965; Raine, Stoddard, Bihrle, & Buchsbaum, 1998), and
longitudinal research indicates that fearlessness, stimulation seeking, and having a low resting
heart rate at age 3 successfully predicts aggression at age 11 (Raine, Venables, & Mednick,
1997). Furthermore, a recent study found that low heart rate was associated with higher levels of
aggression and nonviolent delinquency, and that sensation-seeking mediated the relationship
between heart rate and both aggression and nonviolent delinquency (Portnoy et al., 2014).
It therefore seems likely that this biological predisposition helps individuals with low
autonomic arousal redefine antisocial behavior as gratifying behavior that they enjoy engaging
in. This would result in a person with such a biological predisposition to develop definitions
resulting in criminal and deviant behavior. In this way, the use of psychophysiology to explain
the development of definitions favorable to criminal behavior is compatible with both social
learning and biosocial theories. As this marriage of concepts respects the learned aspect of
definitions, as well as the biological influence behind their formation, the possibility of their
propositional theoretical integration is demonstrated.
The model for the integration of biological predisposition and acquisition of definitions
resulting in criminal behavior is illustrated in the theoretical pathway below.
<INSERT FIGURE 2 ABOUT HERE>
Differential Reinforcement

8
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

SLT principles hold that learning is in part due to the differential reinforcement received
through operant conditioning to various forms of behavior. Such conditioning may be
environmental in nature, in that certain behaviors are rewarded by society and encouraged for the
individual to continue, or they are socially punished, and therefore deterred from being repeated
in the future. While these social reinforcements are those most often associated with
psychology’s operant conditioning principle, Burgess and Akers (1966) allowed for the inclusion
reinforcement other than from social sources. These nonsocial sources of reinforcement, such as
biological impulses and neurological predispositions, may also result in reinforcement for
criminal behavior.
Citing Burgess and Akers’ own example, the act of stealing bread may not receive social
reinforcement, but the nourishment from eating the stolen bread would be sufficient enough to
reinforce the behavior (Burgess & Akers, 1966, p. 128-147). In this instance, the reinforcement
does not involve human interaction, thus opening the door for biological influences to serve as
reinforcement. While the example used by Burgess and Akers refers to non-social reinforcement
as a means to maintain an individual’ behavior, it stands to reason the same type of
reinforcement may initiate criminal behavior as well.
Research suggests there are biological reasons why two people may be exposed to the
same behavior and receive the same reinforcement for imitating the behavior, but only one of
those people will repeat that behavior in the future (Vaske, 2015). For instance, a new line of
imaging genetics research indicates that some individuals are more sensitive to the effects of
social rewards and punishments due to genetic variants in how the brain processes these factors
(Hahn et al., 2011; Nikolova, Ferrell, Manuck, & Hariri, 2011). Specifically, individuals with
genetic variants related to increased dopamine availability (such as the DRD2, DAT1, DRD4,
COMT genes) are more sensitive to the effects of rewards, and therefore are far more likely to
continue their socially-rewarded behavior compared to individuals who do not carry these
genetic variants (Dreher, Kohn, Kolachana, Weinberger, & Berman, 2009; Forbes et al., 2009;
Hahn et al., 2011; Nikolova et al., 2011; Vaske, 2015). This would serve to enhance operant
conditioning for either deviant or non-deviant behavior for an individual with such a genotype,
depending on which behavior the individual is receiving social rewards for.
This variation is referred to as differential susceptibility, which is used to describe when
people with certain genes are “at risk” of the behavior that their environment encourages (Belsky
& Pluess, 2009; Belsky, Bakermans-Kranenburg, & van IJzendoorn, 2007; DiLalla & Bersted,
2015). For instance, DiLalla, Bersted and John (2015) found that children with the DRD4-7R
genetic variant were more likely to engage in negative externalized behavior (e.g., bullying,
delinquency, aggression) when they experienced this behavior, while children with the DRD4-
7R genetic variant who did not experience negative behavior were less likely to engage in
negative externalized behaviors, compared to those without the allele (DiLalla et al., 2015).
In this way, individuals with a genotype for reward sensitivity may be at increased risk
for positive behavior, but only when their environment rewards positive behavior. Conversely,
those with a genotype for reward sensitivity will be at greater risk of negative deviant behavior,
if their environment rewards deviant or criminal behavior. This differential susceptibility model
is consistent with the principles held both by SLT and the biosocial perspective. In such a model,
individuals with genotypes predisposing them to be more sensitive to rewards will have a
stronger sense of social reinforcement than those without this genetic variant. Therefore, when
put in environments that reward criminal behavior, individuals with susceptible genotypes are
more easily conditioned to engage in criminal behavior.
The model for the propositional integration of biological influence and differential
association resulting in criminal behavior is illustrated in the theoretical pathway below.
<INSERT FIGURE 3 ABOUT HERE>
Imitation
The final premise of SLT is imitation, or the concept that an individual may adopt a
behavior after observing and mimicking that behavior in another. While the strongest influence
on whether someone will choose to model another person’s behavior is the characteristics of the
model, SLT does not preclude the possibility that biology may play a part in this imitation
process.
The manner in which biology influences imitation is slightly more complex than it was
for the previous concepts. In this case, biological influence may not play a role in the individual
exhibiting the criminal behavior being examined. Instead, the focus lies on the predisposition and
biology of the individual whose behavior is being modeled. While this pathway may seem
similar to that of the integrated peer association model, two key differences remain. First, in this
model, the individual need not associate with the person whose behavior they are adopting. For
modeling to occur, a person only needs to admire and aspire to imitate another individual’s

9
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

actions. No direct interaction is required. This leads to the second difference in the concept of
imitation from peer association. In the integrated association model, biological influences cause
an individual to self-select others to associate with, who share the same predispositions and traits
as they do. However with the integrated imitation model, biology plays little part in whom a
person chooses to imitate. Instead, the biological influence lies in the likelihood that a person
will admire, and imitate, someone with a deviant or criminal tendency.
An illustration of this concept is the rate of alcoholism across various groups in society.
Multiple studies have shown that the ADH2 polymorphism has a protective factor against
alcoholism, and that this gene is more prevalent in certain ethnic groups than others. Specifically,
this gene occurs at much higher rates among Jewish populations, and far less among Russians,
compared to other populations. The fact that in the United States, American-born Jews tend to
drink less than American-born Russians is thought to reflect the fact that the ADH2 is more
prevalent among Jewish versus Russian people. However, one study examining the drinking
patterns of Ashkenazi and Sephardic Jews in Israel and Russia found that on average, both the
Ashkenazi and Sephardic Jews who moved to Russia had higher drinking rates than their
matched counterparts back in Israel (Hasin et al., 2002; Shanahan & Hofer, 2005). This study
shows support for imitation rather than differential association, as both groups of immigrant Jews
reported a lack of association with the native Russian people. Considering the exposure to heavy
drinking is nearly unavoidable in Russian culture, the Russian Jews would likely admire some
Russian natives with alcoholic tendencies, even if they did not associate with these people
directly. This indicates that the Russian Jews “overrode” their own biological influence to imitate
the biological tendencies of those they admired in society.
While at first this may seem like conclusive evidence against biological influence on an
individual’s behavior, closer consideration shows that it is because of that biological influence
that individuals attain the behavioral tendencies that will be imitated by those without such
biological predispositions. Another example of this power of biological influence in imitation
lies in one of the most heritable traits found in personality and behavioral research: political
affiliation (Shanahan & Hofer, 2005). While there is of course no liberal or conservative gene,
there are genes which cause certain traits and temperaments that make one ideology much more
attractive to a person than another (Olson, Vernon, & Harris, 2001). However, as sociopolitical
affiliation is also shown to be strongly associated with social context, namely parental political
affiliation and region a person lives in, there is undoubtedly an association or imitation factor
involved in this acquisition of political beliefs. While some of this transference must be
attributed to differential association, as the impact of peer groups and families is enormously
strong, some is undoubtedly also due to imitation as well. Even if an individual associates with
others of similar biological disposition and temperament, the admired model of the individual
has a different biological disposition may result in the person imitating the attitudes and actions
of the model’s biological tendencies instead of their own.
In short, whether biological or social factors have the strongest influence on an
individual’s behavior may be a function of whether that individual is a model or imitator in
society. This melding of biology and imitation respects the principles of the biosocial
perspective and SLT, once again allowing the integration of these models to occur.
The theoretical pathway described in the integrated model of genetic influence and
imitation on future criminal behavior is illustrated below.
<INSERT FIGURE 4 ABOUT HERE>
CONCLUSION
Social learning theory has received considerable attention and support in criminology
(Pratt et al., 2010). The more recent biosocial perspective has also shown an extensive catalog of
notable findings, specifically indicating the biological influence on the reason and ease in which
certain people learn certain behavior, including criminality (Beaver, 2009; Ellis & Walsh, 1997;
Rafter et al., 2016, Walsh, 2002a; Walsh & Beaver, 2009). While there is certainly no genetic
polymorphism for jimmying a lock or stealing a car, there is sufficient evidence to suggest that
certain biological conditions have a profound impact on the way an individual reacts and
interacts with their environment (Rowe, 1996). It therefore becomes clear that biology and social
context are not separate entities without any influence each other, as the current theories in
criminology generally reflect. Instead, nearly all research on the subject has indicated that these
two factors are working in concert to form all behaviors an individual will exhibit in life.
As SLT has received considerable support in predicting criminal behavior (Pratt et al.,
2010), there is reason to believe that behavior is learned through observation, modeling,
conditioning, and reinforcement. However, we also know from research in biology, psychiatry,
neuroscience, psychology, and biosocial criminology, that many biological factors influence our
learning, and consequently our behavior. This occurs when biology and genetics alter our

10
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

definitions of what is rewarding, what things we define as pleasurable, and even what people we
choose to associate with and learn from. In this sense, learning influences human behavior, but
biology clearly influences the key facets of learning. Therefore, we must also consider biological
factors in any theoretical framework that uses learning to explain our behavior.
This relationship between biology, social learning, and criminality is analogous to
Gottfredson and Hirshi’s (1990) notion that self-control largely predicts criminality, although
parental practices are primarily responsible for developing the child’s level self-control. To say
that only self-control matters is incorrect, but to say that parenting is what truly matters is also
incorrect. Parenting is the key mediator between self-control and criminality. Similarly, social
learning largely predicts criminal behavior, although growing research indicates that biology
plays a considerable role in what and how we learn. Therefore, by taking biological factors into
account, our theoretical models and understanding of social learning’s influence on criminal
behavior is drastically enhanced. As the principles outlined by social learning theory and the new
biosocial perspective are among the most empirically supported models in their distinct realms of
criminology, it stands to reason that their integration would lead to increased scope, parsimony,
and validity than each theory has individually. In other words, by integrating biosocial principles
into SLT, a more accurate and modern model of criminal behavior will result.
Furthermore, as the quantity of literature on the combined social and biological nature of
crime continues to grow, there needs to be a single model developed to adequately and succinctly
explain the results being found. Overall, it appears that SLT and biosocial factors independently
provide some of the best explanations, and have some of the highest levels of explanatory power
of all the proposed theories and explanations for criminal behavior. Rather than continue on
these two “independent” avenues of research, it would be practical for criminologists to instead
consider the proposed integration of biological factors in social learning theory.
Additionally, as biology, environmental factors, and behavior are clearly intertwined, a
criticism that has been made against biosocial research (see Burt & Simons, 2014), it is only
prudent to include each of these factors in our models of criminal behavior. Excluding one of
these, be it biology or social influence, does not help disentangle these factors, it simply ignores
the fact that the missing factor exists. Therefore, it is only by accounting for both biological
factors and social context that criminal behavior can most effectively, and accurately, be
modeled and understood. Or, as Rutter (2006) noted, this is not about nature versus nurture… it
is about nature and nurture.

REFERENCES
Akers, R.L., & Jensen, G.F. (2006). Empirical status of social learning theory: Past, present,
and future. In F.T. Cullen, J.P. Wright, & K.R. Blevins (Eds.), Taking Stock: The Status
of Criminological Theory, Vol. 15 (pp. 37-76). New Brunswick, NJ: Transaction
Publishing.
Akers, R.L., & Jensen G.F. (Eds.) (2007). Social Learning Theory and the Explanation of
Crime: A Guide for the New Century. New Brunswick, NJ: Transaction Books.
Akers, R.L., & Sellers, C.S. (2008). Criminological theories: Introduction evaluation, and
application, 5th Edition. New York: Oxford University Press.
Akers, R.L., Krohn, M.D., Lanza-Kaduce, L., & Radosevich, M. (1979). Social learning and
deviant behavior: A specific test for a general theory. American Sociological Review, 44,
636-655.
Akers, R.L. (1998). Social Learning and Social Structure: A General Theory of Crime and
Deviance. Boston: Northeastern University Press.
Bandura, A. (1976). Social Learning Theory. Alexandria, VA: Prentice Hall.
Banks, T., & Dabbs, J.M. (1996). Salivary testosterone and cortisol in a delinquent and violent
urban subculture. The Journal of Social Psychology, 136, 49-56.
Barnes, J.C. & Jacobs, B.A. (2013). Genetic risk for violent behavior and environmental
exposure to disadvantage and violent crime: The case for gene-environment interaction.
Journal of Interpersonal Violence, 18, 92-120.
Barnes, J.C., Boutwell, B.B., & Beaver, K.M. (2016). Contemporary biosocial criminology: A
systematic review of the literature, 2000-2012. In A.R. Piquero (Ed.), The Handbook of
Criminological Theory, (pp. 75-99). Chichester, UK: Wiley & Sons.
Barnes, J.C., Boutwell, B.B., Beaver, K.M., Gibson, C.L., & Wright, J.P. (2014). On the
consequences of ignoring genetic influences in criminological research. Journal of
Criminal Justice, 42, 471-482.
Beaver, K.M. (2008). Nonshared environmental influences on adolescent delinquent
involvement and adult criminal behavior. Criminology, 46, 341-369.
Beaver, K.M. (2013). Biosocial Criminology: A Primer, 2nd Edition. Dubuque, IA: Kendall/Hunt.

11
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Beaver, K.M., & Holtfreter, K. (2009). Biosocial influences on fraudulent behaviors. The
Journal of Genetic Psychology, 170, 101-114.
Beaver, K.M., & Wright, J.P. (2005). Biosocial development and delinquent involvement. Youth
Violence and Juvenile Justice, 3, 168-192.
Beaver, K.M., & Wright, J.P. (2007). A child effects explanation for the association between
family risk and involvement in an antisocial lifestyle. Journal of Adolescent Research,
22, 640-664.
Beaver, K.M., Barnes, J.C., & Boutwell, B.B. (Eds.). (2015). The Nurture Versus Biosocial
Debate in Criminology: On the Origins Of Criminal Behavior and Criminality. Thousand
Oaks, CA: Sage Publications.
Beaver, K.M., Boutwell, B.B., Barnes, J.C., & Cooper, J.A. (2009a). The biosocial
underpinnings to adolescent victimization: Results from a longitudinal sample of twins.
Youth Violence and Juvenile Justice, 7, 350-360.
Beaver, K.M., DeLisi, M., Wright, J.P., & Vaughn, M. (2009b). Gene-environment interplay and
delinquent involvement: Evidence of direct, indirect, and interactive effects. Journal of
Adolescent Research, 24, 147-168.
Beaver, K.M., Gibson, C., Jennings, W., & Ward, J.T. (2009c). A gene x environment interaction
between DRD2 and religiosity in the prediction of adolescent delinquent involvement in a
sample of males. Biodemography and Social Biology, 55, 71-81.
Beaver, K.M., Nedelec, J.L., Costa, C.D.S., & Vidal, M.M. (2015). The future of biosocial
criminology. Criminal Justice Studies, 28, 6-17.
Beaver, K.M., Shutt, J. E., Boutwell, B.B., Ratchford, M., Roberts, K., & Barnes, J.C. (2009d).
Genetic and environmental influences on levels of self-control and delinquent peer
affiliation: Results from a longitudinal sample of adolescent twins. Criminal Justice and
Behavior, 36, 41-60.
Beaver, K.M., Wright, J. P., DeLisi, M., Walsh, A., Vaughn, M. G., Boisvert, D., & Vaske, J.
(2007). A gene x gene interaction between DRD2 and DRD4 is associated with conduct
disorder and antisocial behavior in males. Behavioral and Brain Functions, 3, 30-38.
Beaver, K.M., Wright, J.P., & DeLisi, M. (2008a). Delinquent peer group formation: Evidence of
a gene x environment correlation. The Journal of Genetic Psychology, 169, 227-244.
Beaver, K.M., Wright, J.P., DeLisi, M., & Vaughn, M. (2008b). Desistance from delinquency:
The marriage effect revisited and extended. Social Science Research, 37, 736-752.
Bellinger, D., Leviton, A., Alfred, E., & Rabinowitz, M. (1994). Pre- and postnatal lead exposure
and behavior problems in school-age children. Environmental Research, 66, 12-30.
Belsky, J., & Pluess, M. (2009). Beyond diathesis stress: A differential susceptibility to
environmental influences. Psychological Bulletin, 135, 885–908.
Belsky, J., Bakermans-Kranenburg, M.J., & van Ijzendoorn, M.H. (2007). For better and for
worse: Differential susceptibility to environmental influences. Current Directions in
Psychological Science, 16, 300-304.
Berman, M.E., & Coccaro, E.F. (1998). Neurobiologic correlates of violence: relevance to
criminal responsibility. Behavioral Sciences & the Law, 16, 303-318.
Blackburn, R. (1978). Psychopathy, arousal and the need for stimulation. In R.D. Hare & D.
Schalling (Eds.), Psychopathic Behaviour: Approaches to Research. Chichester, UK:
John Wiley & Sons.
Boisvert, D., Boutwell, B. B., Vaske, J., & Newsome, J. (2013). Genetic and environmental
overlap between delinquent peer association and delinquency in adolescence. Criminal
Justice and Behavior, 41, 58-74.
Bouchard, T. J., Lykken, D. T., McGue, M., Segal, N. L., & Tellegen, A. (1990). Sources of
human psychological differences: The Minnesota Study of Twins Reared Apart. Science,
250, 223-228.
Boutwell, B. B., & Beaver, K. M. (2008). A biosocial explanation of delinquency abstention.
Criminal Behaviour and Mental Health, 18, 59-74.
Brotman, L.M., Gouley, K.K., Huang, K.Y., Kamboukos, D., Fratto, C., & Pine, D.S. (2007).
Effects of a psychosocial family-based preventative intervention on cortisol response to a
social challenge in preschoolers at high risk for antisocial behavior. Archives of General
Psychiatry, 64, 1172-1179.
Burgess, R.L. & Akers, R.L. (1966). A differential association-reinforcement theory of criminal
behavior. Social Problems, 14, 363-383.
Burt, C.H., & Simons, R.L. (2014). Pulling back the curtain on heritability studies: Biosocial
criminology in the postgenomic era. Criminology, 52, 223-262.
Burt, C.H., & Simons, R.L. (2015). Heritability in the postgenomic era: The fatal flaw is
conceptual. Criminology, 53,103–112.

12
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Burt, S.A. (2009a). Are there meaningful etiological differences within antisocial behavior?
Results from a meta-analysis. Clinical Psychology Review, 29, 163-178.
Burt, S.A. (2009b). Rethinking environmental contributions to child and adolescent
psychopathology: A meta-analysis of shared environmental influences. Psychological
Bulletin, 135, 608-637.
Caspi, A., & Moffitt, T.E. (1995). The continuity of maladaptive behavior: From description to
understanding in the study of antisocial behavior. In D. Cicchetti & D.J. Cohen (Eds.),
Manual of Developmental Psychopathology (pp. 472-511). New York: Wiley.
Caspi, A., McClay, J., Moffitt, T.E., Mill, J., Martin, J., Craig, I.W., Taylor, A., & Poulton, R.
(2002). Role of genotype in the cycle of violence in maltreated children. Science, 297,
851-854.
Christakis, N.A., & Fowler, J.H. (2014). Friendship and natural selection. Proceedings of the
National Academy of Sciences of the United States of America, 111, 10796-10801.
Cima, M., Smeets, T., & Jelicic, M. (2008). Self-reported trauma, cortisol levels, and aggression
in psychopathic and non-psychopathic prison inmates. Biological Psychology, 78, 75-86.
Cleveland, H.H., Wiebe, R.P., & Rowe, D.C. (2005). Sources of exposure to smoking and
drinking friends among adolescents: A behavioral-genetic evaluation. Journal of Genetic
Psychology, 166, 153-169.
Connolly, E.J., Schwartz, J.A., Nedelec, J.L. Beaver, K.M. & Barnes, J.C. (2015). Different
slopes for different folks: Genetic influences on growth in delinquent peer association
and delinquency during adolescence. Journal of Youth and Adolescence, 44, 1413-1427.
Craig, M.C., Catani, M., Deeley, Q., Latham, R., Daly, E., Kanaan, R., Picchioni, M., McGuire,
P.K., Fahy, T., & Murphy, D.G. (2009). Altered connections on the road of psychopathy.
Molecular Psychiatry, 14, 946-953.
Dabbs, J. M., & Morris, R. (1990). Testosterone, social class, and antisocial behavior in a sample
of 4,462 men. Psychological Science, 1, 209-211.
DeLisi M., Beaver, K.M., Wright, J.P., & Vaughn, M.G. (2008). The etiology of criminal onset:
The enduring salience of nature and nurture. Journal of Criminal Justice, 36, 217-223.
DeLisi, M. (2016). Psychopathy as Unified Theory of Crime. New York, NY: Palgrave
Macmillan.
DeLisi, M., Beaver, K.M., Vaughn, M.G. & Wright, J.P. (2009). All in the family: Gene x
environment interactions between DRD2 and criminal father is associated with five
antisocial phenotypes. Criminal Justice and Behavior, 36, 1187-1197.
DeLisi, M., & Vaughn, M.G. (Eds.) (2015). The Routledge International Handbook of Biosocial
Criminology. New York, NY: Routledge.
DiLalla, L.F., & Bersted, K. (2015). Biosocial foundations of externalizing behaviors. In M.
DeLisi & M.G. Vaughn (Eds.), The Routledge International Handbook of Biosocial
Criminology (pp. 349-364). New York, NY: Routledge
DiLalla, L.F., Bersted, K., & John, S.G. (2015). Peer victimization and DRD4 genotype
influence problem behaviors in young children. Journal of Youth and Adolescence, 44,
1478-1493.
DiLalla, L.F. (2002). Behavior genetics of aggression in children: Review and future directions.
Developmental Review, 22, 593-622.
Dreher, J.C., Kohn, P., Kolachana, B., Weinberger, D.R., & Berman, K.F. (2009). Variation in
dopamine genes influences responsivity of the human reward system. Proceedings of the
National Academy of Sciences, 106, 617-622.
Edens, J.F., Campbell, J.S., & Weir, J.M. (2007). Youth psychopathy and criminal recidivism: A
meta-analysis of the psychopathy checklist measures. Law and Human Behavior, 31, 53-
75.
Ellis, L. (2003). Biosocial Criminology: Challenging Environmentalism's Supremacy.
Huntington: Nova Science Publishers.
Espelage, D. L., Holt, M.K., and Henkel, R.R. (2003). Examination of peer-group contextual
effects on aggression during early adolescence. Child Development, 74, 205-220.
Eysneck, H. (1964). Crime and personality. London: Methuen.
Farrington, D. P. (1997). The relationship between low resting heart rate and violence. In A
Raine, P.A Brennan, D.P. Farrington, & S.A Mednick (Eds.), Biosocial Bases of
Violence (pp. 89-105). New York: Plenum Press.
Ferguson, C.J. (2010). Genetic contributions to antisocial personality and behavior: A meta-
analytic review (1996-2006) from an evolutionary perspective. Journal of Social
Psychology 150, 160-180.
Fishbein, D. (1990). Biological perspectives in criminology. Criminology, 28, 27-72.

13
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Forbes, E.E., Brown, S.M., Kimak, M., Ferrell, R.E., Manuck, S.B., & Hariri, A.R. (2009).
Genetic variation in components of dopamine neurotransmission impacts ventral striatal
reactivity associated with impulsivity. Molecular Psychiatry, 14, 60-70.
Gibson, C.L., & Tibbetts, S.G. (2000). A biosocial interaction in predicting early onset of
offending. Psychological Reports, 86, 509-518.
Gibson, C.L., Piquero, A.R., & Tibbetts, S.G. (2000). Assessing the relationship between
maternal cigarette smoking during pregnancy and age at first police contact. Justice
Quarterly, 17, 519-542.
Gottfredson, M.R., & Hirschi, T. (1990). A general theory of crime. Stanford, CA: Stanford
University Press.
Guo, G., Roettger, M., & Cai, T. (2008). The integration of genetic propensities into social-
control models of delinquency and violence among male youths. American Sociological
Review, 73, 543-568.
Guo, G., Roettger, M.E., & Shih, J.C. (2007). Contributions of the DAT1 and DRD2 genes to
serious and violent delinquency among adolescents and young adults. Human genetics,
121, 125-136.
Hahn, T., Heinzel, S., Dresler, T., Plichta, M.M., Renner, T.J., Markulin, F., Jakob, P.M., Lesch,
K.-P., & Fallgatter, A.J. (2011). Association between reward-related activation in the
ventral striatum and trait reward sensitivity is moderated by dopamine transporter
genotype. Human Brain Mapping, 32, 1557-1565.
Harden, K.P., Hill, J.E., Turkheimer, E., & Emery, R.E. (2008). Gene-environment correlation
and interaction in peer effects on adolescent alcohol and tobacco use. Behavior Genetics,
38, 339-347.
Harris, J.R. (1998). The nurture assumption: Why children turn out the way they do. New York,
NY: Free Press.
Hasin, D., Aharonovich, E., Liu, X., Mamman, Z., Matseoane, K., Carr, L., & Li, T.-K. (2002).
Alcohol and ADH2 in Israel: Ashkenazis, Sephardic, and recent Russian immigrants.
American Journal of Psychiatry, 159, 1432-1434.
Holi, M., Auvinen-Lintunen, L., Lindberg, N., Tani, P., & Virkkunen, M. (2006). Inverse
correlation between severity of psychopathic traits and serum cortisol levels in young
adult violent male offenders. Psychopathology, 39, 102-104.
Iervolino, A.C., Pike, A., Manke, B., Reiss, D., Hetherington, E.M., & Plomin, R. (2002).
Genetic and environmental influences in adolescent peer socialization: Evidence from
two genetically sensitive designs. Child Development, 73, 162-174.
Ishikawa, S.S., & Raine, A. (2002). Behavioral genetics and crime. In Glicksohn, J. (Ed), The
neurobiology of criminal behavior (pp. 81-110). Boston: Kluwer Academic Publishers.
Kendler, K.S., Jacobson, K., Myers, J.M., & Eaves, L.J. (2008). A genetically informative
developmental study of the relationship between conduct disorder and peer deviance in
males. Psychological Medicine, 38, 1001–1011.
Kim-Cohen, J., Caspi, A., Taylor, A., Willams, B., Newcombe, R., Craig, I. W., & Moffitt, T. E.
(2006). MAOA, maltreatment, and gene-environment interaction predicting children’s
mental health: New evidence and a meta-analysis. Molecular Psychiatry, 11, 903-913.
Lacourse, E., Nagin, D.S., Vitaro, F., Cote, S., Arseneault, L., & Tremblay, R.E. (2006).
Prediction of early onset deviant peer group affiliation: A 12 year longitudinal study.
Archives of General Psychiatry, 63, 562-568.
Lombroso, C. (1876). L’uomo delinquente (Criminal man). Milan: Hoepli.
Loney, B.R., Butler, M.A, Lima, E.N., Counts, C.A., & Eckel, L.A (2006). The relation between
salivary cortisol, callous-unemotional traits, and conduct problems in an adolescent non-
referred sample. Journal of Child Psychology and Psychiatry, 47, 30-36.
Lorber, M.F. (2004). Psychophysiology of aggression, psychopathy, and conduct problems: A
meta-analysis. Psychological Bulletin, 130, 531-552.
Mason, D.A., & Frick, P.J. (1994). The heritability of antisocial behavior: A meta-analysis of
twin and adoption studies. Journal of Psychopathology and Behavioral Assessment, 16,
301-323.
May, P. & Gossage, P. (2008). Estimating the prevalence of fetal alcohol syndrome: A summary.
National Institute of Alcohol Abuse and Alcoholism. National Institute of Health.
Retrieved from http://pubs.niaaa.nih.gov/publications/arh25-3/159-167.htm.
Miles, D.R., & Carey, G. (1997). Genetic and environmental architecture on human aggression.
Journal of Personality and Social Psychology, 72, 207-217.
Moffitt, T.E., & Walsh, A. (2003). The adolescent limited life-course persistent theory of
antisocial behavior: What have we learned? In A. Walsh & L. Ellis (Eds.) Biosocial
Criminology: Challenging Environmentalism’s Supremacy (pp. 125-144). Hauppauge,

14
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

NY: Nova Science Publications.


Moffitt, T E., Caspi, A, Fawcett, J.W., Brammer, G.L., Raleigh, M., Yuwiler, A, & Silva, P.A
(1997). Whole blood serotonin and family background relate to male violence. In A
Raine, P.A Brennan, D.P. Farrington, & S.A Mednick (Eds.), Biosocial Bases of
Violence (pp. 231-249). New York: Plenum Press.
Moffitt, T.E. (2005). The new look of behavioral genetics in developmental psychopathology:
Gene-environment interplay in antisocial behaviors. Psychological Bulletin, 131, 533-
554.
Moffitt, T.E., Ross, S., & Raine, A. (2011). Crime and biology. In J.Q. Wilson & J. Petersilia
(Eds). Crime and Public Policy (pp. 53-87). New York, NY: Oxford University Press.
Moore, T.M., Scarpa, A., & Raine, A. (2002). A meta‐analysis of serotonin metabolite 5‐HIAA
and antisocial behavior. Aggressive Behavior, 28, 299-316.
Nedelec, J. (2015, June 18). What is “Biosocial Criminology”? (It’s Science!). Psychology
Today. Retrieved from https://www.psychologytoday.com/blog/the-nature-
crime/201506/what-is-biosocial-criminology-it-s-science.
Needleman, H.L., McFarland, C., Ness, R.B., Fienberg, S.E., & Tobin, M.J. (2002). Bone lead
levels in adjudicated delinquents: A case control study. Neurotoxicology and Teratology,
24, 711-717.
Needleman, H.L., Riess, J.A., Tobin, M.J., Biesecker, G.E., & Greenhouse, J B. (1996). Bone
lead levels and delinquent behavior. Journal of the American Medical Association, 275,
363-369.
Nikolova, Y.S., Ferrell, R.E., Manuck, S.B., & Hariri, A.R. (2011). Multilocus genetic profile for
dopamine signaling predicts ventral striatum reactivity. Neuropsychopharmacology, 36,
1940-1947.
O'Neal, C.R, Brotman, L.M., Huang, K.Y, Gouley, K.K., Kamboukos, D., Calzada, E.J., & Pine,
D.S. (2010). Understanding relations among early family environment, cortisol response,
and child aggression via a prevention experiment. Child Development, 81, 290-305.
Olson, J., Vernon, P.A., & Harris, J. (2001). The heritability of attitudes: A study of twins.
Journal of Personality and Social Psychology, 80, 845-860.
Ortiz, J., & Raine, A. (2004). Heart rate level and antisocial behavior in children and
adolescents: A meta‐analysis. Journal of the American Academy of Child and Adolescent
Psychiatry, 43, 154–162.
Pike, A., McGuire, S., Hetherington, M.E., Reiss, D., & Plomin, R. (1996). Family environment
and adolescent depressive symptoms and antisocial behavior: A multivariate genetic
analysis. Developmental Psychology, 32, 590-604.
Plomin, R., Owen, M.J., & McGuffin, P. (1994). The genetic basis of complex human behaviors.
Science, 264, 1733-1739.
Portnoy, J., Raine, A., Chen, F.R., Pardini, D., Loeber, R., & Jennings, J.R. (2014). Heart rate
and antisocial behavior: The mediating role of impulsive sensation seeking. Criminology,
52, 292-311.
Pratt, T.C., Cullen, F.T., Sellers, C.S., Winfree, L.T., Madensen, T.D., Daigle, L.E., Fearn, N.E.,
& Gau, J.M. (2010). The empirical status of social learning theory: A meta‐analysis.
Justice Quarterly, 27, 765-802.
Pratt, T.C., McGloin, J.M., & Fearn, N.E. (2006). Maternal cigarette smoking during pregnancy
and criminal/deviant behavior: A meta-analysis. International Journal of Offender
Therapy and Comparative Criminology, 50, 672–690.
Pratt, T.C., Turanovic, J.J., & Cullen, F.T. (2016). Revisiting the criminological consequences of
exposure to fetal testosterone: A meta‐analysis of the 2D: 4D digit ratio. Criminology,
54, 587-620.
Quay, H.C. (1965). Psychopathic personality as pathological stimulation seeking. American
Journal of Psychiatry, 122, 180-183.
Rafter, N. Posick, C., & Rocque, M. (2016). The Criminal Brain: Understanding Biological
Theories of Crime, 2nd Edition. New York: New York University Press.
Raine, A. (2013). The Anatomy of Violence: The Biological Roots of Crime. New York:
Pantheon.
Raine, A., Stoddard, J., Bihrle, S., & Buchsbaum, M. (1998) Prefrontal glucose deficits in
murderers lacking psychosocial deprivation. Neuropsychiatry, Neuropsychology,
Behavioral Neurology, 11, 1-7.
Raine, A. (2002). Biosocial studies of antisocial and violent behavior in children and adults: A
review. Journal of Abnormal Child Psychology, 30, 311-326.
Raine, A., Buchsbaum, M., Stanley, J., Lottenberg, S., Abel, L., & Stoddard, J. (1994). Selective
reductions in prefrontal glucose metabolism in murderers. Biological Psychiatry, 36, 365-

15
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

373.
Raine, A., Mellingen, K., Liu, J., Venables, P. H., & Mednick, S. A. (2003). Effects of
environmental enrichment at ages 3-5 years on schizotypal personality and antisocial
behavior at ages 17 and 23 years. American Journal of Psychiatry, 160, 1627-1635.
Raine, A., Park, S., Lencz, T., Bihrle, S., LaCasse, L., Widom, C S., Al-Dayeh, L. & Singh, M.
(2001). Reduced right hemisphere activation in severely abused violent offenders during
a working memory task: An fMRI study. Aggressive Behavior, 27, 111-129.
Raine, A., Venables, P.H., & Mednick, S.A. (1997). Low resting heart rate age 3 years
predisposes to aggression at age 11 years: Evidence from the Mauritius Child Health
Project. Journal of American Academy of Child and Adolescent Psychiatry, 36, 1457-
1464.
Raine, A., Venables, P.H., & Williams, M. (1996). Better autonomic conditioning and faster
electrodermal half-recovery time at age 15 years as possible protective factors against
crime at age 29 years. Developmental Psychology, 32, 624-630.
Raine, A., Venables, P.H., & Williams, M. (1995). High autonomic arousal and electrodermal
orienting at age 15 years as protective factors against criminal behavior at age 29 years.
American Journal of Psychiatry, 152, 1595-1600.
Rhee, S.H., & Waldman, I.D. (2002). Genetic and environmental influences on antisocial
behavior: A meta-analysis of twin and adoption studies. Psychological Bulletin, 128, 490-
529.
Rowe, D.C. (1994). The limits of family influence: Genes, experience, and behavior. New York:
Guilford.
Rowe, D.C. (1996). An adaptive strategy theory of crime and delinquency. In J.D. Hawkins
(Ed.), Delinquency and Crime: Current Theories. Cambridge: Cambridge University
Press.
Rutter, M. (2006). Genes and Behavior: Nature-Nurture Interplay Explained. Malden, MA:
Blackwell.
Sadeh, N., Javdani, S., Jackson, J.J., Reynolds, E.K., Potenza, M.N., Gelernter, J., Lejuez, C., &
Verona, E. (2010). Serotonin transporter gene associations with psychopathic traits in
youth vary as a function of socioeconomic resources. Journal of Abnormal Psychology,
119, 604-609.
Scarr, S., & McCartney, K. (1983). How people make their own environments: A theory of
genotype → environment effects. Child Development, 54, 424-435.
Schwartz, J.A. & Beaver, K.M. (2014). A biosocial analysis of the sources of missing data in
criminological research. Journal of Criminal Justice, 42, 452-461.
Shanahan, M.J., & Hofer, S.M. (2005). Social context in gene-environment interactions:
Retrospect and prospect. Journals of Gerontology, 60, 65-76.
Stretesky, P.B., & Lynch, M.J. (2001). The relationship between lead exposure and homicide.
Archives of Pediatrics & Adolescent Medicine, 155, 579-582.
Sutherland, E.H. (1939). Principles of criminology. Philadelphia: J. B. Lippincott Co.
TenEyck, M., & Barnes, J.C. (2015). Examining the impact of peer group selection on self-
reported delinquency: A consideration of active gene-environment correlation. Criminal
Justice and Behavior, 42, 741-762.
Turkheimer, E. (2000). Three laws of behavior genetics and what they mean. Current Directions
in Psychological Science, 9, 160-164.
Udry, J.R. (2003). The National Longitudinal Study of Adolescent Health (Add Health), Waves I
and II, 1994–1996; Wave III, 2001–2002 [machine-readable data file and
documentation]. Chapel Hill, NC: Carolina Population Center.
van Honk, J., & Schutter, D. J. (2007). Testosterone reduces conscious detection of signals
serving social correction: Implications for antisocial behavior. Psychological Science, 18,
663-667.
Vaske, J. (2015). The integration of biological and genetic factors into social learning theory. In
K.M. Beaver, J.C. Barnes, & B.B. Boutwell (Eds.), The Nurture Versus Biosocial
Debate in Criminology: On the Origins Of Criminal Behavior and Criminality (pp. 125-
141). Thousand Oaks, CA: Sage Publications.
Vaughn, M.G., DeLisi, M., Beaver, K.M., & Wright, J.P. (2009). DAT1 and 5HTT are
associated with pathological criminal behavior in a nationally representative sample of
youth. Criminal Justice and Behavior, 36, 1113-1124.
Vitaro, F., Brendgen, M., Girard, A., Dionne, G., Tremblay, R.E., & Boivin, M. (2016). Links
between friends’ physical aggression and adolescents’ physical aggression: What
happens if gene-environment correlations are controlled? International Journal of
Behavioral Development, 40, 234-242.

16
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Wadsworth, S.J., DeFries, J.C., Fulker, D.W., & Plomin, R. (1995). Cognitive ability and
academic achievement in the Colorado adoption project: A multivariate genetic analysis
of parent-offspring and sibling data. Behavior Genetics, 25, 1-15.
Wakschlag, L.S. Pickett, K.E., Cook, E.C. Benowitz, N.L., & Leventhal, B.L. (2002). Maternal
smoking during pregnancy and severe antisocial behavior in offspring: A review.
American Journal of Public Health, 92, 966-974.
Walsh, A. & Beaver, K.M. (2009). Biosocial criminology. In M. Krohn, A. Lizotte, & G. Hall
(Eds.) Handbook on Crime and Deviance (pp. 79-101). New York, NY: Springer.
Walsh, A., & Bolen, J.D. (2012). The Neurobiology of Criminal Behavior: Gene-Brain-Culture
Interaction. Burlington, VT: Ashgate.
Walsh, A. (2002a). Biosocial criminology: Introduction and integration. Cincinnati, OH:
Anderson.
Walsh, A. (2002b). Companions in crime: A biosocial perspective. Human Nature Review, 2,
169-178.
Walsh, A., Taylor, C.Y., & Yun, I. (2015). The role of intelligence and temperament in
interpreting the SES–crime relationship. In K.M. Beaver, J.C. Barnes, & B.B. Boutwell
(Eds.), The Nurture Versus Biosocial Debate in Criminology: On the Origins of Criminal
Behavior and Criminality (pp. 91–109). Thousand Oaks, CA: Sage Publications.
Wikström, P.-O. (2004). Crime as alternative: Towards a cross-level situational action theory of
crime causation. In McCord, J. (Ed.) Beyond empiricism: Institutions and intentions in
the study of crime (pp. 1–37). New Brunswick, NY: Transaction.
Wood, P.B., Gove, W.R., Wilson, J.A., & Cochran, J.K. (2006). Nonsocial reinforcement and
habitual criminal conduct: An extension of social learning theory. Criminology, 35, 335-
366.
Wright, J.P., & Beaver, K.M. (2005). Do parents matter in creating self-control in their children?
A genetically informed test of Gottfredson and Hirschi’s theory of low self-control.
Criminology, 43, 1169–1202.
Wright, J.P. & Boisvert, D. (2009). What biosocial criminology offers criminology. Criminal
Justice and Behavior, 36, 1228-1240.
Wright, J.P., Barnes, J.C., Boutwell, B.B., Schwartz, J.A., Connolly, E.J., Nedelec, J.L., &
Beaver, K.M. (2015). Mathematical proof is not minutiae and irreducible complexity is
not a theory: A final response to Burt and Simons and a call to criminologists.
Criminology, 53, 113-120.
Wright, J.P., Boisvert, D., & Vaske, J. (2009). Blood lead levels in early childhood predict
adulthood psychopathy. Youth Violence and Juvenile Justice, 7, 208–222.
Wright, J.P., Dietrich, K.N., Ris, M.D., Hornung, R.W., & Wessel, S.D. (2008). Association of
prenatal and childhood blood lead concentrations with criminal arrests in early adulthood.
PLoS Medicine, 5, 732-740.
Yun, I., Cheong, J., & Walsh, A. (2011). Genetic and environmental influences in delinquent
peer affiliation: From the peer network approach. Youth Violence and Juvenile Justice, 9,
241-258.

17
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Figure 1. Integrated Model of Active Gene-Environment Correlation on Future Behavior

ACTIVE GENE-ENVIRONMENT CORRELATION FUTURE


BEHAVIOR
GENETIC PERSONALITY PEER
INFLUENCE TRAITS ASSOCIATION

Genetic pre-disposition Lack of pro-social traits Deviant peer group selection Criminal behavior

18
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Figure 2. Integrated Model of Biological Influence and Acquired Definitions on Future


Behavior

BIOLOGICAL DEFINITION FUTURE


INFLUENCE BEHAVIOR

Predisposition to low autonomic Acquisition of definitions Criminal behavior


activity and underarousal favorable to criminal activity

19
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Figure 3. Integrated Model of Differential Susceptibility and Differential Reinforcement on

Future Behavior

DIFFERENTIAL SUSCEPTIBILITY FUTURE


DIFFERENTIAL
REINFORCEMENT BEHAVIOR
GENETIC ENVIRONMENTAL
VARIANT FACTOR

Predisposition to Environment rewarding Positive reinforcement for Criminal behavior


reward sensitivity criminal behavior criminal activity

20
NATURE OR NURTURE: INTEGRATING BIOLOGY INTO SOCIAL LEARNING

Figure 4. Integrated Model of Genetic Influence and Imitation on Future Behavior

GENETIC OBSERVATION IMITATION FUTURE


INFLUENCE OF BEHAVIOR BEHAVIOR

Genetic pre-disposition Model’s exhibition Imitation of model’s Criminal behavior


of the model of deviant traits observed deviant traits

21

You might also like