Genes, Crime, and Antisocial Behaviors Research Paper

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When it comes to explaining the causes of crime, criminals, and antisocial behavior, there is virtually an endless supply of ideas. Some of these explanations are based on mounds of data, such as theories that focus on the assumption that antisocial behavior is produced by peer pressure or exposure to maltreatment early in life. Other explanations, however, teeter on the absurd, such as the belief that all crime is due to the pursuit of economic gain. The point is that virtually any factor that could be linked to crime has, in some way, been spun into a criminological theory. A perusal of any introduction to criminology textbook is quite revealing by showing the tremendous breadth of factors and explanations that have been advanced to explain crime and that have yet to be falsified by the academic community. Interestingly, the factors that do not seem to get very much coverage by criminologists – at least not in a balanced format – are genetic factors. In fact, most criminologists argue that genetic factors have absolutely nothing to do with the development of criminal involvement and that only environmental factors matter (Wright et al. 2008a). Recent empirical-based research has called into question the assumption that genes have no effect on criminal involvement and instead have revealed that genetic factors are the dominant etiological influence for crime and antisocial behaviors (Ferguson 2010; Moffitt 2005; Rhee and Waldman 2002).

Genetic Effects And Antisocial Behaviors

One of the major obstacles to studying genetic effects is trying to provide accurate and reliable estimates of both genetic and environmental effects on crime and antisocial behaviors. One of the more common ways of accomplishing this goal is by making use of a naturally occurring experiment: twinning. There are two types of twins: monozygotic (MZ) twins and dizygotic (DZ) twins. MZ twins share 100 % of their DNA (i.e., they are essentially genetic clones of each other), and they also share the same environmental upbringings. DZ twins, in contrast, share only 50 % of their distinguishing DNA, but they too share the same environmental upbringings. By comparing the similarity on measures of crime/antisocial behavior of MZ twins to the similarity of DZ twins, it is possible to quantify the proportion of variance that is the result of genetic factors and the proportion of variance that is the result of environmental factors. The more similar MZ twins are to each other in comparison with DZ twins, the greater the genetic effect. Why? – since MZ twins and DZ twins are exposed to similar environments, the only reason that MZ twins should be more similar to each other than DZ twins is because they share twice as much genetic material.

Twin-based research thus provides an estimate of both genetic and environmental effects on variance in antisocial behaviors (Beaver 2008). Technically speaking, the proportion of variance accounted for by genetic factors is known as heritability. Unlike social science research that treats all environments as the same, twin-based research has helped to make the distinction between two types of environments: shared environments and nonshared environments. Shared environments are environments that are the same between twins (or siblings) and that systematically increase their similarity. Nonshared environments consist of any environmental factors that are different between twins and that make them dissimilar (Beaver 2008). For example, as it applies to crime, shared environments might include such factors as being reared in poverty or living in a disadvantaged neighborhood. Examples of nonshared environments might consist of factors such as having different peer groups or being treated differently by parents. When summed together, the effects of heritability, shared environmental factors, and nonshared environmental factors explain 100 % of the variance (Beaver 2009).

There has been a great deal of research using twin-based studies to estimate genetic, shared environmental, and nonshared environmental effects on an assortment of antisocial behaviors, such as crime, violence, aggression, and other types of antisocial behaviors (Beaver 2008; 2011; Miles and Carey 1997). The results of these individual-level studies tend to provide slightly different point estimates of heritability, shared environmental effects, and nonshared environmental effects depending on the sample analyzed and the precise measure of antisocial behavior investigated. When aggregated and averaged together, these studies tend to suggest that genetic factors explain about 50 % of the variance in antisocial behaviors, shared environmental factors explain between 0 % and 10 % of the variance, and nonshared environmental factors explain about 40 % of the variance (Beaver 2009; Ferguson 2010; Moffitt 2005). Instead of genetic factors having no effect like most criminologists assume, genetic factors appear to have the dominant effect on antisocial behaviors.

While twin-based research has been quite valuable in the quest for estimating genetic and environmental effects on antisocial behaviors, there are some limitations to this research design. Opponents of genetic research argue that these limitations are fatal flaws that bias the results and thus any findings generated from twin-based studies are not believable. Fortunately, there are a number of other research designs that can also be used to estimate genetic and environmental effects (Beaver 2009). These alternative research designs, moreover, are not host to the same limitations as twin-based studies and thus they can act as “checks” on the twin-based research designs. As long as the genetic and environmental estimates are relatively consistent across all research designs, then the likelihood that the results are being affected by limitations is low. However, if the genetic and environmental effects vary significantly across different research designs, then this pattern of findings would tend to indicate that the results are being systematically affected by the choice of research designs.

One of the alternative research designs that has been used in place of the traditional twin-based research design capitalizes on a relatively rare occurrence wherein MZ twins were separated at birth, adopted by different families, and raised without even knowing they had a co-twin (known as MZAs [monozygotic twins who were reared apart]). Later in life, they are often told by family and friends or discover through serendipitous events that they were born as part of a twin pair. Upon reuniting, researchers are presented with one of the most effective ways to estimate genetic effects. Since MZAs were reared in different environments and by different families, the only reason that MZAs can be similar to each other is because they share 100 % of their DNA. MZAs obviously are quite rare, but scientists at the University of Minnesota have established the Minnesota Study of Identical Twins Reared Apart (MISTRA) and have located more than 100 pairs of MZAs to interview and study (Bouchard et al. 1990). Upon learning of an MZA, investigators on the MISTRA project invite the twins to participate in their study where the twins undergo a weeklong series of tests designed to measure virtually every human characteristic. Overall, the results of the MZA studies have converged with those of traditional twin-based studies, indicating that genes are highly influential when it comes to crime, aggression, violence, and other antisocial characteristics (Beaver 2009).

Even though twin-based studies and MZA studies reveal results that are relatively consistent, there are still those opponents to genetic research that argue that MZA studies also are host to a number of different flaws. According to such critics, the genetic effects reported in MZA studies are also not believable. Luckily, there is yet another way to estimate genetic effects on antisocial behaviors: adoption studies (Beaver 2009). Adoption studies represent another accurate way to estimate genetic and environmental effects on behaviors and traits. To do so, adoptees are compared to their biological parents (with whom they have had little to no contact) and their adoptive parents (with whom they share no genetic material). The only reason that adoptees should resemble their biological parents on measures of antisocial behaviors is because of the genetic material they share with them. And, the only reason that adoptees should resemble their adoptive parents on measures of antisocial behaviors is because of the environment that they share with them. As with twin-based studies and MZA studies, adoption-based studies have revealed that crime and other types of antisocial behaviors are affected by genetic factors (Beaver 2010; Rhee and Waldman 2002).

Molecular Genetics And Antisocial Behaviors

When the results culled from twin-based studies and adoption-based studies are viewed simultaneously, they paint a very detailed and accurate picture indicating that crime, delinquency, and antisocial behavior in general are influenced in large part by genetic factors. While these studies have provided very compelling evidence establishing the genetic foundations to criminal involvement, they do not provide any information as to the specific genes that are involved in creating crime. The next logical step, therefore, is to uncover the particular genes that are associated with crime and antisocial behaviors. In order to do so, it is first necessary to be exposed to some of the basics of molecular genetics.

Genes are inherited on 23 pairs of threadlike structures called chromosomes. One pair of chromosomes is inherited maternally and the other pair is inherited paternally. Of these 23 pairs of chromosomes, there are 22 pairs of autosomes and one pair of sex chromosomes. For all genes located on the autosomes, there are two copies (one on the maternal chromosome and one on the paternal chromosome). When it comes to the sex chromosomes, there is a slightly different pattern of inheritance. Females have two X chromosomes and thus they have two copies of all genes located on the X chromosomes. Males, however, have one X chromosome (always inherited maternally) and one Y chromosome (always inherited paternally). As a result, males have only one copy of each gene located on the X chromosome and one copy of each gene located on the Y chromosome.

Most of the genes in humans do not vary from person to person which is why, structurally and anatomically speaking, humans look very similar to each other (e.g., two arms, two eyes, two legs, a heart). A small percentage of genes, somewhere around 1–10 % depending on how genetic differences are measured, do vary from person to person (Beaver 2009). Genes that can vary from person to person are known as genetic polymorphisms. For example, genes that are involved in creating height are genetic polymorphisms, which is what produces variation in the height of humans. Alternative versions of genetic polymorphisms are known as alleles (e.g., alleles that make someone tall or alleles that make someone short). Criminologists interested in examining the molecular genetic basis to crime and other antisocial behaviors focus on genetic polymorphisms because only genes that vary can explain variation in antisocial behaviors and traits (otherwise it would be analogous to trying to explain a variable (i.e., crime) with a constant).

Historically there has been much confusion among criminologists and social scientists over how genes ultimately affect criminal behaviors (Wright et al. 2008b). The overarching belief is that there is a single gene that decides whether someone will become a criminal; persons who have this gene will always become a criminal and persons lacking this gene will never become a criminal. This type of deterministic thinking is preposterous. Complex behaviors like criminal involvement are multifactorial meaning that they are produced by a combination of genetic and environmental factors. Moreover, criminal and antisocial behaviors are considered polygenic phenotypes. Polygenic phenotypes refer to human behaviors and traits that are affected by many genes, with each gene having only a small effect on the propensity to engage in crime. Seen in this way, genes work in a probabilistic way, where the presence of certain alleles increase or decrease the probability of an antisocial outcome (Beaver 2009). Each genetic variant, however, would only increase the odds of a crime and antisocial behavior by a relatively small margin, typically less than 10 %. Clearly there is nothing deterministic with this contemporary view of the ways in which genetic factors ultimately affect crime, delinquency, and antisocial behaviors.

During the past decade, there has been a considerable amount of molecular genetic research examining whether the alleles of certain genes predispose someone to engage in crime and violence. Although the results of this line of research have not always been entirely consistent, the main theme running across these studies is that genes that are involved in neurotransmission are the genes most likely to affect criminal involvement. Neurotransmission refers to the process by which neurons communicate with each other. Neurons are brain cells and in order for information to be processed across neuronal networks, adjacent neurons must communicate with each other to pass information from neuron to neuron. Neurons, however, are not physically wired together as there is a small gap – known as a synapse – that exists between neurons. So transmitting information between neurons requires that the synapse be bridged in some capacity.

This is accomplished with neurotransmitters, such as serotonin and dopamine, which are chemical messengers that are released from the presynaptic neuron where they cross the synapse and lock into receptors on the postsynaptic neuron.

After the neurotransmitter has locked into the postsynaptic neuron, the neurotransmitters need to be removed from the synapse. There are two main ways that neurotransmitters are purged from the synapse. The first is through a process called reuptake. With reuptake, transporter proteins are released into the synapse where they seek out neurotransmitters, remove them from the synapse, and return them to the vesicles of the presynaptic neuron. The second way that neurotransmitters are removed is through enzymes that degrade neurotransmitters into inactive particles that are then flushed from the synapse. Both reuptake and enzymatic degradation work simultaneously to regulate levels of neurotransmitters. If something interferes with either of these processes or if either of these two processes is not working efficiently, then levels of neurotransmitters may deviate from normality. Importantly, there is a good deal of research linking variation in neurotransmitter levels to a range of psychopathologies, including aggression, violence, suicide, and crime (Brunner et al. 1993; Beaver et al. 2007).

Genes are involved in coding for the production of transporter proteins that are central to the process of reuptake. This is especially important because some genetic polymorphisms related to transporter proteins are functional, meaning that different alleles correspond to differences in the activity level of the transporter protein. For example, different alleles of a genetic polymorphism that codes for the production of the serotonin transporter protein (5HTTLPR) are associated with different transcriptional efficiencies (functional differences that may ultimately produce different levels of serotonin). Similarly, a gene that codes for the production of the monoamine oxidase A (MAOA) enzyme, which is responsible for breaking down neurotransmitters, also has a functional polymorphism (in the promoter region of the gene). Some alleles of this MAOA polymorphism code for the production of low MAOA activity, meaning that the MAOA is not as efficient at mopping up neurotransmitters from the synapse, while other alleles code for the production of high MAOA activity, which is much more efficient at removing neurotransmitters from the synapse.

Overall, molecular genetic research has provided some evidence tying variants of certain genes, such as dopaminergic genes (e.g., DAT1, DRD2, and DRD4), serotonergic genes (e.g., 5HTTLPR), and genes coding for the production of enzymes (e.g., MAOA and COMT) to various antisocial behaviors (Beaver et al. 2007; Caspi et al. 2002; Brody et al. 2011). These genes tend to have small effects, a finding which is consistent with polygenic explanations of human behavior. Perhaps partially as a result of the small effects associated with genes, genetic association studies are often plagued by an inability to replicate the original results. What this means is that after a study first reports a statistically significant association between a genetic polymorphism and an outcome, replication studies often fail to detect that same association in independent samples. There are a number of potential explanations for a failure to replicate, including the possibility that the original report was a methodological or statistical artifact. Consequentially, replication studies are of utmost importance when attempting to figure out whether a putative candidate gene is indeed related, perhaps causally, to a human trait/ behavior.

Gene-Environment Interplay And Antisocial Behaviors

Although molecular genetic research has revealed that some genes are related to a variety of antisocial outcomes, the most cutting-edge genetic research examines the interplay between genetic factors and environmental factors (Moffitt 2005). There are two main types of gene-environment interplay that have been tied to antisocial behaviors: gene-environment interactions and gene-environment correlations. Gene-environment interactions capture the processes by which genetic effects are moderated by environmental factors and/or by which environmental effects are moderated by genetic factors. In short, gene-environment interactions can explain why two people who encounter the same stimuli may turn out quite differently. An example will help to clarify what is meant by a geneenvironment interaction. Suppose that a study was examining a group of adolescents who were raised in a disadvantaged neighborhood with high rates of crime, poverty, and homelessness. Exposure to this neighborhood is certainly a criminogenic risk factor that heightens the propensity for engaging in crime and disrepute. Evenso, most of the adolescents exposed to such conditions will not turn out to be criminal, but a handful of adolescents will develop into criminals. The million-dollar question, of course, is what accounts for these differential outcomes? The logic of gene-environment interactions can easily answer this question by drawing attention to the fact that for a criminal to develop they must (1) be exposed to a criminogenic environment and (2) have a sufficient genetic predisposition for crime. If either of these two factors is absent, then their independent effects are either muted or attenuated significantly. To summarize, then, gene-environment interactions refer to the fact that genetic effects are strongest when paired with environmental liabilities (and vice versa).

Much of the contemporary genetic research examining genetic effects on antisocial behavior and psychopathologies has been guided by geneenvironment interactions. What this line of research has revealed is that the effects of specific polymorphisms on antisocial behaviors are structured in part by exposure to environmental liabilities and stressors. For example, the MAOA gene has consistently been found to be related to violence and aggression in males (Caspi et al. 2002; Haberstick et al. 2007; Kim-Cohen et al. 2006). Consistent with the logic of gene-environment interactions, however, the effect of MAOA only surfaces among males who have been abused and maltreated as children. For males who have not been abused as children, there is no effect of MAOA on antisocial behaviors. Similar findings have been observed with other genetic polymorphisms linked to antisocial propensities. These findings underscore the mutual interdependence of genes and the environment when trying to understand the etiology of criminal and antisocial behaviors.

Gene-environment interactions may also be integral to understanding why there are some problems with replicating molecular genetic findings. Molecular genetic research is often based on clinical, non-nationally representative samples. This necessarily means that the samples that are used to test for genetic associations are differentially exposed to environmental conditions. The respondents from one sample, for instance, may be exposed to severe poverty, whereas respondents from another sample may have been drawn from a wealthy population. If poverty acts as a trigger for a genetic effect to surface (i.e., a gene-environment interaction), then the genetic effect would be detected in the first sample, but not in the second. So, failing to recognize differential exposure to environmental liabilities may be one additional reason for why there is a failure to replicate some genetic associations with criminal behavior.

The second type of gene-environment interplay that has direct bearing on criminology is known as gene-environment correlation. Geneenvironment correlation captures the effects that genes have on predicting and explaining variance in environmental measures (Beaver and Wright 2005; Scarr and McCartney 1983). To most criminologists and social scientists, even suggesting that an environment could be affected by genetics seems a bit odd. There is, however, a great deal of empirical evidence indicating that almost all environments are influenced, at least in part, by genetic factors (Beaver and Wright 2005). To understand how it is possible to estimate genetic effects on environmental measures, it is essential to revisit the twin-based methodology. Recall that with the twin-based methodology, the similarity of MZ twins on some behavior trait is compared with the similarity of DZ twins on that same behavior/trait. If MZ twins are more similar than DZ twins, there is evidence of a genetic effect on the behavior/trait. This same twin-based methodology can be employed to estimate genetic effects on environmental measures; the only difference is that an environmental measure is used in place of the measure of the behavior/trait. A pool of empirical research has used the twin-based study to estimate genetic effects on environmental measures, and the results have provided strong support in favor of gene-environment correlations for environments related to crime and delinquency (Beaver and Wright 2005; DiLalla 2002). For example, variance in measures of parental socialization (Beaver and Wright 2007; DiLalla 2002), exposure to antisocial peer networks (Beaver et al. 2009), stressful life events (Dick et al. 2006), and various dimensions of family life have all been found to be affected, to varying degrees, by genetic factors. While the precise heritability estimates ebb and flow across the environmental measures, on average, genetic factors account for around 25 % of the variance in most environmental measures (Kendler and Baker 2006). Some environments, such as exposure to delinquent peer groups, have much higher heritability estimates with genetic factors explaining about around 60 % of the variance (Cleveland et al. 2005).

In addition to twin-based studies, a small number of studies have also explored the possibility that certain genetic polymorphisms might explain variance in measures of criminogenic environments. While this line of research is still in its infancy, there is some emerging evidence linking specific genetic polymorphisms, such as dopaminergic polymorphisms, to negative parental socialization, to contact with delinquent peers, and even to the probability of getting married (Dick et al. 2006). As more and more social science datasets begin to include genotypic information, the number of genes that are found to be associated with specific environmental conditions will likely increase.

Establishing a link between genetic variance and environmental variance is important in unpacking the ways in which genes and the environment work together to produce human phenotypic variation. Nonetheless, simply establishing a link reveals nothing about the underlying processes that account for gene-environment correlations. Existing research, however, has delineated three different types of geneenvironment correlations, each of which explains a different mechanism by which genes account for environmental variance (Scarr and McCartney 1983). These three types of geneenvironment correlations are known as passive gene-environment correlation, active geneenvironment correlation, and evocative geneenvironment correlation.

Passive gene-environment correlation is grounded in the fact that parents pass along two entities to their children: genes and an environment. Given that the child is unable to pick and choose their genes and/or their environment, they passively receive these. Moreover, because both genes and the environment are traced to the same source – that is, parents – the two are likely to be correlated (Beaver 2009; Scarr and McCartney 1983). For example, highly aggressive parents are likely to pass along a genetic predisposition for aggression and violence to their children. At the same time, parents who are highly aggressive are also statistically more likely to abuse their children, live in low SES areas, and not supervise their children closely. All of these environments have been shown to increase the probability of antisocial behaviors. With passive geneenvironment correlation, then, children are hit with a “double whammy” of risk factors, wherein they have the genetic predispositions for antisocial behavior and they are also born into an environment that also contributes to antisocial behavior. This process thereby captures part of the reason that criminogenic environments are affected by genetic factors.

The second type of gene-environment correlation is active gene-environment correlation. Active gene-environment correlation avers that genotype pushes or nudges people into certain environments that are compatible with their genetic predispositions (Beaver 2009; Scarr and McCartney 1983). To illustrate, a person who is highly aggressive and violent is likely to seek out environments that are conducive to these predispositions. So, they might join a gang or befriend other people who are violent, too. In this example, choosing a gang is not a random occurrence, but rather is structured in part by the genetic predisposition for violence and aggression. It is important to underscore the fact that there are not genes that are “for” any type of environment; rather, genes operate indirectly, such as via their effects on personality traits. Continuing on with the gang example, a part of the reason a person might choose a gang is because they are genetically predisposed to be violent, not because there is a single gene that tells the person to join a gang.

The last type of gene-environment correlation is known as evocative gene-environment correlation. With evocative gene-environment correlation, genotype elicits certain responses from the environment, which are ultimately correlated with their genotype (Beaver 2009; Scarr and McCartney 1983). A person with a bad temper (a genetically influenced phenotype), for instance, is likely to evoke negative responses from their environment. Evocative geneenvironment correlations are virtually synonymous with child-effects models except that the effect is thought to flow directly from genotype. Consider two siblings: one who is genetically predisposed to be unruly and one who is genetically predisposed to be passive and compliant. The unruly child will likely evoke negative and harsh parenting, such as being spanked, while the compliant child will likely escape such discipline. In this case, parental discipline is differentially invoked against the two siblings, but the reason for this difference is the result of the genetically influenced propensities and temperaments of the two siblings.

The saliency of these three types of geneenvironment correlation waxes and wanes over different sections of the life course. Passive geneenvironment correlation is thought to be most evident early in life, especially during infancy and childhood. During this time period, children are under the control of their parents and have their parents’ environment imposed on them. As children develop into adolescence, they begin to gain more autonomy and thus are able to follow their genetic predispositions without as much guidance and control by their parents. By the time of early adulthood when most children have moved out of their parents’ home, they are able to follow their genetic predispositions without interference. Evocative gene-environment correlation tends to have relatively equal effects throughout life. In childhood, for instance, genetically influenced antisocial traits may elicit negative responses from parents; in adolescence, genetically influenced antisocial traits may elicit negative responses from peers and teachers; and in adulthood, genetically influenced antisocial traits may elicit negative responses from employers and from potential mates.

Taken together, the two types of geneenvironment interplay – gene-environment interaction and gene-environment correlation – draw attention to the very real possibility that genes and the environment do not represent simple dichotomies (Beaver et al. 2009). Instead, a wealth of scientifically rigorous scholarship has shown that there is a close interdependence between genes and the environment and the way to understand the causes of all human phenotypes – including antisocial ones – is to examine these two influences simultaneously and to model directly the various types of gene-environment interplay.

Conclusions And Future Directions

During the past century, the field of criminology has made some enormous gains in terms of identifying the causes and correlates of crime, delinquency, and other types of antisocial behaviors. For the most part, however, all of these advancements have been on discovering the environmental underpinnings to criminal involvement. With the recent mapping of the human genome and with empirical studies strongly implicating genes in all human phenotypes, the time is ripe for criminology to begin to examine the dual influences of genes and the environment in the genesis of antisocial behaviors. Such an approach does not mean that all existing theories need to be abandoned. Instead, such an approach allows for a fuller integration of findings from biological sciences into mainstream criminological theories. This type of theoretical integration would likely pave the way for an explosion of knowledge about the developmental pathways to crime and violence. The knowledge flowing from this research could then be used to open up newer and perhaps more effective avenues for the treatment and rehabilitation of offenders that would ultimately increase public safety and reduce criminal involvement.

Bibliography:

Beaver KM (2008) Nonshared environmental influences on adolescent delinquent involvement and adult criminal behavior. Criminology 46(2):341–369
Beaver KM (2009) Biosocial criminology: a primer. Kendall/Hunt, Dubuque
Beaver KM (2010) Genetic influences on being processed through the criminal justice system: results from a sample of adoptees. Biol Psychiatry 69(3): 282–287
Beaver KM (2011) The effects of genetics, the environment, and low self-control on perceived maternal and paternal socialization: results from a longitudinal sample of twins. J Quant Criminol 27(1):85–105
Beaver KM, Wright JP (2005) Biosocial development and delinquent involvement. Youth Violence Juv Justice 3(2):168–192
Beaver KM, Wright JP (2007) A child effects explanation for the association between family risk and involvement in an antisocial lifestyle. J Adolesc Res 22(6):640–664
Beaver KM, Wright JP, Delisi M, Walsh A, Vaughn MG, Boisvert D, Vaske J (2007) A gene gene interaction between DRD2 and DRD4 is associated with conduct disorder and antisocial behavior in males. Behav Brain Funct 3(1):30–37
Beaver KM, Delisi M, Wright JP, Vaughn MG (2009) Gene–environment interplay and delinquent involvement: evidence of direct, indirect, and interactive effects. J Adolesc Res 24(2):147–168
Bouchard T, Lykken D, McGue M, Segal N, Tellegen A (1990) Sources of human psychological differences: the Minnesota study of twins reared apart. Science 250(4978):223–228
Brody GH, Beach SRH, Chen YF, Obasi E, Philibert RA, Kogan SM, Simons RL (2011) Perceived discrimination, serotonin transporter linked polymorphic region status, and the development of conduct problems. Dev Psychopathol 23(02):617–627
Brunner H, Nelen M, Breakefield X, Ropers H, van Oost B (1993) Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A. Science 262(5133):578–580
Caspi A, McClay J, Moffitt TE, Mill J, Martin J, Craig IW, Taylor A et al (2002) Role of genotype in the cycle of violence in maltreated children. Science 297(5582): 851–854
Cleveland HH, Wiebe RP, Rowe DC (2005) Sources of exposure to smoking and drinking friends among adolescents: a behavioral-genetic evaluation. J Genet Psychol 166(2):153–169
Dick DM, Agrawal A, Schuckit MA, Bierut L, Hinrichs A, Fox L, Mullaney J et al (2006) Marital status, alcohol dependence, and GABRA2: evidence for geneenvironment correlation and interaction. J Stud Alcohol 67:185–194
DiLalla LF (2002) Behavior genetics of aggression in children: review and future directions. Dev Rev 22:593–622
Ferguson CJ (2010) Genetic contributions to antisocial personality and behavior: a meta-analytic review from an evolutionary perspective. J Soc Psychol 150(2):160–180
Haberstick BC, Timberlake D, Hopfer CJ, Lessem JM, Ehringer MA, Hewitt JK (2007) Genetic and environmental contributions to retrospectively reported DSMIV childhood attention deficit hyperactivity disorder. Psychol Med 38(7):1057–1066
Harris JR (1998) The nurture assumption: why children turn out the way they do. Touchstone, New York
Kendler KS, Baker JH (2006) Genetic influences on measures of the environment: a systematic review. Psychol Med 37(5):615
Kim-Cohen J, Caspi A, Taylor A, Williams B, Newcombe R, Craig IW, Moffitt TE (2006) MAOA, maltreatment, and gene–environment interaction predicting children’s mental health: new evidence and a metaanalysis. Mol Psychiatry 11(10):903–913
Miles DR, Carey G (1997) Genetic and environmental architecture of human aggression. J Pers Soc Psychol 72:207–217.
Moffitt TE (2005) The new look of behavioral genetics in developmental psychopathology: gene-environment interplay in antisocial behaviors. Psychol Bull 131(4):533–554
Raine A (1993) The psychopathology of crime: criminal behavior as a clinical disorder. Academic, San Diego
Rhee SH, Waldman ID (2002) Genetic and environmental influences on antisocial behavior: a meta-analysis of twin and adoption studies. Psychol Bull 128(3):490–529
Rowe DC (1994) The limits of family influence: genes, experience, and behavior. Guilford, New York
Scarr S, McCartney K (1983) How people make their own environments: a theory of genotype environment effects. Child Dev 54:424–435
Walsh A (2009) Biology and criminology: the biosocial synthesis. Routledge, New York
Walsh A, Beaver KM (2009) Biosocial criminology: new directions in theory and research. Routledge, New York
Wright JP, Beaver KM, Delisi M, Vaughn MG, Boisvert D, Vaske J (2008a) Lombroso’s legacy: the miseducation of criminologists. J Crim Justice Educ 19(3):325–338
Wright JP, Tibbetts SG, Daigle LE (2008b) Criminals in the making: criminality across the life course. Sage, Los Angeles