Encyclopedia of Law & Society:American and Global Perspectives

Genes and Crime

Contributors: David S. ClarkPrint Pub. Date: 2007Online Pub. Date: September 25, 2007Print ISBN: 9780761923879Online ISBN: 9781412952637DOI: 10.4135/9781412952637Print pages: 635-638

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Willamette UniversityA growing body of empirical evidence over the last decade has shown that geneticfactors play a causal role in the development of antisocial behaviors, many of whichcorrelate positively with crime. While all people occasionally engage in some formsof antisocial acts, a few repeat offenders begin their offenses at an early age and areresponsible for a disproportionate amount of criminal activity. Scholars characterizethese individuals by their impulsivity and aggression; they are more likely to developconduct disorders like antisocial personality.

To the extent that attributes such as violence, aggression, and antisociality areheritable, criminality has a genetic basis. However, adopting this simplified deterministicview of a “gene for crime” would be a mistake. The actual interplay is far more complex.Genes associated with criminal behavior are likely to have small, nonspecific impactsand be entangled in numerous neurobiological pathways. Since the expression of genesinfluencing complex behavior tends to be probabilistic and often modulated by a host ofenvironmental interactions, the causal connections between genes and crime are likelyto be distanced by a few levels of organization; that is, gene → protein → nerve cell →information transfer → higher brain organization → motor action

Rather than highlighting a direct connection between genes and crime, current modelssuggest that genetic variants may influence neurotransmitter pathways in brain regionsassociated with cognitive function and the encoding of emotional intent. These in turnmay lead to an increased predisposition toward violent or antisocial behavior.

Twin Studies

Twin studies give us insight into the overall heritability of an attribute by comparingfeatures of monozygotic twins (MZ), who share a common environment and 100percent of their genes, with dizygotic twins (DZ), who share a common environmentand roughly half of their genes. Comparisons of twin types allow for an estimation of thepercentage of variation of genetic and environmental factors on behavior. For example,to the extent that similarities observed in MZ twins are greater than those observed in

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DZ twins, genetic influences are implicated. Lisabeth Dilalla and Irving Gottesman'sreview of twin concordance rates for adult criminality in nine studies reported an MZconcordance of 51 percent versus 22 percent for DZ twins, a strong indication of geneticeffects. Findings, which subsequent studies support, show heritability for a broad set ofmeasures, including juvenile antisocial behavior and early-onset delinquency. Soo HyunRhee and Irwin Waldman's 2002 meta-analysis reviewing 51 twin and adoption studiesestimated a genetic influence of about 40 percent on antisocial behavior.

Twin and adoption studies provide helpful estimations as to the range of heritabilityfor criminal and [p. 635 ↓ ] antisocial behavior. However, these studies do not identifyunderlying biological mechanisms or individual differences. It is important to notethat for an individual, genetic influences may range from only a small part of theexplanation of behavior to the major influence, with environmental factors explainingthe remainder of the difference. Saying that genetic influences explain 50 percent ofthe variance for a trait between individuals does not mean that for every individualthat is the division of the gene and environment pie. Such is the nature of the strangedance between environment and gene interactions in contributing to complex behaviorsuch as criminality. What twin studies measure are the differences in behavior acrossaverages; for evidence of specific trait variants, it is necessary to look at animal modelsand candidate genes.

Animal Models

Genes involved in the regulation of serotonergic neurotransmitters, particularlymonoamine oxidase A (MAOA), an enzyme that degrades serotonin levels, haveshown the most consistent and meaningful results in both animals and humans.Animal models, particularly mice, provide a method for examining genes that wouldotherwise be inaccessible to human subjects. Researchers base these models, in part,on parallels between the DNA of mice and humans. They use, for example, “knockoutmice,” mice that have had genes made inoperative. They can then identify the functionof specific DNA sequences. For example, mice knocked out for the 5-HT1B

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receptor gene, involved in serotonin modulation, display impaired impulse control andattack intruders with twice the intensity of normal mice. Similar findings of excessiveaggression and impulsivity are seen in both MAOA and other knockout mice associatedwith reduced serotonin receptor function.

In 1993, H. G. Brunner and colleagues published a study on Dutch relatives with a pointmutation in the MAOA gene and a history of antisocial behavior, including attemptedrape, arson, and exhibitionism. A syndrome of borderline mental retardation andimpulsive aggressive behavior affected several males in the family. The researcherstraced the abnormalities to their rare genetic mutation leading to a complete deficiencyof the MAOA enzyme, effectively making them a set of knockout humans.

Candidate Genes

Candidate genes are those whose functions investigators suspect connect to specifictrait variants. Investigators identify them via linkage studies of chromosomal regionslinked to a specific trait as well as knowledge of cellular function associated with a gene.The MAOA gene consists of high and low activity variants. In a study examining thecombined effects of genetic variability and maltreatment on antisociality, AvshalomCaspi and colleagues found that while MAOA activity alone did not significantly affectantisocial behavior, an interaction between MAOA activity and childhood maltreatmentsignificantly increased the incidence of antisocial behavior.

The study presented a model in which subjects with low MAOA activity genotype arepredisposed to antisocial behavior. However, its expression is contingent upon thepresence of childhood maltreatment. Maltreated males with low MAOA activity weresignificantly more likely than maltreated males with high MAOA activity to be convictedof violent crimes (with an odds ratio of 9:8), and 85 percent of severely maltreatedindividuals with the low activity genotype developed some form of antisocial behavior. A2004 study by Debra Foley and colleagues replicated these findings.

Recent studies using functional magnetic resonance imaging have shown associationsbetween the low expression MAOA genotype and activation of the amygdala and limbicregions. These associations are higher in tasks involving emotional arousal, emotional

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memory, and inhibitory control. The integration of brain imaging studies and geneticpolymorphisms are establishing new avenues to improve our understanding of howgenes affect brain activity and function.

Specific Cases

Attempts at using genetic evidence as either exculpatory or mitigating factors in judicialproceedings have for the most part been unsuccessful. The earliest cases of [p. 636 ↓ ]genetic evidence, in the 1970s, involved a few high profile cases of defendants with anadditional Y chromosome, a condition known as XYY syndrome, resulting in argumentsabout a defendant's innate predisposition to crime. Cases such as People v. Yukl (372N.Y.S.2d 715, Sup. Ct., 1975) followed a study that showed an increased prevalenceof XYY syndrome males in selected penal institutions; arguments ensued that carriersof the extra chromosome were prone to greater levels of aggression. For the most part,judges excluded the studies, which scholars later showed to have large methodologicalbiases that led to erroneous findings.

Another well-known case was that of Stephen Mobley, a convicted murderer fromGeorgia whose family history was characterized by four generations of violence andantisocial behavior. Citing Brunner's collaborative research, the defense attempted,unsuccessfully, to establish a basis for appealing the death sentence by having Mobleytested for the MAOA genetic mutation and using the results as evidence. The court, inMobley v. State (426 S.E. 2d 150, Ga., 1993), ultimately declined the request.

Future Directions

Technical and scientific advances in behavioral genetics over the last few decadeshave permitted researchers to investigate the relative contributions of environmentand heredity in criminal behavior. The recent sequencing of the human genome, newdesigns for studying linkage disequilibrium mapping, and general advances in brainimaging technology have led to innovative and increasingly sophisticated tools tounderstand the architecture of more complex behavioral traits.

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Future studies should help advance our understanding of the complex factors involvedin the interplay between genes and environment in general, and genes and crimespecifically. While newfound discoveries in behavioral genetics will undoubtedlyhelp refine and improve our understanding of the etiology of criminal behavior, theiradvancement is also constrained by methodological limitations. Ultimately, modelsevaluating the probability of criminal likelihood as a function of environmental andgenetic determinants cannot conceptually reduce to a purely scientific component.Decisions regarding legal culpability and rehabilitative therapy still require a valuejudgment based on legal, philosophical, and social views.

Salomon Israel, and Richard P. Ebstein

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See also

Further Readings

Bock, Gregory R., ed. , and Jaimie A. Goode, eds. (1996). Genetics of Criminal andAntisocial Behaviour . West Sussex, UK: Wiley & Sons.

Brunner, H., M. Nelen, X. Breakefield, H. Ropers, and B. van Oost. “Abnormal BehaviorAssociated with a Point Mutation in the Structural Gene for Monoamine Oxidase A.”Science vol. 262 (1993). pp. 578–80. http://dx.doi.org/10.1126/science.8211186

Caspi, Avshalom, Joseph McClay, Terrie E. Moffitt, Jonathan Mill, Judy Martin, Ian W.Craig, Alan Taylor, and Richie Poulton. “Role of Genotype in the Cycle of Violence inMaltreated Children.” Science vol. 297 (2002). pp. 851–54. http://dx.doi.org/10.1126/science.1072290

Dilalla, Lisabeth F., and Irving I. Gottesman. “Heterogeneity of Causes for Delinquencyand Criminality: Lifespan Perspectives.” Development and Psychopathology vol. 1(1989). pp. 339–49. http://dx.doi.org/10.1017/S0954579400000511

Foley, Debra L., Lindon J. Eaves, Brandon Wormley, Judy L. Silberg, Hermine H.Maes, Jonathan Kuhn, and Brien Riley. “Childhood Adversity, Monoamine Oxidase

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A Genotype, and Risk for Conduct Disorder.” Archives of General Psychiatry vol. 61(2004). pp. 738–44. http://dx.doi.org/10.1001/archpsyc.61.7.738

Meyer-Lindberg, Andreas, Joshua W. Buckholtz, Bhaskar Kolachana, Ahmad R. Hariri,Lukas Pezawas, Giuseppe Blasi, Ashley Wabnitz, Robyn Hone, Beth Verchinski,Joseph H. Callicott, Michael Egan, Venkata Mattay, and Daniel R. Weinberger.“Neural Mechanisms of Genetic Risk for Impulsivity and Violence in Humans.”Proceedings of the National Academy of Sciences vol. 103 (2006). pp. 6269–74. http://dx.doi.org/10.1073/pnas.0511311103

Rhee, Soo Hyun, and Irwin D. Waldman. “Genetic and Environmental Influences onAntisocial Behavior: A Meta-analysis of Twin and Adoption Studies.” PsychologicalBulletin vol. 128 (2002). pp. 490–529. http://dx.doi.org/10.1037/0033-2909.128.3.490

Rutter, Michael, Henri Giller, and Ann Hagell. (1998). Antisocial Behavior by YoungPeople . Cambridge: Cambridge University Press.

Sluyter, Frans, et al. “Toward an Animal Model for Antisocial Behavior: Parallelsbetween Mice and Humans.” Behavior Genetics vol. 33 (2003). pp. 563–74. http://dx.doi.org/10.1023/A:1025730901955

Taylor, Jeannete, W. G. Iacono, and Matt McGue. “Evidence for a Genetic Etiology ofEarly-Onset Delinquency.” Journal of Abnormal Psychology vol. 109 (2000). pp. 634–43. http://dx.doi.org/10.1037/0021-843X.109.4.634

Viding, Essi, and Uta Frith. “Genes for Susceptibility to Violence Lurk in the Brain”Proceedings of the National Academy of Sciences vol. 103 (2006). pp. 6085–86. http://dx.doi.org/10.1073/pnas.0601350103